Trans Cardio

Medicine II
CARDIOLOGY
Prelim Coverage – Dr. Payawal and Dr. Deduyo
June 23, 30, July 7, 14, 21, 28, 2015 10:00-12:00pm AMS 204
Coverage of Preliminary Examination:

I. Electrocardiography
II. Peripheral Vascular Diseases
III. Cardiac Dysrrythmia
IV. Cardiomyopathies
V. Infective Endocarditis
ELECTROCARDIOGRAPHY
- Electro- means electricity

- Cardio - means heart
- It is the study of the electrical activity of the heart
- Painless procedure; non-invasive; inexpensive
diagnostic modality; readily available
- ECG tracing – up, down, and flat lines which are
interpreted by a physician and can be the basis and
evidence of a diagnosis of a heart condition.
- Before the heart can move or contract, it has to be
stimulated electrically otherwise the heart will not move. Now it is compact, small, portable and can be battery operated.
This electrical stimulus comes from specialized cells
But, ECG machine interpretations are not completely reliable.
within the heart, known as pacemaker cells. The There are some models now that can do interpretation but is not
primary pacemaker of the heart is a real structure
accurate because the machine cannot distinguish artifacts from the
located in the superior fossa of the right atrium, real ones. Do not rely on ECG machine interpretation alone.
known as SA node (Sinoatrial node). If this electrical
stimulus does not occur and the other pacemakers of the
ECG
heart do not function, the heart will not pump or move.
- can see enlargement of heart cavities
This electrical activity is the one represented in the
- non invasive, inexpensive and readily available
electrocardiogram. Electrical activity originates from the
- warning: interpretation of machine is not reliable
pacemakers of the heart.
- R-leg is used only as a ground
- ECG machine is a modified galvanometer. It records
- noninvasive, inexpensive and readily available
these electrical potentials produced by the heart.
- There are electrodes placed on all the extremities as
well as on the chest wall which pick up the electrical
activity of the heart.
Cardiac cycle – electrical events represented in the ECG. Since

we are talking about electrical activity, there is an electrical cardiac
cycle counterpart to that. There are different phases/stages of this
electrical cardiac cycle counterpart of the cardiac cycle. Remember
that electrical events precede cardiac contractile events.
- This phase is called phase 4 or resting phase or
polarized state which is the last phase.
- This is an isolated myocardial cell with a plasma
membrane or cell membrane (this membrane is not only
for the protection of the cell but also has a lot of
receptors and ionic channels for sodium, potassium,
calcium). During this phase, these sodium channels are
closed. There are more sodium outside the cell and
cannot enter. Since sodium carries a positive charge, the
1920s - Patient immerses their extremity in a solution that exterior of the cell is relatively more positive than the
conducts electrical activites and is recorded. inside of the cell. The interior of the cell is relatively more
negative than outside of the cell because the large
proteins (ribosome, endoplasmic reticulum) inside the
1|J KC Pa lo m a r e s
cell are predominantly negatively charged and are big so o Na-K pump restores Na out
it stays inside the cell. o Cell membrane impermeable to Na ions
- Phase 4: Sodium channels are closed o Charge = -90
- After phase 4 is phase 0
The electrical events are produced by the influx and efflux of ions
DEPOLARIZATION-REPOLARIZATION CYCLE of myocardial cells.
(Action Potential)
Phase 0 - Rapid depolarization

- During this phase, the sodium channels that were initially
closed now open up along the cell membrane so that the
sodium that was mainly outside the cell will now move
rapidly into the cell so there is now a surge of sodium
ions inside the cell carrying its positive charge, so that
interior of the cell now becomes positive
- Among pacemaker cells, the predominant ion is calcium
where there are also calcium channels inside the cell
and move slowly inside the cell and this calcium also
carries a positive charge, the interior of the cell also
becomes positive
- Phase 0:
o Na moves rapidly into the cell
o Ca moves slowly into the cell
o Charge = (+)
Normal concentrations of ions in plasma or extracellular fluid:
Phase 1 - Early Repolarization - Na+ = 135 – 140
- Sodium channels close (so they only open transiently) - K+ = 3.5 – 4.5
and with the closure of the sodium channels, there would - Ca++ = 1.7 – 2.6
be a slight drop in the positivity of the interior of the cell These serum electrolytes are usually requested especially in cases
and this s called as Early Repolarization. of abnormalities in the conduction of the heart in patients. It is
- There is also efflux of potassium ions during Phase 1 routinely requested for cases like cardiac arrhythmias
- Phase 1:
o Na channels close Note:
o Transient efflux of K - Resting phase or Phase 4: If you put a microelectrode
o Charge = slight drop in positive charge inside the myocardial cell in the resting phase or phase 4
where the cell membrane is impermeable to sodium,
Phase 2 - Plateau phase there is approximately -90mV (1,000mV = 1V). An ECG
- Plateau means flat because as the calcium continuously machine is needed to appreciate this.
flow in and potassium continuously flows out, since both - Rapid depolarization phase or Phase 0: this is when
carry a positive charge, there will be no net change in the the sodium channel open, and calcium among
charges inside the cell. pacemaker cells. The influx of sodium causes the interior
- Phase 2: of the cell to become positive and becomes
o Ca continues to flow in approximately 30 mV.
o K continues to flow out - Early repolarization or Phase 1: closure of sodium
o Charge = 0 channel and efflux of Potassium ions so there will be a
drop in the positivity
Phase 3 - Rapid Repolarization - Plateau phase or Phase 2: equal influx and efflux of
- This is where large amounts of potassium diffuse out as calcium and potassium ions respectively
all the potassium channels open. The calcium channels - Rapid Repolarization or Phase 3: there is rapid efflux
close so there will be further drop in the charges inside of potassium ions and then goes back to Phase 4 with
the cell and goes to Phase 4 or resting phase the activation of the pump along the cell membrane (Na
- Phase 3: out)
o Large amounts of K diffuse out as all K channels
open Red line - The electrical influxes of these ions are reflected by the
o Inactvation of Ca channels red line.
o Charge = continuous to go down
Blue line – this represents tension created by contraction of the
Phase 4 - Resting Phase myocardial cells. For it to create tension, it has to contract.
- cell membrane becomes impermeable to the entry of
sodium ions X-axis - represents time, so before the myocardial cell can move
- there is a pump that is activated which requires energy or contract, it has to be depolarized first, phase 0 has to occur first
which will extrude sodium out so the interior of the cell before any movement of the heart can be noticed over time. If this
becomes relatively more negative than outside of the does not occur, it will appear flat. With depolarization, there will be
cell. contraction.
- Phase 4:
positive electrode facing a wave of repolarization, it will
Electrical activity precedes contractile events still create a positive deflection but a smaller one
(represented by the T wave). It depends on the
Green line – this is the one seen in the ECG paper orientation or where the electrodes are.
QRS complex – it starts with Phase 0. It actually
represents Phase 0 or rapid depolarization of the
ventricles. This is why the QRS complex starts at the
same time as Phase 0. This occurs first before any
contractile movement of the heart.
ST segment – this is used to diagnose or to look at if the
patient has ischemia (ischemic heart disease) or acute
myocardial infaction or heart attack. Normally, it should
be the same level as the PR segment. This represents
Phase 2 or Plateau phase of the ventricles.
T wave – upward deflection. It represents Phase 3 or
Rapid Repolarization of the ventricles.
P wave – upward deflection. This represents atrial
depolarization which occurs before the ventricles
contract. Atrial repolarization is not seen because it is
buried in the QRS complex. The atrium contracts first
because it is depolarized first because the sinus node ECG STANDARD LIMB LEADS (BIPOLAR) – ORIENTATION OF
is in the atrium. The primary pacemaker of the heart, LEADS
which is SA node, is located in between the atrium. So - During the 1890, it was Dr. Einthoven (Dutch, Father of
the atrium is depolarized first before the ventricle. Electrocardiography) that devised this electrode system.
These electrodes actually represent leads (which is
Absolute Refractory period composed of a positive and negative electrode).
- If the heart is stimulated at this time, the heart will NOT Einthoven devised the first three views of the electrical
respond. The heart cannot be re stimulated. activity of the heart.
- The line that divides the absolute from relative is at the - When we do an ECG, the standard ECG is composed of
middle of phase 3 or the peak of T wave. 12 leads.
Unfortunately, this line has no name but is very important - To be able to appreciate what a lead is, each lead shows
because it is the most vulnerable time during the a certain view of the electrical activity of the heart.
electrical cardiac cycle where any stimulus introduced at Multiple leads oriented differently = better picture of the
this particular moment can be catastrophic to a patient’s heart
heart. It is the deadliest time to stimulate the heart - In ECG, there are 12 leads so there are 12 views of the
that can cause malignant dysrrhytmia which may lead to heart.
sudden cardiac death
Einthoven’s Three Limb Leads (1890)
Relative Refractory period Lead I – from R arm to L arm
- When the heart is stimulated at this time, a stronger o negative electrode on the right arm
stimulus is needed and the response is very weak. o positive electrode on the left arm
Lead II – from R arm to L leg

o negative electrode on the right arm
o positive electrode on the left leg
Lead III – from L arm to L leg

o Negative electrode on the left arm
o positive electrode on the left leg
Note: Right leg is for grounding electrode
EINTHOVEN TRIANGLE HYPOTHESIS

Assumptions:
Note: - Roots of the LA, RA, LL form apices of a triangle.
- Electrodes are placed on the extremities and on the - Electrical forces produced by the heart are represented
chest wall by an equivalent dipole at the center of the triangle.
- Most of these are positive electrodes and some are - Body tissues and fluids in which triangle is located act as
bipolar (meaning these electrodes are both positive and homogenous conductor – because it contain sodium,
negative) potassium, calcium and chloride
- If you put a positive electrode and it faces a wave of - Bipolar limb leads record potential variations of the heart
depolarization, the electrode will create a positive in the frontal plane.
deflection (goes up). Once the whole heart is depolarized Einthoven’s Law: Lead I + Lead III = Lead II
it goes down to baseline. On the other hand, if you put a
If Lead I on the ECG is very big on the ECG paper and Lead III is directed to the left left axis deviation because of the
also big on the ECG paper, Lead II should be taller than Lead I + big left ventricle.
Lead III. If the patient suffered an inferior wall myocardial
infarction, the axis of the heart is directed to the left
If Lead I is very big on the ECG paper and Lead III is inverted, because of the loss of electrical activity of the heart
then Lead II is very small left axis deviation.
Big right ventricle axis of the heart may be directed to
If Lead I and Lead III are both negative, then Lead II is also the right right axis deviation
negative and deeper.
Two main leads: Lead I and AVF
Note: If the QRS complex in Lead I is predominantly upright or Lead I – from R arm to L arm
positive and Lead III is predominantly positive, then Lead II should o negative electrode on the right arm
be taller than the two. If Lead I is predominantly positive and Lead o positive electrode on the left arm
III is negative, then Lead II should be very small. If Lead I is AVF
negative and Lead III is positive, Lead II should be smaller. o up and down
o positive electrode = left leg
ECG AUGMENTED LIMB LEADS (UNIPOLAR)
- Dr. Emanuel Goldberger added more leads, but this If on the ECG paper the QRS of Lead I is predominantly positive
time he only used a unipolar limb leads: or upright and the QRS of Lead AVF is predominantly positive
o positive electrode on the left leg and called this lead or upright the axis of the heart is NORMAL
as AVF where the orientation is up and down
Note: The normal axis is between 0 to 90 degrees but
o Positive electrode on the right arm and called this
some books will say up to -30 is still normal. Normal
lead as AVR. The negative assumed to be at zero
direction is going to the left between (+) 30 degrees and
potential by the machine.
(+) 60 degrees
o Positive electrode on the left arm and called this
lead as AVL. Negative assumed to be at zero
potential by the machine.
If on the ECG paper the Lead I is predominantly positive but Lead
AVF is predominantly negative Left axis deviation
AVF
o up and down
If on the ECG paper the Lead I is predominantly negative but
o positive electrode = left leg
Lead AVF is predominantly positive Right axis deviation
AVR
Lead I and AVF: should have a QRS that is predominantly
o positive electrode = right arm
positive which means axis is between 0-90 degrees which is
AVL
normal
o positive electrode = left arm
Lead I is (+) and AVF is (-) = L axis deviation
Lead I is (-) and AVF is (+) = R axis deviation
Lead I is (-) and AVF is (-) = R axis deviation
Unipolar Precordial Leads/ Chest Leads Landmarks:

V1 - 4th ICS right sternal margin
V2 - 4th ICS left sternal margin
V3 - midway between V2 and V4
V4 - 5th ICS MCL
V5 – AAL same level as V4
V6 – MAL same level as V4
o For male patients – V4 is usually under the left
nipple
Note: If you transpose this to Einthoven’s bipolar limb leads

(Leads I, II, III) over that of Goldberger unipolar limb leads, it will
appear this way. This is called as the Hexaxial Reference System
(aka Cabrera system) which is used to compute for the total
electrical axis of the heart. The normal electrical axis of the heart is Note: Proper placing of electrodes/leads on the chest wall is
directed this way. important.
If the patient for example has a big heart (big LV), and
since it s a big left heart, the axis of the heart may be
o AVF
Note:
- When evidence of inferior wall MI on ECG (represented
by ST segment elevation), the patient’s right coronary
artery has a severe obstruction from a thrombus or a
ruptured plaque. And if I plan to do primary angioplasty,
it is the first thing that I will canulate because I know that
the patient has a problem on the RCA because of the
evident changes on the inferior wall on ECG (inferior wall
receives its coronary blood supply from the RCA.
Note: Cup electrode is used more often. This is used during - If I see changes in the anterior wall or anterolateral wall
threadmill stress test because it is more expensive. or anteroseptal wall which receives its blood supply from
the left anterior descending artery (LAD), it is the one
that I will canulate first to remove the obstruction to
salvage the heart from necrosis.
- It will also tell the extent of the damage to the heart,
pathology involved, example:
o Changes from V1 to V6 (Lead I to AVL) gives an
idea that the lesion is more proximal near the origin
of the left lead because it supplies a bigger area of
the heart.
- Just by looking at the ECG, you can already
prognosticate.
Note:
- The primary pacemaker of the heart is the SA node
Note: located in the superior portion of the right atrium near
- ECG gives you an idea where the pathology is. the entrance of the superior vena cava. This is where the
o In ischemia, you will know which coronary artery is wave of depolarization originates.
involved depending on the wall affected. This is - It depolarizes the atrium through these intranodal tracts
important especially when doing angioplasty. (left atrium and right atrium).
- It will give an idea about the extent of the pathology and - From the atrium it goes to the AV node, a real structure
the prognosis if there are multiple leads affected found on the inferomedial portion of the right atrium
behind the septal leaflet of the tricuspid valve. Along the
cardiac conduction system, the AV node has the
longest refractory period.
- From the AV node, it goes under the cardiac skeleton
and passes the bundle of Hiss or the common AV
bundle or Hiss bundle.
- From the Hiss bundle, it divides into two: a smaller right
bundle and a bigger left bundle (because the left
ventricle is bigger than the right)
- From this bundle branches, it comes out with very minute
Purkinje fibers as they go inside the myocardial muscle.
Note: If you look at the pathway of the cardiac conduction system,
the first one to contract are the atria and the last one to move is the
Note: All of these lead (Einthoven’s, Goldberger, Unipolar chest posterobasal portion of the ventricles because it is the last part
leads) represent specific areas within the heart. to depolarize. The whole heart is depolarized in <0.32 second.
Inferior wall myocardial infarction – look at:
o Lead II Pathway of electrical conduction system of the heart:
o Lead III
SA node atrium AV node Hiss bundle purkinje fibers
ventricles
ECG paper: Note:

- There are small squares and big squares - P wave with 2 small squares (0.04 + 0.04) = 0.08s =
- X axis normal
o Horizontal - P-R interval with 4 small squares (0.04 x 4) = 0.16 =
o Measurement of time normal
o The normal standard ECG machine paper speed is o PR interval is measured from p wave to start ofQRS
25 mm/sec. If it runs in this speed:
1 small square = 0.04 seconds QRS complex
1 big square = 0.20 seconds (5 small - Phase 0 of ventricles
squares) - This was named by Dr. Einthoven during the 1890.
- Y axis - There are so many deflections comprising the QRS but
o Measurement of voltage we need to be precise on what it means.
o 1 mV of electricity = 10 mm amplitude on ECG
paper Q wave
10 mm = 10 squares - Represents the first downward deflection that
This is important to know if the patient’s heart comprises QRS.
is enlarged or not - Normally, Q wave is not seen or detected in ECG
Big heart = big voltage = big QRS because a significant Q wave (1 small square and 1/3 of
Heart is too big = QRS larger than the paper. the QRS complex) means that the patient had an old
o Label ECG paper as half sensitivity to heart attack.
fit the QRS o Example: If a patient has a significant Q wave in
o 1 small square = 0.1 mv Leads II, III, AVF previous coronary thrombosis
of right coronary artery (previous inferior wall MI)
P wave
- represents atrial depolarization R wave
- atrial conduction time - First upward deflection that comprises QRS whether
- normal amplitude is 0.5 to 2.5 mm preceded by a Q wave or not
o If the height is >2.5mm = RA enlargement o smallest in V1 and V2 and becomes taller as you go
- normal duration is up to 0.10s (2 ½ small squares) in to V6
adults o Highest in V4
o If the duration is >0.12s or 3 small squares LA
enlargement or dilatation
- It is usually biphasic (with upward and downward
deflections) in V1 S wave
- 1st half represents RA phenomenon; distal half - downward or negative deflection following the R wave
represents LA phenomenon o deepest in V1 and V2 and becomes shallower as
you go to V6
P-R Interval (PQ interval)
- Represents time interval for impulse to reach ventricles QS wave
from SA node (time from the SA node to the ventricle) - single negative deflection representing entire QRS
- Normal is 5 small squares or 1 big square (0.12-0.20s
in adults (HR = 70-90/min) ) Note: Those who had a heart attack, when there is no R wave and
o If the PR interval is >5 small squares first the whole QRS is represented by the QS pattern, this is strong
degree AV block evidence that the patient had a previous heart attack.
- measured in limb lead with longest PR interval
- Start of P to start of QRS Example:
- QS from V1 to V6 but no R wave previous massive
anterior wall MI (+SOB, + easy fatigue) suffering from
heart failure
Note: Prominent in SOB with LV infarct; If prominent from V1 to V6 o Percarditis causes chest pain and ST segment
may indicate a big part of the heart had an infarct; with previous elevations but does not produce Q wave. Presents
MI; depends where the MI is and what coronary artery is involved with pleuritic pain
- Used to diagnose acute MI. Elevated in acute infarct
R’ wave and S’ wave o Elevated >1mm in acute MI (heart attack)
- other upward deflection after S wave o Elevated >0.5mm in ischemia
o The first downward deflection = Q wave - If elevated but concave upward, could be a normal
o The next upward deflection = R wave variant, electrolyte imbalance or pericarditis
o Negative deflection = s wave o Ex. ST elevation in Leads II, III, and aVF – acute
o More deflection after S wave = R’ wave Inferior Wall infarct Thrombosed Right Coronary
o Another deflection = S’ wave Artery (Blood Supply of inferior wall)
o No R wave = QS pattern - MI: heaviness, feeling of impending death b/c of pain,
- bundle branch block; absent in patients with heart attack. cold clammy extremities, perspiration, SOB
- The more elevated the ST segment is, the bigger the
infarct (massive MI) which, if not treated, can cause
CARDIOGENIC SHOCK (80% mortality)
o Philippines – CVD #1 mortality (9/hour)
o 50% of deaths of CVD is 2˚ to Sudden Cardiac
Death (death within 1 hour after onset of S/Sx)
- Prevention: #1 factor is early recognition - ECG
- Depression of more than 0.5mm is an ischemia.
Q wave without ST elevation = OLD INFARCT

Q wave with ST elevation = RECENT INFARCT
Normal pattern of chest leads
- the R wave is usually smallest in V1 and V2, becomes ST elevation without Q Wave = Acute Infarct
taller and predominantly upright from V1 to V6, tallest in ST elevation and no Q wave = Pericarditis
V4
- The S wave deepest in V1 and V2, becomes shallower
from V1 to V6
ST Segment
- Should be isoelectric (same level as PR segment)
- Represents Phase 2 or Plateau phase of the ventricle
- may be depressed –0.5 mm (half small square) or
elevated by 1mm (1 small square) = normal
- represents period from end of ventricular depolarization
to start of ventricular repolarization
- between end of QRS and start of T wave
- If it is convex upward
o Patient presents with chest heaviness or tightness,
cold hands, sweaty; ECG finding = STEMI
o Not all ST elevations are heart attacks
12-Lead ECG is more expensive
- the long lead is useful in arrhythmias. Lead II is usually
utilized.
- Speed is mentioned in the paper (25mm/s)
o 1 small square = 0.,04
o 1 big square = 0.20
- Voltage – in the limb leads, 1 mV produce 10mm
amplitude.
- In patients with big hearts, some will not fit the ECG
anymore. The machine automatically shifts to a half
sensitivity meaning 1 mV will only produce 5mm
amplitude.
Picture 2 of a 12 lead ECG:
WHAT IS THE ELECTRICAL AXIS OF THIS 12 LEAD ECG? - The axis is normal because Lead I is predominantly
- Is it normal? Is there left axis deviation? Right axis positive and Lead AVF is equiphasic (equal positive and
deviation? Cannot be determined? equal negative) = NORMAL
o Lead I and Lead AVF = Look at the QRS of these
leads Case: ST elevation in Lead II, III, aVR, aVF, V4-V6
If the QRS of this two leads are - Q wave at lead II (old infarct)
predominantly upright or positive - Long lead II shows the Concave upward variant of ST
NORMAL elevation, but since ST elevations are also seen in other
leads, it is more probable that it is a MI
Case: 60 year old man complaining of chest pain with (+) history of - ADMIT
smoking. ECG was done, (result picture below), axis is normal; o Giving MI treatment to a non-MI patient can cause
slightly diabetic; 110/80 death 2˚ to hemorrhagic bleeding
- Send home the patient with medicine? Admit the patient
in Intensive coronary care unit? Admit patient in an Case: 70 y/o woman with severe chest heaviness, cold clammy
ordinary room? sweats, BP 110/90, sweat and SOB
o ADMIT IN ICU - Diagnosis: STEMI involving the anterolateral wall or
- ECG is NOT NORMAL because the patient has Lead 2,3 massive anterior – a big part of the myocardium almost
AVF ST segment elevation 40% of left ventricle is involved.
o Represents the inferior wall of the left ventricle o The more ST elevation seen in more leads, the
having an acute inferior wall MI which is supplied more massive the heart attack is. The more
by the right coronary artery massive the heart attack, the worse the prognosis.
o ST Elevation MI (STEMI) - ADMIT
STEMI and NON-STEMI is managed o Extensive V2,V3 anterolateral wall MI
differently and the prognosis is also different o Cardiogenic shock if not treated aggressively
(80% mortality)
o Immediate tx is needed
Classification for MI is divided into 2 types:
- STEMI
o transmural
o involves whole thickness of myocardium
- NSTEMI
o subendocardial
o only involves subendocardium (outer part; more
prone to ischemic insults)
- has different management (of which will benefit from
thrombolytic agents)
- STEMI has higher short term mortality but after a year
has equal mortality rate with NSTEMI due to high rate of
recurrence of NSTEMI. So management is still
aggressive eventhough the whole muscle is not infarcted T Wave
(only subendocardium). - represents ventricular repolarization
- usually upright in LI, LII and diphasic or inverted in LIII,
V1
ST Segment Depression
- Many interpret inversion of the T wave as a marker for
ischemia but is not always true. The T wave can be
inverted in some patients by
o shifting to another position. (Supine stand up =
ECG may become inverted) so T wave inversion
cannot be used as a marker of ischemia in these
patients.
o The ECG may also be inverted during
hyperventilation.
o Skeletal abnormlaities like pectus excavatum may
also have inverted T wave inversion
o T wave may be inverted up to lead V3 in young
adults
Example: T wave inversion from V1, V2, V3 (Female, young, (-)

smoking, diabetic, hypertensive, strong family history (brother or
father did not have any cardiovascular event: unstable angina,
heart attack, bypass, angioplasty, stroke, peripheral vascular
disease, dialysis, did not die of cardiovascular event at age 55 and
- ST segment depression must be compared with PR younger, etc or mother and sister did not have those events
segment mentioned above at age 65 and younger)
o Picture: 3mm ST segment depression Interpretation: low risk to have ischemic heart disease so read as
- In patients who did not present as a heart attack: NORMAL
complains of chest heaviness without cold clammy
sweats, and relieved in less than 2 minutes Example: Same ECG finding as above but in a 60 y.o. man that
o Patient has coronary heart disease and stable came in to the clinic complaining of chest heaviness on effort/
angina; no heart attack if the cardiac enzymes angina on effort with a BP of 160/100, smoker 1 pack per day,
(troponin (very sensitive), CK-MB) are normal RBS is 250.
- If the presentation is like heart attack; cardiac enzymes Interpretation: Anteroseptal wall ischemia
should be requested
o What time is the onset of severe chest heaviness? It is important to always correlate clinically the ECG finding
No heart attack if the Troponins are still
negative after 12 hours of the onset of chest Non-cardiac conditons can make the T wave inverted (Physiologic
pain. Initial negative cardiac enzyme does not T wave):
rule out MI - body position
o Patient has coronary artery disease without - fever
infarction (Stable angina w/o infarct) - skeletal abnormalities (pectus excavatum)
- hyperventilation
NSTEMI short term prognosis is good (mortality is low) but the - T wave in V6 usually > V1
recurrence rate is very high so the prognosis is the same with
STEMI after a year. QT Interval
NSTEMI – endocardium is infacted which is more - Start of Q wave to the end of T wave
prone to ischemia than epicardium - It is dependent on the heart rate
STEMI – whole thickness of the muscle is infracted o The slower the HR, the longer the QT interval
o If a patient had STEMI and it is a small one and o The faster the HR, the shorter the QT interval
there are no areas that are ischemic, the patient’s - represents electrical systole
chest pain will disappear (ischemic necrotic - measured by counting number of small boxes
dead tissue = no pain)
10 | J K C P a l o m a r e s
- time required for ventricular depolarization and - Normal duration= 2 ½ small squares (0.10 sec)
repolarization o P wave duration > 0.12s (3 small squares or more)
- varies with age sex and heart rate and P wave in V1 (usually biphasic) have a depth of
- normal QT = 0.35-0.44s (adults) 1 small square Left Atrial enlargement or
Hypertrophy or dilatation
Corrected QT or QTc (correction factor) - The terminal half of the P wave represents left atrial
phenomenon.
- The proximal half represents the right atrial phenomenon
which is understandable because the sinus node is in the
right atrium so RA is depolarized first.
- ECG can no longer differentiate hypertrophy from
- measuring QT interval in seconds by the number of small dilatation. (Before a chamber enlarges it usually goes to
squares times 0.04, divided by square root of R-R a process of hypertrophy)
interval in seconds (# small squares times 0.04)
- Biphasic P wave in V1 & V2 with negative terminal
- Prolonged QTc > 0.425s portion having depth of >0.1 Mv
o prone to develop Malignant Arrhythmia (has - if you have a wide P wave particularly in inferior leads
potential to kill) cardiac arrest o 2 ½ small squares or more
o Many drugs can prolong Q-T interval like GI drugs o terminal portion has depth of at least one small
(to improve motility), IV antibiotics, and Cardiac square or more
Drugs o width atleast one small square or more
o + things mentioned aboved
Case: 26 yo female admitted for elective thyroidectomy due to = left atrial hypertrophy or dilatation
non-toxic goiter
- at recovery room: 2-3 hrs after surgery, the patient went
into cardiac arrest
- at ICU: intubated, in respirator, comatosed, on triple
inotropic support (Dopamine, NEP, Dobutamine: these
drugs cause tachycardia or ↑ hr)
- Q-Tc of the patient was prolonged (0.51) but ECG before
surgery was normal so this rules out congenital
prolonged Q-Tc. This signifies acquired prolonged Q-T
syndrome
- request for serum calcium stat very low (only 0.8; N=
1.2 and above)
o Request for serum calcium after thyroidectomy if
you suspect that the parathyroid gland has been
accidentally removed or damaged or the vascular or
nerve supply was cut off during surgery causing
serum calcium to drop and resulted to prolonged Q- LII:
Tc - P wave is more than 3 small squares (at least 0.12 sec.)
U Wave V1
- Seen after the T wave. It usually has the same polarity - P wave is more than 3 small squares
as the T wave. If the T wave is upright, the U wave - Prominent terminal portion which is >1 small square
should also be upright. - Depth and width is 2 small squares
- It is not always present in ECG - meets criteria for left atrial
- If the T wave is upright, and the U wave is negative: enlargement/dilatation/hypertrophy
o A negative U wave is specific for heart diseases **Loud S1 Opening Snap = Mitral Stenosis 2˚ Enlarged RA
but will not tell you what type of heart pathology the
patient has (coronary heart disease, valvular heart
disease, cardiomyopathy, etc). It is just a clue to
investigate further
- It is increased in amplitude in:
o Electrolyte problems (hypokalemia)
o Drugs
o Left ventricular hypertrophy
- It represents repolarization of the Purkinje fibers Lead II - The P wave is widened and is more than 3 small squares.
which innervates the myocardium V1 – P wave is more than 1 small square in depth and in width
- small deflection after the T wave Diastolic murmur heard at the apex; the loud first heart sound
- tallest in V2 & V3 ECG with evidence of left atrial enlargement
- usually does not exceed >1mm in amplitude Diagnosis: Mitral Stenosis
P wave
P wave in Lead V1 is predominantly upright associated with tall
peaked P wave in the inferior leads
- Right atrial hypertrophy or dilatation
Prox ½ of P wave is taller in lead V1
No more terminal half in V1 (not biphasic)
Right Ventricular Hypertrophy (RVH)

- R/S ratio
o R wave in V1 is taller than how deep the S wave is
R wave is usually smallest in Leads V1 and
V2 but if the R wave is very tall in V1 then you
should start to suspect especially when there
is right axis deviation and the S is very small
Axis of 12 lead ECG: Left Axis Deviation
when the S should be deepest in V1
- Lead I is predominantly positive
o The R should be taller than how the S wave is deep
- Lead AVF is predominantly negative
o In Lead VI, the R wave is smallest and the S wave
P wave – dicrotic notch – 3 small squares in Leads II, III, AVF
should be deepest in the normal heart
It is atleast 1 small square in the Lead V1
- Left atrial hypertrophy or dilatation
Example: RAH Patient with holosystolic murmur which increases
on ECG
In contrast to Right atrial enlargement, it is tall and peak in the
inferior leads II, III, and AVF. It is 2 ½ or more small squares. - PE finding on a patient with RVH – apex beat is
The proximal half of the P wave is more prominent in Lead V1 in displaced; Right ventricle is an anterior chamber relative
Right Atrial Hypertrophy or Dilatation. to the left so when it enlarges it moves forward where the
P waves is tall (> 0.25mV) (2.5 mm or more) & peaked in inferior one behind it is the left atrium (Left atrium moves
Biphasic P wave in V1 with first component larger than the second backward)
- RVH = R/S ratio in V1 > 1
o Normally, R wave should be small in V1
o R wave is very tall in RVH; R wave is taller than
how deep the S wave is
- RVH caused the Right Axis Deviation in the patient
- S in V1 < 2mm
- RAD > 110 degrees
- Similar ECG with Bundle Branch Block and Posterior
The height is at least 2 ½ small squares or more Wall MI (Differential Diagnosis)
Duration is not widened
Diagnosis: Right Atrial Enlargement
Example: Holosystolic murmur heard at the left lower parasternal

border which increases in intensity on inspiration and on ECG
there is right atrial enlargement
Diagnosis: Tricuspid Regurgitation
Left Ventricular Hypertrophy

- The sum of the R wave in V5 or V6 plus the S wave in
V1 or V2
LVH (Left Ventricular Hypertrophy)
o If >35 in a patient 30 years and above
o If >40 in a patient 20-30 years old
o If >60 in a patient 6-20 years old
o Values change depending on the age of the patient
Example:
Axis of this 12 lead ECG: Right Axis deviation

- Lead I is predominantly negative
- Lead AVF is predominantly positive
P wave is 2.5mm in Lead II and Lead AVF
Axis of this 12 lead ECG: Normal
- In Lead I, the QRS is still predominantly upright
- Lead AVF is predominantly upright
Diagnosis:
- Left Ventricular Hypertrophy
o S wave in V1 and V2 (deeper S wave - 20)
o R wave in V5 (taller R wave - 27) and V6
20+27 = 47
o >35 so patient has LVH
- The R/S ratio is normal
- ST segment markedly depressed
o 4mm ST segment depression
o In the presence of LVH on ECG, it is hard to say if
the patient has ischemia or coronary heart disease
because the patient may not have ischemia but has
an ST depression because of the LVH sometimes
called the strain pattern of LVH
- Patients with hypertrophy, the hypertrophied muscle
needs more blood supply and is more prone to compress
the small arterioles which means that a hypertrophied
heart is more prone to ischemia even in the absence of
atherosclerosis, coronary heart disease because the
demand is higher and they may be more prone to
compress the arterioles that supplies the heart muscle.
Signs and Symptoms suggestive of Deep Vein
Acute Deep Vein Thrombosis Thrombosis in 160 consecutive patients with negative
Dr. O Deduyo venograms
Take Off Case Signs and Symptoms No. of %
57 year old male patients
pain, erythema and swelling in his right leg for Pain, tenderness and swelling 94 59
two days Pain and tenderness only 35 22
he denies any trauma, fever, or dyspnea Swelling only 18 11
Physical Examination Tenderness and swelling 13 8
tenderness in his right popliteal fossa Other clinical findings:
pitting edema in his right leg
his calf circumference, measured 10 cm below Edema 38
the tibial tuberosity in both legs, is 3 cm greater Homan’s sign 35
in the right leg.
Cord 8
Site
Epidemiology of DVT
Calf only 90 56
Calf and thigh 56 35
VTE
Thigh only 14 9
US Figures: 1, 2
1 per 1000 individuals Hull RD et al. Clinical Validility of a negative venogram
40% DVT in patients
60% PE Clinically suspected venous thrombosis, Circulation
Acute PE’s cause 25,000 deaths per year 64:622, 1981
Untreated proximal DVT is associated with 30-
50% for PE, and 12% mortality rate DVT- Clinical Presentation
Classically= calf pain, tenderness, swelling, redness and
PHIL Data: 3 Homan’s sign
Incidence of DVT in ICU patients is 20.7% Overall sens/spec= 3-91%
Unreliable for diagnostic decisions
Etiology and Pathogenesis Up to 50% have none of these
VIRCHOW’S TRIAD
Well developed and tested in clinical prediction model
for DVT in 1997
Wells PS, Anderson DR, Bormanis J, et al. Value of

assessment of pretest probability of deep vein
thrombosis in clinical management. Lancet 1997; 350
(9094): 1795-8
Clinical Prediction Rules: Wells Clinical Criteria
Table 1: Clinical Model for Predicting the Pretest

Probability of Deep Vein Thrombosis
Clinical Characteristic Score
Active Cancer (patient receiving treatment for 1
cancer within the previous 6 mos or currently
CLINICAL FEATURES AND CLINICAL DIAGNOSIS receiving palliative treatment
Paralysis, Paresis or recent plaster 1
The alternate diagnosis in 87 consecutive patients with
immobilization of the lower extremities
clinically suspected venous thrombosis and negative
Recently bedridden for 3 days or more or 1
venograms
major surgery within the previous 12 week
Diagnosis No. of
requiring general or regional anesthesia
Patients
Localized tenderness along the distribution of 1
Muscle strain 21
the deep venous system
Direct twisting injury to leg 9
Entire leg swollen 1
Leg swelling in paralyzed leg 8
Calf swelling at least 3 cm larger than that on
Venous reflux 6 the asymptomatic side (measured 10cm below 1
Lymphangitis, lymphatic obstruction 6 tibial tuberosity)
Muscle tear 5 Pitting edema confined to the symptomatic leg 1
Baker’s cyst 4
Cellulitis 3 Collateral superficial veins (non varicose) 1
Internal abnormality of knee 2 Previously documented deep vein thrombosis 1
Unknown 23 Alternative diagnosis atleast as likely as deep -2
Total 87 vein thrombosis
A score of two or higher indicates that the
probability of deep vein thrombosis is likely; a
score of less than two indicates that the
probability of deep vein thrombosis is unlikely. A
patient with symptoms in both legs, the more
symptomatic leg is used.
CLINICAL ESTIMATE OF THE PROBABILITY OF DEEP

VEIN THROMBOSIS (DVT)
Wells Clinical Score Interpretation 1997

Total Points Probability of DVT
<0 low
1 or 2 intermediate
>3 high
Wells Clinical Score Interpretation 2003

<2 unlikely
>2 likely
VENOGRAPHY
Considered the diagnostic standard for lower
extremity DVT
Infrequently used today due to its numerous
disadvantages DVT – D-DIMER
Its use is limited to situations of diagnostic Fibrin degradation product elevated in active
uncertainty thrombosis
Negative test can help exclude VTE
Preferred test
- Quantitative Rapid ELISA – sensitivity 96/95% for
DVT/PE
- Other methods include latex agglutination and
RBC agglutination (SimpliRED)
VENOUS DUPLEX SCAN

Accuracy for the diagnosis of DVT in the
iliofemoral and popliteal areas:
Sensitivity and specificity: >90% (approaches
100% in some series)
In patients who are considered clinically

unlikely to have deep vein thrombosis and
who have a negative D-Dimer test, the
diagnosis of deep vein thrombosis can safely
be excluded without the need for further
diagnostic testing.
TREATMENT OF DEEP VEIN THROMBOSIS
TREATMENT RECOMMENDATIONS FOR DEEP VENOUS THROMBOSIS

CHEST
Antithrombotic Therapy for Venous Thromboembolic Disease: American College of Chest Physicians Evidenced Based
Clinical Practice Guidelines( 8th Edition)
Current Approach To Grades of Recommendations

Grade of Clarity of Risk/ Methodological Strength of Implications
Recommendation Benefit Supporting Evidence
1A Clear RCTs without important limitations Strong recommendation: can
apply to most patients in most
circumstances without
reservations
1C+ Clear No RCTs but strong RCT result can be Strong recommendation: can
unequivocally extrapolated or apply to most patients in most
overwhelming evidence from circumstances
observational studies
1B Clear RCTs with important limitations Strong recommendation: likely to
(inconsistent results and apply to most patients
methodological flaws)
1C Clear Observational studies Intermediate strength
recommendation: may change
when stronger evidence is
available
2A Unclear RCts without important limitations Intermediate strength
recommendation: best action
may differ depending on
circumstances or patients or
societal values
2C+ Unclear No RCTs but strong Rct result can be Weak recommendation: best
unequivocally extrapolated or action may differ depending on
overwhelming evidence from circumstances or patients or
observational studies societal values
2B Unclear RCTs with important limitations Weak recommendation:
(inconsistent results and alternative approaches likely to
methodological flaws) be better for some patients
under some circumstances.
2C Unclear Observational studies Weak recommendations: other
alternatives maybe reasonable
ACC/AHA Classification of Recommendations and Level of Evidence
Summary of Recommendations ACCP: Initial Anticoagulation of Acute DVT of the Leg

For patients with a high clinical suspicion of DVT start
ACCP: Initial Anticoagulation of Acute DVT of the Leg Anticoagulants while awaiting the outcome of
For Patients with objectively confirmed DVT: diagnostic tests (Grade 1C)
SC LMWL (Grade A1)
IV UFH (Grade A1) In patients with Acute DVT start with LMWH, UFH or
Monitored SC UFH (Grade A1) Fondaparinux for atleast 5 days and until the INR is >2.0
Fixed-Dose SCUFH (Grade A1) for 24h (Grade 1C)
SC Fondaparinux (Grade A1)
In patients with Acute DVT start VKA together with
ACC/AHA: Initial Anticoagulation of patients with LMWH, UFH or Fondaparinux on the first treatment day
IFDVT (Grade 1A)
1.) In the absence of suspected or proven heparin induced
thrombocytopenia IV UFH for the Initial Treatment of DVT
Intravenous UFH (Class A1) Initial IV Bolus (80 U/kg or 5000 U) by continuous
UFH by Subcutaneous Injection (Class 1B) infusion (initially 18U/kg/h or 1300 U/h) with APTT
LMWH (Class 1A) monitoring (Grade 1C)
Fondaparinux (Class 1A)
SC UFH Compared with IV Heparin for the Initial
2.) Patients with IFDVT who have suspected or proven Treatment of DVT
Heparin-Induced Thrombocytopenia should received a Initial Dose of 17,500 U or 250 U/kg BID, APTT
direct thrombin inhibitor. measured 6h after injection (Grade 1C)
(eg. Argatroban, Lepirudin, Class 1B)
If Fixed-Dose, Unmonitored SC UFH is chosen:
Initial Dose of 333 U/kg followed by 250 U/kg BID
(Grade 1C)
LMWH for the INITIAL treatment of DVT IMMOBILIZATION FOR THE TREATMENT OF ACUTE DVT
-LMWH SC once or twice daily, as an outpatient early ambulation is recommended if feasible
if possible (Grade 1A)
(Grade 1C) or as an inpatient if necessary
(Grade 1A), rather than treatment with IV UFH ELASTIC STOCKINGS AND COMPRESSION BANDAGES TO
-In patients with acute DVT and severe renal PREVENT PTS
failure, suggest UFH over LMWH ( Grade 2c) For symptomatic proximal DVT, elastic
compression stockings with an ankle gradient
DOSE CALCULATION pressure of 30 to 40 mm Hg if feasible (Grade
Enoxaparin twice daily at 1 mg/kg or once daily 1A)
at 1.5 mg/kg, Dalteparin once daily at 200 IU/kg Compression therapy, which may include use of
or twice daily at 100 IU/kg, or Tinzaparin once bandages acutely, should be started as soon as
daily at 175 anti Xa IU/kg feasible after starting anticoagulant therapy and
should be continued for a minimum of 2 years,
FONDAPARINUX for the INITIAL treatment of DVT and longer if patients have symptoms of PTS
-Fondaparinux by SC injection once daily
o 5mg for patient weighing 50 kg Comparison of ACCP and ACC/AHA Recommendations
o 7.5 mg for patients weighing 50 to 100 on Certain Aspects of DVT Management
kg
o 10 mg for patients weighing 100 kg Treatment ACCP 8th ACC/AHA
2008 2011
DURATION OF ANTICOAGULANT THERAPY (IFDVT)
FIRST EPISODE: Catheter Directed Grade 2B Class 1C
-with tramsient (reversible) risk factor Thrombolysis
-unprovoked DVT Balloon Grade 2C Class 2a/bC
angioplasty/Stenting
DURATION OF THERAPY (after CDT)
-3 mos. VKA (Grade 1A) Systemic thrombolysis Grade 2C Class 3A
-at least 3 mos. (Grade 1A) Operative venous Grade 2B Class 2aB
o First unprovoked proximal DVT with no thrombectomy
risk of bleeding and for whom good Percutaneous venous Grade 2C -
anticoagulant monitoring is achievable, thrombectomy
long term treatment is recommended Vena cava filter Against it Class IIIB
(Grade 1A) (IA)
o After 3 months of anticoagulant VCF as substitute Grade 1C Class IB
therapy, all patients with unprovoked because of bleeding
DVT should be evaluated for the risk- Anticoagulation after Grade 1C Class IB
benefit ratio of long term therapy IVC filter placement
(Grade 1C) Early ambulation Grade 1A
o First isolated unprovoked distal DVT 3
Elastic Stockings Grade 1A
months of anticoagulant therapy is
Pentoxyphilline, Grade 2B Class IB
sufficient rather than indefinite therapy
MPFF, Sulodexide in
(Grade 2B)
venous ulcers
INTENSITY OF ANTICOAGULANT EFFECT
RETURNING TO OUR PATIENT
INR of 2.5 (range: 2.0 to 3.0) for all treatment
durations (Grade 1A)
57-year-old male
With unprovoked DVT who have a strong
Pain, erythema, and swelling in his right leg for two days
preference for less frequent INR testing to
He denies any trauma, fever, or dyspnea
monitor their therapy, after first 3 months of
Physical examination:
conventional-intensity anticoagulation (INR
Tenderness in the right popliteal fossa
range: 2.0 to 3.0), low intensity therapy (Range:
Pitting edema of the right leg
1.5 to 1.9) is recommended with less frequent
His calf circumference, measured 10 cm below
INR monitoring over stopping treatment (Grade
the tibial tuberosity in both legs, is 3 cm greater
1A)
in the right leg
FOR PATIENTS WITH DVT AND CANCER
Wells Score 3 – Likely for Acute Deep venous
LMWH for the first 3 to 6 months of long-term
Thrombosis
anticoagulant therapy (Grade 1A)
For these patients, subsequent anticoagulant
therapy with VKA or LMWH is recommended
indefinetely or until the cancer is resolved
(Grade 1C)
D-Dimer for VTE Exclusion: accuracy of assays: meta- Potential difficulties/limitations with the new oral
analysis agents
DVT (49 studies) PE (31 studies) Half life (9-17 hrs): requires adequate compliance for
Se Sp( LR(neg)( Se Sp( LR(neg)( VTE treatment
(% %) *) (% %) *) How to revert or measure the anticoagulant effect?
) ) Immediate post-op use (nausea/vomiting) for
Elisa 96 44 0.10 97 41 0.07 prophylaxis
(VIDAS@) Lower compliance with prescription with unmonitored
Elisa 95 40 0.12 96 51 0.08 pills than with parenterals
(micropla Are these agents really cost effective in routine clinical
te) practice?
Elisa 92 43 0.20 92 55 0.16
(membra Potential difficulties/limitations with the new oral
ne) agents
Latex 86 61 0.23 89 47 0.23
(auto) These drugs behave like circulating anticoagulants and
SimpliRED 86 67 0.20 83 64 0.27 cannot be reversed with blood products
@ Bleeding has been an issue with these new drugs
Latex 79 66 0.32 80 56 0.36 FDA looking into post-market reports of serious
(manual) bleeding events with Dabigatran
Reports of fatal bleeding events in Japan using
(*) Negative likelihood ratio = false negatives/true Dabigatran
negatives = (1-se)/sp Postoperative bleeding a concern in some patients
High sensitivity at the expense of lower specificity

Best safety by VIDAS
o Highest sensitivity; lowest LR(neg)
Characteristics of new oral anticoagulants

Dabigatran Rivaroxaban Apixaban
Mechanism of Direct Direct FXa Direct
action Thrombin inhibitor FXa
inhibitor inhibitor
Oral 6.5% 80% ~50%
bioavailability
Route of Oral Oral Oral
administration
Dosing OD or BID OD or BID BID
Pro-drug Yes No No
Food effect No No No
Renal 85% 36% ~27%
Clearance
Mean 14-17 h 7-11 h ~12 h
Half0Life (patients)
(T1/2)
Tmax 0.5-2 h 2-4 h 3h
Drug P-gp CYP 3A4 CYP 3A4
interactions inhibitors and P-gp and P-gp
P-gp inhibitors inhibitors
inducers CYP 3A4 CYP 3A4
Amiodarone inducers inducers
Advantages with the new agents
Half life (9-17 hrs): OD/BID dosing for prophylaxis

Post operative initiation for prophylaxis
Fixed oral doses for both indications (no weight
adjustment)
Routine monitoring not needed
Few interactions with other medications/food
Potentially better compliance for extended
prophylaxis and treatment than with injections
Pulmonary Embolism
EPIDEMIOLOGY
300,000 hospitalizations and 100,000-200,000
deaths/year
Case fatality of 15% (not changed in last decade)
Majority of emboli from deep veins of the lower
extremity
*437/930 pts with neg D-dimer and low pres-test prob
Majority of deaths in undiagnosed
1 PE in flu; NPV=99.5% Ann Int Med 2001; 135:98
PE risk with proximal LE DVT = 50%
Upper extremity venous thrombosis (rare)
Evaluation : CXR, labs, EKG, Thoracentesis not really
o PE risk = 12-17%
helpful
70% PE deaths not diagnosed prior to death
VENTILATION PERFUSION SCAN (VQ SCAN)
Look for VQ mismatches
(ventilated but non-perfused
areas of lung)
Risk of PE (% probability)
o Normal 0%
o Low <10%
o Intermediate 20-30%
DIFFERENTIAL DIAGNOSIS
o High 90%
(PULMONARY)
40-50% suspected PE’s will have non-diagnostic VQ
Pneumonia
and normal LE evaluation (US/IPG)
COPD/Asthma
Pneumothorax SPIRAL CT
Pleurisy Radiology 1996; 201:467-70
TB VQ vs. spiral CT in 149 patients
Cancer PAgram done if VQ indeterminate
Effective in detecting up to segmental level PE
(CARDIAC) Sensitivity 82% & 94%
Myocardial Infarction
Specificity 93% & 96%
Pericarditis
CHF
Tamponade
VENOGRAPHY OR NON-INVASIVE STUDY OF THE

LOWER EXTREMITY
Same positive findings as for DVT
Positive LE DVT in a suspicious patient is usually
adequate for diagnosis
(MUSCULOSKELETAL)
Costochondritis
Rib Fracture
Myositis
Trigger Point Pain
(OTHER)
Herpes Zoster
Sepsis
Radiation of abdominal pain
PULMONARY ANGIOGRAPHY
Gold standard
Death rate 2-5/1000 TREATMENT OPTIONS
Not widely available Anticoagulation
Consider use if: Thrombolytics
o Low prob VQ in
suspicious patient
o Consideration for
ANTICOAGULATION
use of thrombolytics Prevent further embolization
o Contraindication
IV Heparin for 5 days
to anticoagulants o Or LMWH
Coumadin starting as early as day 1 Heparin with 4
***thrombosed Pulmonary day overlap
V. You can see lysis of the PE o Duration same as for DVT
MR ANGIOGRAPHY
THROMBOLYSIS BENEFITS
PAgram vs MRA Accelerated clot lysis and tissue perfusion
with Gadolinium
Decreased mortality
Three sets of
readings Reversal of right heart failure
Decrease recurrence
Sensitivities
100, 87, & 75% Decrease Pulmonary HTN
Specificities 95,
100, & 95% PROGNOSIS
If untreated survival is 70% (death secondary
Segmental or recurrent PE)
larger vessels
Treated survival = 92%
Source: Ebel MH Majority of deaths occur before therapy initiated or
: condition recognized
PREVENTION
Same as for DVT
Identify high risk patients and institute
recommended protocols
WHAT TO DO WITH THE IDIOPATHIC DVT? (RISK OF

CANCER OR HYPERCOAGULABLE STATE)
HYPERCOAGULABLE W/U
Age < 40
Thrombus in unusual locations
Upper extremity, neck, anterior abd wall, eye, CNS
Recurrent thrombotic events without incident
causation
Recurrent thrombotic events when on
anticoagulants in therapeutic range
Thrombotic events in absence of underlying illness
or medication
Family history of thrombotic events or
hypercoagulability
Bilateral symmetric thrombotic events (bilateral
DVT)
PULMONARY HYPERTENSION
HYPERCOAGULABLE LABS
Ernst von Romberg (1981) –case report of “pulmonary
CBC, PT, PTT
vascular sclerosis”
ANA
Protein C & S Abel Ayerza
APC resistance (Factor V Leiden mutation) 1901- unpublished lecture describing pulmonary artery
Antiphospholipid antibody and right heart disease
Antithrombin III 1913- Dr. F.C. Arrillaga attributed the disease to syphilis
Fibrinogen & plasminogen
Prothrombin 2010A Mutation Oscar Brenner
1940- first detailed pathologic characterization from
RISK OF CANCER? 100 autopsy reports at MGH in the disease in arterioles
Increased risk of discovering cancer in the <60 age
group
Paul Wood
2/3 adenocarcinoma
o GI 25% 1951- clinical cardiologist, elucidated pathophysiology
and clinical characteristics of pulmonary hypertension
o Urogenital F=12%; M=16%
(PH)
o Hematologic 10%
o Highest risk in first 6 months
David Dresdale
o H&P, CBC, ESR, Chem 20, PSA, GUIAC
1951- first reported hemodynamic variables in cases of
o NEJM 1998; 338:1169
pulmonary hypertension without evident etiology and
15,348 DVT & 11,305 PE
coined the name “primary pulmonary hypertension”
1737 cancer (est. 1372)
POST THROMBOTIC SYNDROME

(POST PHLEBITIC SYNDROME)
DEFINITION
Incompetent lower extremity venous valves result in
ambulatory venous hypertension
FINDINGS
Edema
Soft tissue fibrosis
Ulceration
Pain
Questions to address
MANAGEMENT
Compression stockings (20-30 mmHg class 2) How does derrangement of normal pysiology
Surgical (goal is ulcer healing and decreased pain) explain the symptoms and clinical worsening in
o Perforator Interruption PAH?
New laparoscopic technique What do we know regarding the histopathology
o Valve Repair and pathogenic mediators of PAH?
Symptom relief 65% What is the WHO classification for PAH based
Ulcer healing approx 65% (@ 5 yrs) on this underlying pathophysiology?
Major treatment is prevention of DVT How do we differentiate PH from PAH?
More aggressive treatment of DVT Thrombolytics What is an evidence-based approach in the
diagnosis of PAH?
CONCLUSION
Thromboembolism is a common primary care
problem The Problem
Clinical suspicion is still quite important
Careful use of diagnostic exams
Use LMWH
Survey for Hypercoagulability
Pulmonary Arterial hypertension
Is a syndrome resulting from restricted flow
through the pulmonary arterial circulation resulting in
increased pulmonary vascular resistance and ultimately
in right heart failure.
Use of Right Heart Catheterization

PAH: mPAP≥25mmHg plus PCWP≤15mmHg
In previous guidelines, PVR>3 wood units was included
in the definition of PAH.
Clinical Classification of PH (Dana Point 2009)

1. PAH (Our Focus)
- Idiopathic PAH
- Heritable
- Drug and toxin induced
- Persistent PH of newborn
- Associated with:
o CTD
o HIV infection
o Portal Hypertension
o CHD
o Schistosomiasis
o Chronic hemolytic anemia
1’ PVOD and PCH
2. PH owing to left Heart Disease
- Systolic dysfunction
- Diastolic dysfunction
- Valvular disease
3. PH owing to lung disease and/or hypoxia
- COPD
- ILD
- Other pulmonary diseases with mixed
restrictive and obstructive pattern sleep-
disordered breathing
- Alveolar hypoventilationdisorders
- Chronic exposure to high altitude
- Developmental abnormalities
4. CTEPH
5. PH with unclear Multifactorial Mechanisms
- Hematologic disorders/splenectomy
- Systemic disorders
- Metabolic disorders
WHO functional Classes of PAH

Class I patient with (PAH)but without resulting irritation
of physical activity. Ordinary physical activity does not
cause undue dyspnea, chest pain, or near syncope
Class II patients with (PAH) resulting in slight limitation

of physical activity. They are comfortable at rest.
Ordinary physical activity causes undue dyspnea or
fatigue, chest pain, or near syncope
Class III patients with (PAH) resulting in marked

irritation of physical activity. They are comfortable at
rest. Less than ordinary activity causes undue dyspnea
or fatigue, chest pain, or near syncope
Class IV patients with (PAH) with inability to carry out

any physical activity without symptoms. These patients
manifests signs of right- heart failure. Dyspnea and/or
fatigue (including near syncope) may even be present at
rest. Discomfort is increased by any physical activity.
What is the difference between PH and PAH?
Additional Risk Factors for Drugs and Toxins

Associated with PAH
Definite
- Aminorex
- Fenfluramine
1990s for losing weight
- Dexfenfluramine
- Toxic rapeseed oil
Likely
- Amphetamines
- L-tryptophan
Who is at high risk for development of PAH? - Methamphetamines
Possible
- Cocaine
- Phenylpropanolamine
- St. John’s Wort
- Chemotherapeutic agents
- SSRI
Unlikely
- Oral contraceptives
- Estrogen
- Cigarette smoking
Who develops risk for PAH? Other Risk Factors of PAH
Human Immunodeficiency Virus Infection (HIV)

Infection
- Estimated prevalence of PAH in HIV is 0.5%
- Cases of PAH are declining; however, overall
prevalence is similar to periods before HAART
- Treatment with HAART does not appear to
prevent the development of PAH
Schistosomiasis Infection
- Estimated prevalence of PAH in
schistosomiasisis
o Probably the leading cause of PAH
worldwide
- Endemic in developing tropical countries,
affecting million people
- Parasite not found in United States
Hemolytic Anemia From a diagnostic standpoint,
- Estimated prevalence of PAH in hemolytic how do we differentiate PH from PAH?
anemia is inconsistent
o Varies among studies from 2% (in SCD)
to 68% (in thalassemia)
Portal Hypertension
- Prevalence varies with patient population and
method used to diagnose PAH
o Range from 0.78% in autopsy study of
patients with cirrhosis to as much as 12% in patients
being evaluated for orthotopic liver transplants
assessed on 2-diomensional echocardiography
How do we get an Accurate Diagnosis of PAH?
Symptoms at Time of Diagnosis of PAH

1. dsypnea 93% (most common, same in CHF and PE)
2. fatigue 73%
3. chest pain 47%
4. near syncope 41%
5. syncope 36%
6. leg edema 37%
7. palpitations 33%
Common signs of PAH

1. accentuation of P2 93%
2. tricuspid regurgitation 40%
3. right-sided s4 38%
4. peripheral edema 32%
5. right sided s3 23%
6. cyanosis 20%
7. pulmonic insufficiency 13%
Normal sinus rhythm, complete RBBB (Tall R), Biatrial

enlargement (seen in patients with COPD + PAH)
Echocardiographic Features of PH
2-D echo
- Dilated LV and/or LA= LVH
- Variable EF
- RV:LV ratio <1.0
- LV remains round in short axis
Doppler
- Variable PASP
- ≥2+ MR
- E>A (pseudonormal or restrictive)
What is the most appropriate test to conduct to Rule

Out CTEPH?
Non-specific
Is Echo a useful screening tool for PAH?
RVH or RA Enlargement in PAH (not LVH)
Echocardiographic Features of PAH

The Importance of Pulmonary Function Testing in PAH
2-D echo
- Normal LA, LV size, small LV (<3.5 cm) Important in assessing for presence of obstruction or
- No LVH restriction
- Normal to high EF
- RV apex sharing DLco
- Septal flattening (systole>diastole) - Important as it relates to scleroderma patients
- Pericardial effusion Among patients with systemic sclerosis (n=33), DL co
correlates inversely (r=0.60) with invasively measured
Doppler
- Variable PASP sPA
- No MR - These patients should have annual PFTs in
- Stage 1 diastolic dysfunction (E<A) addiction their annual echocardiogram
Right Heart Catheterization Case in Point
- Required to confirm diagnosis, calculate VS was immediately started on evidence-based
resistance, and guide therapy for PAH treatment to stabilize and improve heart
Exudates other etiologies of PH function
- Intracardiac or extracardiac shunts After 2 weeks on medical therapy, VS continued
- Left heart disease experiencing dyspnea on exertions well as
Measures degree of right-heart dysfunction intermittent episodes of exertional presyncope
- Right atrial pressure
- Cardiac output (Animation) Return to pulmonologist, symptoms worse
Physical exam: HR 88, BP 130/90, RR 12, SpO2
Essential Components of Invasive Hemodynamic 91% Room Air 85% with exertion; WHO FC III
Assessment Echo: Normal Left heart structure and function.
- Oxygen saturations (SVC, IVC, RV, PA, SA) Mild to moderate RV dilation, moderate RV
- RAP dysfunction, moderate septal bowing, E/A 0.8
- RV pressure Review of hemodynamics: performed 2 weeks
- PAP, systolic, diastolic, mean prior
- PCWP, LA pressure, or LVEDP
- CO/CI
- PVR
- Systemic blood pressure
- HR
- Response to acute vasodilator
Your role in the Screening and diagnosis of PAH
Summary
Have a high index of suspicion for the disease in high-
risk patient populations
CASE IN POINT
Will the hemodynamics found on repeat RHC “match”

the Echo-Doppler (and clinical) findings under review?
RV dysfunction
o TAPSE 1.6
Grade 1 diastolic Dysfuntion
o E to A reversal
(Animation) Rheumatology appointment What is the most appropriate next step?

Physical exam and preliminary PFTs. A low DLco A. Initiate aggressive diuresis
(55% predicted) was also noted. Pt denies PND B. Continue medical therapy for severe pulmonary
and orthopnea. Pt referred to a pulmonologist venous hypertension
for further w/u of suspected PAH. C. Request hemodynamic tracings for review,
consider repeating Right heart catheterization
(Animation) Appointment with pulmonologist D. Repeat right heart catheterization with acute
Ordered new set of PFTs and an Echo. Following vasodilator challenge to test “reversibility” of
review of rheum and pulmo reports, VS referred pulmonary venous hypertension
to cardiologist for complete cardiac w/u. FC II
(Animation) Appointment with cardiologist #1

W/u included ECG< CXR< repeat Echo and RHC.
PVH diagnosed.
Understand the screening and diagnostic progression
for PAH
- History and physical examination, ECG, and
CXR echocardiography RHC
Be aware of the strengths and limitations of

echocardiography as a screening tool
Be able to accurately interprets results from RHC
RHC is the gold standard for assessment of

hemodynamics in PAH
PAH Treatment Goals

Functional class improvement
Improve exercise capacity
Improve hemodynamics
Delay of clinical worsening
Improved quality of life
Improved survival
Evidence based Therapies for PAH

Prostacyclin derivatives
- Inhaled
- Subcutaneous/IV
Endothelin Receptor Antagonists
- Oral
Phosphodiesterase Type-5 inhibitors
- Oral
- IV
Benefits of a Multidisciplinary Approach

All physicians are important in the screening of
PAH patients
o This includes pulmonologists,
cardiologists and rheumatologists who
frequently see patients at high risk for
PAH
A coordinated and collaborative diagnostic
process:
How can we optimize the cooperation amongst o Reduces confusion
specialties in the management of a PAH patient? o Helps optimize the overall PAH
Pulmonologist screening, diagnostic treatment and
Cardiologist follow-up plan
Rheumatologist
Future Directions in PAH
- New diagnostic /prognostic tools
o Imaging (MR), biomarkers
- Long term event-driven trials
- Combination therapy
- Emerging therapies:
o Guanylate cyclase stimulator
o Kinase inhibitors
o Elastase inhibitors
o Surviving inhibitors
o NO coupling agents
o Prostacyclin receptor agonists
o Metabolic modulators
o Statins
o Anti-inflammatory/immunomodulat
ory agents
- Endothelial cell replacement:
o Stem/progenitor cells
END
Acute DVT
Totally from PPT only
PE and PAH
Orig trans by KCL and UERA,
Jessica Antoinette S.
Those in red are additional notes,
Most of the pics are recent.
Kung may kulang, typo errors, o malabong pics,

pagpasensyahan nyo na po…
Combined powers na po ito =D.
Thank You
Cardio Team
bam, cathy, erick, jhigz, jhoey, lar, rowel™
###good4urheart =D
Conclusion
“There are three things that will last forever –
Hope, Faith and Love – and the most
PH and PAH share many overlapping features important of which is Love.” – 1 Corinthians
The Echo-doppler exam is an essential part of the initial
workup for screening a patient with PH ##KeeptheFAITH™
- RHC is the gold standard for assessment of
hemodynamics in PAH
A multidisciplinary approach is a critical period of the

diagnostic evaluation and differentiation of PH and PAH
ARRYTHMIA (Part I) 2014 -2015
Dr. Payawal
ARRYTHMIA
o Abnormal cardiac rhythm

o Proper term is dysrrhytmia but they are interchangeable terms
because there are several kinds of cardiac arrythmia
o it is important to distinguish benign from malignant [has capacity o IRREGULAR
to kill Px} -R-R intervals not same
the #1 killer in Philippines is cardiovasculat disease (9 die
every hour)
50 % of deaths from cv disease are sudden cardiac
death [death within one hour of symptom onset]
Majority of sudden cardiac death is caused by o IRREGULAR
arrythmia [arrythmic death]
-in Px with acute coronary syndrome
STEPS IN ARRHYTHMIA RECOGNITION
Cardiac Rhythm Identification

Regularity o IRREGULAR
o Regular
o irregular 2. HEART RATE
Cardiac rate based on ECG 2 methods to get the heart rate:
o Tachycardia MATH
o bradycardia Heart rate = 1500
Pattern of the rhythm # of small squares (0.04s)
o Normal Sinus Rhythm or not? Count the number of small squares(0.04) between 2
o Is rhythm coming from sinus node? R waves (ventricular) or 2 P waves (atrial)
Are there QRS complexes? -use this number to divide with 1,500
o Normal or abnormal? -1,500 because 1 small square is 0.04; 1,500 x 0.04 =
Are there P waves? 60; there are 60 seconds in 1 minute
o Normal or abnormal? Non-MATH
What is the relationship between P and QRS complexes? Sequence method: 300, 150, 100, 75, 60, 50
P-QRS-T -just memorize this sequence
o does it follow the normal pattern? Math method and Sequence Method is applicable for
Clinical correlation? regular only
Intervals: PR, QRS, QT If irregular, count # of R-waves in a 3 (or 6)-second strip, X
20 (or 10)
1. REGULARITY
Beat to beat interval (R to R or P to P intervals) the same BASIC ECG INTERPRETATION
Use a calliper to have an exact measurement
Regular: same interval R-R or P-P
Gold standard to measure regularity: measure R-R or P-P
intervals
o regular: same measurement
It is possible to have a rapid beat with regular rhythm
Determination of Rate
IF RHYTHM IS REGULAR
ECG paper:
Count the # of small squares between 2 R waves
Long lead II = 23
REGULAR 1500/23 = 65 bpm
Sequence method:
If R wave falls on a thick line on big square, the rate would
be 300. Next 150, then 100.. 75..60..50.
This one is between 60 and 75 but nearer to 60 so it is
around 65.
st
1 arrow: 300
REGULAR 1: 150
Magno Opere Somnia Dura Page 1 of 10

Dr. Payawal
2:100
3:75
4: 60
nd
2 arrow: approx. 65
IF RHYTHM IS IRREGULAR
Also estimate
Count the number of big squares in a 6-second strip
*there are 5 big squares in 1 second
*30 big squares in 6 seconds
Regular
P waves normal
HR: around 60-70
PR interval IS normal ;is 0.12 sec. or more
There is the presence of a P wave, followed by a QRS
complex at a regular rate
3 second strip (15 big squares is 3 seconds)
Rate/min = # of complexes multiplied by 20 ECG LeadII
Count the number of R waves in 15 big squares This is a Normal sinus Rhythm:
Presence of P wave
6 second strip (30 big squares is 6 seconds) P wave is followed by QRS
Rate/min = # of complexes (Rwaves) multiplied by 10 Rate is between 60-100
Count the number of R waves in 30 big squares Divide by 22 = 68
Remember: 5 big squares is 1 second
In the example given:
Counted 7 R waves
7 x 10 = 70 beats per minute
3. NORMAL SINUS RHYTHM

Criteria:
There should be a P wave (normal: upright) followed same contour in same lead?
by a QRS complex at a regular rhythm and normal rate Upright in I, II, aVF & left precordial leads
o Normal HR: 60-100bpm followed by QRST?
o Tachycardia: > 100
o Bradycardia: < 60 Review…
o Pacemaker impulses are initiated in the SA node.
Travelling through atrial pathways at a frequency
between 60-100 bpm
cycle length do not vary by 10%
o if cycle varies by >10%: sinus arrythmia
Regular Rhythm
Rate (75 using sequence method)
P wave upright
Followed by QRS (which is narrow or normal)
*Wide QRS= 0.12 seconds or more [3 small squares or
more]
P-R interval normal (0.60)
Therefore Normal sinus rhythm
ACLS Rhythms [Advanced Cardiac Life Support]
Arrhythmias are now being taught in the ACLS class because

st
arrhythmia is a common cause of death in the 1 48 hours
after a heart attack.

Dr. Payawal
Id an arryhtmia is recognized early, you can resuscitate the
patient. Knowing how to recognize an arryhtmia will improve SLOW ARRYTHMIA
MI patient survival
So even non-doctors can learn cardiac arrythmia [nurses,
paramedics, med tech, therapists..]
TYPES OF RHYTHM
THE ACLS ARRHYTHMIA

SLOW RHYTHMS (HR: <60)
o Sinus Bradycardia
o Sinus Pause
o Escape Rhythms:
Junctional rhythm
Idioventricular rhythm
- when sinus node fails to fire (no depolarization), Px does
not go to cardiac arrest immediately because heart
has back-up pacemakers and it will be the one
initiating
AV node: junctional rhythm
ventricle: idioventricular rhythm
o Heart Blocks
FAST RHYTHMS (HR: >100)
o Sinus tachycardia
o Suprventricular tachycardia [SVP]
-above ventricle
o Atrial fibrillation
o Atrila flutter
o Multifocal atrial tachycardia
o Ventricular tachycardia
ARREST RHYTHMS
o Asystole
-(flat line) WILL be in the exam!
o Ventricular Fibrillation
o Pulseless VT (ventricular tachycardia)
o Pulseless Electrical Activity (PEA)
-Px has electrical activity but has no pulse
-easiest to recognize
-causes sudden cardiac death
BENIGN RHYTHMS
o PREMATURE ATRIAL COMPLEX (PAC)
o PREMATURE VENTRICULAR COMPLEX (PVC)
MISCELLANEOUS
o Artificial pacemaker rhythm
-pacemaker in patients esp. those with heart blocks
o Preexcitation/wpw pattern (wolff parkinson white syndrome)
-rare; congenital
-there is an accesory pathway excitation
*do not mind, di lalabas sa exam :D
1. SEPARATE RHYTHMS, either:

FAST (HR > 100)
SLOW (HR <60)

Dr. Payawal
SINUS BRADYCARDIA SINUS PAUSE/ARREST
Sinus bradycardia follows all criteria for normal sinus rhythm Cause: if SA node does not fire
except for the rate There is a pause
Always ask for drug history (drugs that slow down HR) No P wave (as opposed to AV Block)
nd
o Beta blockers *2 degree AV block has P wave but no QRS
o Anti-arrythmic drugs No QRST
Always ask if he’s athletic, especially in young patients
*athletes also have bigger hearts (LVH) but not sick
ECG paper: lead I

Rate = 48/min
65 y.o man with same ECG (as athletic’s)
Frequent
- Near-syncopal attack (nagdilim paningin) <1 sec
Irregular because there is a pause
- Sedentary lifestyle (not athlete)
Normal then pause then again normal beat
- No drugs that slows down HR
Sinus bradycardia due to sinus node dysfunction No P wave, no Q wave
-consider a pacemaker implantation What is the interval between the previous peak and the next
peak following the pause?
Interval is less than twice the normal interval between
beats
-this interval where the pause is, is shorter than the
2 normal beats
-the one with the pause is twice shorter than the 2
normal interval
AV BLOCKS
FIRST DEGREE AV BLOCK
Measure from start of P wave up to start of QRS

Sinus Bradycardia PR> 0.20 sec –> only criteria
If P-R interval is prolonged (more than 5 small squares or 1 big
square): FIRST DEGREE AV BLOCK
Correlate clinically
Can be caused by drugs (digitalis)
Case: SA node does not fire. No P, no QRS

Interval less than 2x the normal
I2 cycles is always longer than the cycle with a pause

Dr. Payawal
SECOND DEGREE AV BLOCK
P-R interval= 8 small squares x 0.04

= 0.32 (which is longer than 0.20 sec)
HAS TWO TYPES:

-need to distinguish because have different prognosis
-Different from each other
o PR interval not the same
o Has P wave with no QRS
o Cycle repeats itself: shorter PR interval.. longer PR.. then
non-conductive P wave.. repeat..
Second Degree
Atrioventricular Block
n Type I - Mobitz type I or Wenckebach
Transcient/temporary
No aggressive measures needed
n Type II - Mobitz type II
Usually goes into complete heart
block/asystole/arrest
Prepare Px for pacemaker already
Type I Type II
Temporary Goes into complete heart
block
From 1 cycle to next until the PR interval is constant and
drop beat then drop beat
Prepare for pacemaker
implants
Normal sinus rhythm with first degree AV block

Dr. Payawal
2° Type II
non-conductive P-wave (drooped beat): has P wave but no QRS
MOBITZ TYPE I
Prolongation in PR interval
Non-conductive P wave (dropped beat)
MOBITZ TYPE II
No prolongation of PR interval; constant
Just have dropped beat
THIRD DEGREE/COMPLETE AV BLOCK
More advanced block

Atrium is controlled by sinus node
Ventricle do not get depolarized from the sinus node
anymore
Ventricle has its own pacemaker
o AV node
o Bundle of His
o Bundle branches
o Ventricle itself
-So you will have different rates already
AV node pacemaker:
QRS will not be wide
rate= 40-60 bpm
pacemaker from ventricle itself:
QRS is wade (0.12 sec or more)
rate <40bpm
Ventricular rate usually slower
-depend on where is the pacemaker of ventricle
-back-up pacemakers of heart are not as efficient (slower
compared to sinus node)
More P wave than QRS

-Because in complete heart block, the atrial rate is usually
faster than the ventricular arte
P wave do not cause QRS anymore
Measure P-P interval: it is constant

Sometimes P wave is buried in T wave, in QRS, depending on
atrial beat
P-P = atrial rate constant

R-R = ventricular rate constant
BUT atrial and ventricular rate is not the same

Dr. Payawal
In AV block, complete heart block. Normal atrial rate is
faster/greater than ventricular rate
Clinically: if complete heart block, but rate is coming from AV
node, it will respond to mediastinum
If from ventricle, pacemaker is needed, does not respond to
mediastinum
Symptom: hypotension, Syncope – magdidilim paningin
If QRS is narrow: may respond to drugs (Dopamine, etc.)
If rate <40 and QRS is wide: will not respond to drugs; need
pacemaker already
Ventricle-independent from poor SA node

AV node: QRS not wide
Ventriclr itself – Wide QRS, rate <40
Atrio-ventricular Dssociation
P-P and R-R intervals are constant
Arrows are pointing to P waves

o Buried in QRS, T wave, etc.
o If you measre P-P interval, it is constant
o Does not cause QRS
o HR: <40 (pacemaker is in the ventricle)

Dr. Payawal
FAST ARRYTHMIAS
SINUS TACHYCARDIA
Has same criteria as Sinus rhythm except that rate is >100bpm

Not necessarily mean there’s a problem in the heart
*you have sinus tachycardia during exams
Always correlate clinically
-know what patient is tachypneic about
-Consider conditions that will increase heart rate like stress,
fatigue, emotional disturbance, fever
Lead I rate = 111/min

Dr. Payawal
BENIGN ECTOPIC RHYTHMS PREMATURE VENTRICULAR COMPLEX (PVC)
PREMATURE ATRIAL COMPLEX (PAC)
Ectopic focus comes from ventricles

Ectopic focus outside that of the sinus node comes from QRS complex is wide because the ventricle is a wider chamber
atrium -markedly different
-If in Lead II = ectopic focus on right atrium that fired - >0.12 sec or more
When you see premature beat (beat occuring earlier than it No P wave usually because it came from the ventricles
should be), usually in V2? You scrutinize it: With compensatory pause
o Does it have a wide or narrow QRS? -either a pause after PVC
*here it is narrow: 2 small squares (0.08 sec) -compensate for two normal beats
o Look if there is a P wave before the QRS of that *if you measure interval from beat before and after PVC, it’s
premature beat the same as 2 normal beats
*here, there is a P wave T wave is opposite from QRS complex
o Does the P wave differ from the sinus beat? -If ORS is predominantly upright, T wave is negative
*here, it looks different -If QRS predominantly negative, T wave will be upright
Criteria for PAC: -opposite polarity
o P-R interval is often long [>0.12 sec] instead of 0.10 sec Many physicians are scared to see PVCs
- Long here is diff. from that of first degree AV block
-distinguish PAC from PJC (premature junctional CRITERIA
complex?) o Markedly different (wider than usual beat)
-ectopic focus comes from AV node o No P wave
o P wave different in configuration but predominantly o T wave opposite polarity of QRS complex
upright o There is a pause
o Narrow QRS
P waves are different but upright

PR interval is > 0.12 sec (0.16 or 4 small squares)
QRS narrow
meets criteria for PAC

Dr. Payawal
Others: (hindi nabanggit ang classification sa lecture)

Dra. Deduyo CARDIOLOGY 9TH October 2018
UPDATES ON THE MANAGEMENT OF practice to designate patients with persistent chest discomfort or
other symptoms suggestive of ischaemia and ST-segment
PATIENTS WITH STEMI and NSTEMI elevation in at least two contiguous leads as STEMI. In contrast,
patients without ST-segment elevation at presentation are usually
designated as having a non-ST-segment elevation myocardial
infarction (MI) (NSTEMI) and separate guidelines have recently
been developed for these. Some patients with MI develop Q-
waves (Q-waveMI), but many do not (non-Q-wave MI).
Worldwide, Ischemic Heart Disease is the single most

common cause of death, and its frequency is increasing, however,
in Europe, there is an overall trend in reduction of Ischemic Heart
Disease mortality over the past decade. Why? They are able to do
reperfusion therapy immediately, and of course, the government
is responsible for that. The relative incidence of STEMI against
NSTEMI are decreasing and increasing. There is a consistent
pattern for STEMI to be relatively more common in the younger
than in the older people, and more common in men than in
women. And that is true even here in our country, it is true that
So, these are updates on the management of patients presenting with
STEMI, and this is based on the different clinical trials that had been we have more young patients having STEMI, and even Stroke than
made. So the class I evidence, that evidence and/or general agreement older individuals and several recent studies have highlighted a fall
that a given treatment or procedure is beneficial, useful, effective. So in in the acute and long term mortality following STEMI in parallel to
class I, it is proven recommended, and beneficial. Looking at a research, the greater use, we are emphasizing on Reperfusion Therapy like
you are looking at a class I evidence. Class II, conflicting evidence and/or PTCA, modern anti-thrombotic therapy, as well as secondary
a divergence of opinion about the usefulness, efficacy of the given prevention.
treatment/procedure. So class II evidence is maybe good, but class I is
There are two kinds of Reperfusion. One is Angioplasty,
the best.
and the other is Coronary Artery Bypass Graft Surgery. Still,
mortality remains substantial. The in-hospital mortality of
unselected patients with STEMI in the National Registries in
European Countries varies within 4 and 12%, while reported 1-
year mortality in Angiography Registry is approximately 10%,
although Ischemic Heart Disease develops, on average 7-13 years
later in women, compared with men.
Acute Coronary Syndrome gives importance in men than
in women who are below 60 years, but after the age of 75, women
represent the majority of patients, and tend to present with atypical
symptoms up to 30% in some registries and tend to present
And of course, Level of Evidence A are data derived from various clinical greater than men, it is therefore important to maintain a high
trials and meta-analyses. degree of awareness for Myocardial infarction in women, with
Looking back at the definition of Acute Myocardial Infarction, it potential symptoms of Ischemic Heart Disease.
should be used when there is evidence of Myocardial injury, so that if there The manifestation is more of a chest discomfort. Be aware that is
is myocardial injury, it means that there is elevation of the cardiac troponin
should be more a heaviness, not a pain, because there is no
values, Troponin I or Troponin T, with at least 1 value about the 99th
percentile upper reference limit with necrosis in the clinical setting,
inflammation in the musculoskeletal system. The majority of
consistent with Myocardial Ischemia. For the sake of immediate treatment, patients would come to us that there is a chest pain. If it is a chest
strategies such as reperfusion therapy, it is a useful practice to designate pain, try to evaluate. Is it a pain or a heaviness? If it is a heaviness,
patients with persistent chest discomfort, or other symptoms suggestive I’d always ask them, for how long did it occur? If they tell you it
of ischemia and ST segment elevation of at least 2 contiguous leads as has been three days, if it is MI, they would be dead by that time.
STEMI. I have given you samples of ECG, where you have various findings So we are very sure that it is not MI, because you know, if it is a
of ST segment, and I have emphasized on you that when you are looking STEMI or NSTEMI, it is highly progressive. Chest discomfort, cold
at an ECG tracing, you are to look at the ST segment. Whenever you have
sweating, and pallor. Immediate Electrocardiogram should be
an ST elevation, of > 2mm, (you talk about voltage) or even greater, and
there is still no evidence of a Q wave, then that patient is a candidate
done.
for thrombolysis or thrombolytic therapy. However, when we have a
patient who comes in with ST elevation, but there is a peaked Q wave, it
means that the patient already has fibrosis. This patient is no longer a
candidate or thrombolytic therapy. So reperfusion therapy will be
recommended.
The term acute myocardial infarction (AMI) should be used when

there is evidence of myocardial injury (defined as an elevation of
cardiac troponin values with at least one value above the 99th
percentile upper reference limit) with necrosis in a clinical setting
consistent with myocardial ischaemia. For the sake of immediate
treatment strategies such as reperfusion therapy, it is usual
1ST Semester Section A OLFU MD 2020

But the question here now is, is
it Permanent? You have heard
about patients who have
undergone 2 rounds of
angioplasty, or a bypass and
had angioplasty. There are five
arteries, the most common, the
Left Anterior Descending
Coronary Artery, it is a must
that this patient should be told,
and advised that drugs should
be continued. Of course,
patients who have undergone
revascularization think they are
permanently cured. There is no
permanent cure for a patient
with Atherosclerosis. We know
in pathology that it is
permanent. The basic
pathology in patients with
Coronary Artery Disease is the
atherosclerotic plug. Patients
should undergo continuous
treatment. If they are
Hypertensive, give anti-
hypertensives; if they are
diabetic, give anti-DM drugs, it
could be Insulin or other oral
medications. A permanent anti-
Platelet therapy should also be
in place. During the first year of
revascularization, Triple Anti-
Platelet are given: Aspirin,
Clopidogrel, and Ticagrelor, not
Bivaluridin, but Ticagrelor.
Usually, Ticagrelor is given for 3
months, but the Aspirin, and
Anti-Platelet are given for a
prolonged period of time. But
What is New in the 2017 Guidelines for STEMI? they should be warned of side
First I would just like to tell you that before, we used the effect of aspirin, especially, Upper Gastrointestinal Bleeding
Femoral approach, now we use the Radial approach. If it is caused by mucosal irritation. They should be warned about this.
Angioplasty, means that we will insert a catheter, and through that Many patients are being admitted for severe anemia, only to find
catheter, what is inserted? It is a stent, and the stent used now is out that they had been taking aspirin for a long period of time.
a Drug-Eluting Stent, before it was a bare metal stent. It was found Check for blood in the stool. If it is black (melena) that could be
out that with the bare metal stent, it imbibes thrombus formation. indicative of an Upper GI Bleed. The recommended PPi,
With a drug-eluting stent, it does not. It maintains the patency of pantoprazole. Until maybe a later study would prove that there
the stent after angioplasty. Using this, there is complete could be other drugs that could be given for the GI bleed from the
revascularization. They can also do thrombus aspiration, or antiplatelet therapy. And, of course, what is given for a long period
sometimes, if there is a hardened thrombus, they would use a drill, of time to stabilize the clot? It is Statin Therapy. It could be either
like a typical electric drill to dissolve that very hard blood clot that Itorvastatin or Rosuvastatin.
is found in the artery, we call it a rotablator. The purpose of which
is to dissolve the thrombus. After that, we give Bivaluridin and The treatment for Unstable Angina, Non ST Elevation MI, and ST
Enoxaparin, and they would recommend early hospital Elevation MI are all the same. Are they all candidates for
discharge. In the U.S., if they have done it in the morning, the next Revascularization therapy, the answer is YES. So, if you would
day the patient will be discharged. This is for angioplasty, not ask, ‘Are All patients undergoing Revascularization?” the answer
bypass. I hope that you do understand the difference between is, sadly a No. PhilHealth cannot sustain the expenses for
angioplasty and a bypass done on the heart. In a bypass, you have Revascularization. Maybe for Angiogram, yes, but for angioplasty,
a scar. The thorax is opened, and the bypass is done. It is more the amount to be paid will be dependent on the stent, and the
expensive and, of course, there is a higher risk of post-operative stent is considered a treatment. Up to now, PhilHealth does not
infection and complications, a more serious outcome on a patient cover treatment but it covers hospitalization and the diagnostics,
having a bypass surgery. But true enough, when patients of STEMI but not all. Maybe in the future there may be changes in the
or NSTEMI that have undergone revascularization would live long. Universal Health Insurance Program.

injured, that muscle would not contract effectively. Bomba ang problema.
CONGESTIVE HEART FAILURE There is a problem on Ejection itself. Where is the blood retained? It is
Definition of Heart Failure inside the ventricular cavity. And there is a continuous filling of blood
• All the guidelines define Heart Failure as a clinical syndrome because of the cardiac cycle. So in early diastole, there is a small
which patients have typical symptoms and signs resulting from amount blood still in the heart, which causes resistance to early
an abnormality of cardiac structure or function, which impairs ventricular filling. Doon kayo mag-simula sa decrease in cardiac output.
the ability of the ventricle to fill with, or eject blood. Bakit bumaba ang cardiac output? Because there is systolic failure. Why?
so there are two functions of the ventricle, one in diastole, wherein the The muscle is injured, then the muscle could not contract effectively. But
the ventricle fills with blood and in systole, wherein the blood is the cardiac cycle continues so your left ventricular cavity will fail, with a
ejected. So that we have two kinds of failure, diastolic failure (failure to fill more amount of blood retained. So in the early ventricular filling, you should
expect an S3 gallop. What part of your stethoscope will you use, it is your
up), and systolic failure. Sometimes, they occur at the same time, but I
have seen patients wherein the diastolic failure and then goes into systolic bell, because it is a low-pitched heart sound.
failure. Is a murmur always present? The answer is No. But there could be an
acute onset of mitral regurgitation, why? Because the ventricular
• Symptoms: (e.g. breathlessness, orthopnea, paroxysmal
muscle is dilated, and when it dilates, the anterior and posterior leaflets of
nocturnal dyspnea, ankle swelling, fatigue, and reduced the Mitral valve would fail to coarctate or close tightly.
exercise tolerance) Of course, you have the right side of the
You would ask, which of them is symptomatic? Both of them are Normal CO: 5-7 L
heart, the pulmonary artery and the in Heart Failure: ~3 L
symptomatic. In diastolic failure, if there is decreased LV filling, what pulmonary veins, so what is happening, Normal Stroke Volume:
will be the consequence? What will be the effect on cardiac output, if the probably a problem in the muscles. So 70-80 mmHg
LV filling is decreased? it will decrease. The stroke volume will also be in heart failure: ~40
cardiac output is decreased, as well as stroke mmHg
decreased. So the symptoms of breathlessness, orthopnea, paroxysmal volume. Because there is a problem, (check EF: >55%
nocturnal dyspnea, ankle swelling or edema, fatigability, and reduced box) so, as blood is retained, lalong lumalaki
exercise tolerance are the major symptoms that you would look for in a yan eh narito ang posterior and anterior leaflet
patient in heart failure. If your CAD patient is complaining of chest mo, anong mangyayari, itutulak niya, it will not coarctate. Ito yung anterior
discomfort, this patient who is in failure complained of breathless, and posterior, lumaki, hindi magco-coarctate. So you’ll have mitral
orthopnea, and PND. Orthopnea, and PND are the initial symptoms regurgitation. Most often, you’ll hear a systolic murmur, and that is
preceding full blown heart failure by 2-3 years. But before that, the holosystolic, pansystolic. Remember, systolic murmurs are holosystolic
patient will complain of easy fatigability, and then the ankle swelling and and ejection murmur. Go back to your Barbara Bates!
reduced exercise tolerance manifests. How will you understand the patient you see if it so happens that you
• Signs: (e.g. elevated jugular venous pressure, hepatojugular found the patient with heart failure? So I’m just trying to emphasize. No.1
reflux, third heart sound [gallop rhythm], cardiac murmur, and to look for in auscultation is the S3 gallop. Di ko pa tinatanong sa inyo,
displaced apex beat) what will happen to the 1st and 2nd heart sounds. If you have pulmonary
In having a patient with edema, what would be the next thing that you hypertension because of pulmonary congestion, what will be the effect
would look for in the evaluation of patient, ano ang titingnan nyo? Tingnan on the S2, soft or loud? LOUD. Upon auscultation, you’ll hear lub-DUB,
nyo agad ang neck. Look at the neck of the patient and you will see the and if there is an S3, lub-DUB-dub.
distention of the jugular pain, especially if that distention occurs while • Acute HF is recognized as a separate entity by the guidelines.
the patient is sitting. Naka-upo lang siya, bakit naman galit nag alit ang AHF is defined as the rapid onset of (de novo), or change in,
kanyang jugulars, and you have ankle swelling. In a patient who comes to signs and symptoms of HF (decompensated HF) requiring
you complaining with PND and orthopnea. With that, you should also do urgent evaluation and treatment, typically leading to urgent
hepatojugular reflux? Ask your patient to lie down, maybe 45° and then hospital admission.
press on the liver area. By that you squeeze blood coming from the liver
The current definition of HF restricts itself to stages at which
going into the IVC, towards the Right side of the Heart wherein there is
clinical symptoms are apparent. Before clinical symptoms become
increased pressure in the Right Atrium and ventricle, so that pressure is
apparent, patients can present with asymptomatic structural or functional
transmitted to the region of the neck, with pressure from the liver, you
cardiac abnormalities [systolic or diastolic left ventricular (LV) dysfunction],
expect dilatation of the jugulars, and that is hepatojugular reflux.
which are precursors of HF. Recognition of these precursors is important
On examination of the apex beat, what would you expect on
because they are related to poor outcomes, and starting treatment at the
palpation? Of course the patient with failure, remember Starling’s Law,
precursor stage may reduce mortality in patients with asymptomatic
when the cardiac output goes down, there would be stretching of the
systolic LV dysfunction.
myocardial fibers, in physiology, so you’ll expect your heart to be
Demonstration of an underlying cardiac cause is central to the
enlarged, and your apical beat is displaced sideward. Not downward.
diagnosis of HF. This is usually a myocardial abnormality causing systolic
There will be displacement downward if you have a valvular disease, like
and/or diastolic ventricular dysfunction. However, abnormalities of the
aortic regurgitation. Because of volume overloading, and you will be valves, pericardium, endocardium, heart rhythm and conduction can also
confused. In volume overloading, the cardiac output is high because of the
cause HF (and more than one abnormality is often present). Identification
increase in the amount of blood inside the left ventricle, but the usual
of the underlying cardiac problem is crucial for therapeutic reasons, as the
cause, the most common cause of Heart failure is Hypertension and precise pathology determines the specific treatment used (e.g. valve repair
Coronary Artery Disease. Having a patient with failure, you would like to
or replacement for valvular disease, specific pharmacological therapy for
know, if your patient has Hypertension, or CAD, then mind you, patients
HF with reduced EF, reduction of heart rate in tachycardiomyopathy, etc).
who come in with Acute Coronary Syndrome could also manifest heart
failure at the same time. Displacement of the apical beat to the side,
maybe at the anterior axillary, the worst thing that could happen is that
the displacement would be at the mid-axillary in patients with dilated
ischemic cardiomyopathy.
On auscultation, what do you look for? Do you look for a murmur? You
look for an S3 Gallop. What is the cause of S3 gallop? It is the resistance
to early ventricular filling. In heart failure, why is there resistance to early
ventricular filling? The hemodynamic abnormality in Heart failure is a
reduction in the cardiac output and stroke volume, so what is
happening in the left ventricle? The blood is retained inside the ventricle
because the muscle could not eject blood. There is a little amount of blood
that gets out. How would cardiac output be affected? When the muscle is

Chronic HF has a devastating impact on Long-Term Heart Failure with Reduced Ejection Fraction
Prognosis HFrEF (Systolic HF)
• Male sex
Etiology/Risk
• Myocardial infarction (STEMI > NSTEMI)
Myocardial cell death
Factors
•
• Smoking
• Aging
• Obesity
• Elevated NT-proBNP
• Myocardial injury leads to pathologic remodeling of
physiology
All patients with HF, regardless of their symptoms, have a poor the LV, with dilataton and impaired contractility
Patho-
prognosis. Within 3 years, 34% of NYHA class I and class II • Further cardiac events, in combination with
patients, and 42% of NYHA class III and IV patients die. systemic responses to reduced systolic function,
lead to progressive worsening of the disease.
< 40%
EF
Class III are those with very mild activity, and Class IV are those bound to
bed, and still they are very symptomatic.
Hospitalization for Acute HF is associated with Significant

Mortality
Heart failure with REDUCED Ejection Fraction is our SYSTOLIC Heart

Failure. so this is a normal heart (middle), and this is the heart on systolic
heart failure (left) you can see that the left ventricular segment is thinned
out and the caliber is increased.
Heart Failure with Preserved Ejection Fraction

HFrEF (Diastolic HF)
• Female sex
Etiology/Risk
• Atrial Fibrilation
Renal Dysfunction
Factors
Heart Failure Classification •

(According to Left Ventricular Ejection Fraction) • Urinary Albumin Loss
• Aging
HFrEF • Obesity
• Elevated NT-proBNP
Heart Failure with Reduced Ejection Fraction
(LVEF < 40%)
physiology
• Characterized by diastolic LV dysfunction – slow LV

Patho-
HFmrEF relaxation and filling, and increased diastolic LV

stiffness
Heart Failure with Mid-Range Ejection Fraction
(LVEF 40-49%)
> 50%
EF
HFpEF Heart failure with Preserved Ejection Fraction is our Diastolic Failure. You
Heart Failure with Preserved Ejection Fraction would see in diastolic failure, the ventricular caliber is small, and there is
(LVEF ≥ 50%) thickening of the Left ventricular segment. So there is stiffening of the
muscle, and it cannot relax properly, so it can only accommodate a small
So what is the usual normal ejection fraction? It is usually at 55%, you amount of blood in diastole.
could also have it at 60%, 65%, 70%, the higher it is, the better. Comparing HFrEF, HFmrEF, HFpEF on the symptoms and signs, HFmrEF
may be positive or negative, HFpEF may be positive or negative, but they
are differentiated by the ejection fraction. The reduced EF (<40), there
could be elevated NT-proBNP. The criteria plus at least one criterion. There
should be a relevant cardiac structural defect, either LVH or LA
enlargement, and the diastolic function is also impaired. In HFpEF, relevant
structural impairment is the same with HFmrEF, but the diastolic function
is very prominent. (see table on next page)

is hypertension, we control the hypertension. In refractory heart failure,

they are symptomatic even at rest. Class IV NYHA.
Heart Failure Definition: ESC Guidelines
The main terminology used to describe HF is historical and is based Symptoms and Signs
on measurement of the LVEF. HF comprises a wide range of patients, from
those with normal LVEF [typically considered as ≥50%; HF with preserved EF The symptoms and signs of HF are fairly non-specific, making
(HFpEF)] to those with reduced LVEF [typically considered as ,40%; HF with diagnosis difficult. Once diagnosis has been confirmed, symptoms
reduced EF (HFrEF)]. Patients with an LVEFin the range of 40–49% represent a may be used to classify the severity of HF and to monitor response
‘grey area’, which we now define as HFmrEF. Differentiation of patients with HF to treatment.
based on LVEF is important due to different underlying aetiologies,
SYMPTOMS
demographics, co-morbidities and response to therapies.6 Most clinical trials
published after 1990 selected patients based on LVEF [usually measured using Typical Less Typical
echocardiography, a radionuclide technique or cardiac magnetic resonance • breathlessness • nocturnal cough
(CMR)], and it is only in patients with HFrEF that therapies have been shown to • orthopnea • wheezing
reduce both morbidity and mortality
• paroxysmal nocturnal • bloated feeling
.
The diagnosis of HFpEF is more challenging than the diagnosis
dyspnea • loss of appetite
of HFrEF. Patients with HFpEF generally do not have a dilated LV, but • reduced exercise tolerance • confusion (especially with
instead often have an increase in LV wall thickness and/or increased left • fatigue, tiredness, increased elderly)
atrial (LA) size as a sign of increased filling pressures. Most have additional time to recover after exercise • epression
‘evidence’ of impaired LV filling or suction capacity, also classified as • ankle swelling • syncope
diastolic dysfunction, which is generally accepted as the likely cause of HF • benopnea
in these patients (hence the term ‘diastolic HF’). However, most patients
* for weight gain, consider edema.
with HFrEF (previously referred to as ‘systolic HF’) also have diastolic
* remember the difference of crackles between heart failure and
dysfunction, and subtle abnormalities of systolic function have been shown
pneumonia. In heart failure, the crackles are coarse moist and bilateral. if it
in patients with HFpEF. Hence the preference for stating preserved or
is pneumonia, crepitant crackles, unilateral, at the side where there is
reduced LVEF over preserved or reduced ‘systolic function’.
pneumonia.
SIGNS
Heart Failure Classification More Specific Less Specific
(Based on Clinical Progression)
• Elevated jugular • Weight gain • Tachycardia
• ACCF-AHA 2013 Guidelines classify patients with HF based on
venous pressure (>2kg/wk) • Irregular pulse
the development and progression of HF
• Hepatojugular • Weight loss (in • Tachypnea
• These stages provide complementary information to the NYHA
reflux advanced CHF) • Cheyne-stokes
Classification regarding the severity of HF
• Third heart sound • Cardiac murmur respiration
Stages Development and Corresponding (gallop rhythm) • Peripheral edema • Hepatomegaly
of HF Progression of HF NYHA Class • Laterally- • Pulmonary • Ascites
At risk for HF, but without displaced apical crepitations • Cold extremities
A structural heart disease or None impulse • Reduced air entry • Oliguria
symptoms of HF and dullness at • Narrow pulse
Structural disease but without percussion in all pressure
DfB I
signs symptoms of HF lung bases
Structural heart disease with I
C prior or current symptoms of II
HF III
Refractory HF requiring
D IV
specialized interventions
Stage A: only at high risk of Heart Failure, maybe they had an Acute
Coronary Syndrome, or they have chronically uncontrolled Hypertension.
But still without structural heart disease or symptoms of HF, so they are
not classified by the NYHA.
Stage B: there is already a structural Heart Disease: LVH, LA enlargement.
But still they don’t have signs and symptoms of HF, Class I, no symptoms,
but hey have cardiac hypertrophy already. Probably these are the people
with uncontrolled hypertension.
Stage C: there is structural heart disease and are symptomatic. They may
have orthopnea, easy fatigability, palpitations, etc, so class II.
Stage D: what is refractory? Always in heart failure.
In patients with heart failure, we try to identify the etiology. If the etiology is
CAD, these are the people whom we advise revascularization. If the cause



Are we suspecting that the patient has chronic heart failure? Assess the • Useful for suspected HF in the acute setting and for
patient if he has clinical history of CAD, arterial hypertension, exposure to
identifying an alternative, pulmonary explanation for a
cardiotoxic drugs, especially shabu (illicit drugs), or radiation among
patients who have cancer, or even the drugs used in chemotherapy. The patient’s symptoms and signs
use of diuretics, orthopnea and PND. On PE, look for crackles bilateral BNP/NT-proBNP – Should be Considered
ankle edema, presence of a murmur if there is, and most of all, look at the • Where available, BNP/NT-proBNP levels have been
neck if there is jugular venous distention in an upright position, or 45°, 60°,
shown to be a useful initial diagnostic marker of HF
90°, and a laterally displaced apical beat. An Echocardiogram, if it is CAD,
it would be abnormal, and if there is left ventricular hypertrophy by voltage, • Patients with normal plasma BNP/NT-proBNP
you will be able to see it. We then try to assess the natriuretic peptide. If concentrations are unlikely to have HF.
we suspect our patient to be in HF, we request for an NT-proBNP. If it is
≥125 pg/mL or ≥BNP of 35 pg/mL, so the greater the value, (we have DRUG CLASSES
seen 2000 pg/mL, 3000pg/mL, 5000 pg/mL,) the more serious the Drug Class Drugs
condition, and the more serious the injury there is on the muscle, together Captopril, enalapril, Lisinopril, Ramipril, tandolapril,
if troponin is positive. So patient should be undergoing Echocardiography, ACEi
fosinoprill, quinapril, perindopril
just like our CAD patient so that we can be able to evaluate the cardiac Beta Bisoprolol, carvedilol, carvedilol CR, metoprolol
output, the stroke volume, and the ejection fraction. If the Natriuretic succinate (CR/XL), nevibolol
Blockers
Peptide is negative, but with positive history, consider other diagnoses.
ARBs Candesartan, valsartan, losartan
The natriuretic peptide confirms the diagnosis of heart failure. It also ells of
ARNI Sacubitril/Valsartan
the severity of the heart failure.
MRAs Eprlerenone, spironolactone
• Loop diuretics: Forsemide, bumetanide, torsemide
DIAGNOSIS • Thiazides: Bendroflumethiazide, hydrochlorthiazide,
• Clinical suspicion of HF may be based on symptoms, metazolone, indapamide, chlorthiazide,
Diuretics
signs, and the results of investigations – attention should chlorthalidone
be paid to potential risk factors, such as previous MI, • Potassium-sparing diuretics:
spironolactone/eplerenone, amiloride, triamterene
hypertension or AF.
H-ISDN, digoxin, ivabranide, anticoagulants (warfarin,
• Definitive diagnosis is made using echocardiography, Other drugs dabigatran, apixaban, or rivaroxaban), omega-3 fatty
which provides objective evidence of a structural or acids.
functional cardiac anomaly that is thought to account for If the patient is coughing, we don’t give ACEi. The new drug is
Sacubitril/Valsartan, and we call it Enprestol. This is a wonder drug, the
the patient’s symptoms and signs.
latest in the treatment of patients with HF, and with ischemic
On Echo, we can see the enlargement. The ECG will not tell us if the heart
cardiomyopathy. Intake of this drug for about a month will make the patient
is enlarged, because if there is diminished contractility, it does at low
feel better. In patients with PND, orthopnea, with crackles all over, what
voltage. It doesn’t say if the heart is large with ECG. It is good in showing
can make them comfortable are the Diuretics. MRAs in the long run. Beta
ST-segment abnormalities.
Blockers can only be included in the DRY STATE of HF. There should be
no pulmonary congestion. But if we are using already ARNI, there is no
Echocardiography BNP need for beta blockers.
HFrEF Treatment Algorithm
12-lead ECG Chest X-ray
• The following diagnostic tests are recommended for the
initial assessment of a patient with newly-diagnosed HF:
o Hemoglobin and WBC
o Sodium, Potassium, Urea, Creatinine (with eGFR)
o Liver function tests (bilirubin, AST, ALT, GGPT)
o Glucose, HbA1c
o Lipid profile
o TSH
o Ferritin, TSAT = TIBC
ECG – Recommended
• ECG is highly sensitive (81-89%) for HF
• HF is unlikely in patients presenting with a completely
normal ECG. Therefore, routine use of ECG is
recommended to rule out HF (if the cause is CAD)
• ECG may guide decisions about treatment and provide
clues as to etiology
Chest X ray – Should be Considered
• CXR is of limited use in the diagnostic work-up of patients
suspected with HF
• Features of HF may be identified on CXR, including
pulmonary venous congestion or cardiomegaly
note: use of all three of an ACEi, MRA, and ARB is not recommended

Primary care physicians should refer to cardiology at any point where they ACCA-AHA 2013 HF Guidelines
do not feel comfortable managing the patient’s condition.
Therapeutic algorithm for a patient with symptomatic heart failure with reduced
ejection fraction. Green indicates a class I recommendation; yellow indicates a
class IIa recommendation.
• Symptomatic NYHA Class II-IV.
• HFrEF. LVEF,40%.
• If ACE inhibitor not tolerated/contra-indicated, use ARB.
• If MR antagonist not tolerated/contra-indicated, use ARB.
• With a hospital admission for HF within the last 6 months or with elevated
natriuretic peptides (BNP. 250 pg/ml or NTproBNP. 500 pg/ml in men and
750 pg/ml in women).
• With an elevated plasma natriuretic peptide level (BNP ≥ 150 pg/mL or
plasma NT-proBNP ≥ 600 pg/mL, or if HF hospitalization within recent 12
months plasma BNP ≥ 100 pg/mL or plasma NT-proBNP ≥ 400 pg/mL). In
doses equivalent to enalapril 10 mg b.i.d.
• With a hospital admission for HF within the previous year.
patients with asymptomatic ischemic cardiomyopathy who are at least 40 days post-MI
• CRT is recommended if QRS ≥ 130 msec and LBBB (in sinus rhythm). CRT have an LVEF of 30% or less, are on appropriate medical therapy, and have feasible
should/may be considered if QRS ≥ 130 msec with non-LBBB (in a sinus expectation of survival with a good functional status for more than 1 year
rhythm) or for patients in AF provided a strategy to ensure bi-ventricular
capture in place (individualized decision).
ACCF/AHA//HFSA Focused Update 2017
HFrEF

Initiating Diuretic Therapy Initiating Beta-Blocker Therapy
Recommended in all patients with symptoms and signs of Recommended, in addition to an ACEi (or ARB if ACEi not
congestion, irrespective of EF tolerated/contraindicated, for patients with stable,
Check Renal function and Electrolytes symptomatic HFrEF (NHYA Class II-IV)
Start with low dose in a stable condition and double the dose at not
less than 2-week intervals
Start with low dose and adjust according to symptoms and signs of
congestion, BP, and renal function. Use the minimum dose necessary
to maintain euvolemia (dose may need to be increased or decreased Aim for the target dose if possible, otherwise ain for the highest
according to patient’s volume status) tolerated dose
Re-check blood chemistry 1 – 2 weeks after initiation and after any Monitor heart rate, blood pressure, and clinical status (symptoms,
dose increase (urea/BUN, creatinine, K
+ signs – especially signs of congestion, body weight)
Diuretics: Dosing Beta blockers Starting dose (mg) Target dose (mg)
Loop Diuretics Initial dose (mg) Usual daily dose (mg) Bisoprolol 1.25 OD 10 OD
Furosemide 20 – 40 40 – 240 Carvedilol 3.125 BID 50 BID
Bumetanide 0.5 – 1.0 1–5 Carvedilol CR 10 OD 80 OD
Torasemide 5 – 10 10 – 20 Metoprolol 12.5 – 25 QD 200 QD
Thiazides Initial dose (mg) Usual daily dose (mg)
Bendroflumethiazide 2.5 2.5 – 10 Initiating MRA Therapy
Hydrochlorothiazide 25 12.5 – 100 Recommended for patients with HFrEF, who remain
symptomatic (NYHA class II-IV) despite treatment with an ACEi
Metolazone 2.5 2.5 – 10
(or an ARB if an ACEi is not tolerated/is contraindicated) and a
Indapamide 2.5 2.5 – 5
beta-blocker
Potassium- Initial dose (mg) Usual daily dose (mg) +
Check renal function and electrolytes (particularly K )
sparing + - + -
Diuretics ACEi/ARB ACEi/ARB ACEi/ARB ACEi/ARB
Spirinolactone
12.5 – 25 50 50 100 – 200 Start with low dose and consider dose up-titration after 4-8 weeks
/Eplerenone
Amiloride 2.5 5 5 – 10 10 – 20
Triamteride 25 50 100 200
Check blood chemistry at:
• 1 and 4 weeks after starting/increase dose
Initiating ACE Inhibitor/ARB Therapy • 8 and 12 weeks
ACEi: recommended, in addition to a beta-blocker, for symptomatic • 6, 9, and 12 months
patients (NYHA Class II-IV) with HFrRF • 4-monthly thereafter
ARB: recommended in symptomatic patients unable to tolerate an
ACEi (patients should also receive a beta blocker and an MRA)
May be considered in patients who are symptomatic despite + +
K >5.5 mmol/L K > 6.0 mmol/L
treatment with a beta blocker
or or
Check renal function and electrolytes creatinine >221 μmol/L (2.5 g/dL) creatinine >310 μmol/L (3.5 g/dL)
or or
2 2
eGFR <30 mL/min/1.73m eGFR <20 mL/min/1.73m
Start with low dose and double the dose at not less than 2-week
intervals
Halve dose and monitor blood Stop MRA immediately and
chemistry closely seek specialist advice
Aim for the target dose if possible, otherwise aim for the highest
tolerated dose
ARB Starting dose (mg) Target dose (mg)
Spirinolactone 12.5 – 25 QD 25 QD or BID
Eplerenone 25 QID 50 QD
Re-check blood chemistry (urea/BUN, creatinine, ) 1-2 weeks after
initiation and 1-2 weeks after final dose titration
Monitor blood chemistry 4 monthly thereafter

ACE Inhibitors/ARBs: Dosing
ACE Inhibitor Starting dose (mg) Target dose (mg)
Captopril 6.25 TID 50 TID
Enalapril 2.5 BID 20 BID
Lisinopril 2.5 – 5.0 OD 20 – 35 OD
Ramipril 25 OD 10 OD
Trandolapril 0.5 OD 4 OD
ARB Starting dose (mg) Target dose (mg)
Candesartan 4 – 8 OD 32 OD
Valsartan 40 BID 160 BID
Losartan 50 OD 150 OD

Initiating Sacubitril/Valsartan Therapy
given at 50-100mg BID
MEDICATIONS TO AVOID IN HFrEF

Recommendations:
• Thiazolidinediones (glitazones) are not recommended, as they increase
the risk of Heart Failure worsening and HF hospitalization
• NSAIDs or COX-2 inhibitors are not recommended, as they increase the
risk of HF worsening and HF hospitalization
• Diltiazem or Verapamil are not recommended, as they increase the risk
of HF worsening and HF hospitalization. Negative inotropic effect.
• The addition of an ARB (or renin inhibitor) to the combination of an ACEi
AND an MRA is NOT recommended because of the increased risk of
renal dysfunction and hyperkalemia
end of lecture
Black – powerpoint
Green – journal
Blue – recording
Sources:
ESC Guidelines for the diagnosis and treatment of acute and
chronic heart failure
2017 ESC Guidelines for the management of acute myocardial
infarction in patients presenting with ST-segment elevation
2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA
Guideline for the Management of Heart Failure
HAPPY ARAL!
Dr. Strange

ARRYTHMIA (Part II) 2014 -2015
Dr. Payawal
SLOW ARRYTHMIA SA Fails to fire

Inverted P wave has better prognosis,
<60 bpm
ESCAPE RHYTHMS
JUNCTIONAL RHYTHM
o Recall: when Px has sinus arrest or pauses that’s prolonged, a Px

does not necessarily go into cardiac arrest because. that Px usually
has back-up pacemakers that take over from sinus node if there is
sinus arrest/pause.
-e.g. if there is a pacemaker in AV node which is in the AV
junction, this is how it would look like. [junctional rhythm]
CRITERIA:
o QRS is narrow
- <0.12 sec or < 3 small squares
QRS not widened (0.04 sec)
o P wave can appear in 3 different ways: P wave follows QRS
“the wandering pacemaker” Rate= around 50; 1500 divided by 28
- pacemaker of heart keeps on changing from within AV
junction IDIOVENTRICULAR RHYTHM
-sometimes can be from sinus??
Before QRS but Inverted this is usually what we see in a dying heart, wherein you can see
-pacemaker comes from upper portion of AV junction the rhythm on ecg or cardiac monitor but you cannot feel the pulse
Absent of the Px
-bec. It is buried in the QRS o because usually this is an evidence of substancial
-pacemaker from middle portion of AV junction myocardial damage;
Follow qrs o QRS is already damaged and ventricle is poorly functioning;
will definitely go into asystole and DIE
-pacemaker from lower portion of AV junction
-means that the atrium is depolarized after the ventricle -but not all flat line is asystole, electrodes might just have
o P-R interval is short been removed :P for the nth time, CORRELATE CLINICALLY
- < 0.12 sec :D #umay :P
most difficlut cardiac arrythmia
- Distinguishes it from PAC which also has narrowed QRS
o Rate is usually 40-60 per min
Compatible with life
that’s the one facing the whole heart which faces both atrium
and ventricle instead of the sinus node when there is prolonged
sinus arrest/pause (ano daw? Haha!)
the one facing the whole heart comes from the ventricle (may be
from L or R)

Dr. Payawal
looks like a PVC o sometimes they go into bradycardia, tachycardia, with no
-QRS is widened apparent reason
-rate is <40 o some may possess prolong sinus pauses
CRITERIA
o QRS is widened
o no P wave
-because it comes from ventricle
o rate is <40 (in junctional it is 40-60)
Massive heart damage

Ventricular pacemaker
Widened QRS
ALGORITHM FOR SLOW HEART RATES (BRADYCARDIA)
[please refer to the algorithm on the ‘Arrythmia (part I)’ trans to better
MEMORIZE this kasi this will come out on the exam daw]
SINUS BRADYCARDIA
Slow (<60bpm)
Regular
There is P-wave before QRS
JUNCTIONAL RHYTHM
slow
regular
no P wave before QRS
QRS narrow
IDIOVENTRICULAR RHYTHM
slow
regular
no P wave before QRS
QRS wide
THIRD DEGREE/COMPLETE AV BLOCK

slow
regular
no P-QRS relation (P does not cause the QRS)
ATRIAL FIBRILLATION
slow
irregular
no P wave
SECOND DEGREE HEART BLOCK

slow
irregular
with P wave
abnormal PR
group beating
SINUS SYNDROME
o in Px with sinus node disease?

Dr. Payawal
FAST RHYTHMS SINUS TACHYCARDIA

o Narrow QRS
o Regular
o P wave followed by QRS
1. determine if QRS is:
o narrow SUPRAVENTRICULAR TACHYCARDIA
-rate: >100 o No P wave
o wide
-0.12 sec or more / 3 small squares or more VENTRICULAT TACHYCARDIA
o Wide QRS
ALGORITHM FOR FAST RHYTHM (TACHYCARDIA)
MAT
o Narrow QRS
[again, please refer to the previous trans for fast rhythm algorithm to o Irregular
memorize this easier] o Fast
o Diff. P wave morphologies
*just look at QRS and regularity
ATRIAL FLUTTER
TACHYCARDIA; REGULAR; NORMAL/UPRIGHT P WAVE; NARROW o Irregular
QRS: o No p wave
Sinus tachy o Flutter waves
Paroxysmal supraventricular tachycardia
Atrial flutter ATRIAL FIBRILLATION
To differentiate: o Irreg
Do CAROTID SINUS MASSAGE o No p
-Px in tachy and you want to slow down HR or bring back o Rapid
rate to normal sinus
-only done in Px with narrow QRS tachycardia
-only on one side for 20 sec PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
-increases vagal tone: stimulate carotid sinus (SUPRAVENTRICULAR TACHYCARDIA)
-more common among young ladies (20-40)
Paroxysmal Supraventricular Tachycardia (PSVT/SVT) Arrhythmia that originates above the ventricles
o (supra): arrythmia comes above ventricle Regular rhythm
o 25% Pz will have normal sinus Very rapid HR with narrow QRS (normal in contour and duration)
Sinus tachy o 150-250 bpm
o may slow down upon carotid massage o 180-200 bpm in adults
Atrial flutter cannot exactly see P wave
o if you increase AV block o P waves might be buried in the QRS complex or in T wave
o saw-tooth appearance of P waves if you do carotid o may be seen just prior to or just after the end of causes
massage o alteration in the QRS complex that results in a pseudo-R
Sudden onset and termination
TACHYCARDIA; NARROW QRS; IRREGULAR Sometimes on P wave
Multifocal atrial tachycardia [MAT]
o there are more than 3 kinds of P wave you can see Supra ventricular = Class 4 only supra
(inverted, tall, small, flattened, etc.) Class 1a = causes torsades pointes
o in Px with severe pulmonary disease (chronic Class 1c = not recommended for PVC therefore supra
hypoxemia due to COPD) Class 1 b = ventricular only
Atrial fibrillation
o no P wave
o one of the most common cardiac arrythmias;
usuallyin adult >80 y.o
TACHYCARDIA; WIDE QRS

(90%) VENTRICULAR TACHYCARDIA until proven otherwise
o DDx: supraventriculat tachycardia with abberant
conduction?
MANAGEMENT OF SINUS TACHYCARDIA

[all of the above] haha sorry po di ko nasulat :>

Dr. Payawal
QRS becomes small.. big.. then becomes
small again.. big.. small..
this was the cause of death of that lady
who had prolonged QTc after
thyroidectomy :’(
VT and PVC are all deadly

o VT more dangerous
No P wave
o Blabla phenomenon causing V tach
Example case 1:
VENTRICULAR TACHYCARDIA (VTACH) -Did not have previous heart attack, good LV func.
-developed multiform PVC which may progress to V tach
-sometimes they may just complain of palpitations and BP
may be a bit lower
give trial of antiarrythmic drug
Example case 2:
-Previous heart attack, has LV dysfunction
-developed sustained V tach (>30 sec)
-will go into arrest (no BP or pulse)
-V tach can kill instantaneously esp. in those with
previous asdfg ugh di ko marinig haha!
MULTIFOCAL ATRIAL TACHYCARDIA (MAT)
CRITERIA:
o Irregular
o Narrow QRS
o Has P waves but looks different from each other
-bec. it comes from different ectopic foci in atrium
WIDE QRS TACHYCARDIA Related to COPD: correct oxygenation

Three or more PVC in succession Impulse originate irregularly and rapidly at different parts of
<3o sec: non-sustained v tach (an emergency) the atrium
>30 sec: sustained
KINDS OF VTACH
Monomorphic
o looks the same (in same lead)
Polymorphic
o some wide, some narrow (not look the same)
Torsades de pointes (Torsa de pwa) :D
another kind of polymorphic VT

Dr. Payawal
-first time Px discover he has AF: may be paroxysmal
AF (not always there)
-so Tx: anticoagulation
-warfarin
-NOACS (novel oral anticoagulants)
-new drugs
-Dabigatran
-Diparoxaban?
-Apixaban?
Control ventricular rate response
o count rate on an irregular rhythm (get 30 big squares and
count # of R waves x 6= estimated ventricular rate)
60-100: controlled/moderate ventricular response
<60: slow
“asdfg”: drug w/c slows down ventricular rate in AF (sorry di ko
talaga maintindihan hihi)
ATRIAL FLUTTER
(will be in the exam)

Flutter waves
Regular or Irregular Very rapid atrial rate
o depending on AV conduction RR may or may not be regular due to long refractory period
o may be irregularly irregular
QRS not widened o P-P interval (1500 div 4= >300)
Saw-tooth appearance of P waves -atrium is contracting more than 300x per minute
There are more P waves than QRS o The atrium which should be conducting this way is moving this
atrial rate= 250-350 per min way [refer to the heart image above]
o Ventricle rate is slower bec AV node has the longest
refractory period, which is good to Px
-so even if atrial rate of Px is >300, pulse rate will only be
70-80 bec. ventricle is the one that gives pulse
That’s why Tx for AF is DIGOXIN
-prolong refractory period of AV node
Difficult to treat. Hard to convert. Many go into atrial fibrillation
later on
May be compatible with life
Problem is when Px had previous heart attack or LV dysfunction
and develops AF. they usually decompensate (go to heart failure,
pulmonary edema, orthopnea, etc.) bec. atrial contraction
contributes 15-30% of cardiac output; decrease CO= heart failure
Put Px back to sinus rhythm: drug, cardioversion (kukuryentehin
puso)
More common complication of AF: high risk for Cardiac embolism
o when atrium just moves this way and it is not contracting,
blood inside atrium rarely moves and just swirls around
- relative stasis of blood in atrium= high risk to form clot
or thrombus inside
- 80% of time, clot from atrium goes to brain= massive
stroke

Dr. Payawal
-After 10 min and you did nothing, V fib deteriorate to
ARREST RHYTHMS asystole. When asystole occurs, death!
-Early recognition is important
-We do not defibrillate asystole! (what we see on tv again).
-Will just make bad worse.
ASYSTOLE
*we only defibrillate pulseless VT and Vfib
Asystole (flat line) WILL be in the exam!

Aka Ventricular Standstill
(di nakunan ng pic, basta wavy line lang on ECG)
VENTRICULAR FIBRILLATION
there are so many ectopic fossa firing at the same time

ventricle just moving this way rather than the usual contraction
-will not produce any significant cardiac output
-no pulse, no BP, no perfusion to brain and will collapse
not see p wave, qrs, t wave (not contract much)
V TACH & VF
o most common sign of cardiac arrest
o in Px with heart attack/ACS, the kind of arrythmia that will
kill them will be either V tach or VF (VoyFriend) :P
o most common initial rhythm in cardiac arrest among
non-traumatic adults[18 and above]
see at ER lifeless, no pulse, no bp, no breathing

-ecg: fibrillatory waves
initial step: cardiodefibrillation (the one you see in tv :>)
-in Px who are practically dead already
-360 joules is the maximum
-if you are able to defibrillate this lifeless Px in less than 1 min
after onset of VF, chances of survival is >90% yeeey! :>
*For every minute delay, chances of survival goes down by
10%

Dr. Payawal
BENIGN RHYTHMS MISCELLANEOUS
PREMATURE VENTRICULAR COMPLEX ARTIFICIAL PACEMAKER RHYTHM

(PVC)
[this was discussed na sa first part so yung mga references ng pictures

pa-refer nlng sa part 1 ng trans. Thank you ]
COUPLETS
o 2 PVCs in succession
BIGEMINY
o PVC occur every after normal beat
TRIGEMINY
o PVC comes after 2 normal beats
o Complex; we do not see contraction in ecg; uniform PVC
QUADRIGEMINY
o PVC comes after 3 normal beats
PVCs do not look similar (on SAME ECG LEAD)

o You should not compare PVCs of different leads because PVCs
really appear differently in different leads
o from several diff. foci within ventricle
Coupling intervals are not the same

o Coupling interval: interval bet. normal beat and PVC
In Px who suffer from complete heart block, or those in blabla
sinus syndrome, we put an artificial pacemaker usually in RV
MULTIFORM PVC (on same lead)
apex?
o increases risk of Px to have sudden cardiac death even if the Px is
you can set rate
young, physically active and w/o Sx
-If heart beats more than what you set, it would not fire.
o Distinguish. bec. not all PVCs are lethal/dangerous.
-If lower, it will firE
-It can be caused by that moment when exams are coming and
o Rate here: around 80
students have increased sympathetic tone and under stress
(inc. noradrenaline level)
-can infuse cardiac arrythmia (multiform PVC)
R or T PHENOMENON
*Recall: boundary bet. Absolute refractory period and relative
refractory period in ventricle [Phase 0,1,2..]
At the peak of T wave or at the middle of Phase 3 of ventricle
-most dangerous time to stimulate heart bec it is the when
some part of ventricle is in absolute refractory period and
some are still in the relative refractory period (there is
electrical heterogeneity in ventricle at this time)
-most vulnerable period of heart
so if you have PVC that occurred at peak of T wave, that’s
the most dangerous PVC= can trigger malignant arrythmia
which can kill instantaneously

Dr. Payawal
CLASS 1B
o most popular: Lidocane (also use for local anesthesia)
o for ventricular arrythmias
o only available here: lidocane. tocalnide
o do not use lidocaine routinely for it can cause bradycardia
-> asystole
CLASS 1C
o only available here:flocainide, propafenone
o oral form
o only recommended for supraventricular arrythmias
CLASS 2 (Beta blockers)

o one of the most utilized cardiac drugs
Accurate ecg interpretation o potent antiarrythmic (sympatolytic)
Determine cause of arrythmia o also used for ischemic heart disease, heart failure, htn
o not all arrythmias are due to cardiac pathology o for both supra and vent
o order for Ca, Na, K, Mg
-corerct electrolyte then arrythmia disappears CLASS 3
o pulmo disease( hypoxemia) o Amiodarone is widely utilized
-get O2 sat or ABG esp if you see MAT o for both supra and vent
Nature of underlying disease
-get cardiac function CLASS 4 (Ca blockers)
Consequences of arrythmia *but not all ca blockers have anti-arrythmic properties
o Asymptomatic PAC is benign: Go on with you life and take -Mifedipine: widely used but does not have anti-arrythmia;
your exams :D actually induces tachycardia
-Only give medication if has bothering Sx o Only Verapamil and Diltiazem have anti-arr but useful only
o even Tx is clinically correlated for supra
ADENOSINE
o For supra
DIGITALIS
o AF!!
Know what type of arrythmia first before giving drugs. Because

sometimes it’s the drug that kills.
[TAKE NOTE OF INDICATIONS. IF FOR SUPRA ONLY, FOR BOTH SUPRA

AND VENT, ETC.]
Sorry madami pages hiniwalay ko kasi per classification para madali

aralin :>
TO GOD BE ALL THE GLORY!
Traditional way of classifying anti-arrythmic drugs
CLASS 1A
o prolong QT interval
o already banned in first world countries
o monitor Px QTc. If prolonged: stop or dec. dose
o for supra and ventricular arrythmias

Medicine II
CARDIOLOGY Worldwide the level of BP control is far from ideal
Finals Coverage – Dr. Deduyo
AMS 204 Note: If the hypertension level is 140/90 and higher, below 140/90
BP is said to be a controlled level except for the diabetic
Coverage of Final Examination: population. In the diabetic population, the BP of 130/80 or higher is
I. Hypertension already considered to be hypertension. If the person has already
II. Atherosclerosis and CAD achieved the goal, it doesn’t mean that the treatment should be
III. Acute Coronary Syndrome stopped.
IV. Congestive Heart Failure
V. Venous Thromboembolism and Pulmonary Hypertension management comparison, developing versus
Hypertension – Dr. O. Deduyo developed countries
Note: The data is almost the same for both.

HYPERTENSION
Hypertension profile in the Philippines
- Terms:
Hypertension is the leading cause of death globally,
especially in Asia. o Prevalence – incidence
o Treated – patients taking the medication
Note: It is not the hypertension that is the cause of death but its o Compliant – patients are following the dosage
prescribed by the physician
complications. Smoking and second-hand smoke is the second
o Controlled – because of compliance,
leading cause of death. Factors: Diets low in fruits, high BMI, high
blood glucose (diabetes), physical inactivity or low physical activity, controlled level is achieved
high dietary salt, etc.
Profile of anti-hypertension treatment
CVD risk doubles with each 20/10 mmHg BP increment - No medication = 44%
- Medication = 56%
Note: For every increment of 20 systolic BP and 10 diastolic BP,
Treatment Compliance
the CVD (Stroke, heart attack, heart failure) risk doubles
- Mostly
Example: - Sometimes
- Rarely
115/75mmHg (relative risk = 1)
- Never
135/85mmHg (RR = 2)
155/95mmHg (RR = 4)
Treatment compliance versus BP control
175/105mmHg (RR = 8)
- The compliant are 66% controlled and 55% uncontrolled
o The problem could have been the drug itself or
The higher the BP, the higher the risk of developing CVD
the dosage
BP is strongly and directly related to vascular mortality - The non-compliant are 34% controlled and 46%
uncontrolled
without any evidence of threshold down to at least
115/75mmHg
Number of anti-hypertensive drug used
- Type of medications:
Note: Vascular cerebral artery, coronary artery, and also the
peripheral vascular diseases. o Beta blocker – cheapest
o Calcium channel blockers
o ARBs
Stroke and Ischemic heart disease mortality linked to SBP
levels o ACE inhibitors
o Centrally acting drug (Clonidine)
- Number of hypertensive drug used
Note: The leading cause of death is stroke and ischemic heart
o Monotherapy – majority
disease (complications of hypertension). As the BP increases, the
o 2 drugs – 11%
higher is the mortality both for stroke and ischemic heart disease.
o 3-4 drugs – 0.4%
Hypertension prevalence does not discriminate by gender,
Note: When we first determine and recognize the presence of
geography, or income level
hypertension, we try to categorize whether it is Grade 1 or Grade
2. If the BP is more than 160/100mmHg it cannot be managed by
Prevalence of hypertension in developing countries from
only one drug, it should be 2 or more. But if the BP is 140/90mmHg
National Surveys
to 159/99mmHg then 1 drug can be given.
Note: The prevalence in both developing and developed countries
is the same.
Prevalence of hypertension in adults >18 years old
Note: The nationwide registry showed that from 11% in 1992

25% rapid rise to 28% in 2013 (Presyon 1 to Presyon 3)
1|JKCP Villarama
BP control versus Drug Combination Note: There are several types of BP, not only Stage 1 and Stage 2
- Drug combination gives a better control than a single (by ACC and AHA) or Grade 1, Grade 2, Grade 3 (by European
drug Society of Cardiology), there are also:
- The number of anti-hypertensive drugs would tell - Excessive BP variability
whether a control level would be achieved - White coat hypertension
- Masked hypertension
The many causes of uncontrolled BP - Non-dipper/Reverse dipper
o BP is more elevated during nighttime than
Diverse pathogenesis and etiology during the day
- RAAS
- Salt-sensitive, volume of body - Morning surge
fluid
- Sympathetic nerve activity Besides staging, we must also know these by doing 24h
- Sleep apnea syndrome ambulatory BP monitoring. According to the latest ESC, all
- Secondary forms
hypertensive patients are advised to undergo 24h ambulatory BP
UN
monitoring to be able to determine the type of BP.
Important therapeutic regimens C Poor Adherence to anti-
- Low renin activity O hypertensive medications Measurement of the BP can be done in the office or the clinic, and
Lifestyle (sodium intake) N
-
T
- Reduced self CV the out-of-the-office which is the home of the patient.
- Interfering substances R perception
- Fail to adjust drug species or O - forget
dosage timely L - Adverse drug reaction 2013 Europe hypertension guidelines: ESH/ESC emphasize
L - Poor therapeutic effects out of office BP measurement
E
D
BP The task force for the management of arterial hypertension of the
European society of hypertension and cardiology tells us about the
BP Types emphasis in the out-of-office BP measurement.
- Excessive BP variability
o White coat and masked Values:
hypertension
o Non-dipper/reversed dipper - Separating from medical environment better reflects true
(nighttime) hypertension BP condition than office BP
o Morning surge - Use out of office BP for risk stratification
- Patients with high office BP but normal out-of-office BP is
Note: There are many causes of uncontrolled BP. There is diverse termed as white coat hypertension
pathogenesis and etiology. - Those with white coat hypertension have a lower
- There is a need to determine the diverse pathogenesis cardiovascular risk than patients whose BP is elevated at
and the etiology of the elevation of the blood pressure. home but normal or low in the clinic or in the hospital.
o RAAS activation give anti RAAS This is called as masked hypertension. It is frequently
o Excess volume or body fluid give diuretics associated with cardiovascular risk factors and has
o Increased sympathetic nerve activity give increased risk of cardiovascular events.
beta blockers
o Sleep apnea syndrome is different. In the time Lower CV Risk White coat hypertension
of apnea, there is irregularity in breathing and it Higher CV Risk Masked hypertension
can be monitored in the sleep center.
o It can also be secondary: pheochromocytoma, - There is a close association with hypertension induced
renal artery stenosis, because it is not organ damage especially left ventricular hypertrophy
controlled it can lead to uncontrolled BP or among patients with masked hypertension more than the
hypertension. white coat hypertension.
- Proper therapeutic regimen - There is a better prediction of CV morbidity and mortality
o Is there low renin activity? than the office BP thus the emphasis of out of office BP
Try to determine what is the level of measurement.
renin
o Lifestyle (Sodium intake) Poor compliance is a global problem
o Interfering substances - 1/3 of patients will discontinue the initial therapy within 6
Frequent use of NSAIDs interfere months after treatment and only ½ of patients will
with the drug continue treatment after 1 year
o Fail to adjust drug species or dosage timely - Self-monitoring of BP is an important means of
- Poor adherence to the anti-hypertensive therapy is very improving adherence
common o Disadvantage: Patient takes medication only
o Reduced self CV perception – very common when the BP is elevated. The anti-hypertensive
especially in the young adults drug is treating the atherosclerotic problem that
o Forget – long acting preparation should be is going on in a patient with hypertension. It is
given important that the patient is educated.
o Adverse drug reaction – usual side effects
should be disclosed to the patient Comprehensive BP management
o Poor therapeutic effect - Focusing on patients and confining doctors as well as
communities
2|JKCP Villarama
- Self-monitoring of BP is a key component of Clinical Indications for Out-of-office BP Measurements for
comprehensive BP management Diagnostic Purposes
Definitions of HPN by Office and Out-of-office BP levels
Note: There are different values! We say that there is hypertension

in the office if the BP is = or > 140/90mmHg. In an ambulatory BP,
it is divided into daytime BP (awake period) and nighttime BP
(asleep period). The average of the two is taken (24h BP).
HPN definitions
- White coat HPN
o A discrepancy of >20/10 mmHg between the
clinic and average daytime ambulatory BP
monitoring (ABPM) or average home BP Note: Clinical indications for HBPM (Home BP Monitoring) or
monitoring at the time of diagnosis ABPM (Ambulatory BP Monitoring). BP variability – every time the
BP is taken it is different. There is a significant difference in the
Example: If the average daytime
level of the BP.
ambulatory BP is 130/80 and 160/90
in the clinics
Risk of Mortality with Isolated and/or Combined Elevated
- Masked HPN – with higher cardiovascular risk Office, Home and Ambulatory BP — PAMELA study
o The converse of white-coat hypertension. A - The analysis of the Presyon done in Italy compared the
subject with masked hypertension has normal office, home, and ambulatory BP values between 1990
BP measurements in office or clinic but w/ and 1993 with cardiovascular and non-cardiovascular
episodes of elevated BP outside of the death:
clinical environment o 69 Cardiovascular
o 233 All cause death
Note: For people identified as having white coat hypertension and
- The increase in home BP shows a greater risk of
masked hypertension, consider day time ambulatory BP monitoring
cardiovascular mortality
or home BP monitoring as an adjunct to the clinic BP
measurement to monitor the response to the treatment. o Increase home and 24 hour BP had the greater
risk of cardiovascular and all cause death than
The normal circadian rhythm of BP has a nocturnal decrease of the increase in office BP
15% to 25% in BP compared with the awake BP values. This is - The risk of mortality is higher w/ a combination
called as the dipping pattern.
BP Dipping Status Predicts CV events
- Non dipping - CV events are higher in reverse dippers as compared
o Defined arbitrarily as BP reduction during with non-dippers, dippers and extreme dippers
sleep is <10% compared to the BP during o Reverse dippers – very high BP during
awake period nighttime
o Non-dippers – 10% reduction in the nighttime
o Occurs in about 25-40% of patients w/ HPN
BP compared to daytime BP
- Reverse dipping o Dippers – Normal
o Significant increase in BP when asleep or o Extreme dippers – very low BP during
when in supine position compared to the BP nighttime
while awake.
o Also called a riser pattern Blood Pressure Variability
Example: 170/110mmHg at night and - BP normally fluctuates during the day and can vary from
140/90mmHg during daytime day-to-day in response to environmental challenges
(stress, activities, etc.)
- Pronounced fluctuations in BP can occur over a short
term and long term observation period
o BPV has been observed over a 24hour period
ABPM, showing hour-by-hour variability
3|JKCP Villarama
o There can also be a visit-to-visit variability Note: Subclinical organ damage – the organ damage of patients
either short term or long term with hypertension without clinical event
- Episodic HPN is common - Heart – LVH
o In a cohort of patients with previous TIA, only - Arteries – Atherosclerosis
12% has stable HPN while 69% has episodic o Can be determined by carotid duplex scan
HPN - Kidneys – proteinuria in urinalysis but with normal
creatinine
some systolic BP of less than or
equal to 140mmHg and some with
There is organ damage but is subclinical. For it to be clinical, LVH
greater or equal to 140mmHg
angina pectoris, ischemic heart disease, or the patient is in
- BP variability is difficult to measure in routine clinical failure. Carotid atherosclerosis Intima media thickness is
practice and there is no clearly defined or widely adapted greater than 1cm affecting the lumen of the carotid artery which is
diagnostic definition or treatment goal a gateway towards the brain
o BPV is best determined through ABPM
- ABPM can identify patients with the so-called ―morning Note: BP Variability can also lead to a clinical event and it is quite
surge‖ and predicts CV events better than the office BP increased especially when there is decreased arterial compliance.
level Decreased adherence to AHT is the worst. To summarize BP
- High blood pressure measurement is a good alternative variability, there could be increased risk subclinical organ damage
to a 24h ABPM and variability has been correlated with but there is also an increased risk for a clinical event which is a
target organ damage, CV outcome and stroke mortality patient in failure that goes into mortality, CVA that goes into fatal
- Standard deviation and co-efficient of variation of BP condition, or a patient having albuminuria which leads to ESRD.
measurements are commonly used as parameters
- Variation independent of the mean is a transformation of
the standard deviation uncorrelated with the mean blood
pressure
BP Variability over different time periods has been evaluated

in several clinical trials
Note: Different trials have been conducted and they have proven
that BP variability indeed exists especially among patients who had
undergone 24h ABPM.
Mean Determinants of Increase in BPV

- Short term monitoring
o Hour-to-hour
- Day-to-day home BP monitoring
- 24 h monitoring
- Visit-to-visit monitoring
Determinants and Prognostic Relevance of BPV
4|JKCP Villarama
Pronounced fluctuations in BP can occur over short-and-long Morning BP surge
term observation periods - Morning BP surge is associated with increased risk of
- There is a well-established morbidity and mortality stroke by 22%
associated with BP variability whether it is short term or
long term monitoring. Which class of anti-hypertensive drug is best suited to treat
- Increased 24 hour BP variability has been associated the morning BP surge?
with cardiovascular damage. - The long-acting preparation is preferred.
- Rate and severity of target organ damage o Take effect for the whole 24 hours or beyond
- mild to moderate hypertension o Examples:
- increased awake systolic BP variability correlates with Calcium channel blockers
subclinical target organ damage 34 - 36hours
- Day to day BP variability is an independent predictor of Drugs:
cardiovascular event and stroke mortality after o Amlodipine
adjustment from BP and other confounders than in o Nifedipine
Japan among Japanese residents ARBs
- The visit to visit increase in BP and BP variability 36 hours
increases cerebrovascular risk in 683 non-dependent Drugs:
subjects whose age is more than 65 years of age. o Telmisartan
- The difference in BP and uncontrolled BP will predict that
there will be an increase cardiovascular mortality. Note: Beta blockers have 4-6 hour peaks. Beta blockers only
- Comparing visit to visit variability: 3 drugs decrease the heart rate and it has nothing to do with endothelial
o Chlorthalidone (Diuretics) function. But there are vasodilating beta blockers like carvedilol
o Amlodipine (CCB) and nevibolol which has an anti-oxidant effect and improves
o Lisinopril (ACE inhibitor) endothelial function. ACE inhibitors are good anti-hypertensive
drugs but with cough as side effect.
Note: ACE inhibitor is the best drug for hypertension. Side effect:
cough Summary
- The guidelines continue to recommend the office BP for
Example of 24hr BP screening and diagnosis of hypertension and it is
- 6pm midnight 6am noontime recommended that the diagnosis of hypertension be
- When a patient is about to sleep the systolic BP goes based on at least 2 BP measurements on separate visits
down and then increases at midnight to the awake - Out-of-office BP should be considered to confirm the
period. This is called as the morning surge diagnosis of hypertension
- Identify the type of hypertension and detect hypertensive
Morning BP surge
episodes and maximize prediction of cardiovascular risk
- Morning BP surge is defined as the morning BP (average
of 2 hours after arising) minus the nighttime lowest BP - For out-of-office BP measurement, ambulatory BP
(average of the 3 BPs nighttime) monitoring, home blood pressure monitoring may be
- Finding: patients with sleep-trough surge of >55mmHg considered depending on indication, availability, ease,
were classified as a morning BP surge cost of use, and if appropriate, the patient’s preference.
- Reducing morning hypertension may also prevent - There is increasing evidence that high morning BP is
cardiovascular outcome. associated with increased stroke risk, damage to the
- Reducing the morning BP surge as well as the mean BP heart, atherosclerosis and organ damage
in hypertensive patients has been suggested as a - High morning BP is increasingly being recognized as an
potential therapeutic target to prevent vascular outcome important aspect in managing hypertension
particularly acute coronary syndrome, cardiac - Studies have been conducted to investigate the
arrhythmias, and sudden cardiac death on all cause determinants of high morning BP and how control rates
mortality. differ between the clinical population.
- Meta analysis of randomized studies established the
prognostic value of the morning BP surge in the general
Note: Differential effect of CCB compared with other agents like
population.
ACE, Beta blockers for BP variability may account for the disparity
in observed efficacy in reducing the risk of stroke. It is not only
Example: If there is a rise in BP during the morning, the drug is
CCB but also ARBs especially Telmisartan which has the longest
administered before going to sleep knowing the peak plasma level.
half life
An exaggerated morning BP surge, exceeding the 90th percentile
of the population, is an independent risk factor for mortality and CV
and cardiac events, especially in smokers.
The rapid rise of BP in the morning is one of the critical risk

variables for CV events
- BP form of untreated hypertension patient
- Incidences of MI and stroke at different time intervals
have demonstrated that there is a rapid rise of BP early
in the morning.
5|JKCP Villarama
Case # 1 Case # 2
Mr. S, a 36 year old male salesman who reported to a doctor’s Mr. MDC, a 75 year old male known hypertensive for the last
clinic for a problem of hypertension which was detected about a 10 years with poor compliance to medication. (The patient
month ago. He thought that the elevated BP was due to his work knows that he is hypertensive but he does not take it regularly.
for he is emotionally stressed (increased sympathetic aNS This is a very common scenario). He took his antihypertensive
activity) because he cannot achieve the sales quota set by his medication only when he thought his BP is elevated. About 3
employer. However he is also afraid because his father died of months prior to admission in the hospital, he began to suffer from
CVA secondary to hypertension at the age of 56 and his only easy fatigability but no chest pain. Such symptoms he attributed
brother died of a heart attack at the age of 46. His mother also to his age.
died at the age of 56 due to heart failure secondary to
hypertension (Strong family history). Smokes half-pack of Note: Nape pain has nothing to do with the BP, it is not
cigarette for the last 10 years and drinks beer on occasion. related. Hypertension is without symptoms unless there
Complains of palpitations especially when stress and after is clinical organ damage. If there is subclinical organ
drinking coffee and soda (both contains caffeine which causes an damage, the patient is still asymptomatic. When
increase in heart rate). symptoms begin to appear, this is because of the target
organ complications. Any pain can elevate the systolic
PE showed: BP due to increase in sympathetic drive. The expression
BP – 160/92 mmHg, sitting on both arms. of fatigability is due to a low cardiac output.
If seeing the patient for the first time, take it on both However about 3 weeks prior to admission he had episodes of
arms. A difference of greater than 10 mmHg in systolic paroxysmal nocturnal dyspnea and orthopnea (awaken at night
blood pressure, there could be a vascular problem; ask if because of difficulty in breathing and stays in a sitting position
the patient is taking BP at home to r/o white coat overnight) He felt very weak and walking for a minute or two
hypertension; this is a candidate for ABPM makes him very tired. Meantime he noticed bilateral pedal edema
and he spends the night sleeping using 3-4 pillows to support his
HR – 110 bpm back. Thus he decided to consult at the emergency room.
RR – 18 cpm
BMI – 26 PE showed:
Fundoscopy - did not reveal retinal exudates or other signs of BP – 160/96 mmHg
retinopathy. HR – 120 bpm and regular, no arrhythmia
RR – 26cpm
Note: Evidence of atherosclerosis can be seen through (+) Jugular venous engorgement at 60 degrees position
fundoscopy (+) Hepatojugular reflux
(+) Bilateral crackles occupying (1/2) on both lung fields.
Eyes are the window of the Heart: check for retinopathy Bilateral crackles is not pneumonia, that is usually heart failure
or a hypertensive fundus, presence of atherosclerotic
plaques Heart: Apical beat is visible and palpable at the 5th ICS LAAL
and sustained. (There is obvious displacement of the apical beat)
Auscultation of the carotid arteries did not reveal any bruit on Heart sounds revealed tachycardia at 120bpm but normal rhythm.
both sides. Increased S1, Normal S2, (+) S3 gallop noted at the left ventricle.
Note: If there is bruit (like amurmur because of a Note: This patient has a very big heart because his
turbulence) it means to say that the carotid artery is apical beat is already displaced.
>50% occluded. If it is totally occluded, there is no bruit
heard. Always check for bruit because it is a sign of Abdomen: Unremarkable
turbulence. If there is more than 50% stenosis in the Extremities: Cold with bilateral pedal edema extending up to
carotid artery, there will be bruit. below the knee. (diminished CO diminished peripheral perfusion)
Heart: Apex beat is palpable on the 5th ICS LMCL and is Note: This is a description of a patient with organ
sustained with regular rhythm. HR is 110bpm with increased S1, damage. The heart is enlarged and it is symptomatic of
normal S2, no gallop and murmur present. He has good peripheral heart failure.
pulses.
Note: S1 and S2 loudness can be affected by the heart

rate. It can also be affected by the presence of valvular
diseases, arrhythmia, etc.
ECG: reveals an axis of -30 degrees with borderline voltage

criteria for left ventricular hypertrophy
Note: There is already evidence of subclinical organ

damage.
6|JKCP Villarama
Pathophysiology of Hypertension - Alterations in adrenergic receptors that influence heart
rate, inotropic properties of the heart, and vascular tone;
and altered cellular ion transport.
Note: Atherosclerosis is a disease of the blood vessel wall and not

of the lumen.
What factors would affect endothelial dysfunction?

- Environmental stress
- Genetic
- Angiotensinogen, etc.
- CNS sympathetic activation
- Cardiac diminished cardiac output
- Renal sodium retention
- GI Obesity
- Endocrine insulin
- Age Note: The determinants of the blood pressure would be the
cardiac output and the total peripheral resistance. If there is
Note: All of these causes malfunctioning of the endothelium. When increase in the TPR (Total Peripheral Resistance) or SVR
nitric oxide is diminished, there is increased substance P, CGRP (Systemic Vascular Resistance) even in the presence of a normal
and natriuretic peptide. cardiac output, there would be hypertension.
- Increased sympathetic nervous system activity causes Difference between the two major kinds of hypertension
an elevation of the BP (targeted by beta blockers, to
reduce heart rate)
- Heightened exposure or response to psychosocial stress
- Overproduction of sodium retaining hormones and
vasoconstriction
- Long-term high sodium intake
- Inadequate dietary intake of potassium and calcium
- Increased or inappropriate renin secretion with resultant
increased production of angiotensin II and aldosterone
o Because of a decrease in cardiac output, there
would be diminished renal blood flow that
would stimulate renin release
o The end result would be angiotensin II and
aldosterone and anti-diuretic hormone
o This explains the presence of edema in the
patient
- Deficiencies of vasodilators such as prostacyclin, nitric
oxide, the natriuretic peptides and a variety of other
vasodilator peptides inducing angiotensin (1-7) peptide,
calcitonin gene-related peptide (CGRP), substance P,
and adrenomedullin
- Alterations in expression of the kallikrein-kinin system
(part of RAAS) that affect vascular tone and renal salt
handling (targeted by ACE and ARBs) Note:
- Abnormalities of resistance vessels, including selective - Primary or essential hypertension – majority of
lesions in the renal microvasculature (targeted by patients presenting in clinics
vasodilators like CCBs) - Secondary hypertension – there is a known medical
- Diabetes mellitus condition that causes the elevation of the BP. This is only
- Insulin resistance considered when the patient has been given four anti-
- Obesity hypertensive drugs but the BP is still elevated.
- Increased activity of vascular growth factors
7|JKCP Villarama
The Natural History of Untreated Hypertension
Low moderate, high, and very high risk refers to 10 years risk of a
CV fatal or non-fatal event. The term ―added‖ indicates that in all
categories risk is greater than average
Note: There is subclinical target organ damage (LVH, etc.) at first Note: Risk factors include family history of the patient, age, DM,
but these can be determined through examination and diagnostic dyslipidemia, sedentary lifestyle, excessive alcohol intake, etc. If
tests. Then after some time, the patient would be clinically relevant the BP is 120/80 to 129/84, it is considered by the ESC as normal.
(stroke, MI, etc) which can lead to death. When patients are seen If with comorbidities, even at low BP there is already moderate
at this point, we want to at least prevent them to go into the clinical added risk so the BP must already be managed at this point
event. together with the metabolic syndrome especially in patients with
very high added risk.
The Benefits of Antihypertensive Treatment
- Effective antihypertensive treatment can reduce stroke
and CAD
- For both systolic & diastolic hypertension and isolated
systolic hypertension: stroke and all other cardiovascular
diseases can be controlled as long as the blood pressure
is controlled.
Note: As for fatal and non-fatal events and mortality, it can reduce
stroke by 42% and coronary heart disease by 40%; mortality all
causes 14% cardiovascular 21% non cardiovascular. For isolated
systolic increase, fatal and non fatal events and mortality, stroke
can be reduced by 30%; 23% all cause mortality, cardiovascular
event and non-cardiovascular event.
Note: Hypertensive treatment strategy: there should be a broad

range of anti-hypertensive drugs that should be used.
Choice of antihypertensive therapy: ESH/ESC 2007

- Main benefit are due to BP lowering
- Specific drug classes may differ in their effects
- Drugs are not equal in adverse event profiles
- Major drug classes are suitable for initiation and
maintenance of therapy
- Choice of drug will be influenced by patient experience
and preference, concomitant conditions and cost and risk
profiles
- Long-acting drugs that provide once-daily, 24 – hour
efficacy are preferable (CCBs: Amplodipine and
Nifedipine: 36 hours, ARBs: Telmisartan)
8|JKCP Villarama
The goals of antihypertensive treatment
- In hypertensive patients, the primary goal of treatment is
the maximum reduction in long-term total risk of
cardiovascular disease requiring:
o A reduction in raised blood pressure
o Treatment of all associated reversible risk
factors (obesity, smoking, and High salt intake)
Note: Diabetes and Dyslipidemia are not included because they

are not reversible but controlled.
The projected mortality

- As the BP goes up, there is a high mortality risk
- Raised BP has a high global mortality and it is the
leading CV mortality
- 7.1 million Asians die because of hypertension each year
- Asians are more prone to fatal and non-fatal coronary
artery disease compared with the Caucasians.
Note: When we treat hypertension, always tell the patient that we

can prevent MI by 20 to 25% and stroke by 30 to 35% and CKD by
47%. Other risk factors should also be treated.
9|JKCP Villarama
ISCHEMIC HEART DISEASE protected and also the growing children from atherosclerotic
(Coronary Artery Disease and Atherosclerosis) changes.
- There would be smooth muscle migration, foam cell formation,
Note: There are two things to consider in IHD: coronary artery and activation of the T cell, adherence of the platelet, the
myocardium. The coronary artery is the blood supply of the heart aggregation of the platelet, as well as the aggregation of the
specifically the myocardium and the structures inside the chambers of the many leukocytes.
heart.
Advanced Plaque
Definition: - There is accumulation of macrophage, formation of a necrotic
- Coronary Artery Disease core, and fibrous cap formation which is a thin fibrous cap (a
o refers to the atherosclerosis of the coronary arteries vulnerable plaque because the cap is very thin and can be
that may result in significant obstruction to the subjected to rupture)
coronary blood supply leading to myocardial
ischemia Atherosclerosis: a generalized and progressive process
- It is a progressive course
Note: It refers to the presence of atherosclerosis. Hypertension is a risk - From the 1st decade of life, you can see that there is a
for the development of atherosclerosis because of impulses beginning. On the 2nd decade of life onwards, atherosclerosis
malfunctioning of the endothelium. There is endothelial dysfunction in can set in.
atherosclerosis. This is the reason why we need to control the elevation of
the blood pressure to prevent further damage and malfunctioning of the Atherosclerosis can set in the 2nd or 3rd decade
endothelium. - Unstable angina
- MI
- Myocardial ischemia - Ischemic stroke/ TIA
o Refers to a condition in which there is an imbalance - Critical leg ischemia
between the oxygen supply (carried by the coronary - Cardiovascular death
artery) and oxygen demand of the myocardium
usually due to a severe fixed or dynamic obstruction Note:
of the myocardial blood supply, or an increase in - When there is thrombus formation because of plaque rupture,
myocardial oxygen requirements, or both. there will be an acute coronary syndrome in the form of:
o Unstable angina
Note: One of the reasons why there is an increase in myocardial oxygen o MI
requirement by the heart is the presence of hypertrophy which is a o STEMI
consequence of a chronic uncontrolled hypertension. A concentric left o NSTEMI
ventricular hypertrophy and may exceed the concentric form into an - It does not only affect the heart when there is rupture of the
eccentric form becoming bigger, heavier, with a very thick myocardial plaque.
segment. The bigger the muscle, the bigger will be the requirement. o It can circulate and gain entrance into the brain
causing ischemic stroke or TIA, or
Coronary Arteries o In the peripheral vascular system causing critical leg
- Two main coronary arteries: ischemia especially among those whose comorbity
o Left coronary artery is DM on top of hypertension.
Divides into: o The usual death of patients is the presence of
Circumflex coronary artery arrhythmia in the form of ventricular fibrillation
Left anterior descending - At first there is stable angina in the heart. In the peripheral
coronary artery vascular system, there is intermittent claudication.
o Most often o Stable angina in the coronary artery in the
damaged myocardium where the chest discomfort is
o When there is a precipitated by effort which further increases the
clot or thrombus myocardial oxygen demand. There is a chest
that will be discomfort which is relieved by rest.
released because o Intermittent claudication is pain in the leg muscles.
of a rupture of the (gastrocnemius muscles become painful upon
atherosclerotic walking). Upon resting or sitting, there will be a
plaque, it finds its decrease in the demand and the symptom will be
way more into the relieved.
left side (LADCA)
o Right coronary artery Pathophysiology of MI
Supplies the right side of the heart and
the posterior portion of the heart. Oxygen requirement Oxygen supply
Pathogenesis of Atherosclerotic Plaque: endothelial dysfunction and Ischemia

inflammation
- Leukocyte migration Lactic acidosis ST segment change contractility Angina
- Increase adhesion of the endothelium
- Platelet aggregation
Note: It is something that increases the oxygen requirement in the heart
Note: These happen in the wall of the artery. There is presence of plaque. (LVH, increased HR, etc). The oxygen supply is the status of the coronary
artery. When there is an imbalance between the requirement and supply,
Fatty streak there will be ischemia of the myocardium. When there is ischemia, the
- First lesion muscle will suffer and there will be lactic acidosis. There will be reduction
- Fatty streaks have been seen even in the infants born from in the contractility, changes in the ST segment of the ECG. If there is
parents with family history of hypertension. Babies are not severe injury, ST segment elevates. In ischemia, there will be depression
of the ST segment. This is clinically significant because of the presence of
angina pectoris.
10 | J K C P V i l l a r a m a
o It could also be a musculoskeletal pain
Spectrum of CA disease - Constant pain lasting for several days
- Very brief episodes of pain lasting and few seconds
Asymptomatic CAD o It could also be caused by anxiety
- Pain radiation to the lower extremities
Stable angina pectoris o It could also be neuropathy in the presence of DM
Unstable AP Physical Exam in Chronic CAD

- Many patients with CAD have normal physical findings
Non-STEMI - General: corneal arcus (in a young individual), xanthomas
and xanthelasma (these are cholesterol deposits that suggests
STEMI that the cholesterol level is elevated), retinal arteriolar
changes (atherosclerotic changes seen in the retinal lateral
Sudden death vessels during fundoscopic exam), elevated BP (considered as
a risk factor), diagonal earlobe crease (prone to heart
Note: Asymptomatic CAD there is already a coronary atherosclerosis attacks), diminished arterial pulses and bruits (by
but there is still a balance between oxygen supply and myocardial auscultating the carotids, abdomen in the renal arteries which
demand. Until the time when there is imbalance, there is stable angina will suggest that there is a concomitant atherosclerosis or
pectoris or stable ischemic heart disease where the symptoms are felt aneurysm).
during activity because it further increases the demand and is relieved by - Cardiac examination: during an episode of angina pectoris, one
rest. Chest pains that are not relieved by rest are unstable angina, may detect an S3 paradoxical splitting of S2, transient systolic
NSTEMI, and STEMI which are all very symptomatic. Stable angina lasts murmurs, and pulmonary rates. A displaced left ventricular
for 5-10 minutes then disappears. Unstable anginas are felt even at rest. impulse suggests ventricular dysfunction.
This lasts for about 30 minutes. Chest pain of NSTEMI is continuous and
progressive with cold sweats. Note: When you examine a patient, usually there is a normal physical
examination finding. There are some clues to the presence of
Acute CAD versus Chronic CAD atherosclerosis such as those stated above.
- Acute – event is sudden - Cardiac findings:
- Chronic – event is gradual o S3 gallop
Suggests that there is a LV systolic
Clinical Manifestations of Chronic CAD malfunctioning
- Symptoms Hallmark to diagnose the presence of a
- PE heart failure
- Biochemical tests o Paradoxical splitting of S2
- ECG o Transient systolic murmur or crackles due to the
- Other ancillary tests diminished LV function
o Displaced LV impulse which means that the heart is
Note: Chronic CAD is also called as chronic stable ischemic heart enlarged
disease or stable ischemic heart disease
Biochemical tests in chronic CAD
Angina Pectoris - Lipid profile
- AP is a discomfort of the chest or adjacent areas caused by o Total cholesterol >190mg
myocardial ischemia o LDL >70mg
- Usually brought on by exertion or stress o HDL <50 in male; <40 in female
- Described as constricting, crushing, heavy (on the sternum), o Triglycerides >150mg/dL
squeezing in character
- Retrosternal in location but may radiate to other areas of the Note: In atherosclerosis, when there is endothelial
chest, ulnar surface of the arms, more commonly the left arm, dysfunction where the endothelium becomes permeable,
epigastrium, and mandible. the LDL is able to enter and penetrate the endothelium.
- It begins gradually and reaches its maximum over a few The macrophages will engulf the LDL transforming it into
minutes before it dissipates. foam cells and then continuous smooth muscle cell
- It may be associated with dyspnea, vagueness, easy fatigue, migration and the end result is the fibrous plaque. The
and ____ because of the stress and anxiety why the symptoms presence of a low HDL and high triglycerides usually is
appeared but is not related to the condition. usually suspicious of a patient with DM.
Note: There is no pain felt because there is no inflammation. If there is - Fasting Blood Glucose
inflammation, there will be pain which is persistent for several days o Normal <100mg/dL
(costochondritis, myosiitis). It is precipitated by exertion. o Impaired fasting glucose 100 -125mg/dL
Indicative of insulin resistance
Symptoms NOT suggestive of AP Equivalent to pre-diabetes
- Pleuritic pain, brought on by respiratory movement or cough o Level suggestive of DM >126mg/dL
o Always try to differentiate if it is cardiac or - Other biochemical markers
pulmonary o Lipoprotein Lp(a)
Pulmonary – related to a pulmonary o Homocysteine level
symptom (most common: cough) o High sensitivity C-reactive protein
Cardiac – related to cardiac symptoms Indicative for the presence of
(most common: chest discomfort) atherosclerosis
- Pain located in the middle or lower abdomen In other words, maybe a person is not
o if it is located on the right or left and aggravated by diabetic, no increase in the level of
deep breathing or coughing, it is a pleuritic chest cholesterol or even the LDL, but there is
pain a high sensitivity C-reactive protein =
- Pain localized in one finger atherosclerosis
- Pain reproduced by movement or palpation of the chest wall
ECG in Chronic CAD
- Resting ECG is normal in 50% of patients with chronic stable Stress Testing
angina pectoris - Treadmill exercise test
- Most common ECG findings in chronic CAD are non-specific - Bicycle ergometer
ST-T wave changes with or without Q waves.
o ―medyo bumaba pero hindi ganun kababa and Abnormal Stress ECG
without significan Q wave and T wave medyo - Horizontal downsloping of ST segment
bumaliktad pero mababaw‖ - very significant lowering of ST segment
- Various arrhythmia, especially ventricular primitive beats may
be seen Other forms of non-invasive stress testing
o It is not common but it may be seen - Those patient with nonspecific changes in ECG but
symptomatic and you want to prove there is a CAD
Note: In any patients complaining of chest pain especially when there is a
suspicion of risk factors, always request for ECG. Note: If the exercise tests did not show any abnormalities, do other forms
of non- invasive stress testing.
ECG tracing
- Our attention should be on the ST segment Nuclear cardiology techniques
- Stress myocardial perfusion imaging
o Uses either thallium, Tc99 sestamibi, or Tc99
tetrofosmin
- Pharmacologic nuclear stress testing
o For patients unable to exercise adequately
Ex. Stroke patients with chest discomfort;
advanced age who can’t do physical
tests such as treadmill
o May use dipyridamole, adenosine, or dobutamine
to ―Stress‖ the heart
These increase the contractility of the
heart. There would be an increase in the
myocardial oxygen demand using these
drugs.
- Positron emission tomography
- Map the myocardial segments: o Useful to detect myocardial viability of the injured
o I, AVL, V5, V6 – lateral portion of the heart heart (myocardium)
If there is something wrong or if there is o expensive
less perfusion of that portion of the
myocardium, there will be changes in the Stress Echocardiography
ECG - Exercise echocardiography
o II, III, AVF – inferior portion of the heart - Looks at wall motion
o V1, V2, V3, V4 – anterior and septum portion of the - Pharmacologic stress echocardiography
heart
Note: Echo done during rest and will look at the wall motion, during
Note: There could also be a combination because there could be two or exercise, and post exercise. Look for abnormalities in the contraction of
more vessels affected so more changes in the ECG. the heart.
Non-invasive Stress Testing Nuclear Gamma Camera

- Provides useful information to establish the diagnosis and
estimate the prognosis in patients with chronic stable angina Radionuclide Myocardial Perfusion Imaging
- Most helpful in patients considered to have a moderate - Looks at the perfusion of the myocardium.
probability of CAD based on clinical symptoms, normal ECG, - If there is less perfusion, refer the patient for angiogram.
and risk factors. o If positive in angiogram, you can immediately do
o A normal ECG will not rule out the possibility of dilatation of the artery by inserting a stent.
CAD.
Stress Echocardiography (wall motion and diminished contractility)
Note: If the patient has normal ECG but is symptomatic and presents with - Exercise echography
the risk factors seen in the biochemical tests and PE, subject the patient to - Pharmacologic stress echography
non-invasive stress testing. - Abnormality in wall motion
- Thin cannot contract effectively
Exercise ECG
- Most widely used test to diagnose CAD Note: There is an abnormality in the wall motion and thinning wherein it
- Usually performed on a treadmill or bicycle ergometer (two cannot contract effectively.
equipments used)
- Gives information not only the presence or absence of ECG Newer non-invasive imaging technologies for CAD diagnosis
evidence of ischemia but also on exercise capacity, BP and HR - Computed Tomography (CT Scan)
responses to exercise o Electron beam CT coronary calcium scoring
- ECG findings of horizontal or downsloping ST segment Looks at the coronary calcium scoring
depression is indicative of myocardial ischemia (>2mm small Calcium is needed for the contractility of
square) the muscle (ex. Striated muscles of the
o ―bumabagsak yung ST segment‖ heart)
- Accuracy of ECG diagnosis may be limited in patients with o Multi-slice CT coronary angiography
abnormal baseline ECG (right bundle heart block configuration) - Magnetic resonance imaging
o ―Meron namang abnormal pero yung mga normal
have to undergo further testing‖
- Statins (HMG CoA reductase inhibitors) are drug of choice
Invasive Testing in CAD o Atorvastatin – good statin for CAD. There is
- Cardiac catheterization and coronary angiography superior reduction with high dose atorvastatin.
o Definitive diagnosis of CAD
o Precise assessment of anatomical severity of It lowers LDL and cholesterol
CAD The most important effect is stabilization of plaque.
o Assessment of LV function It will not rupture which may release thrombus that my occlude the arteries
o Requires the insertion of a catheter in a peripheral In patients with CAD in high risk category, high intensity lipid control is
artery (radial artery is used because it is shorter needed meaning the highest dose of statins should be maintained to
compared to the femoral artery) which is advanced control dyslipidemia and stabilized the plaque.
intravascularly to the heart under fluoroscopic
guidance. Extra-cardiac factors which may provoke angina
- IVUS (Intravascular ultrasonography) - Fever (increase HR)
o Myocardium is seen - Hypertension (LVH)
- Anemia(increase HR)
Note: The hallmark on the diagnosis of coronary artery disease leading to
ischemic myocardium is seen with cardiac catheterization and coronary - Hypoxia ( decrease O2)
angiography. Cadiac catheterization (for coronary arteries) and IVUS (for - Tachyarrhythmias
myocardium) are done simultaneously - Thyrotoxicosis
- Illicit drug use - direct injury to the myocardium
IVUS
- The wall of the coronary artery and the presence of Pharmacologic Therapy of CAD
atherosclerotic plaque can be seen in IVUS - Anti-platelet agents
o Aspirin – drug of choice; cheapest
Management of CAD can cause gastric irritation to the gastric
- Lifestyle modification mucosa specially aspirin use PPI:
- Control coronary risk factors Pantoprazole
o DM, hypertension, hyperlipidemia, etc. The use of omeprazole decrease the
- Management of extracardiac contributing factors efficiency of clopidogrel by 50%
- Pharmacologic therapy o Clopidogrel (Plavix)
- Coronary revascularization o Ticlopidine (Ticlid)
o Significant test but not an ultimate therapy - Anti-ischemic drugs – diminishes oxygen demand by
because you cannot control atherosclerosis decreasing the end-diastolic volume
o Tries to enhance coronary blood supply but o Nitrates – In the acute stage, this is given
atherosclerosis remains to be present sublingually and maintain an oral long-acting
The patient should be under medication preparation of Isosorbide mononitrate for prevention
indefinitely More on venous dilatation to decrease
return to the RA and RV. Dimished return
Non-pharmacologic measures in the management of CAD to the left side lessen end diastolic
- Lifestyle modification volume (from 80%-50%) lessen the
o Maintain ideal BMI myocardial work load
BMI = weight (kg)/height(m2) Form of Isosorbide that is rapid in action
Regular aerobic exercise (to improve is dinitrate. Dinatrate is given for acute
blood flow) minimum 30-45 minutes four attacks – short-acting
times a week (30mins of walking 4x a o Beta blockers
week) Decrease HR decrease oxygen
o Healthy heart diet - low salt, low fat, high fiber demand decrease cardiac workload
o Smoking cessation No effect on vessels. It has no effect on
o Control coronary risk factors endothelial function.
- Hypertension Side effects: asthma – provoke the
o Goal is to maintain BP < or = 130/80 attack
o In patients with CAD, beta blockers, CCB (calcium What can be given is
antagonists), or ACE inhibitors preferred. diltiazem or isoptin verapamil
Beta blockers, ACE or ARBs are more but these two have (-)
preferred inotropic effect in the heart.
Calcium antagonists: dihydropyridine and Vasodilator beta blockers: carvedilol
non-dihydropyridine and nebivolol. (Included in studies
Non-dihydropyridine which regarding heart failure and not in CAD)
has a similar effect as beta Carvedilol - with alpha
blocker: verapamil and blocker as vasodilator
diltiazem
Nebivolol – has nitric oxide
- DM
which is a powerful
o Maintain normal fasting and post-prandial glucose
vasodilator and enhances
and glycosylated hemoglobin; ACE or ARB
endothelial function.
inhibitors preferred
o CCB
Glycosylated hemoglobin tells us the
Verapamil and diltiazem
control of diabetes.
(-) inotropic effect
- Dyslipidemia
o ACE inhibitors
o Goals are more stringent in patients with CAD
Total cholesterol = <200%
LDL = <70mg
HDL = >45
Tg = <150mg
Pharmacologic therapy of ischemic heart disease: antiplatelet agents Pharmacologic Therapy of CAD: Anti-ischemic agents
Agent Action Usual dose Side effects Agent Indication Dosage A/E or C/I
Aspirin Inhibits GI irritation Diltiazem Diltiazem is Angina pectoris The most
cyclooxygenase 80-325mg od indicated for – initially commonly
Ticlopidine Inhibits ADP Neutropenia unstable angina 120mg/day in observed side
(Ticlid) – mediated platelet 250mg BID pectoris including equally divided effects were
not activation withdrawn from angina die to doses. Optimum edema,
available in the market coronary artery dose range: 180- asthenia,
the market spasm, or 360 mg/day in flushing, sinus
Clopidogrel Same same following MI. It is divided doses bradycardia,
(plavix) 75mg OD also indicated for first degree AV
chronic stable Hypertension – block,
angina, Initially 12-240 headache,
Note: To prevent GI irritation, what can be given are PPIs like hypertension, and mg/day in nausea, rash,
Pantoprazole which does not affect the strength of the Clopidogrel. for the prevention divided doses. joint swelling,
Omeprazole decreases the effect of Clopidogrel by 50%. of graft failure Usual dose fatigue and
following kidney range: 240-360 dizziness.
Effect of anti-ischemic drugs transplantation mg/day in divided
doses
Agent HR Contractility BP LV Coronary Collate
vol. blood rals Kidney
flow transplantation
Nitrates NC – initially 120
Beta NC NC NC mg/day in two
blockers or equally divided
doses. Optimum
CCB or NC NC NC dose range 180-
(Non-D) 300 mg/day in 3
equally divided
Pharmacologic Therapy of CAD: Anti-ischemic agents doses
Verapamil Treatment of Verapamil 40-80 Edema,
Agent Indication Dosage A/E or C/I coronary artery mg q 6-8h asthma,
Nitroglycerines Ischemic, SL: 0.4mg Headache, disease including flushing, sinus
(Isosorbide) hypertension ISDN: 5-10mg TID BP, crescendo angina bradycardia,
(because it (short-acting/rapid) hypoxemia, pectoris at rest, first degree AV
decreases the ISMN: 30-60mg BID caution with vasospastic angina block,
BP), CHF (long-acting - for RV infarct or Prinzmetal headache,
(which is d/t prevention of chest angina, and post-Mi nausea, joint
IHD) discomfort) infarction angina in swelling, rash,
NTG patch: 5-10mg patients with heart fatigue,
OD (applied over the failure if beta dizziness
chest for 12h and blockers cannot be
then remove then given
reapply to prevent
nitrate tolerance)
Metoprolol: Anti-ischemic, IV not available Bradycardia, Pharmacologic therapy of IHD: ACE Inhibitors
other beta anti- PO: 25-50mg q6h, AV block,
blockers hypertensive, then 50-100 mg BID CHF, asthma Agent Indication Dosage A/E or C/I
anti-arrythmic Captopril LV dysfunction 6.25mg initially; Renal failure,
Diltiazem: Ischemia not Diltiazem CHF, with CHF titrate to 50mg low BP, cough
verapamil responsive to 30-90 mg q6-8hrs LVEF<40%; TID
beta blockers, AV block; Enalapril Same 6.25mg initially Same
(N-d CCBs rapid AF Verapamil 40-80 mg low BP, titrate to 10-20
NOT Nifedipine without CHF q6-8hrs avoid mg BID
and Amlodipine nifedipine Lisinopril Same 6.5mg initially Same
which are D titrate to 10-20
CCBs) Not given in mg OD
patients with
HF with an Metabolic approaches to MI
ejection - Preconditioning (nicorandil)
fraction - Sinus node inhibition (Ivabradine)
<40% o This has a study in heart failure by inhibiting the
because it sinus node and therefore decreasing the heart rate
has a (-) without the side effect of beta blockers, ACE
inotropic inhibitors, or non-dihydropyridine CCBs.
effect - Late sodium current inhibition (ranolazine)
o In myocardial ischemia, there is inhibition in the
action potential (late sodium current). With inhibition
of the late sodium current, there is an increase in
the calcium that would promote more contractility
and stiffness of the myocardial segment. There is
LV diastolic dysfunction. If this is given, calcium will
be blocked and so there will be more expansion
during the period of diastole.
o People with LV diastolic dysfunction have a low
cardiac output and low stroke volume but ejection
fraction is normal. Because of the low cardiac output
and low stroke volume, the patients will feel easy
fatigability.
o The symptom of easy fatigability is controlled with
this ranolazine
- Metabolic modulations (trimetazidine)
o Increasing oxygenation of the myocardium
Non-pharmacologic therapy of IHD

- Percutaneous transluminal coronary angioplasty (PTCA)
with or without coronary stent implantation (to maintain the
patency)
- Coronary artery bypass grafting (CABG)
o Even in a stable IHD, this is the treatment of choice.
o This is done when the patient have been
bombarded with all the different drugs but the
patient remains to be symptomatic and ECG shows
ST segment depression with concomitant T wave
inversion seen from V1 to V6 carotid
angiography is done to see how severe the
obstruction of the coronary artery is and a
consequent angioplasty.
Post MI Risk Assessment

- Treadmill stress test
- ECG
- Radionuclide ventriculography
- Holter monitoring; signal averaged
o For 24h ECG monitoring
- Dipyridamole or adenosine thallium testing
- Coronary angiography
o If the patient is positive, another coronary
angiograpy is warranted.
Secondary prevention of MI
- Aspirin – indefinitely
o Counterpart is Clopidogrel
- Beta blockers – 2 years to indefinitely
- Converting enzyme inhibitors – all patients with or without LV
dysfunction; indefinitely
- Diet and lipid lowering therapy – statins; indefinitely
- Exercise and rehabilitation
- Smoking cessation
Note: If the patient survives the attack and the patient responded to the
optimum medical therapy or the patient had undergone more invasive
procedures such as angioplasty and bypass procedure, indefinite
prevention must be followed. It is a lifetime disease and a lifetime intake of
medications. Patient education is a must!
ACUTE CORONARY SYNDROME - There are two types of plaque:
- Severe form of ischemic heart disease o Stable plaque
The fibrous cap is thick with a lipid core
ATHEROTHROMBOSIS o Disrupted plaque
- Acute thrombosis occurring in the presence or pre-existing Plaque having a narrower cap containing
atherosclerosis produces acute ischemic strokes, acute the lipid core
ischemic syndromes of peripheral arteries (called peripheral There is a site of rupture
arterial disease or peripheral arterial occlusive disease) and Thrombus or blood clot
acute coronary syndrome including unstable angina,
myocardial infarction (NSTEMI and STEMI based on Pathologic and Clinical Presentation of Acute Coronary Syndromes
electrocardiogram) and sudden death
Burden of Acute Coronary Syndrome

- Significant public health problem both in industrialized and
developing countries
ACUTE CORONARY SYNDROME

- Unstable angina is a non-ST elevation MI
o There are 1.43 million hospitalizations in the US
- ST Elevation Myocardial Infarction (STEMI)
o 1,680,000 hospitalization for ACS in 2001
o 30% of ACS patients have STEMI
o 500,000 STEMI events per year in USA
ATHEROSCLEROSIS TIMELINE
Case: Patient has ischemic discomfort (discomfort in the region of the

chest). It is described as heaviness, squeezing, or something that
compresses the region of the chest. There is no pain because it is just a
very uncomfortable feeling. The working diagnosis is acute coronary
syndrome.
Note: The kind of ACS depends upon electrocardiogram and the

biochemical markers to be able to reach the final diagnosis.
- We look at the ECG and look for the ST segment if there is
elevation or not.
o If it is not elevated NSTEMI or unstable angina
o If it is elevated STEMI
Note: It starts during the first decade of life and the artery is still well- - STEMI and NSTEMI are formerly referred to as:
dilated. There are already beginning atherosclerotic changes in the form of o Non Q MI
a fatty streak which is the early stage of atherosclerosis. On the second o Q wave MI
decade, it becomes bigger. On the third decade, it also becomes bigger
and thicker and the artery becomes narrower. In the later part of the third CARDIAC BIOMARKERS - UNSTABLE ANGINA vs NSTEMI
decade there will be an atheroma or the plaque is already formed. On the
fourth decade, a fibrous plaque is well-formed and the artery is narrow
and there is a rupture of the plaque. When it ruptures, a lot of thrombus
or clot will circulate. It depends upon where it will land and how big is the
clot when an event happens. When it goes to the brain into the cerebral
artery it will produce stroke in the form of an infarct. Similar to this, when it
lands to the heart into the coronary artery it will produce. The more
arteries affected, the more segments affected. It is a thrombus that
basically semi-occluded or occluded therefore diminishes or stops blood
flow to that myocardial segment necrosis fibrinoid degeneration.
It will affect the overall function of the heart which is pumping blood in
order to perfuse the peripheral arteries.
Atherosclerosis to atherothrombosis
Note: To differentiate between the two, it is based on the biochemical

cardiac markers.
- Unstable angina and NSTEMI
o Both do not present with ST elevation
- It can be a non-occlusive thrombus or there is a vasospasm on
top of a non-occlusive thrombus. When the artery becomes
spastic it becomes narrow even if the thrombus is not occlusive
(not occluding completely the artery that has been affected) it
will be similar to a complete or partial occlusion of a coronary Note: On the first several days, the site of necrosis does not extend on the
artery. whole extent of the myocardial segment. After several weeks or months,
o If it is a non-occlusive thrombus there will be less there will be fibrinoid degeneration. Some subendocardial muscle will die
severe ischemia and less myocardial damage but the lesion does not extend throughout the entire myocardial segment
Unstable angina or the wall.
o Non-occlusive + vasospasm: there would be
severe ischemia and more myocardial damage ECG
NSTEMI
- When there is myocardial damage, there will be necrosis
followed by fibrinoid degeneration. During necrosis, the
cardiac myocytes will release troponins (troponins located in
the thin filaments: Troponin T, Troponin I, Troponin C). It
serves as a clue to the severity of the damage. Tropinin is the
one that would differentiate NSTEMI from Unstable angina.
History:
- severe localized chest or arm pain at rest or on minimal
exertion > 20mins crescendo pattern
Physical exam:
- pulmonary edema new or worsening MR, S3, new or worsening Note: The point that we are looking for is the ST segment.
rales
- First several days
Note: sometimes there will be crackles due to pulmonary edema, apical o Some subendocardial muscle dies (necrosis,
systolic murmur, or S3 gallop on auscultation decrease perfusion, not enough blood in
myocardium), lesion does not extend through the
ECG: entire heart wall
- transient ST segment changes (>0.05mv), new bundle branch o In terms of electrocardiogram, what we can see are:
block, sustained ventricular tachycardia R wave persists but may diminish
somewhat
Note: The ECG shows some ST segment changes but is only 0.05mV. Q wave not significant—significant if it is ¼
For it to be significant, it must be 2 or more mV. Both have the same of the height of R wave.; necrosis
presentation and what would separate the two would be the cardiac ST segment often returns to baseline
markers. T-wave inversion may occur
- After several weeks or months
Cardiac Markers o Lesion heals. Some subendocardial fibrosis may
Unstable angina NSTEMI occur but does not involve the entire thickness of
Shows no elevation of Troponin I, Troponin T, CKMB (creatinine heart wall so the heart can still contract.
Troponin. There could kinase and myoglobin are also released by the Q wave not significant
be troponin up to 50 cardiac myocytes in response to the presence ST segment and T wave may or may not
nanogram per deciliter. of necrosis but this is not used nowadays return to normal. T wave is upright.
because it does not last long). In early
necrosis, myoglobin is elevated but it lasts for
only a few minutes to hours. CKMB will be
elevated on the 2nd day. Troponin I and
Troponin T are elevated during the 1st day.
- CKMB lasts for 24 hours
- Trop I lasts for 6-7 days
- Trop T lasts for 10 days
Note: Troponins further increases in the presence of necriosis. They have
longer stay in the plasma as a manifestation that there is a myocardial
damage. The presentation of unstable angina and NSTEMI is the same
but what differs is the level of Trop I and Trop T. Note:
- There are other markers called high sensitive Troponin T and Location ECG leads Blood supply
high sensitive Troponin I Inferior wall lead II, III, AVF RCA/LCX
Lateral wall lead I, AVL, V5 and V6 LAD/LCX
PATHOLOGIC and ECG changes in NSTEMI
Anterior wall V3 and V4 LAD
Anteroseptal V1 and V2 LAD
- Posterior wall is represented by reciprocal changes
What do we look for in the ECG?

- ST segment: elevated, depressed, or at the baseline (normal)
- T wave: inverted or upright
- Q wave: can be deep or ¼ of the size of the R wave or wide
more than 0.4seconds
Note: ECG
- When we refer to the timing, it is horizontal.
- When we refer to the voltage, it is vertical.
ECG changes in Unstable Angina/NSTEMI Note: These are the reasons why the troponins are markedly elevated
- ST segment depression (30%) signifying the severity of damage in the myocardium. Refer the patient
- T-wave inversion (20%) immediately to the cardiac cath lab for emergency angiogram and a
- Transient ST-segment elevation (5%) possibility of bypass operation due to widespread damage.
PATHOLOGIC and ECG changes in STEMI
- ST segment depression at V4, V5, V6

- T wave inversion at Lead I, AVL It affects the whole or entire segment of the myocardium because of total
occlusion necrosis (black). Because there is necrosis:
Note: In II, III, AVF involvement, 2 out of 3 or all of the three must be - First and second days
present to consider an inferior wall involvement. In I and AVL, both must o Transmural infarction nearly complete. Some
be present to consider a lateral wall involvement. ischemia and injury may be present at borders
o R wave gone or nearly gone
o Significant Q wave
o ST elevation may decrease
o T wave inversion beginning
- After 2 or 3 days
o Transmural infarction complete
o No R wave
o Deep T wave inversion
o Marked Q wave
o ST may be at baseline
- After several weeks or months
o Infracted tissue replaced by fibrous scar, sometimes
bulging (ventricular aneurysm)
There is fibrinoid degeneration or
fibrosis
- Significant T wave inversion – deep and symmetrical at V2, o Some R wave may return (but is not tall)
V3, V4, V5, and V6 o T wave often less inverted (smaller)
- No ST segment elevation or depression o Significant Q wave usually persists
- With small Q wave (the elevation should be >2mv) o ST elevation
Note: V2 – V6 changes = anteroseptal wall and lateral wall involvement STEMI ECG findings
diffuse myocardial ischemia
ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

- There is total occlusion
- Clinical Diagnosis
o History
Accelerating Angina and rest pain
(>30mins)
Constricting, crushing, compressing,
heaviness, choking
Retrosternal radiating to ulnar aspect of left
arm
Atypical presentation
- Physical exam
o Soft S1, S3, S4, Mitral regurgitation due to papillary - At least 2mm ST segment elevation in two or more precordial
muscle dysfunction, pericardial friction rub leads
o Hypotension, tachycardia, bradycardia - ST segment elevation of at least 1 mm in two or more leads
- ECG
o ST Segment Elevation, Q waves (signifies necrosis) Note:
- Cardiac Markers
- 2mm ST segment elevation in V2, V3, and V4 there is
o Troponins (cTnT, cTnI), CK-MB mass, Myoglobin
occlusion of the left anterior descending coronary artery. If it is
- Pathological Diagnosis
the only one occluded and angiogram and immediate
There is total occlusion
angioplasty is done, the patient will recover.
o Prolonged ischemia
- ST elevation in II, III, AVF + depression in I and AVL which
o Myocyte Death
is significant? Inferior changes are more significant and in
o Coagulation Necrosis
the leads opposite the site there are depressions and these
o Myocytolysis
are called reciprocal changes.
Myocardial Ischemia, Injury and Infarction ST Segment changes in infarct
- ST segment elevation indicative of injury

- Disturbance in current flow across the membrane
Note: This is a typical ST segment elevation because there is an acute

injury to the myocardium. There is a disturbance in the current flow across
- Zones: the membrane. The Q is not significant so it means that this is a recent
o Infarction infarction (4-6 hours). At this point, thrombolysis can still be done because
o Injury there is an acute injury with significant elevated ST segment.
o Ischemia
PRIMARY AND RECIPROCAL ST CHANGES IN ACUTE PHASE
INFARCTION
Myocardial ischemia T wave inversion
Before Infarct In acute phase infarction
Myocardial injury Elevation of the ST segment
(Injury)
Infarction Significant Q wave appears Lead facing infarct zone ST elevation typical primary
ST segment elevation change
Q wave persist s, ST goes back to normal Lead opposite infarct zone ST depression Typical
reciprocal change
Note: If you see an ST elevation + the patient has chest discomfort
thrombolysis (best thrombolytic agent is rtPA) can still be done to Note: If you see a ST elevation, it is the one that is significant. If you see a
dissolve the thrombus. If there is already occlusion and the presence of Q depression, it is the reciprocal change.
wave don’t do thrombolysis.
T wave changes in Myocardial Infarction
Reciprocal effect on the opposite side of the infarct - Deep symmetrical T wave inversion
- Since there is elevation in one side, there is depression on the - ―Symmetry‖ refers to the equality of the angles of downstroke
opposite side because the QRS axis is moving to the opposite and upstroke of the T wave
side away from the site of injury.
o If there is elevation, the reciprocal change is a Evolution of ECG changes in Acute STEMI
depression.
QRS Complexes in Infarction

- Normal QRS progression
- Height of R wave is related to thickness of viable myocardium
o If there is a small R wave, this means that there is a
site of injury. In echo, there is thinning of the
myocardial segment because there is a site of
injury.
- Full thickness infarction show abnormal Q waves and QS
complexes
o If there is a negative wave immediately after the P, it
is the Q wave
o If there is a negative wave after the R wave, it is the
S wave. - Normal
o No contraction - In hours ST elevation
- Extent of wall thickness involved in infarction determines R o In about 4-6 hours
wave voltage and abnormal Q waves. o Thrombolysis can be done (within golden period)
- In days Q waves, Small R, ST elevation
Abnormal Q waves o Thrombolysis cannot be done anymore because of
the presence of Q wave
- In weeks Q waves, Small R, ST isoelectric, Deep T
inversion
- In months Q waves, small R, ST isoelectric, T wave upright
Note: Q wave signifies that there is already a fibrosis (lifetime)
- Duration: >0.04sec
o The duration is more than one square moving
horizontally
- Depth: >25% of the height of R wave
o The depth is more than ¼ of the height of R wave
INFARCT, LOCATION AND ECG LEAD INVOLVEMENT
Location of infarction Leads showing primary

changes
Anterior Infarction
Anteroseptal V1, V2, V3
Anterior V1-V3, V4-V6
Anterolateral V4-V6, I and AVL, possibly II
Extensive Anterior V1- V6, I and AVL
High Lateral AVL (plus high precordial leads)
Inferior infarction
Inferior II, III,AVF
Inferolateral-Apical II, III, AVF, V5, V6 and
sometimes also I and AVL Occlusion of the right coronary artery, where is the significant lesion?
Inferoseptal II, III, AVF, V1-V3 - Reciprocal change in V1, V2, V3, V4
Other changes - No significant elevation of the ST segment
Posterior infarction V1, V2( inverse of usual changes - II, III, and AVF – QS wave (inferior wall)
elsewhere) - Injury in the posterior wall
Subendocardial Infarction Any lead (usually multiple leads)
Early intervention + medical management should be given!
Note: The posterior portion of the heart is supplied by the right coronary
artery, including the inferior. Since we know that in V1 and V2 are CASE 1: 55 year old male bank executive experienced severe constricting
negative waves (P wave, small R, S, upright T), the wave of depolarization chest pain radiating to the back after a heated discussion. 3 hours later
is moving away from it moving to the left. Therefore, we use the reciprocal was brought to the ER because of persistent chest pain
changes. In V1 and V2 there is inversion as the usual change elsewhere.
There is a tall R and ST depression and T wave inversion. Reciprocal
change seen in V1 and V2, (and sometimes V3), it is a reciprocal change
of an infarction affecting the posterior portion of the heart supplied by the
right coronary artery.
Subendocardial symmetrical T wave inversion (diffuse ischemia)
Anteroseptal Wall STEMI
There is occlusion of a branch of the left anterior descending coronary

artery, where is the significant lesion?
- ST elevation V1, V2, and V3
(+) Q wave – thrombolysis cannot be done anymore
CASE 2: 65 year old female obese diabetic was awakened early in the
morning becayse of severe epigastric pain radiating to the anterior chest
There is occlusion of the left anterior descending coronary artery, where is

the significant lesion?
- Q wave in I and AVL
- V2, V3, V4, V5
Occlusion of the right posterior descending coronary artery, where is the dDx: GERD, Acid peptic disease, cholelithiasis
lesion? (+) risk factors for atherosclerosis – age, obese, diabetic
- II, III, and AVF ECG: ST elevation in II, III, AVF; reciprocal changes in I and AVL
- Reciprocal changes in I and AVL (-) Q wave – can still perform thrombolysis
CASE 3: 53 year old female diabetic, meat vendor complained of on and Note: Aspirin should be chewed and absorbed under the tongue for
off chest pain for the last 3 days. Persistence of pain prompted to consult immediate effect. During the acute attack/rupture, there would be platelet
cardiologist where an ECG was done. adhesion and aggregation that contribute to the size of the thrombus.
Aspirin is the anti-platelet drug of choice. Aspirin + 4 tablets of Clopidogrel
swallowed.
PCI (percutaneous coronary intervention) with possible angioplasty or

bypass
Further tests include treadmill or stress echo or nuclear imaging. Echo
looks at the wall motion and nuclear looks at the myocardial perfusion and
angiogram looks at the lumen of the coronary artery (coronary angiogram
+ intravascular ultrasound done to look into the wall of the heart)
Results should be correlated clinically
Acute coronary syndrome/ acute myocardial infarction Algorith

(PHA council on CardioPulmonary Resuscitation)
ACUTE CORONARY SYNDROME

- Most common proximate cause of sudden cardiac death
(+) Risk factors: age, diabetic, possible dyslipidemia due to occupation - Manifested as a chest pain
ECG: peaking of T wave, symmetrical T wave inversion, (+) Q wave - With ECG changes
(days) [recent is ST elevation] - Cardiac markers
Dx: Inferior wall myopcardial infarction
Tall T wave of hyperkalemia, stress, etc Treatment objective
- Reduce myocardial necrosis
CASE 4: 45 year old male surgeon, smoker complains of retrosternal - Prevent major adverse cardiac events
chest pain with choking sensation lasting for 30 minutes. o ACS
fatal arrhythmias – sudden cause of death
goes into heart failure
aneurysm
cardiogenic shock
Manifestation of cardiogenic shock to
differ it with circulatory or neurogenic
is progressive lowering of blood
pressure, urine output, and
confused.
Stage 1 to 4
o 1 – responds to
treatment
o 2 – chest pain but able
to tolerate it
o 3 – pulmonary edema
o 4 – cardiogenic shock
Risk factors – male, age, stress
- Treat life threatening complications (pulmonary edema or
ECG: No ST elevation, ST depression in V4, V5, and V6 (significant/true)
cardiogenic shock)
Dx: To consider Unstable angina or NSTEMI, lateral wall (request for
cardiac markers to confirm)
ST segment
MANAGEMENT
Infarct – ST elevation
Ischemia – ST depression
Unstable angina
Note: End result of these is that the myocardium becomes ischemic or

necrotic
CASE the workload and cannot dilate the
- 55y/o man damaged coronary artery. Vasodilating
- Hypertensive, diabetic, smoker effect is on the venous and in the normal
- High cholesterol coronary artery but not in the damaged
- Severe substernal chest heaviness> 30 minutes, ―crushing‖, coronary artery. It can promote collateral
―squeezing‖ circulation (Isosorbide + Beta blocker)
o Clopidogrel
What do you do? o Heparin (UFH or LMWH)
a. Assess ABCs To prevent coagulation
b. Insert IV line Promote reduction of the symptoms of the
c. Give oxygen per nasal canula patient
d. Get a 12 lead ECG o ACE inhibitors (or ARB)
Choice
Chest pain (Suggestive of ischemia) Within the 24 hours onset + HMG CoA
A. Immediate assessment 80mg Atorvastatin can be given
- Vital sign, O2 saturation
- IV access If there is a ST depression and dynamic T wave inversion, management is
- 12 lead ECG the same!
- Brief history and PE
- Cardiac Markers STEMI or NSTEMI or unstable
- Electrolytes, coagulation and portable CXR - select reperfusion strategy
- Begin fibrinolytic checklist in order to determine if thrombolysis - -be aware of reperfusion goals
can be done or not (if there is tendency for bleeding) o Door to balloon inflation(PCI) goal of 90 min
o Door to needle (fibrinolysis) goal of 30 mins
B. Immediate general treatment o Continue adjunctive therapies and HMGCoA
- Oxygen 4LPM reductase inhibitor(statin)
- ASA 160-325mg Statin of choice is Atorvastatin
- Nitroglycerin SL or spray
o Isosorbide dinitrate Time onset of symptoms
- Morphine - >12 hours
o Best given for the relief of the discomfort o Monitor the patient in the emergency room and
assess risk status
MONA - Morphine, Oxygen, NTG, ASA - <12 hours
- Cardiac cath lab unit or notify receiving hospital o Select reperfusion strategy
C. Assess initial 12L ECG If there is cardiogenic shock or contraindications to fibrinolysis, reperfusion
(surgical) is needed. PCI is the treatment of choice. If PCI is not available,
A. Assess the Initial ECG use fibrinolytics.
12L ECG is central to triage of ACS in the ER. Classify patients
as being 1 to 3 symptoms within 10 minutes of arrival Fibrinolytic therapy selected
a. STEMI - Altapase
ST-segment elevation - Streptokinase
Or new or presumably new LBBB - APSAC
b. High risk unstable (NSTEMI) - Recombinant tissue plasminogen activator
ST-segment depression o Best
Dynamic T-wave inversion
c. Intermediate/ low risk unstable angina Absolute contraindications to beta blockers
Non-diagnostic ECG - heavy failure
ST depression 0.5-1mm - pulmonary edema
T-wave inversion or flattening or flattening - bradycardia (HR <60)
in leads with dominant R waves - Hypotensive
o Systolic BP <100
Note: Before we do other tests, do cardiac markers. If normal, do other - Signs of poor peripheral perfusion
tests. Flattening of ST segments is suspicious so treadmill tests are - Presence of a 2nd or 3rd degree heart block
usually done.
Fibrinolytic
Q: Small R wave, widened QRS, V5 and V6 - Contraindications:
A: LBBB – manifestation of ST elevation MI o Very high blood pressure
- Even though it is a manifestation of STEMI with increase in o Recent surgery
Troponins, we cannot do thrombolysis because there is no o Bleeding tendency
elevation. There is no clue whether the infarct is recent or not
(within the 4-6 hours after the rupture of plaque). No
Dynamic T wave inversion
thrombolysis for LBBB! RBBB is usually insignificant and is not
included in STEMI.
High risk group
A. ST elevation or new LBBB/ ST elevation AMI - Ischemic chest discomfort (recurrent)
- Treatment - V-tach – prelude to ventricular fibrillation
o Start Adjunctive Treatment (within 24hrs of onset/ - Hemodynamic instability
stable) - Heart failure
o B-blockers - Early invasive strategy
Decreases the heart rate/workload similar to o Cardiac catheterization and revascularization within
the effect of nitroglycerine that decreases 48h of MI
Main Objective is
Treatment for STEMI and NSTEMI is the same! - to reduce necrosis that affects the myocardium
- prevent major cardiac event and ventricular aneurysm, cardiac
In general, treat these patients with anti-thrombin, heparin, and anti- arrhythmia, rupture of chorda tendinae and most common
platelet agents complication (Heart failure) and most common cause of death
(Cardiac arrhythmia)
Persistent symptoms, recurrent ischemia, diffuse or widespread ECG
abnormalities, depressed LV function, heart failure, serum cardiac Start adjunct tx:
markers needs reperfusion therapy - NTG
- Betablocker
Who stays in the ICU? - Clopidogrel-less expensive, for three months
- No persistent symptoms - Heparin
- Symptoms disappear - Glycoprotein IIb/IIIa
Optimum medical management can be given: High risk subgroup:

- refractory ischemic chest pain
- Anti-platelet
- recurrent/persistent ST deviation
- Clopidogrel
- Hemodynamic instability
- ACE or ARBs
- Pump failure
- Beta blockers
- Nitrates or Isosorbide dinitrate
Early invasive strategy includes cathetherization and
- Glyc IIb/IIIa inhibitor revascularization.
EXTRA NOTES: Prevention:
- Clopidogrel and Aspirin - within 90mins of thrombus formation - Clopidogrel-less expensive,( FOR LIFE)
- New antiplatelet: PRASUGREL AND BRELINTA
Why do we give beta blockers? - Statin therapy high dose(FOR LIFE)
- It decreases the HR - ACE/ARB(FOR LIFE)
- increased HR more oxygen consumption needed
Contraindications of Beta blocker :

- pulmonary edema
- heavy failure
- bradycardia
- hypotensive
- complete heart block
Contraindications of Fibrinolytic therapy (streptokinase, Tissue

plasminogen activator)
- (+) bleeding episode
- CVA hemorrhage
In short the patient needs to undergo REVASCULARIZATION
Primary PCI selected

- Experienced operators
- High volume centers
- Cardiac surgical capability
Fibrinolytic therapy selected

- Altapase
- Streptokinase
- APSAC
B. ST depression/ dynamic T-wave inversion (High risk UA/ non-

STEMI)/ ST elevation or new LBBB/ ST-elevation AMI
C. Non-diagnostic ECG
- ST depression 0.5-1mm
- T wave inversion or flattening in leads with dominant R waves
- Intermediate/low risk unstable angina
Absolute contraindications to beta blocker therapy

- Severe LV failure and pulmonary edema
- Bradycardia(heart rate < 60bpm)
- Hypotension( SBP < 100mm Hg)
- Signs of poor peripheral perfusion
- Second or third-degree heart block
If there is ST elevation, initiate Ischemic therapy and non dx ECG.

Combine ECG and serum markers
adiuvante Dei gratia doctorum factionis 2014-2015
CARDIOLOGY: CARDIAC DR. MOISES
BARTOLOME, MD
TUMORS
CARDIAC TUMORS CLINICAL MANIFESTATIONS
Cardiac and non-cardiac manifestations

Primary tumors of the heart RARE (.0017 - .28%) o When you say cardiac, murmurs, heart failure
Often BENIGN (75%) – usually myxoma o Non cardiac – anemiaa fever etc
Potential for life-threatening complication if thaht goes to
the brain, stroke, to heart, MI Location and size of tumor the major determinants of
Curable by surgery specific signs and symptoms
Most common cause of primary tumor is myxoma
Followed by rhabdomyomas – infants and children o halimbawa, sa pericardium (most common area
Myxoma is the most common primary tumor of the heart the tumor goes into the heart) , end up problems
Myxoma is the most common primary BENIGN tumor of the like pericarditis and pericardial tamponade
heart
Sarcomas (angiosarcoma) - most common primary malignant o If it is in SA node, end up having AV blocks
tumor of the heart and is the second most common primary
tumor of the heart after myxoma o If in intramyocardium, end up with congestive
In children infants you have rhabdomyosarcoma and malignant heart failure because of inadequate contraction
teratoma to think of and relaxation of the heart
SIGNS AND SYMPTOMS SIMILAR TO ALL FORM OF HEART DISEASE
Chest pain – different hard to differentiate from other

Syncope – loss of consciousness; inadequate perfusion to
the brain.
o Heart attack and then having ventricular
arrhythmia no CO inadequate perfusion to
the brain syncopal attack
o if obstruct carotid arteries inadeaute perfusion
to the brrain syncopal attack
o If tumor obstruct outflow tract (area before aorta)
syncopal attack
Heart failure
o Right sided – neck vein distention, ascites,
o Left sided – dyspnea, orthopnea, nocturnal
paroxysmal dyspnea
Murmurs
o Systolic – aortic stenosis, pulmonic stenosis,
mitral and tricuspid regurgitation
o Diastolic – aortic regurg, pulmonic regurg, mitral
and tricuspid stenosis
Arrhythmias
o Example: Ventricular arrhythmia
o Ventricular tap vs supraventricular tap in ECG
unless theres no bundle branch block – you look
at QRS. QRS in supraventricular is narrow,
ventricular wide QRS
Conduction disturbance
o AV blocks
Pericardial effusion or tamponade
Diagnosis: SIGNS AND SYMPTOMS
Essential is positive imaging for characteristic cardiac
masses and biopsy of that masses
Have to open up the patient
MYXOMA
Most common type of primary cardiac tumor (1/3 to ½ of all

cases)
rd th
Most commonly in 3 – 6 decade; female > male
Sporadic vs familial
Majority sporadic; some are familial (autosomal dominant
transmission) or part of a syndrome
Carney complex – spotty skin pigmentation, myxomas,
endocrine overactivity, schwannomas
NAME syndrome – nevi, atrial myxoma, myxoid
neurofibroma, ephelides
LAMB syndrome – lentigines, atrial myxoma, blue nevi
CLINICAL PRESENTATION
Systemic or cardiovascular findings
Pulm hypeetension – R sided failure

Pulmonary emboli- difficulty of breathing, if obstruct pulm
artery -> RV sided failure
Anemia, elevated ESR, Raynaud’s, clubbing, elevated
Autosomal dominant – investigate the whole family,
globulin you can think of SLE
diagnostic procedure to use: echo
most common primary cardiac neoplasm--an atrial Cardiovascular findings:
myxoma.
These benign masses are most often attached to the atrial 1. Atrial
wall, but can arise on a valve or in a ventricle. • s/sx resemble mitral valve disease most
They can produce a "ball valve" effect by intermittently common clinical presentation
occluding the atrioventricular valve orifice. • Stenosis – tumor prolapse into the mitral
Embolization of fragments of tumor may also occur. orifice during diastole, mas common
Myxomas are easily diagnosed by echocardiography. stenosis kesa sa regurg
• Regurgitation – injury to the valve by
tumor-induced trauma, itf theres
destruction of the valves
2. Ventricular – outflow obstruction syncope
DIAGNOSIS
1. Two-dimensional transthoracic or trans-

esophageal echocardiography
• Determine site of tumor attachment

and tumor size
Don’t let anyone look down on you because you are
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young, but set an examples to the believers in speech, in life, in love, in faith and in
purity 1 Timothy 4:12
Page 2 of 12
st
• Screening of 1 degree relatives for • Benign connective tissue tumor
familial or syndrome myxoma
• Associated with calcification
2. CT scan and MRI
• Occur in the ventricle and IVS
• Tumor size, shape, composition, and
surface characteristics • s/sx secondary to mechanical interference with cardiac
flow, ventricular contraction abnormalities, conduction
3. Cardiac catheterization disturbance
• Done if theres Risk of tumor emboli; for PAPILLARY FIBROELASTOMA

suspected CAD
RHABDOMYOMAS
• Common findings on cardiac valves or the adjacent
endothelium at post-mortem
• Most common in infants and children (75% < 1 y/o)
• Seldom result in clinical manifestations
• Most common in ventricles s/sx due to mechanical
obstruction mimic valvular stenosis, CHF, restrictive or • Growth may cause mechanical interference with valve
hypertrophic cardiomyopathy, & pericardial constriction function -> regurg problems
• Multiple in 90% of cases • Found in elderly population (mean age 60 y/o)
• May be associated with tuberous sclerosis, adenoma HEMANGIOMAS AND MESOTHELIOMA

sebaceum, benign kidney tumors
CARDIAC LIPOMAS
• Generally small tumors
•
nd
2 most common benign tumor • Most often intra-myocardial in location
• Usually incidental post mortem findings • May cause atrioventricular (AV) conduction disturbances
and sudden death due to predilection for region of AV node
• Usually solitary; grow as large as 15 cm -- AV blocks
• Clinical: SARCOMA
Symptoms due to mechanical interference with

cardiac function
nd
• Most common malignant tumor; 2 most common primary
Arrhythmias tumor of heart
Conduction disturbances • Common in male (3:1)
Abnormality of cardiac silhouette on CXR • Characterized by rapidly downhill course leading to

patient’s death weeks to months from time of presentation
• If subepicardial due to:
Compression of the heart 1. Hemodynamic compromise
Pericardial effusion 2. Local invasion
If subendocardial 3. Distant metastases
With intracavitary extension, may produce • Histologic types:

symptoms characteristic of their location
1. Angiosarcomas – most common
Most common chambers affected: LV, RA, Interatrial
septum 2. Rhabdomyosarcoma
FIBROMAS 3. Fibrosarcoma
4. Osteosarcoma
nd
• 2 most common in pediatric age group
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5. Characterized by rapid growth 2. Signs of pericarditis (triad of pericarditis)
• At presentation, often spread extensively for surgical a) Chest pain aggravated by coughing, inspiration or
excision recumbency
• Commonly involve RA & pericardium right-sided failure, b) Pericardial friction rub on auscultation
pericardial disease, vena cava obstruction
c) Characteristic ECG changes
• May occur in left side mistaken for myxoma
3. Cardiac tamponade
TREATMENT AND PROGNOSIS
a) Increased JVP
• Surgery not effective to establish diagnosis b) Pulsus paradoxus
• Occurrence of distant metastases Look for the pulse, palpate it, if nawala
in neck vein engorgement
• Poor prognosis
c) To confirm: Echo evidence of RA and RV collapse
CARDIAC METASTASIS (metastatic to the heart)
CARDIOVASCULAR MANIFESTATIONS OF SYSTEMIC DISEASES
• 40x more common than primary tumors

DIABETES MELLITUS
• Occurs in 1-20% of all tumor types
• Malignant melanoma – highest predilection for cardiac 1. Increased incidence of CAD most common cause of death
metastasis (50-65%) can go to heart and cause problems, in adults with DM
kala niyo ganun ganun lang yung melanoma.
o CAD is the most common cause of death in adult
• Most common from breast (if female) and lung CA (if male) DM patients
o Equivalent ang survival rate with DM patient vs
• Almost always occur in the setting of widespread primary patient with MI
disease
• Two types of vascular disease
• May be the initial presentation of tumor elsewhere
a) Macrovascular
• Reach the heart via bloodstream, lymphatics or direct
invasion Atherosclerosis &
arteriosclerosis - CAD
• Usually present as small, firm nodules in the pericardium (
most common kasi) Cerebral circulation TIA,
stroke
LOCATION
>50% of DM have CAD; >50%
of DM ending up with stroke
• Pericardium – most common
Lower limb circulation
• Pericardial tamponade claudication, ulceration,
gangrene
• Myocardium
b) Microvascular
• Rarely, endocardium and cardiac valves
Retinopathy (number 1 cause
CLINICAL PRESENTATION of blindness) , nephropathy
(number 1 cause of dialysis),
neuropathy, small artery
• Depends on location and size of tumor occlusions of the heart
• Signs & symptoms occur only in 10%; non-specific • MI more frequent but also tend to be larger in
size and more likely to result in complications
• Usually occurs in the setting of recognized neoplasm such as heart failure, shock, and death
(stage 4 carcinomas)
1. Dyspnea – most common

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• Abnormal or absent pain response to myocardial MALNUTRITION AND VITAMIN DEFICIENCY
ischemia due to generalized autonomic nervous
system dysfunction up to 90% silent ischemias
KWASHIORKOR OR MARASMUS OR BOTH
When you have DM, threshold to test
for ischemia is low.
ECG, stress test Heart becomes thin, pale, and flabby with
Angina equivalent – no chest pain, but myofibrillar atrophy and interstitial edema
come to you with dyspnea, and sa ECG
may infarction na Low systolic pressure and cardiac output
• Presentation of ischemia may be: Narrow pulse pressure
a) Exertional or episodic dyspnea Generalized edema due to:
b) Flash pulmonary edema Reduced serum oncotic pressure
c) Arrhythmias – ventricular arrhythmia – Myocardial dysfunction

request for stress test. If may block,
check for CAD. Effects of starvation on the heart:
d) Heart block Decreased contractile force

decreased cardiac output
e) Syncope
Diminished diastolic compliance
RESTRICTIVE CARDIOMYOPATHY
Clinical:
• Myocardial dysfunction in the absence of large-
Bradycardia
vessel CAD
• Abnormal relaxation of myocardium elevated Hypotension

left ventricular filling pressure
ECG: NSSTTWC, ectopic rhythm
• Diastolic heart failure
MVP
AUTONOMIC NEUROPATHY
Decreased exercise capacity
• Secondary to autonomic denervation Heart failure, worsened or precipitated

by feeding
• Manifested as fixed tachycardia (>90 bpm
usually)with subsequent parasympathetic damage Heart becomes thin, pale, and flabby with
decreased heart rate (give beta blockers) myofibrillar atrophy and interstitial edema
• Complete autonomic denervation HR no longer Low systolic pressure and cardiac output
responsive to physiologic stimuli
Narrow pulse pressure
• All DM patients should receive statin therapy
unless contraindicated Generalized edema due to:
• All receive anti thrombotic unless contraindicated Reduced serum oncotic pressure
• Target BP: below 135/85 Myocardial dysfunction
• Best drug for DM patients: ACEI or ARB Effects of starvation on the heart:
• Cholesterol: <80 Decreased contractile force

decreased cardiac output
Diminished diastolic compliance
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• Clinical: The acute administration of thiamine to these patients
increases the left ventricular ejection fraction and the
a) Bradycardia excretion of salt and water.
b) Hypotension Characteristic cardiovascular syndrome:

• Heart failure with increased cardiac output high output
c) ECG: NSSTTWC, ectopic rhythm
due to vasomotor depression leading to reduced systemic
d) MVP vascular resistance
• Tachycardia
e) Decreased exercise capacity • Elevated filling pressures in the left and right sides of the
heart
f) Heart failure, worsened or precipitated
by feeding
DIAGNOSTIC CRITERIA
• Decreased intake also seen in:
Clinical features
a) Chronic disease – AIDS, PTB
• Dependent edema
b) Semi-starvation – anorexia nervosa • Low peripheral vascular resistance, decreased minimum BP,
increased pulse pressure
c) Severe CHF – GI hypoperfusion and
venous congestion anorexia and • Hyperkinetic circulatory state (mid-systolic murmur and S3)
malabsorption • Enlarged heart
• T-wave changes on ECG: inverted, diphasic, depressed
• Treatment should be gradual rapid expansion • Peripheral neuritis
leads to stress to heart heart failure • Dietary deficiency for at least 3 months or chronic
alcoholism
THIAMINE DEFICIENCY (BERIBERI)
May occur in the presence of adequate intake of calories and Presence of thiamine deficiency
• Decreased blood thiamine concentration
protein if polished rice is used
• Decreased ESR
Deficiency common among alcoholics
Don’t forget there is such a thing as thiamine deficiency or
Improvement after adequate thiamine therapy
beriberi heart disease.
The major cause of the high-output state is vasomotor
This is common in alcoholic patients
depression leading to reduced systemic vascular resistance, the
Probably those who are nagaavoid ng four legged animals. precise mechanism of which is not understood.
May ituturo ako sa inyo, you know, best food for patients The cardiac examination reveals a wide pulse pressure,
with increased cholesterol, you should avoid 4 legged tachycardia,a third heart sound, and, frequently, an apical
animals. Baka, baboy, lahat ng 4 legged animals, mataas ang systolic murmur.
cholesterol. Sarap sarap ng baboy ano? Advise them to eat The electrocardiogram (ECG) may reveal decreased voltage, a
2 legged animals. Pag 2 legged animals, kita mo, mababa prolonged QT interval, and T-wave abnormalities. The chest x-
ray generally reveals cardiomegaly and signs of congestive heart
ang cholesterol mo. Turkey, chicken
failure (CHF).
Clinical:
The response to thiamine is often dramatic, with an increase in
• Generalized malnutrition systemic vascular resistance, a decrease in cardiac output,
• Peripheral neuropathy clearing of pulmonary congestion, and a reduction in heart size
• Glossitis often occurring in 12–48 h
• Anemia
OBESITY
Don’t forget in Beriberi heart disease there is generalized
malnutrition, peripheral neuropathy, glossitis, anemia. Increased CV mortality and morbidity
What is glossitis? Tama din yung mga Chinese, tinitingnan Increased prevalence of
yung dila, may sakit ka, di ba? Tapos pulang pula. So that is
• Hypertension
your P.E.
• Glucose intolerance
When thiamine stores are measured using the thiamine-
pyrophosphate effect (TPPE), thiamine deficiency has been • Atherosclerotic coronary artery disease
found in 20–90% of patients with chronic heartfailure. Obesity can have problems, alam niyo naman yun pag
This deficiency appears to result from both reduced dietary obese, increased cardiovascular mortality and
intake and a diuretic-induced increase in the urinary morbidity because they have more likely to have
excretion of thiamine. hypertension, more likely to have diabetes,
atherosclerosis.
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+ +
• Increase synthesis of myosin, Na ,K - ATPase
Distinct CVS abnormalities • Increase density of myocardial ß-adrenergic receptors
• Increased total and central blood volumes
• Increased cardiac output and LV filling pressure HYPERTHYROIDISM
Pag walang mantika ang pagkain hindi masarap dib a? That
is your lifestyle now. You don’t have exercise anymore. Yun
Essentials of Diagnosis:
ang problem sa pasyente niyo ngayon. So, laging lifestyle
modification ang sinasabi. Don’t forget the obesity; you • Low TSH levels
should able to control that. Later, you have to master how
to advise them regarding diet therapy, and don’t forget that • Increased T3, T4, iodine uptake
patient with obesity, there will be increased total and
central blood volumes, increased cardiac output and LV So how do you diagnose hyperthyroidism? Examination
filling pressure and laboratory test. The most essential is to request for T3,
T4, and TSH
• Hypertension
o Eccentric LVH General Considerations:
o Pickwickian syndrome – cor pulmonale,
apnea, hypoxemia • Increased levels of thyroid hormone hyperdynamic CVS
What is Pickwickian syndrome? Basically the
Increased cardiac output, contractility;
development of cor pulmonale in obese patient, there
tachycardia
can be primary pulmonary problem because of being
obese, nagkakaroon ng obstructive sleep apnea that • Decreased SVR
end result to cor pulmonale. Sila yung mga obese
patients, matataba tapos nangingitim ngitim pa yan.
o Heart failure – (+) crackles, inc. JVP, S3, S4 SIGNS AND SYMPTOMS
o Edema
o Exercise intolerance
TREATMENT
Systemic s/sx
Weight loss
Weight reduction – most effective Increased appetite
Resting tremors of the hand
The most important effective way of preventing Nervousness, anxiety, insomnia, mood swings,
complications in obesity is lifestyle modification irritability
Heat intolerance & sweaty skin
Digitalis
Proximal muscle weakness & wasting
Sodium restriction Increased bowel movement or diarrhea
Diplopia
Diuretics Periodic paralysis
And when you say periodic paralysis, bigla
So how do you prefer to treat a patient with hypertensive nanghihina ang extremities mo. Kaya kailangan
obesity? so what will be your drug of choice probably? kumain kayo ng saging. Sa mga low
You have to give diuretic therapy. Sisikat ka pa. Bakit socioeconomic status, ang ulam ngayon, high
kamo? Aba, kapag umihi ang pasyente mo, bagsak ang carbo and high sodium intake. Pag nag high
timbang niya. Bumaba na yung blood pressure mo, carbo ka, bakit di bumababa potassium mo?
bumaba pa timbang mo. Because of insulin secretion. Kung alam mo
yung pinapakain mo sa pasyente mo.
THYROID DISEASE
Cardiovascular s/sx
Physiologic effects of thyroid hormone: Palpitations
• Increased total body metabolism and oxygen consumption Dyspnea – with or without LV failure
Increase workload on the heart Atypical chest pain
• Direct inotropic, chronotropic, and dromotropic effects Cardiac arrhythmias – AF, PACs
Tachycardia, increased cardiac output
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The most common dysrhytmia or rhythm Thyroid function test – T3, T4, TSH, RAIU
disturbance in patient with hyperthyroidism is
sinus tachycardia – PLEASE TAKE NOTE OF THAT! Initial Diagnosis:
Common cardiovascular manifestations of Atrial arrhythmias
hyperthyroidism include palpitations, systolic Cardiac enlargement
hypertension, and fatigue. Ventricular failure
Sinus tachycardia is present in ~40% of s/sx of hyperthyroidism
hyperthyroid patients, and atrial fibrillation in
~15%. You label your patient with thyrotoxicosis that is
hyperthyroidism that is what we called now
Apathetic hyperthyroidism thyrotoxic heart disease. If your patient has atrial
Elderly patient arrhythmias, cardiac enlargement, ventricular
o Present only with CV manifestations of
failure, s/sx of hyperthyroidism with biochemical
thyrotoxicosis such as AF (resistant to
therapy until hyper-thyroidism is evidence of hyperthyroidism and there is also
controlled) reversal of findings after treatment, you called it
Apathetic hyperthyroidism is very common in elderly thyrotoxic heart disease.
patients, these are patients with weight loss and atrial
fibrillation, isolated systolic hypertension Definite Diagnosis:
o (+) signs and symptoms
Elderly patients with hyperthyroidism may present with o Biochemical evidence of hyperthyroidism
only cardiovascular manifestations of thyrotoxicosis such as o Reversal of findings after treatment
sinus tachycardia, atrial fibrillation, and hypertension, all of
which maybe resistant to therapy until the hyperthyroidism
is controlled. TREATMENT
Directed at improving s/sx, reducing the demands to the

PHYSICAL EXAMINATION heart
• Anti-thyroid drugs
o Stare, lid retraction, exophthalmos • Thyroid ablation
o Skin – soft and velvety • Steroids – hydrocortisone 50-100 mg q 6-8 hours
o Goiter – audible bruit • Beta blockers if without CHF – Propanolol 20-30
o Precordium mg 4x/day
Inspection – hyperdynamic precordium • Digitalis
Auscultation – loud S1, systolic ejection • Anti-coagulation
murmur you should have beta blockers for them, digitalis especially
Palpation – rapid & bounding pulse those with atrial fibrillation
o Proximal muscle weakness
Hyperreflexic DTRs HYPOTHYROIDISM
Physical examination may reveal a hyperdynamic Essentials of Diagnosis:

precordium, a widened pulse pressure, increases in the • Increased TSH
intensity of the first heart sound and the pulmonic • Low T3, T4, FTI
component of the second heart sound, and a third heart
sound General Considerations:
An increased incidence of mitral valve prolapse has been • Given to any form of TH deficiency
described in hyperthyroid patients,in which case a • Myxedema – TH deficiency with profound
midsystolic murmur may be heard at the left sternalborder hypothermia, hypoventilation, hypotension, CNS
with or without a midsystolic click. A systolic signs (coma)
pleuropericardial friction rub (Means-Lerman scratch) may • Associated with accelerated athero-sclerosis
be heard at the left second intercostal space during • Angina uncommon due to decreased metabolic
expiration and is thought to resultfrom the hyperdynamic demand
cardiac motion.
You have high TSH levels, associated with accelerated
atherosclerosis, most of these patients with signs and
DIAGNOSTIC STUDIES symptoms of pleural effusion
CLINICAL FINDINGS
ECG – sinus tachycardia, AF
Echocardiography – hypercontractility, increased
LV mass & hypertrophy Systemic signs and symptoms
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o Weight gain, weakness, lethargy, fatigue, Initial Diagnosis:
depression Pericardial effusion or decreased contractile
o Constipation, cold intolerance, dry skin, coarse performance
hair Clinical suspicion of hypothyroidism
o Menstrual disorders, impotence or decreased
libido Definite Diagnosis:
o Clinical findings
Cardiovascular signs and symptoms o Biochemical evidence of hypothyroidism
o Decreased CO, SV, HR o Reversal of abnormalities after treatment with
o Loss of inotropism and chronotropism thyroid hormone
o Heart failure rare – decreased CO match
metabolic demands TREATMENT
Cardiac manifestations of hypothyroidism include
a reduction in cardiac output, stroke volume,
heart rate, blood pressure, and pulse pressure. Thyroid hormone replacement
Pericardial effusions are present in about one- • If > 50 y/o – judicious & slow replacement
third of patients, rarely progress to tamponade, To prevent exacerbation of angina or
and probably result from increased capillary precipitation of AMI
permeability. ¼ of the usual replacement dose (25
Other clinical signs include cardiomegaly, mg/day)
bradycardia, weak arterial pulses, distant heart
sounds, and pleural effusions. So when you start giving supplementation for thyroid
Although the signs and symptoms of myxedema hormone in a pt. more than 50 years old, you should give
may mimic those of CHF, in the absence of other judiciously and slowly. Bakit kamo? Siyempre hindi na
cardiac disease, myocardial failure is uncommon. normal takbo ng puso ng pasyente niyo kasi hypothyroid na
dib a? Mabagal. Pag binigyan mo ng thyroid hormone,
DIAGNOSTIC STUDIES
mghyperactive yung systole nila. Di ba sinabi natin usually
they are associated with accelerated atherosclerosis so may
ECG probability na may significant coronary artery disease
• sinus bradycardia obstruction, pag binigyan mo, bibilis, may bara. Kaya dapat
• prolonged PR & QT interval dahan dahan.
• low voltage complexes
• flattened or inverted T waves
Before treatment with thyroid hormone, patients with
• Atrial, ventricular or interventricular delay
hypothyroidism frequently do not have angina pectoris,
presumably because of the low metabolic demands caused
The ECG generally reveals sinus bradycardia and low voltage
by their condition.
and may show prolongation of the QT interval, decreased P-
wave voltage, prolonged AV conduction time,
intraventricular conduction disturbances, and nonspecific However, angina and myocardial infarction may be
ST-T-wave abnormalities. precipitated during initiation of thyroid hormone
Chest x-ray may show cardiomegaly, often with a “water replacement, especially in elderly patients with underlying
bottle” configuration; pleural effusions; and, in some cases, heart disease. Therefore, replacement should be done with
evidence of CHF. care, starting with low doses that are increased gradually.
Echocardiography – pericardial effusion, ASH

MALIGNANT CARCINOID
Laboratory findings
• Low T3, T4; high TSH levels Associated with right sided murmur especially tricuspid
• Increased cholesterol & triglyceride regurgitation
• Hyponatremia
• Increased CK-MM but not CK-MB • Tumors that elaborate vasoactive amines (eg serotonin),
• anemia kinins, indoles responsible for diarrhea, flushing, labile
BP
Pathologically, the heart is pale and dilated and • Gastrointestinal carcinoids
often demonstrates myofibrillar swelling, loss of Almost exclusively in the right side
striations, and interstitial fibrosis. Occur only with hepatic metastases substance
responsible for the cardiac lesions inactivated by
Patients with hypothyroidism frequently have
passage through liver and lungs
elevations of cholesterol and triglycerides,
resulting in premature atherosclerotic CAD.
• Left-sided lesions occur when
1. there exists a right-to-left shunt, or
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Page 9 of 12
2. tumor is located in the lungs pressure. It is very important how you define hypertension.
3. Lesion: fibrous plaques on the endothelium of Alam niyo ba yung hypertension, pwede mawalan ng
cardiac chambers, valves, and great vessels tarbaho ang isang pasyente. Pag sinabi ninyo na high blood,
result in distortion of the cardiac valves there are some companies that when you have
hypertension, they do not hire you.
CLINICAL SYNDROME SIGNS AND SYMPTOMS
o Tricuspid regurgitation, pulmonic Systemic signs and symptoms:

stenosis or both Attacks of headache
o High-output cardiac state may occur – Palpitations
due to decrease in systemic vascular resistance Tachycardia
o Coronary artery spasm due to a
Sweating
circulating vasoactive substance
Irritability
CVS signs and symptoms:

Inc. HR, contractility, conduction velocity
Orthostatic hypotension
Hypertension (85%) – sustained or paroxysmal
LVH
LV failure – due to focal myocardial necrosis
Pulmonary edema
ACROMEGALY
Excessive growth hormone (problem)

o CHF due to high cardiac output
o Diastolic dysfunction due to ventricular
hypertrophy – increased LV chamber size or wall
thickness
o Global systolic dysfunction
In some cases a high cardiac output state may occur,
o Suppression of renin-aldosterone axis
presumably as a result of a decrease systemic vascular
increased total body sodium and plasma volume
resistance resulting from vasoactive substances released by
hypertension
the tumor.
Treatment with somatostatin analogues (e.g., octreotide) or
Hypertension occurs in up to one-third of patients with
interferon α improves symptoms and survival in patients
acromegaly and is characterized by suppression of the
with carcinoid heart disease but does not appear to
reninangiotensin- aldosterone axis and increases in total-
improve valvular abnormalities.
body sodium and plasma volume.
In some severely symptomatic patients, valve replacement
Some form of cardiac disease occurs in about one-third of
is indicated.
patients with acromegaly and is associated with a doubling
Coronary artery spasm, presumably due to a circulating
of the risk of cardiac death.
vasoactive substance, may occur in patients with carcinoid
syndrome.
RHEUMATOID ARTHRITIS
PHEOCHROMOCYTOMA
Inflammation of any or all anatomical parts of the heart
• High circulating levels of catecholamines labile or usually pancarditis
sustained hypertension LVH
• May cause direct myocardial injury Pericarditis
Focal myocardial necrosis and inflammatory cell Most common cause of clinically apparent disease
infiltration (50% of patients) contribute to Found by echocardiography in 10-50% of patients,
significant LV failure and pulmonary edema particularly those with sub-cutaneous nodules
LV function and CHF may resolve after removal of Usually benign course but may progress to cardiac
tumor tamponade or constrictive pericarditis
Sympathetic tumor so clinical manifestation of your patient Coronary arteritis

with hypersympathetic activity 20% of cases; rarely results in angina or MI
It is secondary cause of hyoertension, usually it is
paroxysmal hypertension. Cardiac valves
Paano ninyo idedefine yung hbypertension? How do you Mitral or aortic regurgitation
make a diagnosis of hypertension? Yes, we check the blood Inflammation and granuloma formation
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• SLE with elevated antibody to cardiolipin high
Myocarditis incidence of valvular disease
Rarely result in cardiac dysfunction • Younger patients with active disease, 5 yrs.
Pericardial fluid Libman-Sacks lesion

Exudate, dec. conc. complements, dec. Glucose, Characteristic endocardial lesion
elevated cholesterol Wart-like lesions most often located at
The high circulating levels of catecholamines resulting from angle of the valves or ventricular surface
a pheochromocytoma may cause direct myocardial injury. of MV
Focal myocardial necrosis and inflammatory cell infiltration
are present in ~50% of patients who die with • Hemodynamically important valcular lesions rare
pheochromocytoma and may contribute to clinically
significant left ventricular failure and pulmonary edema. Coronary Artery Disease
In addition, associated hypertension results in left • Secondary to arteritis of large coronary arteries,
ventricular hypertrophy. Left ventricular dysfunction and embolism
CHF may resolve after removal of the tumor. • Also due to atherosclerosis related to
hypertension or glucocorticoid therapy
Thrombotic Disease
• Deep venous thrombosis
• Pulmonary, peripheral or cerebral thrombosis
• Associated with anti-phospholipid antibodies
produce endothelial dysfunction
Two-dimensional color and spectral Doppler echocardiographic

studies of patients with rheumatic heart disease show moderate to
severe aortic valve insufficiency with no stenosis (A, arrow) and
bowing of the anterior mitral leaflet with severe insufficiency and no
stenosis (B, arrow).
TREATMENT
• Treat underlying RA
• Glucocorticoids
• Pericardiectomy
SYSTEMIC LUPUS ERYTHEMATOSUS
It is also pancarditis – pericardial involvement, myocardial

involvement
Pericarditis
• 2/3 of patients
• Benign course
• Rarely tamponade or constriction
Myocarditis
• Seen in autopsy in up to 80%
• Only 20% clinically detected
• Parallels the activity of the disease
• Seldom results to clinical heart failure, unless
associated with hypertension
Valvular Heart Disease

• Clinically most important and frequent SLE-
associated CV manifestation
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Medicine II Deflation rate – the recommended deflation of
CARDIOLOGY the BP apparatus should be 2-3mmHg/sec
Midterm Coverage – Dr. Bartolome >2-3mmHg/sec – diastolic pressure will
AMS 204 be higher
Korotkoff sound
Coverage of Midterm Examination: 1st sound – Systolic BP (Korotkoff 1)
I. Rheumatic Fever, Valvular Heart Disease Last sound – Diastolic BP (Korotkoff 5)
II. Pericardial Diseases o RR
III. Congenital Heart Disease in Adult o PR/HR
IV. Diseases of the Aorta (Dr.Deduyo) Normal – 60-100 bpm
V. Cardiac Tumors, Cardiac Manifestation of o Temperature
Systemic Diseases or Traumatic Cardiac Injury
PE of the Heart
- Inspect the precordium
INTRODUCTION o By merely looking at the patient, you can assess
the probability of disease in the patient.
Definition of terms: Examples:
- Orthopnea - shortness of breath (dyspnea) which occurs If the arm length is greater than the
when lying flat, causing the person to have to sleep height and the patient complains of
propped up in bed or sitting in a chair. dyspnea, the patient may be suffering
- Platypnea - refers to shortness of breath (breathlessness) from valvular heart disease;
that is relieved when lying down, and worsens when sitting if there is chest pain the patient may be
or standing up. suffering from aortic dissection;
if there are low set ears the patient may
Chest pain be suffering from a ventral septal
- Always be guided by the mnemonics for pain: defect or endocardial cushion
defect
P – What Provokes? if with ear crease, the patient is high
P – What Palliates? risk for developing coronary artery
Q – What is the Quality? disease
R – Region/Radiation? o Check for the apical beat
S – Severity? Normal location of apical beat – 5th ICS LMCL
T – Timing? and is <2.5cm in diameter
If it is displaced laterally inferiorly or it is
Five Fingers of the Diagnosis in Cardiovascular Medicine >2.5cm in diameter most likely there is
- All patients should have adequate history, adequate PE, cardiomegaly
imaging studies (x-ray), ECG, and specific laboratory tests o Look for abnormal pulsations
to confirm the diagnosis of the problem Normal: no abnormal pulsations seen in the
- Example: In most cases in order to confirm the diagnosis aortic, pulmonic, tricuspid, and mitral area
an echocardiogram is needed especially in valvular heart Cardiac auscultatory areas:
diseases. Aortic area – 2nd RICS
Pulmonic area – 2nd LICS
History Tricuspid area – 4th ICS left
- The history (and its components: general data, CC, HPI, parasternal border
PMH, PS, FH) of the patient is very important because it Mitral area – 5th ICS LMCL
would give clues (ex. risks) to the diagnosis. If you have a Abnormal pulsations:
certain risk you are more likely to end up with a certain Aortic area – caused by a dilated aorta
problem. Pulmonic area – caused by a dilated
pulmonary artery
Example: Atherosclerotic Heart Disease Tricuspid area – caused by a dilated or
- Risks: enlarged right ventricle
o Modifiable (smoker) - Palpate
o Non-modifiable (Old age:>45y/o, male, w/ family o Check for apical beat
history, hypertension, dyslipidemia) o Check for heaves, thrills, and lifts
- If you have the non-modifiable risk factors, you are more Significance of heaves (use heel of hand)
likely to end up with the heart disease.
Types:
o Right Ventricular heave -
Physical Examination
occurs in the setting of right
- Start with the vital signs
ventricular enlargement
o BP
(sustained impulse). Example:
1|J KCP Vil la r a m a

valvular disease (pulmonary Abnormal
valve), respiratory disease o Fixed splitting of the 2nd heart
(pressure in the pulmonary sound
artery becomes elevated – Patients with ASD (Atrial
COPD), Cor pulmonale, mitral Septal Defect)
stenosis, and dilated right S3 and S4
ventricular myopathy (vigorous Best appreciated using the bell
and brief). Either (+)present or (-)absent
o Left Ventricular heave - o Murmurs
occurs in the setting of left Murmurs are characterized either as systolic or
ventricular enlargement diastolic, location, grade, pitch, and timing
Significance of thrills (use proximal palm) Pitch
It signifies the presence of a palpable o If loud using the diaphragm –
murmur (minimum murmur grade: 4/6) high-pitch murmur
- Auscultate o If loud using the bell – low-
o Use of stethoscope: pitch murmur
Diaphragm – firm application Location
For high pitch sounds o If you hear the murmur at the
o S1 aortic area – aortic
o S2 systolic/diastolic murmur
Bell – light application; pressing of bell firmly o If you hear the murmur at the
mimics the function of the diaphragm pulmonic area – pulmonic
For low pitch sounds systolic/diastolic murmur
o S3 o If you hear the murmur at the
o S4 tricuspid – tricuspid
o Auscultatory areas systolic/diastolic murmur
Aortic o If you hear the murmur at the
Pulmonic mitral area – mitral
Tricuspid systolic/diastolic murmur
Mitral Timing
o If you hear a murmur that starts
Note: Aortic and Pulmonic areas produce the 2nd heart sound. The from S1 and ends up after S2 –
1st heart sound is produced by the closure of the AV valves. When Continuous murmur
you auscultate, you have to identify first the 1st heart sound. Example: ASD (Atrial
Septal Defect)
o Heart sounds o If you hear the murmur between
S1>S2 – apex S1 and S2 – Systolic murmur
S1<S2 – base of the heart o If you hear the murmur between
S2 and S1 – Diastolic murmur
Note: S1 is simultaneous with the pulse. After identifying S1 and S2,
you can identify the S3 which occurs after S2 and S4 happens just Note: Basically, between S1 and S2 are all systolic events and
before S1. between S2 and S1 are all diastolic events. S3 and S4 are heard
between S2 and S1 so it is a diastolic event.
Check also for the intensity of the heart sound
(loud or soft or normally accentuated) o Valves
Loud S1 – associated with Mitral Systole
stenosis The aortic and pulmonic valves
Soft S1 – associated with Mitral (semilunar valves) should be open
regurgitation during systole
Take note also for the physiologic splitting of o If there is a turbulent blood flow,
the second heart sound constriction or narrowing of the
Rationale: aortic opening or pulmonic
o when you inspire, the A2 P2 opening, it would produce a
coupling widens turbulent blood flow. This is
o when you expire, the A2 P2 called as aortic stenosis or
coupling narrows pulmonic stenosis.
There is physiologic splitting of the 2nd The tricuspid and mitral valves
heart sound because when you inspire (Atrioventricular valves) should be
there is an increase in venous return closed during systole to prevent
which causes delayed closure of the regurgitation of blood coming from the
pulmonic valve. ventricles going to the atria.
o The tricuspid and mitral should To appreciate the presence or absence of
prevent regurgitation of blood. If aortic bruits
there is a regurgitant blood o Renal artery
volume coming from the atria To appreciate the presence or absence of
going to the ventricle passing renal artery bruits
through the tricuspid and mitral, o Iliac artery
it is called as tricuspid To appreciate the presence or absence of iliac
regurgitation or mitral bruits
regurgitation during systole. - Palpation
Diastole o Pulses – weak or strong (+1, +2, or +3)
The semilunar valves should be closed Radial
o If there is an obstructed valve, it Brachial
produces a turbulent blood flow Femoral
and this is called as mitral Popliteal
stenosis or tricuspid Dorsalis pedis
stenosis. Posterior tibialis
AV valves should be open to allow Located in the medial malleolus
ventricular filling. o If the patient is hypertensive, upper and lower
o There should be no regurgitant extremities pulses should be compared
blood from the aorta to the left Upper extremity pulse>lower extremity pulse –
ventricle and from the consider a secondary cause of hypertension
pulmonary artery to the right like coarctation of aorta
ventricle. If there is, this is If a patient has chest pain and there is a
called as aortic regurgitation difference with right and left pulses called as
or pulmonic regurgitation an asymmetrical pulse – the patient may be
o Friction Rub suffering from an aortic dissection which is a
Present in the pericardial diseases medical emergency
Best heard in an upright leaning forward
position with held respiration (patient in expired Note: The heart sound should be short and snappy
breathing)
Best heard using the diaphragm because it is a
high-pitch sound
o Positioning of the patient
The leaning forward position is the best
position for you to appreciate aortic and
pulmonic sounds.
The left lateral decubitus position is the best
position for you to appreciate mitral sounds
Summary:
- Auscultation
o Apical beat – location, size
o Pulsations in the aortic, pulmonic, tricuspid, and
mitral
o Heaves, lifts, and thrills (using bell)
o S1>S2 apex; S1<S2 base
o S3 and S4 (using the bell)
o Murmurs (using diaphragm and bell)
o Friction rub (using diaphragm)
o Rate
Normal – 60-100bpm
Tachycardia – >100bpm
Bradycardia – <60bpm
o Rhythm
Regular
Irregular
o Neck
To appreciate the presence or absence of
bruits
o Epigastric area

VALVULAR HEART DISEASE MITRAL STENOSIS
(Included here are those that are not in the hand-out/previous trans)
- Common condition among the female population
Definition of terms: - Secondary to rheumatic heart disease
- Stenosis o These patients usually have a recurrent acute
o narrowing or constriction of the diameter of a bodily rheumatic fever
passage or orifice - End result of this condition is a rigid valvular cusps
o produces pressure on the chamber prior to the causing narrowing of the funnel-shaped mitral valve
stenotic area - Echocardiogram – confirms the presence of a thickened
- Regurgitation anterior and posterior mitral valve (AL and PL) with a
o Backward flow of blood through a defective valve dilated left atrium and doming motion of the mitral
o Regurgitant volume produces volume overload on valve
the chamber before and after the valve - Problem in mitral stenosis:
o Blood flow that would happen from LA to LV
Example: only if it is propelled by the abnormally elevated
- Mitral stenosis left atrio-ventricular pressure gradient –
o There is NO enlargement of the left ventricle. hemodynamic hallmark of mitral stenosis
You cannot appreciate LVH in a patient with pure
mitral stenosis. There is enlargement of the left Note: There is a need to generate pressure for the blood to go from
atrium. LA to LV. If there is an increase in pressure in the LA (left atrial
- Tricuspid stenosis hypertension) and the blood goes back to the pulmonary vein then
o There is NO enlargement of the right ventricle. there will be pulmonary venous hypertension. If it goes back to the
There is right atrium enlargement. capillaries then there will be pulmonary capillary hypertension
- Mitral regurgitation transudation of fluid pulmonary edema or congestion. The
o There is enlargement of the left ventricle and the pressure will then be transmitted from the capillaries to the
left atrium pulmonary arteries then there will be pulmonary arterial
- Tricuspid regurgitation hypertension. This pressure then goes to the chamber with the
o There is enlargement of the right atrium and lesser pressure (RV) causing right ventricular hypertension
ventricle right atrial hypertension pressure goes to the veins causing
venous hypertension left sided and right sided failure
manifestations.
Left-sided failure manifestations:

Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Right-sided failure manifestations:

Neck vein engorgement
IVC hypertension
CPC
Inadequate production of albumin Venous
hypertension ascites
Femoral venous hypertension Transudation
of fluid edema
Note: The atrial enlargement cannot be appreciated during physical

examination. It is only the ventricles that you can appreciate because o Elevated pulmonary venous and pulmonary
the atria are supero-posteriorly located. During physical arterial wedge pressure reduced pulmonary
examination, the most anterior part of the heart being presented to compliance exertional dyspnea
you is the right ventricle and part of the left ventricle. o Increased heart rate shortens diastole
proportionately more than systole + diminishes time
Principle of Valvular heart disease: available for flow across the MV further elevation
- Stenosis – chamber prior the valve is affected of LA pressure
- Regurgitation – chambers before and after the valve are
affected Note: If the heart rate is rapid, less blood will go from the LA to the
LV because there is less time for ventricular filling leading to
congestion. In patients with mitral stenosis, slow down the heart rate
to prevent tachycardia. End result right sided and left sided
failure manifestations

- Cardiac output in this condition may be normal initially but - PND
later becomes abnormal during exertion. - Pulmonary edema
- Pulmonary arterial hypertension (due to backward - Palpitation
pressure discussed above) - Hemoptysis
o Physical sign of PAH: - Rare: Fever and anemia
Loud 2nd heart sound (Loud P2)
o Other causes: #2 Pulmonary changes
Passive backward transmission of elevated LA Note:
pressure
Pulmonary arteriolar constriction triggered by - Pulmonary changes
LA & pulmonary venous hypertension (reactive o End result fibrotic changes in the pulmonary
pulmonary hypertension) parenchyma
Interstitial edema in walls of small pulmonary o Further reduce oxygen tension and blood flow
vessels - Patients with mitral stenosis are also prone to develop
Organic obliterative changes in pulmonary thrombi and emboli
vascular bed o Fibrillating heart inadequate contraction
o Later develop pulmonary arterial thrombosis of the blood emboli
vasoconstriction - Example: Young individual who suffered from stroke
Triggered in greater increase in pressure auscultate the heart it may be mitral stenosis especially
Called as reactive pulmonary if with atrial fibrillation.
hypertension
o Inflammation of the pulmonary capillary vessels or #3 Physical findings
rigid blood vessels in the lungs will not permit the Note:
usual blood flow from the pulmonary artery going to - JVP is prominent
the lungs Right-sided failure - BP may be normal or slightly low
- (+) RV heave in the left sterna border (tricuspid area)
Note: - (+) Diastolic thrill at the apex (mitral area)
- Circulation:
Vein RA RV Pulmonary artery Lungs Pulmonary Typical physical signs of MS
vein LA LV o Loud S1
- Congestive heart failure o Accentuated loud P2 because of pulmonary
o Systolic and diastolic dysfunction hypertension
- Organic obliterative changes in pulmonary vascular o Most important examination finding of MS:
bed helpful to a patient with mitral stenosis Appreciation of a low-pitch sound diastolic
o In this condition, less blood will go to the left side so murmur best heard at the apex in a patient in
the left atrium is protected from volume and lateral recumbent position.
pressure overload. Theoretically, the dyspnea will o Duration of the murmur correlates with the severity
disappear and recurrent pulmonary edema of a Holodiastolic
patient with mitral stenosis. It can be protective. From S2 to S1 (severe MS)
Less blood no volume overload no
pulmonary edema Other associated problems:
o Development of tricuspid regurgitation
#1 Symptoms o Development of pulmonic regurgitation
Note: o MS:
End result increase in HR LAH
Pulmonary venous hypertension
Increase in heart rate increase in left atrial pressure pulmonary Pulmonary capillary hypertension
congestion Pulmonary arterial hypertension
- Example: Pregnant patient with dyspnea (hingal) RV hypertension
auscultate the heart because it may be a case of mitral Pressure within the RV is increased
stenosis which leads to enlargement of RV
- Example: Female patient with hemoptysis can also be a RVH tricuspid valve widens
case of mitral stenosis. inadequate closure of tricuspid valve
- Don’t fprget to auscultate the apex of the heart in a patient tricuspid regurgitation in MS
with hemoptysis, dyspnea especially if the patient is
pregnant may arrest need to decongest the patient #4 Auscultation
(furosemide) Note:
- is it systolic or diastolic?
Other manifestations: o Systolic murmurs
- Limitation of daily activities Aortic stenosis
- Orthopnea Pulmonic stenosis
Tricuspid regurgitation #6 dDx
Mitral regurgitation
o Diastolic murmur Note:
Pulmonic regurgitation - Mitral regurgitation
There is left atrial hypertension o Systolic murmur
venous hypertension capillary - Atrial regurgitation
hypertension pulmonary arterial o Diastolic murmur best heard at the upper sternal
hypertension pulmonic valve border
enlarges inadequate pressure in the - Atrial septal defect
pulmonic valve PR o A congenital heart disease associated with right
- Is it a right sided murmur or a left sided murmur? ventricular enlargement and accentuation of the
o Right sided murmur pulmonary vascularity because of increase in
Murmur coming from the pulmonic and pulmonary blood flow
tricuspid area o In this condition, there is NO left atrial enlargement
If you ask the patient to inspire and the because the blood flow in atrial septal defect is from
intensity of the murmur increases it is pulmonary vein LA and part of the volume goes
considered as a right sided murmur to the RA that is why LA is decompressed no
There is a positive Caraballo sign enlargement of LA in a patient with ASD
except in pulmonic stenosis o Associated with fixed splitting of 2nd heart sound
- Left atrial myxoma
Summary for the Physical Signs of MS: o Tumor within the left atrial cavity
o Irregular pulse o When there is opening of the mitral valve the tumor
o JVP distended in the left atrium will go to the mitral valve orifice
o RV heave causing obstruction of the mitral valve opening and
o Loud S1 can produce the mitral valve stenosis physiology
o Opening snap o There is an increase in left atrial pressure because
o Diastolic murmur of MS the blood cannot flow through from the LA to LV in
patients with left atrial myxoma
#5 Examination o This condition is associated with platypnea while
mitral stenosis is associated with orthopnea.
Note: Platypnea is dyspnea on upright position
- In MS, there are: The atrium is located supero-posteriorly or
o Left atrial hypertension Left atrial enlargement above the ventricle. By gravity, when a patient
o Enlargement of pulmonary vein stands the left atrial tumor goes down causing
o Transudation of fluid pulmonary edema obstruction to the blood flow from the LA going
o Pulmonary arterial hypertension dilatation of to the LV. This is why the patient is more
pulmonary artery symptomatic in an upright position as
o BP goes to RV RVH RAH compared to an MS wherein the patient
- ECG Pattern becomes less symptomatic in an upright
o Enlarged LA position.
o Enlarged RA o Associated with systemic diseases
Widening of the P wave and then the height of SLE
the P wave for RAH biphasic P wave V1 Connective tissue disorder
P wave in Lead II, Lead III, aVF >2.5mm or With fever, anemia, etc
2.25mV
o Enlarged RV #7 treatment
Presence of prominent R in V1 Note:
- X-ray - Since it is an anatomical problem then the solution is also
o LA enlargement anatomical. But, the anatomical solution may either be:
Straightening of left heart shadow o Replace the valve
- Echocardiogram o Repair or enlarge the valve (valvotomy)
o To confirm the diagnosis - Medical treatment may also be helpful especially in those
o It can visualize thickening of the mitral valves who cannot undergo valve replacement or valvotomy
o Gold standard for cardiomegaly next to opening up o You need to give patients Penicillin prophylaxis
and measuring it especially those with recurrent acute rheumatic
It has an accuracy rate of 95-99% for fever to reduce the probability of developing
enlargement of the heart rheumatic heart disease
- Cardiac catheterization Theory: the more rheumatic fever you have,
o Done in patients who are candidates for valve the more likely that you will end up having
replacement valvular heart disease

Rheumatic heart disease is rare nowadays MITRAL REGURGITATION
because of a better antibiotic coverage - Systolic murmur best heard at the apex
The main problem in acute rheumatic fever is - Frequently, it is secondary to MI and mitral valve prolapsed
the development of self against self - Another frequent cause of MR is hypertrophic
o Give prophylaxis for infective endocarditis cardiomyopathy
All patients with valve disease or congenital - One of the common causes of MR is MI
heart disease should be given prophylaxis for o MI Inadequate perfusion to papillary muscles
infective endocarditis for any surgical or dental inadequate contraction of the muscles
manipulation because in these procedures, it inadequate mitral valve closure development of
produces bacteremia which can go to the MR (one mechanical complication of myocardial
enodocardium causing inflammation of the infarction)
endocardium and cause infective endocarditis - Problem with MR:
which is very hard to treat because there is o Blood coming from the LV LA so when LA
continuous pumping of the blood so less direct contracts more blood goes to the LV end up with
effect of antibiotics LA and LV volume increase. The LA and LV will
enlarge because of this
Note: o MR LA and LV enlargement
- Problem of MS: Increase HR increase in pressure - MR
volume overload congestion o Acute MR
There is no time for the body to compensate
If the patient has volume overload: There is sudden regurgitant volume coming
- Restrict sodium because where sodium is water is from the LV going to LA LA pressure
- Give diuretic therapy suddenly increases. With the sudden increase
- Slow down the heart rate so that you will allow more in LA pressure, the pressure goes to the
ventricular filling time so more blood goes from LA to LV pulmonary vein and pulmonary capillaries
NO CONGESTION End result: acute development of acute
o The drug that can decrease the heart rate or with (-) pulmonary congestion/edema (volume
chronotropic effect: overload in the lungs) neck vein
Beta blockers (B1) engorgement due to increase venous
Non-selective beta blockers cannot be pressure
given in patients with bronchial asthma Example: Destruction of mitral valve (due to MI
with MS because of the possibility of V- destruction of papillary muscle); valvular
tach infection (endocarditis mitral valve)
Non-dihydropyridine calcium channel blockers Management: reduce the regurgitant blood
Verapamil volume by reducing the afterload; give a drug
Diltiazem that decreases the afterload by giving
Digitalis vasodilator therapy (nitroglycerin, nitropruside)
Best given in a patient with rapid heart o Chronic MR
rate in atrial fibrillation There is time for the body to compensate
DOC if patient is in A-fib There is already enlargement of the left
Anti-thrombus agents ventricle
If the patient has thrombus formation LV enlargement can be appreciated by
you can give: PE where in there is the presence of
o Warfarin displaced apical beat
The size of apical beat may be >2.5cm
Note: Not all patients with MS are candidates for mitral balloon There could also be LV heave
valvuloplasty. There are only subsets of patients who are candidates Cannot be appreciated by auscultation
for this procedure. If the mitral valve is already highly calcified, this is
the tiem that you should do valve replacement. If the calcifications Acute MR
were disrupted, it may go the LV and to the arterial circuit and goes - There is sudden increase in LV volume increase
to the brain and end up having stroke if it goes to heart you’ll end up pressure in LA pulmonary venous hypertension
with MI. If it goes to the superior mesenteric artery which supplies the pulmonary capillary hypertension pulmonary congestion
foregut you’ll end up with bowell ischemia. dyspnea
- There is a decrease in cardiac output because of
regurgitation.
- There is a decrease in forward ejection fraction and the
end result is a decrease in CO
o There is LOW BLOOD PRESSURE

Chronic MR - X-RAY
- There is time for compensation o Ratio of more than 0.5
- Initially, if the MR is significant, all the enlargement patterns - Echocardiogram
can be seen o Confirm the diagnosis of MR
- Increase LV end-diastolic filling pressure LA
hypertension capillary hypertension congestion Medical treatment of MR:
right-sided failure manifestations Decrease the afterload; no resistance =
- Drug: forward flow
o With (+) inotropic effect Afterload is the pressure where the
Sympathomimetic drugs myocardium will pump on = Systemic
Dobutamine vascular resistance
Dopamine o There is a need to lower down
Epinephrine/NEP the SVR
- Heart transplantation is possible o In order to do this, give a drug
o Problem: cost and rejection with artery dilating effect which
reduces SVR (vasodilator
Note: drugs)
- MR ACE inhibitors
o With left sided failure manifestations then later right Calcium channel blockers
sided failure manifestations If there is volume overload volume
o PE: restriction. If still with volume overload give
Severe MR Initially with increased BP diuretics and vasodilator drugs
Acute MR hypotension because there is no Digitalis glycosides are given to enhance
time for compensation contraction
JVP increased initially in acute MR IV nitroprusside – potent afterload unloader;
Because all of a sudden there is left potent venous afterload unloader
sided heart failure right side heart Venous unloader
failure venous hypertension o If you dilate the veins
neck vein engorgement (capacitance vessels), less
Systolic thrills of MR blood will go to the right side
Appreciated in the apex less blood will go to the left side
LV heave of MR no congestion
Appreciated in the apex Afterload unloader
Significant MR will be in the axilla 6th o Enhance forward flow
ICS or lower sufficient blood flow and less
RV heave of MR will go to the lungs
Very rare o If there is a problem of
Auscultate for: pulmonary congestion, you
S3 need to venodilate, enhance
S1 in this condition is soft contraction, and then afterload
unloader.
Loud S1 in MS
ACE inhibitors
Most important PE finding is the presence of a
apical murmur that radiates to the axilla Potent vasodilator drugs
Systolic murmur Has some venounloading capacity
Endocarditis prophylaxis
Note: Anticoagulants and leg binders
- Aortic stenosis is a systolic murmur
- Mitral regurgitation is a systolic murmur that radiates to the Note: Best position for a patient in pulmonary congestion is standing
axilla position or sitting position and put an alternating tourniquet in a
patien in pulmonary congestion. If there is an anatomical problem,
Clinical signs of chronic MR the solution is usually anatomical also.
o Prominent distinct apical beat
o Systolic thrill at apex MR
o LV heave - Repair the mitral valve
o Soft S1 - Replace the mitral valve
o Systolic murmur at apex
o Presence of S3
ECG
o Enlargement

CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I
• Can you imagine a stenotic valve? A thickened

arortic valve.. can you imagine yung bisagra?
AORTIC STENOSIS Ayaw bumukas kasi matigas na sya. So even if you
ETIOLOGY contact, hirap na hirap lumabas kasi yung bisagra
matigas na (yun po yung joint ng door haha)
• Occurs in about ¼ of patients with chronic valvular heart disease • Yung sinabi na systemic vascular resistance is
• Approximately 80% are male another cause of increased afterload. This time it
• Causes: is the aorta that produce the after load problem.
1. Adults - degenerative calcification of the aortic cusps • Peak systolic pressure gradient > 50 mmHg with normal cardiac
2
Age-related degenerative calcific AS (senile or output or an effective aortic orifice less than 1.0 cm or < 0.6
2 2
sclerocalcific AS) – most common cause of AS in cm /m body surface area = severe obstruction to LV outflow
adults in North America & Western Europe • Elevated LV end-diastolic pressure in severe AS signifies LV
Risk factors same as those for atherosclerosis dilatation and/or decreased compliance of hypertrophied LV wall
30% of persons > 65 y/o with aortic valve sclerosis increased myocardial oxygen demand
2% with frank stenosis • What would be the problem of the patient with
2. At birth - Congenital increased oxygen demand? They could be
Stenosis present at birth become progressively complaining of chest pain. And your patient will
more fibrotic, calcified and stenotic end up having Myocardial Ischemia
Congenital valve deformity – normally it is • Cardiac output at rest within normal but fails to rise normally
tricuspid, but in this condition, usually bicuspid, during exercise
without serious narrowing of aortic orifice during
childhood, but they are later prone to develop
calcific changes
Most common congenital disease
3. Rheumatic endocarditis of aortic leaflets
Produce commissural fusion, resulting in bicuspid
valve leaflet more susceptible to trauma
lead to fibrosis, calcification and further
narrowing
Almost always associated with involvement of
mitral valve and severe AR
SYMPTOMS
• Rarely of clinical importance until valve orifice has narrowed to

2 2
approximately 0.5 cm /m body surface area in adults
th th
• Symptoms gradually appear until 6 – 8 decades
1. Reduced compliance elevated LV diastolic pressure
elevated pulmonary capillary pressure exertional
dyspnea
2. Inc. Myocardial oxygen demand + reduced O2 availability
angina pectoris
3. Vasodilation in exercising muscles & inadequate
vasoconstriction in non-exercising muscles decreased
PATHOPHYSIOLOGY arterial pressure exertional syncope
• Once you have all these three, these are
indications for you to replace your
• (+) obstruction to LV outflow produce systolic pressure
aortic valve
gradient between the LV and aorta
• If you have syncopal attack and angina
• There is increased afterload. What do you mean
pectoris and will not replace the valve,
by afterload? Miki?hahaha
FRED
Page 1 of 9
CARDIOLOGY: DR.
BARTOLOME
within 2-3 years time, 50% of them will 5. Late stages of AS – pulse pressure reduced pulse
die amplitude small
• On the other hand, if you have the left 6. Bulging, hypertrophied intraventricular septum
sided failure manifestation like the diminished distensibility of RV cavity accentuated a wave
exertional dyspnea 50% of them will die in the jugular venous pulse
within 1 year if you don’t change the 7. LV impulse active and laterally and inferiorly displaced
valve (+) LVH PMI is more than 2.5cm
• It is important to undergo left heart 8. Double apical impulse with the patient in the left lateral
catheterization to identify the severity recumbent position
of the aortic stenosis and identify if ever 9. Systolic thrill at base of heart, in the jugular notch, and
they have CAD. Class magkaiba pa yung along carotid arteries
CAD at yung aorti stenosis. Magkaiba • You can appreciate thrills on aortic and pulmonic
nnamng gastos yun area and in the carotid
• CO at rest usually well maintained until late in the course -right sided and left sided failure manifestation
Marked fatigability Auscultation
Weakness 1. Early systolic ejection sound (OS of the aortic valve) in
Peripheral cyanosis children and adolescents with congenital non-calcific
Other manifestations of low CO valvular AS – disappears when valve becomes calcific and
• Advanced stages – symptoms of LV failure rigid
Orthopnea 2. Paradoxic splitting of S2
Paroxysmal nocturnal dyspnea 3. S4 audible at apex – reflects presence of LVH and elevated
Pulmonary edema LV end-diastolic pressure
• Isolated, severe AS Eccentric LVH –lumalakinat kumapal ang puso
Severe pulmonary HPN leading to RV failure Concentric LVH – kumakapal lang
Systemic venous HPN Dilated LV – lumaki lang, you see in MI kasi dead
Hepatomegaly heart muscles na.. di na sya naghyhypertrophy
AF and TR 4. (+) S3 when LV dilates
• AS + MS decreased pressure gradient across the aortic valve 5. Murmur
clinical findings produced by AS are masked • Ejection mid-systolic murmur
• Left heart catheterization helpful in defining the relative • Commences shortly after the S1
importance of each valvular abnormality • Ends just before aortic valve closure
• Low-pitched, rough and rasping in character,
PHYSICAL FINDINGS loudest at the base of the heart, most commonly
nd
in 2 right intercostal space
1. Rhythm generally regular until late in the course • Transmitted upward along the carotid arteries
• (+) AF suggests associated MV disease • At least grade III/VI with severe obstruction
2. Systemic arterial pressure usually within normal limits • Best heard on a leaning forward position and you
• In late stages – stroke volume decreased dec. need to use the bell because it is low pitched
Systolic pressure + narrowing of pulse pressure
Example of narrowing of pulsepressure
110/100 binibigyan kayo ng clue non
actually, mas malaki ang pulpressure
nyo ibigsabhn you heart is still
contracting and there is a large amount
of fluid coming out. Diastolic pressure is
the minimum pressure in your counduit
then on the other hand, your systolic
pressure is the cardiac output plus your
minimum pressure.
3. Peripheral arterial pulse rises slowly to a delayed sustained
peak - pulsus parvus et tardus –basta pag aortic class, there
are a lot of peripheral signs
4. Palpable systolic arterial pulse (bisfiriens pulse) excludes
pure or predominant AS; signifies dominant AR
FRED
Page 2 of 9
CARDIOLOGY: DR.
BARTOLOME
LABORATORY EXAM
ECG
1. Left ventricular hypertrophy – key finding
2. Advanced cases
• ST-segment depression and T-wave inversion (LV
“strain”) in leads I and aVL and in left precordial leads
• When will you say that it is LV? Pag matanda more that
35.. pag bata morethan 40. (height sae cg yata tong
tinutukoy no doc)
Two-dimensional ECHOCARDIOGRAPHY
• Eccentric aortic valve cusps – characteristic of
congenital bicuspid valves
• Can identify cardio megaly. Ang ganda no? kasi ang
goldstandard autopsy haha Chest x-ray: May show a dilated aorta. Calcification of the aortic valve
may be seen. In late disease, pulmonary oedema ("fluid on the lung")
Doppler echocardiography may be seen.
• Estimate transaortic valvular gradient
• LV dilatation and reduced systolic shortening reflect Catheterization and coronary arteriography
impairment of LV function • Indications:
1. Patients with clinical signs of AS and symptoms of
myocardial ischemia – coronary artery disease
suspected
2. Patients with multivalvular disease
3. Young, asymptomatic patients with non-calcific
congenital AS – to define the severity of obstruction to
LV outflow
4. Patients in whom it is suspected that the obstruction
to LV outflow may not be at the aortic valve but rather
in the sub- or supravalvular regions
Thickened and stenosed aortic valve seen in parasternal long axis

view on echocardiography. Both the mitral and aortic valves are in
near closed position. IVS: interventricular septum; Ao V: aortic valve;
LV: left ventricle; MV: mitral valve; LA: left atrium.
Roentgenogram
• LVH without dilatation produce some rounding of
the cardiac apex
• Critical AS associated with post-stenotic dilatation of
AVA, aortic valve area; BP, blood pressure; CABG, coronary artery
ascending aorta
bypass graft surgery; echo, echocardiography; LV, left ventricle;
• Aortic calcification apparent on fluoroscopic
Vmax, maximal velocity across aortic valve by Doppler
examination
echocardiography. (From Bonow et al. Modified from CM Otto: J Am
Coll Cardiol 47:2141, 2006.)
FRED
Page 3 of 9
CARDIOLOGY: DR.
BARTOLOME
TREATMENT a. Cystic medial necrosis of ascending aorta

b. Idiopathic dilatation of the aorta –in severe HPN
Medical c. Osteogenesis imperfecta
1. Avoidance of strenuous physical activities in patients with d. Severe hypertension
2 2
severe AS (< 0.5 cm /m ) e. Syphilis
2. Sodium restriction f. Rheumatoid ankylosing spondylitis
3. If with CHF – diuretics and digitalis glycosides
4. Nitroglycerin – for angina pectoris
5. HMG CoA reductase inhibitors (“statins”) – for slower
progression of leaflet calcification and aortic valve area
reduction –hindi ko sinabing standard therapy to, but
probably for patients who are not seeing surgery in the
future, you may want to give this, because thin CAN delay
the problem
6. Digitalis if there is weak contraction of the heart
Surgical: Aortic Valve Replacement (AVR)

• Indications:
2
1. Patients with severe AS – valve area < 1.0 cm or
2 2
0.6 cm /m body surface area who are
symptomatic
2. Patients who exhibit LV dysfunction
3. Patients with an expanding post-stenotic aortic
root, even if asymptomatic
AORTIC REGURGITATION
Diastolic murmur
Causes:
1. Primary valve disease –destruction of the valve, thus
inadequate coarctation or there is an opening within the
AV. Any inflammation of the AV can produce the problem
• Males – pure or predominant valvular AR
• Females – primary valvular AR with associated MV
disease
a. 2/3 of patients – rheumatic in origin
thickening, deformity and shortening of individual
aortic valve cusps prevent proper opening
during systole and proper closing during diastole
b. Congenital membranous subaortic stenosis – thick
aortic valve leaflets valves susceptible to
endocarditis
c. Rheumatoid spondylitis
d. Congenital bicuspid aortic valves
e. Infective endocarditis PATHOPHYSIOLOGY
• Can develop on a valve previously affected
by rheumatic disease • Increased total stroke volume ejected by LV
f. Traumatic rupture of aortic valve – uncommon Entire LV stroke volume ejected into the aorta
cause increased LV end-diastolic volume (increased
preload) major hemodynamic compensation
2. Primary Aortic Root Disease for AR
• Aortic root disease without primary involvement of During diastole, there is a regurgitant blood
valve leaflets volume coming from the aorta going to the
• Dilatation of aortic annulus may occur secondarily ventricle. You must remember that it is during
and intensify the regurgitation diastole you have left verticular filling. So ang
• Patients with marfan’s syndrome
FRED
Page 4 of 9
CARDIOLOGY: DR.
BARTOLOME
daming volume na nangagaling sa ventricle, so it • Rapidly rising “water-hammer” pulse – collapses

will make your left ventricle enlarged now. suddenly as arterial pressure falls rapidly during
• Dilatation and eccentric hypertrophy of LV – allows LV to late systole and diastole (Corrigan’s pulse)
eject a normal effective forward stroke volume and a • Capillary pulsations
normal left ventricular EF • Corrigan’s pulse
• As LV function deteriorates end-diastolic volume rises • Capillary pulsations
further & forward stroke volume and EF decline • Quincke’s pulse – alternate flushing and paling of
• Deterioration of LV function precedes development of the skin at the root of the nail while pressure is
symptoms applied to the tip of the nail
• Reverse pressure gradient from aorta to LV falls • Traube’s sign – booming “pistol-shot” sound over
progressively during diastole account for the the femoral arteries
decrescendo nature of the diastolic murmur • Duroziez’s sign - to-and-fro murmur audible if the
• Patients with severe AR – effective forward CO usually femoral artery is lightly compressed with a
normal or only slightly reduced at rest but fails to rise stethoscope
normally during exertion 4. Palpation
• Elevated myocardial oxygen requirements due to LV • Heaving LV impulse that is displaced laterally and
dilatation and elevated LV systolic tension myocardial inferiorly
ischemia • Diastolic thrill palpable along left sternal border
• Prominent systolic thrill in the jugular notch and
HISTORY transmitted upward along the carotid arteries
Due to markedly increased blood flow across
• Patients with acute, severe AR the aortic orifice
Failure of LV to dilate sufficiently to maintain stroke • With pure AR or with combined AS and AR
volume carotid arterial pulse is bisfiriens (two systolic
LV diastolic pressure rises rapidly with associated waves separated by a trough)
increase of LA and PA wedge pressures 5. Auscultation
Pulmonary edema and/or cardiogenic shock rapidly • With severe AR aortic valve closure sound (A2)
develop usually absent
• S3 and systolic ejection sound
SYMPTOMS • Murmur
1. high-pitched, blowing, decrescendo diastolic
• Patients with CHRONIC, severe AR murmur
rd
Long latent period – asymptomatic for 10-15 years Heard best in 3 intercostal space along
1. Uncomfortable awareness of heartbeat especially on left sternal border
lying down – early complaint 2. Mid-systolic ejection murmur heard best at
2. Sinus tachycardia during exertion or with emotion, base of heart & transmitted along the carotid
or PVCs produce uncomfortable palpitations and vessels
head pounding 3. Austin Flint murmur – soft, low-pitched,
3. Diminished cardiac reserve first symptom is rumbling mid-diastolic bruit
exertional dyspnea followed by orthopnea, PND, If murmur is soft – heard best with diaphragm of
and excessive diaphoresis stethoscope and with patient sitting up, leaning
4. Anginal chest pain at rest and during exertion forward, and with breath held in forced expiration
5. Systemic fluid accumulation, including congestive If AR due to primary valvular disease – diastolic
hepatomegaly and ankle edema murmur louder along left rather than right sternal
6. Left and right sided manifestations border suggests that AR caused by aneurysmal
dilatation of aortic root
PHYSICAL FINDINGS
• Patients with severe AR

1. Jarring of entire body and bobbing motion of the head
with each systole –parang naghehead bang..
2. Abrupt distention and collapse of the larter arteries
easily visible
3. Arterial pulse
FRED
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CARDIOLOGY: DR.
BARTOLOME
Eccentric jet of aortic regurgitation cursing along the posterior margin

• Severe, ACUTE AR of the left ventricular outflow tract (anterior mitral leaflet).
• There is sudden regurgitant blood volume fro the
aorta going to the left ventricle you up have 3. Roentgenogram
sudden elevated end diastolic pressure then LA • Apex displaced downward and to the left
HPN thenP venous HPN then P arterial HPN the P • Cardiac shadow extends below left diaphragm
edema. • LV enlargement in left anterior oblique and lateral
Elevated LV end-diastolic pressure lead to projections LV displaced posteriorly and
early closure of mitral valve (+) mid-diastolic encroaches on spine
sound
Soft or absent S1
Soft, short diastolic murmur of AR
Walang time mag compensate ang puso nyo
Acute pulmonary edema- primary
manifestation
You end up having patient with cardiogenic
shock
LABORATORY EXAM
1. ECG
• Severe, chronic AR ECG signs of LVH
• ST-segment depression and T-wave inversion in
leads I, aVL, V5 and V6 (LV “strain”)
• Left axis deviation and/or prolonged QRS –
denote diffuse myocardial disease poor
prognosis
2. Echocardiogram
• Rapid, high-frequency fluttering of anterior mitral
leaflet a characteristic finding
1. Produced by impact of regurgitant jet
• Useful in determining cause of AR, by detecting
dilatation of the aortic annulus
• Color flow Doppler – very sensitive and helpful in
assessing severity
FRED
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CARDIOLOGY: DR.
BARTOLOME
• Generally rheumatic in origin commonly associated with

some degree of TR; females > males
• Does not occur as an isolated lesion usually associated with
MS
• (+) diastolic pressure gradient between RA and RV
Mean diastolic pressure gradient of 4 mmHg sufficient to
TREATMENT
elevate mean RA pressure systemic venous congestion
(+) ascites and edema
Medical-prevent regurgitant blood volume-goal
• Patients with sinus rhythm RA a wave extremely tall and may
-reduce afterload, that’s the time you reduce your systemic
approach the level of the RV systolic pressure
vascular resistance.
• CO at rest usually depressed and fails to rise during exercise
1. Digitalis glycosides – patients with severe regurgitation
Low CO normal or slightly elevated LA, PA, and RV
and dilated LV without frank LV failure
systolic pressures despite presence of MS
2. Salt restriction
Presence of the TS masks the hemodynamic and
3. Diuretics
clinical features of the MS
4. Vasodilators, especially ACE inhibitors
5. Antiarrhythmics
SYMPTOMS
6. Long-acting nifedipine – delay the need for operation
• Development of MS precedes that of TS initial symptoms of
Surgical – definitive treatment –following the 55 rule
pulmonary congestion
• Consider two points in deciding on advisability and proper
• Characteristically complain of relatively little dyspnea for the
timing of surgical treatment:
degree of hepatomegaly, ascites, and edema
Patients with chronic AR usually do not become
• Low CO fatigue
symptomatic until after the development of myocardial
• Discomfort due to refractory edema, ascites, and marked
dysfunction
hepatomegaly
When delayed too long, surgical treatment often does
• Suspected if symptoms of RV failure persist after an adequate
not restore normal LV function
mitral valvotomy
• Operation should be carried out even in asymptomatic
patients with progressive LV dysfunction and a left
ventricular ejection fraction < 55% OR a LV end-systolic PHYSICAL FINDINGS
2
volume > 55 mL/m “55/55 rule”
• Patients with acute, severe AR require prompt surgical • Severe TS
treatment 1. Marked hepatic congestion resulting in cirrhosis, jaundice,
serious malnutrition, anasarca, and ascites
TRICUSPID STENOSIS 2. Congestive hepatosplenomegaly with prominent pre-
systolic pulsations of the enlarged liver
3. Distended jugular veins with giant a waves (in patient with
• diastolic mumur
sinus rhythm)
• right or left sided murmur?
4. Auscultation
Right sided (pulmonic and tricuspid are right sided
• Pulmonic valve closure sound not accentuated
murmurs)
• Diastolic murmur with many of the qualities of the
Bakit may tinatawag tayong right sided murmurs?
diastolic murmur of MS
Dun pumapasok yung caravllo sign ninyo. When
• Murmur heard best over left lower sternal margin and
you ask the patient to inspire and the murmur
over the xiphoid process – most prominent during
and the intensity of the murmur
presystole in patients with sinus rhythm
increases(murmur becomes louder), most
• Murmur augmented during expiration and during the
probably that is a right sided murmur
strain of Valsalva maneuver
• where will you appreciate the murmur?
Left Lower sternal border
• Will there be a right ventricular enlargement in TS? LABORATORY EXAM
• Will there be asignificant right sided failure manifestation in TS?
Tandaan nyo, hindi makapass ang blood from RA ECG
to RV. • RA enlargement – tall, peaked P waves in lead II with
So YES merong right sided failure manifestation. prominent, upright P waves in lead V1
You will have RA HPN and then venous HPN
• More common in tropical and subtropical climates
FRED
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CARDIOLOGY: DR.
BARTOLOME
• Absence of ECG evidence of RVH in a patient with right- intensified during inspiration
sided heart failure believed to have MS should suggest Reduced during expiration and Valsalva maneuver
associated tricuspid valve disease • AF usually present
Chest roentgenogram – combined TS and MS LABORATORY EXAM

• Prominence of RA and SVC without much enlargement of
the PA ECG
• Changes characteristic of MI or severe RVH
Echocardiogram
• Thickened tricuspid valve Echocardiography
• RV dilatation and prolapsing or flail tricuspid leaflets
TREATMENT • Diagnosis made by color flow Doppler echo
Medical Roentgenogram
• Intensive salt restriction and diuretic therapy – required • Enlargement of both RA and RV
during preoperative period to improve hepatic function
Surgical TREATMENT
• Carried out preferably at time of mitral valvotomy in
patients with moderate or severe TS • No operation needed in the absence of pulmonary HPN
• Open heart repair OR replacement of TV with a large • Treatment of underlying cause of heart failure – reduce
bioprosthetic valve severity of functional TR
• Surgical treatment should be carried out in patients with
TRICUSPID REGURGITATION severe regurgitation secondary to deformity of the TV due
to rheumatic fever
• Systolic murmur
• + caravallo’s sign PULMONIC VALVE DISEASE
• Always associated with left sided malfunctions or valvular
problems • Less affected by rheumatic fever
• Usually functional and secondary to marked dilatation of • Pulmonic regurgitation – most common acquired
the tricuspid annulus abnormality affecting the pulmonic valve
• May complicate RV enlargement of any cause Secondary to dilatation of the PV ring as a
• Commonly seen in late stages of heart failure due to consequence of severe pulmonary HPN
rheumatic (TR with TS) or congenital heart disease with (+) Graham Steell murmur
severe pulmonary HPN High-pitched, decrescendo, diastolic blowing murmur
• Other causes: ischemic heart disease, cardiomyopathy, cor along left sternal border difficult to differentiate from
pulmonale, infective endocarditis, tricuspid valve prolapse, murmur of AR
trauma, carcinoid heart disease Usually of little hemodynamic significance
• Reversible if pulmonary HPN is relieved
CLINICAL FEATURES
JONES CRITERIA FOR RHEUMATIC FEVER
• Clinical features result primarily from systemic venous
congestion and reduced CO
Major Criteria Minor Criteria
• TR in patients with pulmonary HPN – symptoms of
pulmonary congestion diminish but clinical manifestations
of right-sided heart failure become intensified
Distended neck veins with prominent v waves Carditis Clinical
Marked hepatomegaly, ascites, pleural effusion, Migratory polyarthritis Fever
edema Sydenham’s chorea Arthralgia
Systolic pulsations of liver Subcutaneous nodules Laboratory
(+) hepatojugular reflux Erythema marginatum Elevated acute phase
• Prominent RV pulsation along left parasternal region reactants
• Blowing holosystolic murmur along lower left sternal Prolonged PR interval
margin
FRED
Page 8 of 9
CARDIOLOGY: DR.
BARTOLOME
Plus
Supporting evidence of a recent group A streptococcal infection
(e.g. (+) throat culture or rapid antigen detection test; and/or
elevated or increasing streptococcal antibody test)
To fulfil the Jones Criteria, either 2 major criteria or 1 major criterion
and 2 minor criteria PLUS evidence of an antecedent streptococcal
infection are required (p1977-1979) read this topic dw haha
Involvement of heart in rheumatic fever is called
pancarditis. There is involvement of the endo, epi and
myocardium.
They can have
o CHESTPAIN
o MYOCARDIAL DYSFUNCTION
o Either SYSTOLIC OR DIASTOLIC PROBLEMS
o Most of the time its CONTRACTION PROBLEMS-
there is inadequate contraction of the heart, so
the patient will start complaining of heart failure
o VALVULITIS – namamaga yung mga valves nyo..
hindi pa naninigas yan initially.
During acute rheumatic fever you do
not develop stenotic valve. It is later
after how many years that you develop
stenosis. 15 to 30 years
MIGRATORY POLYARTHRITIS
-involves the large joint and it is migratory
-asymmetrical usually
DERMATOLIGIC MANIFESTATIONS
-nodules
-erythema marginatum
OTHER MANIFESTATION
Arthralgia and fever
- Magkaiba ang arthralgia at ang arthritis.
- In ARTHRALGIA there is only pain
- In ARTHRITIS there is inflammation
LAB
-CBC –increase in WBC
- ESR
-C REACTIVE PROTEIN
-ECG - PROLONGED PR INTERVAl
SUPPORTING EVIDENCES OF GROUP B STEP INFECTION
AGES 15 TO 5 YEARS OLD ARE COMMON
FRED
Page 9 of 9
CARDIO:PERICARDIAL DISEASES Dr. Bartolome
Pericardial Diseases Essentials of Diagnosis

Pericardium
Visceral and Parietal Pericardium Central chest pain aggravated by coughing, inspiration, or
recumbency
Visceral pericardium is a serous membrane separated from the Pericardial friction rub on auscultation
parietal pericardium by a small quantity (15-50ml) of fluid.
Characteristic ECG changes
Inside the pericardial cavity (space between visceral and parietal
pericardium) is pericardial fluid of about 50-70cc (ibasa notes…)
Prevalence
Functions of Pericardium
Admitting diagnosis in 0.1% of hospital admissions
1. Prevents sudden dilation of the cardiac chambers during exercise More common in men than in women
and with hypervolemia In pericarditis class, there is chest pain but you must remember that
2. Restricts the anatomic position of the heart when you see a patient having a chest pain you should know the
3. Minimizes friction between the heart and surrounding structures risk probability of the patient having that condition.
4. Prevents displacement of the heart and kinking of the great vessels Eto, katuladnitongbatangetopag nag-chest pain (simiki? )
5. Retards the spread of infections from the lungs and pleural cavities anongiisipinnyo? Iisipinnyobana may ischemic heart disease sya?
Unlikelydiba? That’s why you always have to remember the risk
factors for the development of heart disease.
Hindi nyodapatkinakalimutanang modifiable and non-modifiable
risk factors diba?
So what are the modifiable risk factors?
Hypertension
DM
Hyperlipidemia
Smoking
obesity
Sedentary lifestyle
And the non-modifiable risk factors are as follows:
45 yo male or 55 yo female
Early history of CAD
Eto, katuladnito (miki again? ) pwede bang ischemic heart disease
yan? Rheumatic heart disease pwede pa.
At the ER you should be able to diagnose ischemic heart disease
within 10min., and then do the PE… you have to rule out allthe
things that can cause death.
Anobayung chest pain napwedengmamatayyung patient mo?
Myocardial ischemia or infarction
Pneumothorax
Aortic dissection
Acute pulmonary embolism
All of these can cause acute chest pain and dyspnea and all are life
threatening condition.
Then, history, risk factors, diba?
Prolonged chest pain, more than 20 minutes will you consider it to
be MI? How do you diagnose a patient with MI? 1, 2, 3 anoyun?
Prolonged chest pain of more than 20 min
Acute Pericarditis You have to request for ECG and lastly
Definition Cardiac enzymes
So how about pulmonary embolism? Another term for acute PE is
acute corpulmonale. So you know that there is a risk for developing
inflammatory process involving the pericardium DVT…anobayungmga risk factors for developing DVT? Patients who
results in a clinical syndrome with triad of chest pain, pericardial are immobile, have prosthesis, those who underwent orthopedic
friction rub, and changes in the ECG surgery, cancer patients…and then all of a sudden may dyspnea…
so for pericardial diseases actually we’re talking about so, where will that be lodge? SaPulmonary artery, that’s why it is
inflammation and we call that pericarditis. And this pericardial called pulmonary embolism. So, when you obstruct the pulmonary
inflammation can be acute or chronic. And that inflammation may artery what will happen next? You’ll end up having pulmonary
have complications later and these are as follows: arterial hypertension, R ventricular hypertension, and venous
pericardial effusion or hypertension.So what is the physical examination? So you end up
constrictive pericarditis having R sided PE findings like neck vein engorgement in a patient
Pericardial effusion may be small in amount or large in amount, if it who is hypotensive???
is in large amount it may become what you call cardiac tamponade Another thing that you have to rule out is the possibility of having
disorders. pneumothorax, what do you expect to see? There is lagging of the
So basically the problem in pericardium is inflammation and that affected side; by percussion will you be able to appreciate
inflammation can later produce effusion and then constriction. pneumothorax? There will be what? Hyper-resonance on the
affected side; now in auscultation? There will be absence of breath Viral Pericarditis
sound on the affected side. That’s why in the ER you request for ECG
and Xray. Peronakitamonahindinagumagalaw, anonguunahinmo, Most common causes: coxsackievirus B, echovirus – usual cause of
ECG or Xray? sipon and uboubonyo.
Sa aortic dissection? What is the presentation? Prolonged chest 4-fold increase in antiviral titer required for diagnosis
pain… masyadongmatagal like 2 hours or 3 to 4 hours. What is the withprodrome of URTI – mga 1-2 weeks that later complaints of
PE finding of aortic dissection that differentiates it with other severe pleuritic chest pain.
diseases mentioned? You have to palpate the pulses. Patients with Prognosis good →usually self-limited
aortic dissection haveassymetrical pulse, but with normal ECG. You
can also request for chest Xray. Anongmakikitanyo? There’s Purulent Pericarditis
widening of the mediastinum.
So yanyungsinasabikosainyonaapatnapwedemagcausengdeath, but This is the one that causes problem compared to viral in origin.
not acute pericarditis. Predisposing Factors:
1. Thoracic Surgery
Common Causes of Pericarditis and Pericardial Effusion 2. Chemotherapy
3. Immunosuppression
Idiopathic – the most common cause is idiopathic in origin. The 4. Hemodialysis
problem is that probably most of these are secondary to viral Acute onset: high fever, chills, night sweats, dyspnea; chest pain or
infection. It’s very hard to document a viral infection. Sino friction rub rare
nanakakitasainyong viral titer result?Nakikitakolangsalibro. That’s Cardiac tamponade common (42%-77%) – don’t forget that
why probably this idiopathic cause is due to viral infection. Puro purulent pericarditis is associated with cardiac tamponade. You
clinical tayosapinas. really need to document if it is really purulent.
Infectious – bacterial, viral, fungal, HIV Paanomosususpentyahinna may purulent pericarditis yan? So,
Myocardial Infarction yanyungmga people prone to have infection later developing
Radiation cardiac tamponade. Once you have cardiac tamponade it is a
Postoperatively after open heart surgery medical emergency. Additional medical emergency,
Chest trauma – blunt, sharp kaninaapatdiba? Oh, plus one!
Malignancy High mortality rate – kasiyungmga patient immunosuppressed.
1o – Mesothelioma, angiosarcoma Hospital admission with immediate pericardiocentesis + IV broad
Metastatic – lung, breast, bone, lymphoma, melanoma spectrum antibiotics mandatory → followed by early surgical
Collagen vascular disease –RA, SLE drainage.
Metabolic – uremia, hypothyroidism Kailangantanggalinyung fluid agad and then give anitbiotics.
Pharmacologic – penicillin, phenytoin, procainamide, hydralazine,
minoxidil, cromolyn Na, methysergide, doxorubicin Tuberculous Pericarditis
Para saanang hydralazine? Hydralazine is for
hypertension specifically for pregnant patient. 1%- 2% of cases of PTB
Cromolyn Na for allergy. You must be careful. Increased risk in patients who are immunocompromised or HIV (+)
– if patient have Tuberculous pericarditis, you always have to rule
Signs and Symptoms out the possibility of having HIV. Actually for patient suffering from
TB not in Philippines, the probability that that patient is suffering
Most common symptom: chest pain from HIV is very high! More than 30-40%. Sa US now, pag positive
- Described as pleuritic in nature. TB ka, kahit PTB lang, automatic nagpapoHIV test na din sila. Satin,
- severe, sharp, retrosternal hindikapinoypagwalang TB. LOL
- often radiating to the neck, shoulder, or back Slow development of non-specific symptoms; chest pain and
- worsens in the supine position and with inspiration friction rub often absent
- Improved with sitting upright and leaning forward – but not always Chest radiography useful when findings of PTB present
present. Hospital admission indicated + anti-TB therapy (e.g. Rifampicin,
- Now, don’t forget your PPQRRST, for any kind of pain you use this INH, streptomycin, ethambutol) started promptly
as a guide. You can do this in 1 minute. Pericardial fluid analysis: very high specific gravity, very high
- How will you differentiate MI from unstable angina pectoris? That’s protein (>6 g/dL), & predominantly lymphocytic cells
why it is important to use that guide. Pericardial biopsy with acidfast bacilli PCR recommended
Friction Rub
- Scratchy, grating, high-pitched friction rubs (“squeak of leather of Uremic Pericarditis
a new saddle”)–walangkabayosi doc so hindinyaalamyan
- Due to fibrous deposits in the pericardial space Incidence: 6%-10% of patients with advanced renal failure before
- With three components: initiation of dialysis
1. atrial systole BUN usually >60 mg/dL
2. ventricular systole Large hemorrhagic effusion due to impaired platelet function
3. early ventricular diastole common
- best heard during inspiration at left lower sternal border, with Dialysis indicated
patient leaning forward
- That’s why pagnagPE kayo you always have to do this. Actually this Dialysis - Associated Pericarditis
is the best position for you to appreciate aortic and pulmonic
sounds and also at the same time the friction rub.so you have 3. An irony, since patient with uremic pericarditis needs dialysis.
- Ano daw Brazilian? LOL Si Santillan girl or boy…? waaaah! The main problem here is inadequate dialysis treatment.
Ditokasisapinas 2x a week lang, and ideally dapat minimum of 3x a
Specific Types week yan.
Idiopathic Pericarditis Cause by fluid overload →fluid usually serous
Intensification of hemodialysis indicated
Cause difficult to establish Improvement in 1-2 weeks
Most common diagnosis
Shiela and Young

Work hard in silence
let success make the noise Page 2 of 8
Treatment is give NSAID peropwedeng acute pericarditis yun
Post MI Pericarditis because of the trauma, but one thing about costochondritis is you
can localize the pain now.
Common complication in patients with MI (25%-40%)
1. within 3-10 days after MI Diagnosis
2. development correlates with extent of necrosis
more frequent with anterior than inferior infarcts Remains a clinical diagnosis based on:
Happens esp. in large anterior infarction, so pag may post MI 1. History
pericarditis ka, ibigsabihin nun malakiang infarction. The size 2. PE
depends on what artery is affected. 3. ECG – there is typical ECG changes in acute pericarditis.There is
associated with a higher 1-year mortality rate and incidence of CHF diffuse ST segment elevation in acute pericarditis. Dibarinurule out
Diagnosis requires: natinsyasa MI? anobayungsa MI, diffuse or localized? Localized. It
1. Symptoms or a new pericardial friction rub only involves the arterial supply affected. Remember anatomy.
2. ECG changes Aside from that, there is also PR segment depression in acute
typical ST elevation seen with acute pericarditis pericarditis. In MI, it doesn’t happen except if you have auricular
persistently positive T waves more than 2 days post-MIor infarction.
normalization of previously inverted T waves Other imaging studies: CT scan, MRI, Echocardiography – not really useful
so, pericarditis has chest pain, what differentiates it from MI? except if with pericardial effusion.
one is pleuritic the other is not
MI has ECG changes while pericarditis none
Another is Cardiac enzyme but you have to know its
release pattern.
CKMB – 6-8hours present in blood; peak- 24-
48 hours and would last for 72 hours
Troponin T/I - 6-8hours present in blood;
peak- same but would last for 10-14 days
Can I use trop T if may chest pain on 5th day? No. kasi
positive pa sya. You will use CKMB, kasiwalanasya after
3 days. (diko gets, pabasana lang.)
Actually class if you have to request for cardiac
enzymes, dapat serial yun, 0, 6, 12, and 14. Kaya
langpagsiguradonayung doctor hindinasiniserial.
Pagnatitipid pa yun, kungnakitanana may ST elevation
yunhindinamagrerequestyun.
Post Cardiac Injury Pericarditis
Dressler’s syndrome
occurs 2-3 weeks after MI or open heart surgery
Autoimmune component and possibly a latent viral infection
implicated
consists of pleuritic chest pain, fever, leukocytosis, and a
pericardial friction rub
Malignancy - Associated Pericarditis
caused mostly by metastatic disease – mostly with tumor

metastatic to the heart. Nagkakaroonnang cardiac tamponade
physiology.
Bronchogenic or breast carcinoma, Hodgkin’s disease and
lymphoma are common –you have to rule this out immediately.
Diagnosis is based on analysis of pericardial fluid cytology
sensitivity ranging from 70% to 90%
specificity of up to 95% to 100%
Radiation Pericarditis
Recent or remote mediastinal radiation

Any time from weeks to months after the exposure
Paminsannakaligtaan to. Pag may history ng malignancy yung
patient mo, don’t forget to ask if nagkaroonbang radiation
treatment before. Can be used as ddx. - In AP, concave. In MI convex, payong.
Trauma Pericarditis
May accompany sharp or blunt trauma and even a minimally

invasive procedure such as cardiac diagnostic or interventional
catheterizations
Iba pa yungcostochondral fracture/ inflammation
Shiela and Young

Stage I Acute Pericarditis Colchicine – for persistent or refractory cases of
Dressler’s syndrome and idiopathic pericarditis
Anticoagulants avoided during acute phase →reduce
bleeding and tamponade
Pericardiectomy
Indications:
1. development of pericardial constriction
2. recurrent pericarditis – rare
most definitive procedure
30-day perioperative mortality rateis about 5%
Outcome
Patients with uncomplicated acute pericarditis should have regular

follow-up after the initial visit to ensure resolution of symptoms
and rule out the development of constrictive symptoms.
PERICARDIAL EFFUSION
Myocardial Infarction Definition
increased amount of pericardial fluid
Essentials of Diagnosis
echocardiographic demonstration of pericardial fluid
Echocardiogram- to confirm the diagnosis
Acute Pericarditis: Chest Radiography

May be entirely normal unless there is a pericardial effusion
causing cardiomegaly or changes caused by underlying disease
Acute Pericarditis: Echocardiography

Indications:
1. symptoms persisting for longer than 1-2 week
2. presence of hemodynamic abnormalities
3. clinical suspicion of a large or increasing pericardial effusion, or
4. recent cardiac surgery
Treatment
most cases uncomplicated and self-limited – kahitwalanggagawin,

but don’t forget that acute pericarditis is with pain and
inflammation. So, what can you give to reduce pain and
inflammation? So you give drug with analgesic and anti-
inflammatory property. And that is NSAIDs. Most common causes of large effusions are:
Indications for an imaging modality, hospital admission, or both: 1. Malignancy (25% of cases)
1. clinical suspicion of a large effusion
2. Infection (27%) –most common cause is secondary tuberculosis
2. hemodynamic instability
3. Collagen vascular disease (12%)
3. severe pain or other symptoms
4. suspicion of a serious underlying condition, or 4. Chest radiation (14%)
5. any other signs or symptoms of clinical instability or Most common Cardiovascular manifestation of acquired immunodeficiency
impending deterioration syndrome – worse outcome ( BOARD EXAM QUESTION)
HIV + pericardial effusionassociated with poor prognosis,
Medical Management WHY? Actually it is not secondary to AIDS that produces Pericardial
Treatment of underlying disease- mainstay inflammation,
NSAIDs for pain relief it its secondary to secondary problem of HIV infection
1. Ibuprofen 400 mg q8h , it is secondary to pneumocystis or Kaposi sarcoma or tb going to
2. Ketorolac tromethamine – parenteral pericardium,
3. Contraindicated in the early period (<7-10 days) after MI (may so ibig sabihin niyan talagang highly immunosupress yung patient,
predispose to cardiac rupture) → use aspirin instead –why? konting sipon lang ng rhinovirus, deads na!
You give it as an anti-inflammatory drug and as an
antithrombotic, not as analgesic.
Prednisone – high dose → taper over 3 weeks
1. if pericarditis recurs (20%-30% of patients OR
2. response to NASAIDs is poor
Shiela and Young

Pathophysiology
Pericardial sac normally contains 15-30 ml of fluid → can hold 80-200ml

of fluid acutely and even up to 2L if the fluid accumulates slowly
development of tamponade depends on the rate of accumulation rather
than on the volume of the effusion typically, signs of right ventricular
diastolic failure develop first, followed by left-sided symptoms
Symptoms
Arise from the compression of surrounding structures (lung, stomach, phrenic

nerve) or diastolic heart failure
Include:
1. Chest pressure or pain
2. Dyspnea
3. Nausea, abdominal fullness, and dysphagia
4. Phrenic nerve irrirtation may cause hiccup Echocardiography
Hiccup- merong patient dati hiccup ng hiccup, wala daw nagtatanong Echo-free space between visceral and parietal pericardium → the
sa PE, eh yung patient nag underwent nuclear ablation of thyroid extent of the space defines the size of the effusion
gland,
Large effusions may produce the picture of a “swinging heart”
so pinaxray, ang laki ng heart! Yun pala yung patient is suffering
severe hypothyroidism tapos walang nagbother to look up the neck Imaging modality of choice for diagnosing a pericardial effusion
, eh 1 week na yung patient, nalusutan na daw lahat, yung but may miss small loculated effusions
clerk,intern, 3 residents, and even the consultant and the another
consultant., eh nagtamponade yung patient, Sizing of Small Medium Large
Kaya daw ipractice yung P.E….. may medical officer pang di nag PE, Pericardial
tapos after 1 hr, deads yung patient. Effusion by
NO ONE CAN ARGUE ON YOUR PE,! In short mag P.E. or change your Echocardiogra
course.( halerrrr!!! Third year na kaya! ) phy Size
Vol (ml) <100 100-500 >500
Physical Examination Localization Localized Circum- Circum-
ferential ferenial
Small effusion – PE unremarkable ,asymptomatic Width <1 1-2 >2
Large effusion:
1. Muffled heart sounds Analysis of Pericardial Fluid
2. Ewart’s sign (dullness to percussion, bronchial breath sounds, and egophony 1. CBC
below the angle of the left scapula) – rare 2. Chemistry panel
3. With increasing volume of the effusion, signs and symptoms of cardiac 3. ESR
tamponade may occur
Diagnostic pericardiocentesis done if the cause is unclear or any of the
Diagnosis following is suspected
1. Malignancy
Electrocardiography 2. TB
Low voltage & electrical alterans 3. Fungal or bacterial infection
Therapeutic pericardiocentesis done for large effusions that are

increasing in size or causing tamponade
Diagnostic pericardiocentesis done if the cause is unclear or any of the

following is suspected
1. Malignancy
2. TB
3. Fungal or bacterial infection
Therapeutic pericardiocentesis done for large effusions that are increasing in
size or causing tamponade
Chest Radiography
Cardiomegaly occurs if there is more than 250 ml of fluid in the
pericardial sac
Shiela and Young

Exudate vs. Exudate Transudate Pericardial tamponade end up in having Venous Hypetension
Transudate
Parameter Essentials of Diagnosis
Cause Malignancy Radiation
Infectious, Uremia Increase jugular venous pressure with an obliterated y descent
parainfectious Hypothyroidism Pulsus paradoxus
Postpericardiotomy Trauma Echocardiographic evidence of right atrial and ventricular collapse
syndrome
Equal diastolic pressures in all four cardiac chambers
Collagen vascular
disease
Spg (g/ml) >1.015 <1.015 Pathophysiology
Elevated intrapericardial pressure → progressive limitation of mostly early
Total protein >3.0 <3.0
diastolic ventricular filling → low cardiac output
Fluid-to-serum >0.5 <0.5
protein ratio
Symptoms
Fluid-to-serum LDH >0.6 <0.6
Symptoms resulting from decreased cardiac output and congestion:
Fluid-to-serum <1.0 >1.0 dyspnea,
glucose ratio
chest discomfort
weakness restlessness
Treatment
Agitation
Medical Management
Diuretics →help decrease the intensity of fluid overload symptoms if present Drowsiness
Effusions causing pretamponade or tamponade →immediate drainage Oliguria
Volume expansion and inotropic → for hemodynamic stabilization pending anorexia
drainage If the tamponade develops acutely as a complication of an acute MI (free
wall rupture) or trauma → catastrophic, with sudden death or shock and
Pericardiocentesis high mortality
Echocardiographically guided pericardiocentesis is safe and
effective Physical Examination
Indications: Classic findings – Beck’s triad (10% to 40% of patients):
1. A large effusion with hemodynamic compromise or tamponade 1. Hypotension
2. For diagnostic purposes 2. JVD
3. Muffled heart sounds
Surgical Treatment Manifestations are right sided(neckvein engorgement,ascites, and
1. Percutaneous Balloon Pericardiotomy bipedal edema)
Least invasive Other things that produced your massive pleural effusion
Used mostly for neoplastic effusion with a poor prognosis as a can also produce these clinical manifestations such as muffling of
palliative treatment
the heart sound bec of that fluid
Success rate for relieving re-accumulation of pericardial fluid is 85%
Since there is fluid in between the precordium, dati kasi walang
to 92% at 30 days
2. Subxiphoid Pericardiostomy fluid, now there is a large fluid , it will muffles the heart sound s the
Known as a “pericardial window” transmission on the stethoscope Muffling of the heart sound-
May be done under local anesthesia humihina yung heart sounds to the point na hindi mo marinig
High success rate, with few complications talaga.
Recurrence of fluid accumulation is rare
Ewart sign- dullness to percussion ,brochial breath sound
Cardiac Tamponade ,egophony in the angle of scapula-
Definition where will you look for this sign?BACK,LEFT, kasi andun yung
heart... lumaki yung cardiac silhouette , so nacompress yung
Occurs when fluid accumulation in the finite pericardial space lungs cardiac t
causes an increase in pressure, with subsequent cardiac
compression and hemodynamic compromise Ewart's sign is a set of findings on physical examination in people
Pag nagka effusion,lalaki yan,magkakaroon ng pericardial space with large collections of fluid around their heart (pericardial
with fluid inside, effusions).
and that’s fluid inside will have increase intracardial pressure Dullness to percussion (described historically as "woody" in
quality), egophony, and bronchial breath sounds may be
and it will compress the heart.
appreciated at the inferior angle of the left scapula when the
In the left heart, which is much thicker than your right heart,
effusion is large enough to compress the left lower lobe of the lung,
and that’s why when you have compreesion, the one that will be causing consolidation or atelectasis.
easily compress is your right side of the heart( the right ventricle
and the right autirum) Tachycardia, tachypnea, hepatomegaly common
It will not allow blood flow coming from the veins going to the Pulsus paradoxus – inspiratory decline in systolic BP of more than 10
right atrium and right ventricle mmHg due to compression and poor filling of the LV caused by
And it will Decrease preload, decrease CO, Decrease BP and as increased venous return to the right side of the heart
-during inspiration tapos medyo nawala-wala pa—it is pulsus
compensatory mechanism it will dec your heart rate Pericardial
paradoxus or alterans
tamponade with Tachycardia
Since your not allowing blood flow from great arc veins going to
right atrium venous hypertension
Shiela and Young

Hyoptension, neck veing engorgement, muflled heart
sound + narrow pulse pressure+ pulsus paradoxus
Pericardial tamponade(MEDICAL EMERGENCY)
Diagnosis
Electrocardiography
Abnormal findings may include:
1. Electrical alternans - height of QRS varies like 3 mvolt, 5,8 millivolts.
Check the height of ECG.
It is commonly seen on pt with neck vein engorgement,
cardiomegaly SUSPECT CARDIAC TAMPONADE
Massive pericardial effusion
you need at least 250 cc of pericardial fluid for you to
produce Cardiomegaly secondary to Pleural effusion,
Cardiothoracic ratio of >0.5 or something like 0.7
Typical water bottle configuration
2. Low voltage
3. Changes associated with acute pericarditis
Since there is a fluid in between the transmission of electrical potential
going to the ECG DOUBLE lean lead ecg? ??? ano d daw? Sorry ..
QRS is small
Lean? Leads- at least 5 millivolts( para hind maconsiderdouble...)
Chest lead- V1-V6- 5 millivolt;
Lead II and V -7 millivolts
Lead 3 and 4 –9millivolts
IF hindi ganito yung value, we can consider na meron Double ...
Transthoracic Echocardiography
Sensitive finding for tamponade physiology is inferior vena
cava plethora, with absent inspiratory collapse
Pericardial Constriction/ Constrictive Pericarditis
Right ventricle and atrial collapse on echocardiography is the
most accurate finding for diagnosis Definition
ECHOCARDIOGRAPHY- confirms the dx of pericardial
effusion and cardiac tamponade and to the point that An abnormal thickening of the pericardium, resulting in impaired
effusion is called swimming heart ventricular filling and decreased cardiac output
Most cases idiopathic
Right Heart Catheterization May have history of acute or chronic pericarditis
Most typical finding: equalization of mean right atrial, right ventricular
and pulmonary artery diastolic, and mean pulmonary capillary wedge Essentials of Diagnosis
pressures. Markedly elevated JVP with accentuated x and y descent and
Kussmaul’s sign
Treatment Kussmaul’s sign- enlargement of neck vein during deep inspiration (
Medical emergency Normal:collapsed neck vein )
Remove the fluid Kussmaul's sign is a paradoxical rise in jugular venous
Immediate hospital admission and prompt pressure (JVP) on inspiration.
pericardial drainage by pericardiocentesis It can be seen in some forms of heart disease and is
If follow-up echocardiography documents fluid re-accumulation usually indicative of limited right ventricular filling due
→pericardial window should be considered to right heart failure.
Infection risk associated with a pericardial drain increases after 48 hours Pericardial knock on auscultation
MRI, CT or echocardiographic imaging showing a thickened
Differential Diagnosis pericardium
1. Right-sided heart failure
2. Right ventricular infarction
3. Constrictive pericarditis Pathophysiology
4. Pulmonary embolism
Initiating event causes a chronic inflammatory pericardial process → fibrinous
Treatment thickening & calcification of pericardium → limitation of intrapericardial
Immediate hospital admission and prompt pericardial drainage by volume → impaired ventricular filling → decreased cardiac output → right and
pericardiocentesis left ventricular failure
If follow-up echocardiography documents fluid re-accumulation
→pericardial window should be considered
Infection risk associated with a pericardial drain increases after 48
hours
Shiela and Young

Calcification of the pericardium by CT
Physical Examination
Increased ventricular filling pressures cause:
1. Jugular vein distention
2. Kussmaul’s sign – absent inspiratory decline of jugular venous distention
Auscultation: muffled heart sounds and occasionally a
characteristic pericardial knock (60-200 milliseconds after the
second heart sound)
Diagnosis
ECG
Non-specific but low voltage of QRS complex may be seen
Laboratory tests
Brain natriuretic peptide (BNP) – serum biomarker; distinguish
constrictive from restrictive pericarditis →higher in resetrictive
Echocardiography
Best imaging modality for assessing
hemodynamic parameters non-invasively
Doppler echocardiographic
findings have the highest sensitivity and specificity for detecting
constrictive physiology
MRI & CT
CT is the imaging modality of choice to evaluate the
pericardium
Pericardial calcifications may easily be identified on CT
Finding of thickened pericardium on the CT or MRI is specific
for constriction
Treatment
Medical treatment is difficult and does not affect the natural
progression or prognosis of the disease
Diuretics and a low-sodium diet for patients with mild to moderate
(New York Heart Association [NYHA] Class I or II) symptoms or
contraindications to surgery
For most patients, pericardiectomy is advised, with 80% to 90% of
patients experiencing improvement and 50% complete relief of
symptoms
remove the pericardium
Shiela and Young

CARDIOLOGY: DISEASES OF
DR. ORLANDO DEDUYO
THE AORTA
DISEASES OF THE AORTA Causes of AA:

ANATOMY OF THE AORTA Degenerative diseases
Inherited or developmental diseases ( Marfan ‘s
The aorta is the conduit through which blood ejected from the syndrome)
left ventricle is delivered to the systemic arterial bed Infections ( syphilis, TB)
diameter is approximately 3 cm at the origin Vasculitis
ascending portion- 2.5 cm Trauma
descending portion in the thorax- 2.5 cm Inflammation, proteolysis, and biomechanical wall stress
abdomen- 1.8-2 cm contribute to the degenerative processes that characterize most
Aortic wall consist of a thin intima composed of: aneurysms of the abdominal and descending thoracic aorta.
Tunica intima- composed of endothelium, These are mediated by B and T cell lymphocytes, macrophages,
subendothelial connective tissue and an internal elastic inflammatory cytokines, and matrix metalloproteinases that
lamina degrade elastin and collagen and alter the tensile strength and
Tunica media- composed of smooth muscle cells and ability of the aorta to accommodate pulsatile stretch.
extracellular matrix
Tunica adventitia- composed primarily of connective DEGENERATIVE AORTIC ANEURYSM (AA)
tissue enclosing the vasa vasorum and nervi vascularis
The viscoelastic and compliant properties of the aorta serves as a Factors associated with degenerative aortic aneurysms:
buffering function. Aging
The aorta is distended during systole to allow a portion of the Cigarette smoking
stroke volume and elastic energy to be stored, and it recoils Hypercholesterolemia
during diastole so that blood continues to flow to the periphery Male gender
Due to its continues exposure to high pulsatile pressure and Family history of aortic aneurysm
shear stress, the aorta is particularly prone to injury and disease Atherosclerosis - most common pathologic condition associated
resulting from mechanical trauma with degenerative aortic aneurysm.
It’s also more prone to rupture especially with the development High risk condition such as high blood, DM age 50 and above are
of aneurysmal dilation, since its wall tension will be increased, as high risk in developing Aortic aneurysm
governed by Laplace’s law (proportional to the product of Screened for AA
pressure and radius) Female > 65 years old are also high risk
Age>40 above
AORTIC ANEURYSM
CYSTIC MEDIAL NECROSIS
Aneurysm – pathologic dilatation of a segment of a blood vessel.
True aneurysm – involves all three layers of the vessel Cystic medial necrosis – histophatologic term used to describe
wall and is distinguished from a pseudoaneurysm the degeneration of collagen and elastin fibers in the tunica
Pseudoaneurysm- intimal and medial layers are media of the aorta, as well as the loss of medial cells that are
disrupted and the dilatation is lined by adventitia only replaced by multiple clefts of mucoid material.
and, at times, by perivascular clot. Affects the proximal aorta, results in circumferential weakness
Ectasia- arterial dilatation < 150% of normal artery and dilatation, and leads to the development of fusiform
diameter aneurysms involving the ascending aorta and sinuses of Valsalva
TYPES in terms of SHAPE
o Fusiform aneurysm – affects the entire This condition is particularly prevalent in patients with:
circumference of a segment of the vessel, Marfan syndrome
resulting in a diffusely dilated artery. Ehlers-Danlos syndrome type IV
o Saccular aneurysm – involves only a portion of HPN
the circumference, resulting in an out pouching Congenital bicuspid aortic valves- sometimes these
of the vessel wall. patients has no symptoms and they are referred for
Aortic aneurysms are also classified according to location, i.e. presence of murmur only
abdominal vs. thoracic. Familial thoracic aortic aneurysm syndromes.
Sometimes it appears as an isolated condition in
ETIOLOGY Patient without any other apparent cause.
Aortic aneurysms result from conditions that cause degradation

or abnormal production of the aortic wall’s structural
components, elastin and collagen.
INFECTIOUS CAUSES THORACIC AORTIC ANEURYSM (TAA)
Infectious causes of AA: Clinical manifestations and natural history depend on their
Syphilis location
TB ( most common in the Philippines) Cystic medial necrosis is the most common cause of ascending
Other bacterial infections aortic aneurysms, whereas atherosclerosis is the condition most
frequently associated with aneurysms of the aortic arch and
Syphilis descending thoracic aorta.
relatively uncommon cause Average growth rate of thoracic aneurysms: 0.1 – 0.2 cm/year.
Syphilitic periaortitis and mesoaortitis damage elastic Risk of rupture is related to:
fibers, resulting in thickening and weakening of the size of the aneurysm
aortic wall. The presence of symptoms, ranging approx. from 2-
Approximately 90% of syphilitic aneurysms are 3% per year for thoracic aneurysms <4.0 cm in
located in the ascending aorta and aortic arch. diameter to 7% per year for those >6 cm in diameter.
Tuberculous aneurysms The bigger the aneurysm increase manifestation or
Typically affect the thoracic aorta and result from symptoms increase risk for rupture
direct extension of infection from hilar lymph nodes Borderline in requesting surgery for patient with
or contiguous abscesses, or from bacterial seeding. Thoracic aortic aneurysm is 5.5 cm diameter and for
Loss of aortic wall elasticity results from patient with Marfan syndrome and congenital
granulomatous destruction of the medial layer. bicuspid aortic valve the cu-off is lower 5 cm
So if you have patient with multidrug resistance Most thoracic aortic aneurysms are asymptomatic
tuberculosis and develop chest pain you have screen However, compression or erosion of adjacent tissue by
patient and you will see in the x-ray that there is aneurysms may cause symptoms such as
widened mediastinum so you will suspect aortic 1. chest pain (MOST COMMON)
aneurysm 2. shortness of breath
Mycotic aneurysm 3. cough
is a rare condition that develops as a result of 4. hoarseness
Staphylococcal, Streptococcal, Salmonella or other 5. Dysphagia.
bacterial or fungal infections of the aorta, usually at But the manifestation is not specific because it can
an atherosclerotic plaque. mimic other diseases such as TB, emphysema,
These aneurysms are usually saccular pericarditis. So put together the history, P.E and
Tx: prolonged IV antibiotics Laboratory examination to diagnose the patient
Aneurysmal dilatation of the ascending aorta may cause
VASCULITIS Congestive Heart Failure as a consequence of aortic
regurgitation (warning sign)
Vasculitides associated with aortic aneurysm include Marked compression of the superior vena cava may
Takayasu’s arteritis produce congestion of the head, neck, and upper
giant cell arteritis extremities.(edematous upper extremities)
which may cause aneurysms of the aortic arch and descending Chest X-ray may be the first test to suggest the diagnosis of a
thoracic aorta. thoracic aortic aneurysm. Findings include
Spondyloarthropathies, such as ankylosing spondylitis, Widening of the mediastinal shadow
rheumatoid arthritis, psoriatic arthritis, relapsing polychondritis, Displacement or compression of the trachea or
and Reiter’s syndrome, are associated with dilatation of the left mainstem bronchus.
ascending aorta 2D-echo, particularly transesophageal echocardiography, can be
Behcet’s syndrome causes thoracic and abdominal aortic used to assess the proximal ascending aorta and descending
aneurysms. thoracic aorta.-
So for simple 2 D ECHO (surface echo) you can see
TRAUMA only up to the root of the aorta. Yung transesophageal
Echo pinapasok sa bibig and you can visualize your
Traumatic aneurysm may occur after penetrating or non- proximal ascending and descending thoracic aorta
penetrating chest trauma Contrast-enhanced computed tomography (CT), Magnetic
Most commonly affected is the descending aorta just beyond the resonance imaging (MRI), and Conventional invasive aortography
site of insertion of ligamentum arteriosum are sensitive and specific tests for assessment of aneurysms of
the thoracic aorta and involvement of branch vessels.
In asymptomatic patients whose aneurysms are too small to
justify surgery, noninvasive testing with either contrast
enhanced Ct or MRI should be performed at least every 6-12
months to monitor expansion.
Page 2 of 11 Jay and Miki

Malayo ang mararating ng ating pangarap kung sasamahan ng pagsisikap!
SURGICAL PROCEDURE FOR TAA .001) and treatment with conventional open
repair (P = .02).
Operative repair with placement of a prosthetic valve Conclusion
Indicated in patient with symptomatic thoracic aortic o An endovascular approach for the ruptured
aneurysm (non-traumatic) descending thoracic aorta
Ascending aortic diameter is > 5.5-6 cm reduces early morbidity, mortality, and duration
Aneurysm that has increased by > 1 cm per year of hospitalization, while providing equivalent
Endovascular repair is an alternative for some patients with late outcomes even in an older group largely
descending thoracic aortic aneurysm considered high risk for open repair. These data
Complication of surgery support a paradigm shift, with TEVAR emerging
Increase risk of paraplegia or stroke as the preferred therapy for all patients
- Increase risk heart attack for patient with distal presenting with descending aortic rupture.
abdominal aorta 32% o Based on the guidelines open surgery is on level
Neurologic deficit 1A evidence that’s why still this is the treatment
Acute renal failure or CKD of choice while TEVAR is level 2A evidence.
- 38% mortality for patient with renal disease
- 13% mortality for patient with no renal disease RUPTURED ABDOMINAL AORTIC ANEURYSM
- 30 day mortality occur for patient with low GFR ( th
patient with stage 3A) 27% 10 leading cause of death in Men
- Stage IV- dialysis is needed 2:1-4:1 M-F predominance
Cardiac failure 50% undetected
Infection Occur more frequently in males than females
TH
Respiratory failure 13 leading cause of death
24,000 deaths/year
DESCENDING THORACIC AORTIC ANEURYSM (DTAA) Increase incidence with age- 6-7 decade of life
AAA ≥ 4.0 cm may affect men older than 50 years old
90% of all AAA > 4 cm are related to atherosclerotic disease and
Type C: 54% - extensive (MOST COMMON)
most of them are below the level of renal arteries
Type A: 33% (proximal only)
Prognosis is related to both the size of the aneurysm and the
Type B: 13% (distal part)
severity of coexisting coronary artery and cerebrovascular
disease
30d mortality:8%
The risk of rupture increases with size
Neurologic deficits: 23%
Many complications < 5 cm- 1-2%
HF, Renal failure, Infections > 5cm in diameter- 20-40%
6cm diameter: exponential increase
THORACIC ENDOVASCULAR AORTIC REPAIR ( TEVAR) 10cm diameter: 50% chance of rupture
5.5cm decide if patient undergo open surgery or
Analogous to angioplasty TEVAR
Benefits in comparison with open surgery Increase high operative mortality maybe because of
Attractive option late detection
Less invasive 50% die before they reach the hospital
40-50% die before they reach surgery
Minimal blood loss
High mortality and high operative mortality due to late
Minimal pulmonary complication
detection and diagnosis
Decrease risk of paraplegia
Quick recovery
IMAGING MODALITY
Anatomical criteria
Proximal and distal diameter- 23-37 cm
Information needed from diagnostic studies
Proximal landing zone- ≥ 2cm
Length and size of the aneurysm
Distal landing zone
Proximal extent (infra, supra, or juxtarenal)
Candidate for TEVAR
Supre/juxta-complex and extensive
dissection
A comparative analysis of open and endovascular repair for the
Obligatory renal ischemia time due to
ruptured descending thoracic aorta ( taken from journal)
clamping above the renal arteries.
Result
Distal extent, aneurysm or occlusive disease of the
o By multivariate analysis, independent predictors
iliofemoral segments.
of a composite outcome of early mortality,
Status of the suprarenal-visceral vessels
stroke, permanent spinal cord ischemia, or need
(dilatation/stenosis of coeliac, mesenteric)
for dialysis or tracheostomy included the
Presence of anatomical variant (horseshoe
presentation with hemodynamic instability (P <
kidney,retroaortic renal vain, IVC duplication)
Leak or rupture
For thoracic aortic aneurysm the imaging modality of choice is
chest x-ray and for
Abdominal aneurysm if patient present with pulsatile mass on
periumbilical area you have to suspect
ABDOMINAL ULTRASOUND
Most practical screening tool readily available

Sensitivity: 88-99%; specificity: 100%
Fast and accurately defines aneurysm size within +/-
0.3 cm
Fairly defines proximal extent (infra, supra, juxta
renal) – improved by DUPLEX UTZ
Fairly defines status of suprarenal/visceral segments
– improved by DUPLEX UTZ
Distal extent poorly defines (dilatation/stenosis of
iliofemoral segments)
Poorly defines presence of anatomic variants
(retroaortic renal veins, IVC duplication)
Cannot identify leak or rupture.
COMPUTED TOMOGRAPHY SCAN
Sufficient as a stand-alone modality for vital information

Extremely accurate in diagnosis & sizing with accuracy within +/-
0.2 cm
Provides better definition of proximal extent of aneurysm and
local anatomical relationship of the visceral & renal vessels
Provides information regarding the presence of anatomical
Example of suprarenal abdominal aneurysm
variants (horsehoe kidney, retroaortic renal vein, IVC
duplication)
MAGNETIC RESONANCE ANGIOGRAPHY (MRA)
Provides information for iliofemoral aneurysmal extension
Identifies leak or rupture
Excellent modality for monitoring changes in aneurysm size Alternative to CT scan for preoperative evaluation in elective
cases in those with incipient renal insufficiency (Px w/ CKD)
Extremely accurate for sizing
Correctly defines proximal and distal extent of disease in >80%
of cases
Defines anatomical variants
Identifies leak or rupture
Time consuming, expensive and not readily available.
AORTOGRAPHY (invasive)
Excellent in vascular roadmapping especially with suspected

concomitant renal and iliofemoral stenosis.
Leak or rupture may be seen with extravasation of contrast
medium.
Underestimates aneurysm size in the presence of non-opacified
mural thrombus lining the walls.
SPIRAL CT WITH 3D RECONSTRUCTION Cannot identify anatomical variants.
Time consuming
Provides 3D images or aorta & its branches Mobilizes many personnel
Better definition and roadmapping for surgical strategy Entails a lot of cathlab preparation
May be time-consuming for urgent or emergent AAA Invasive, potential catheter insertion – related complications
(hematoma, dissection, ect.)
Largely supplanted by high-definition CT
So if patient is for TEVAR you start with CT contrast and do
aortography prior to placement of stent

Analogous to coronary angiogram but the dye is injected to the CONSERVATIVE TREATMENT for LOW RISK RUPTURE
aorta from proximal carotid vessel, renal vessel, & aortic iliac
vessel No conservative tx for elimination of aneurysm
Hypertension Control
RISK FOR RUPTURE o Beta blockers (reduces expansion rate
independent of hemodynamic effects)
Estimated Rupture Risk o Target SBP of 110-120mmHg and HR of 60-
70bpm
AAA DIAMETER ( CM) RUPTURE RISK( % /YEAR) o Higher BP, higher HR – higher shear stress
<4 0 o If Px is asthmatic and COPD –
4-5 0.5-5 Verapamil/Diltiazem or Digoxin for HR control
5-6 3-15 o (--ra---in) New agent that controls only HR and
6-7 10-20 not BP
7-8 20-40 o The new agent should not coexist with
>8 30-50 verapamil/diltiazem beacause it will prolong QT
interval → high risk for sudden cardiac death
AAA diameter best predictor of rupture risk (just like drinking coffee w/ energy drink!)
Rupture risk very low for <5 cm (1.5%), increase substantially by Smoking cessation
6 cm Cessation of steroid treatment for COPD
Current evidence 5.5 cm best threshold for repair for “average” Modify/treat risk factors (DM, Dyslipidemia, etc.)
patient UTZ surveillance
Independent predictors of AAA rupture in 4-5.5 cm size Recommendations for UTZ Surveillance
(Society for Vascular Surgery and the Society for Vascular Medicine
PARAMETERS RELATIVE RISK and Biology)
FEMALE GENDER (ACS higher 3X
independent risk) < 3cm No further testing
LARGER INITIAL DIAMETER 2.9X per cm 3-4 cm Annual US
CURRENT SMOKING 1.5X 4-4.5 cm US every 6 months
WORSE COPD 0.6X per L FEV1 > 4.5 cm Referral to a vascular specialist
HIGHER MAP 1.02X per mmHg
AVERAGE OR HIGH RISK RUPTURE
Observation that not all AAA rupture at the same size threshold.
Unfortunately, there is no precise formula that incorporates the Assess life expectancy
risk factors to calculate rupture risk. Risk factors used in If short, i.e. terminal malignancy, irreversible severe
combination to estimate rupture risk and categorize patients as CAD, cardiomyopathy, etc.;
low, average or high risk. If average or long, assess operative risk
Conservative management
Factors Influencing Risks of Aneurysm Rupture if Px will undergo TEVAR or Open Surgery, most likely
this patients will die
Low risk Average risk High risk (for
TEVAR)
Diameter < 5 cm 5-6 cm >6 cm
expansion < 0.3 cm/yr 0.3-0.6 cm/yr >0.6 cm/year
Smoking/COPD None, mild moderate Severe/steroids
Family history No relatives 1 relative Numerous
relatives
Hypertension Normal BP controlled Poorly
controlled
shape Fusiform saccular Very eccentric
Smoking/COPD – bad predictors (longer time extubating patient

during surgery)

- Example of open repair
OPERATIVE MORTALITY FOR OPEN REPAIR X
Elective= 1-3 (4-6%)

Urgent= 19%
Ruptures (massive blood loss/transfusion, intraoperative
MI, DIC, ARDS, Renal Failure, etc.) = 40-50%
Age is not an absolute contraindication for the procedure
ENDOVASCULAR ANEURYSM REPAIR X
GOOD OR MODERATE OPERATIVE MORTALITY
Emerged in the early 1990’s as an alternative treatment for AAA
Open Repair (Gold standard) IA level of evidence Studies have demonstrated equivalent early safety/efficacy of
Endovascular Aneurysm Repair (EVAR) (Alternate procedure) 2A EVAR
level of evidence EVAR short term benefits of reduced ICU and hospital stays,
EVAR mortality lower mortality than open repair in RAAA reduced blood loss, fewer major complications, and more rapid
recovery.
EVAR midterm (3-6 years) result favourable with limitation of AAA
HIGH OPERATIVE MORTALITY RISK expansion 80-90%, and rupture prevention 95-98%
Has a higher reintervention rate, increases surveillance burden, and
Conservative management a small but ongoing risk of AAA rupture.
Endovascular aneurysm repair (Px w/ high income who insists Px’s preference is important (EVAR vs. Open Repair) for those with
they want to live) good or moderate operative risk.
Preferred intervention for those with high operative risk who
satisfy the EVAR anatomic criteria
Presently, there are no randomized control trials comparing EVAR
vs. Open repair

Anatomic Criteria SYMPTOMATIC
1. Proximal neck length >1.5 cm
2. Proximal neck diameter <2.8 cm Steady gnawing pain in the hypogastrium or lower back that lasts
for hours or days
3. Distal cuff length >1 cm
Leak or heralds impending rupture
4. Distal cuff diameter <2.8 cm Diagnostic test: CT scan
5. Angulation/tortuosity <60 degrees Indication for surgery:
6. Iliac artery diameter >7 mm Any size especially if saccular, mycotic or inflammatory
7. Mural thrombus attachment site Timing: urgent
not present
8. Iliac site attachment – common iliac RUPTURED ANEURYSM
artery
9. Associated mesenteric disease not Pathognomonic Triad
present 1. Pulsatile abdominal mass
2. Hypotension
3. Abdominal/back pain (1/3 of cases)
MANAGEMENT
Rx: no work-up needed, emergent intervention
Acute abdominal or back pain which is generally sudden in onset,
Goal of Repair
or worsening pain
Most aneurysm repairs aim to prevent rupture Often associated with light headedness or collapse (most likely
(rupture operative mortality risk 50%) stroke or involvement of carotid vessels)
Most effective if performed when rupture risk is high
compared to elective operative risk (1-5%) in patients
Known AAA Px, STABLE
who will live long enough to enjoy the longterm
benefits ECG (to r/o ACS)
Thus decision influenced primarily by estimates of: CT Scan
Aneurysm rupture risk o Ruptured: Emergent intervention (unstable &
Elective operation mortality hypotensive)
Life expectancy o Non-ruptured: Evaluate for early repair
Patient preference
Known AAA Px, UNSTABLE (Hypotension)
STENT PLACEMENT Emergent intervention
Undiagnosed AAA Px, STABLE

ECG, CT Scan (UTZ)
o Ruptured: Emergent intervention
o Non-ruptured: Evaluate for early repair
Undiagnosed AAA Px, UNSTABLE

Rx: ECG, Resuscitate
o If stabilized: CT scan (UTZ)
If not AAA: evaluate other causes
Ruptured AAA: Emergent intervention
Non-ruptured AAA: Evaluate for early
repair
o Remain unstable: Emergent intervention
***NOTE: Study this part because Doc will give cases and
necessary management will be based on this.(dati pa to hehe,
not sure if applicable to satin)

Ruptured Abdominal Aneurysm
AORTIC DISSECTION
Considered emergency
Uncommon
Potentially catastrophic disease if not recognized early and treated
promptly
Diagnosis often requires clinical suspicion
th th
Peak incidence is the 6 to 7 decade of life
Has a 3:1 male preponderance
ANATOMIC CLASSIFICATION (Debakey)
hematoma
CURRENT RECOMMENDATIONS FOR AAA REPAIR X

Type I – Entire length (proximal-distal)
Report of a subcommittee of the Joint Council of the American Type II – Proximal
Association for Vascular Surgery and Society for Vascular Surgery
Type III – thoracic
1. Single threshold diameter for elective AAA repair not applicable to
all Pxs, decision for repair must be individualized in each case SPECTRUM of AORTIC DISSECTION
2. RCT’s have shown rupture risk of small (<5cm) AAA is quite low, Ascending aorta – 65%
and a policy of careful surveillance up to a diameter of 5.5 cm is safe, Descending aorta – 25%
unless rapid expansion (>1cm/yr) or symptoms develop. Aortic arch – about 10%
Abdominal aorta – 5%
However, early surgery is comparable to surveillance with later
surgery, so that Px preference is important, especially for AAA 4.5 CLINICAL MANIFESTATIONS
to 5.5 cm in diameter.
Based on the best available current evidence, 5.5 cm diameter Severe pain
appears to be an appropriate threshold for repair in an average Px.
Most common presenting symptoms of acute aortic
However, subsets of younger low-risk Pxs, with long projected life
dissection
expectancy, may prefer early repair.
In up to 96% of cases
Typically severe and of sudden onset
3. If the surgeon’s personal documented operative mortality rate is
“tearing”, “ripping”, “sharp” and “stabbing”
low, repair may be indicated at smaller sizes (4.5-5.5 cm) if that is the
Px’s preference. Migratory pain in 17% of cases
Mean age 63.1%
4. For women, or with AAA greater than average rupture risk, Mostly Males
elective repair at 4.5-5.0 cm is an appropriate threshold for repair. PE
5. For high-risk Pxs, delay in repair until larger diameter is warranted, Any reported pain 96%
especially if EVAR is not possible. Abrupt onset 85%
Chest pain 73%
6. In view of its uncertain long-term durability and effectiveness, as Anterior 61%
well as the increased surveillance burden, EVAR is most appropriate Posterior 36%
for Pxs at increased risk for conventional open aneurysm repair. Back pain 53%
Abdominal pain 30%
7. EVAR may be preferred treatment method for older, high risk Pxs, Hypotensive 8%
those with hostile abdomen or other clinical circumstances likely to Shock 8.4%
increase the risk of conventional open, repair, if their anatomy is Murmurs (mostly AR)
appropriate. CHF 7%
8. Use of EVAR in Pxs with unsuitable anatomy markedly increases the

risk of adverse outcomes and need for conversion to open repair.

PRACTICAL ASSESSMENT of DIAGNOSTIC RELIEF
Location of pain
Anterior – involvement of ascending aorta, likewise pain in ADVANTAGES AO CT MRI TEE
the neck, throat, jaw or face (like ACS involving the L. main
Readily Fairly Quite Fairly Very
coronary – high risk for sudden cardiac death)
available
Interscapular – involvement of the descending thoracic
aorta (back pain) Rapid Fairly Quite Fairly Very
o Signs of AR: bounding pulse, wide pulse pressure, Performed at No No No Yes
diastolic murmur beating along the R. parasternal bedside
border, evidence of CHF Noninvasive No Yes Yes Yes
Symptoms of life-threatening complications involving dissection of
the ascending aorta No IV contrast No No Yes Yes
Congestive Heart Failure (7%)
Cost High Reasonable Moderate Reasonabble
o Almost invariably due to severe aortic regurgitation
Syncope (9%)
o May be an ominous sign suggesting a surgical
emergency due to carotid artery dissection
Cerebrovascular accident (5%)
Cardiac arrest or sudden death due to coronary artery
involvement
Signs of tamponade due to pericardial effusion
(hypotensive, very faint or no pulse)
Ischemic peripheral neuropathy
Paraplegia
THORACIC AORTIC DISSECTION
Mortality rate of untreated ascending aorta

st
80% - 1 6hrs
st
21% - 1 24hrs
st
15% - 1 2 days
Acute Severe AR
Coronary occlusion
Pericardial rupture
Arc branch lesion
VITAL INFO needed for MANAGEMENT of STRATEGY
1. Involvement of the ascending aorta

2. Dissection involving coronaries
3. Severity of AR
4. Presence of Pericardial effusion/tamponade
5. Distal extent of the dissection with occlusion
6. avulsion of visceral branches (coeliac, mesenteric, renal) /
iliofemoral vessels (ischemia/insufficiency)
Lumen that supplies the visceral organs (true or false lumen)

Dissection of Ascending Aorta
XR – widened superior mediastinum w/ pleural effusion
Dissection of Descending Aorta
XR – widened mediastinum w/ widened descending aorta
IMAGING TESTS
Transesophageal Echocardiography (TTE) – 32%

CT Scan – 62%
MRI/MRA – 2%
Aortography – 4%
You can see more of THROMBUS
More branch vessel involvement (also in MRI)

PROTOCOL Chronic (2 weeks and above)
Formation of aneurysm from aortic dissection to a size of 6
cm and above
Rapid expansion of aneurysm 0.5 cm/6 months
TRAUMATIC AORTIC RUPTURE

BLUNT AORTIC INJURY: Epidemiology
nd
2 most common cause of death (after head injury)
Majority caused by automobile crashes
Rapid deceleration of the body (vertica or horizontal plane)
Isthmus
Most common site
Deceleration differential forces between various tissues
Strain: points of junction
This portion is mobile
MANAGEMENT PLAN
Initial management
Resuscitation
INITIAL MANAGEMENT Investigation: CXR, CTA, aortogram
Treatment of associated injuries
Elimination of pain (IV morphine) BP management
Reduction of systolic BP to 100 to 120 mmHg (mean of 60-75
mmHg) Diagnosis
Arterial dP/dt should be reduced through the use of beta-blocking CXR
agents o Wide mediastinum – 85%
Serial Hgb and Hct monitoring o Indistinct aortic knob – 24%
Repeat Ct scan after 5-7 days o Pleural effusion
May be adequate Rx for Stanford B (descending thoracic aorta CT-Scan
dissection)
*once stable and associated injuries are treated:
URGENT or EMERGENT SURGERY for STANFORD A involving
ASCENDING AORTA
(mas Emergency compared to B)

Acute severe AR
Presence of pericardial effusion (rupture)
Symptomatic arch branch occlusion (vessels to upper extremities
and head) Conclusion
Leak or rupture Short-term results appear favorable
st Patient selection critical
More than 25% of all Pxs died within the 1 24 hours after
the onset of dissection (more than 1% /hr) Surveillance imaging required
st
More than 50% died within the 1 week Long-term results pending
More than 75% died within 1 month Follow ups remain a challenge
More than 90% died within 1 year Future generation
AORTITIS
SURGICAL INDICATIONS for STANFORD B AORTIC DISSECTION
(DESCENDING THORACIC AORTA) Inflammatory disease of the aorta
CAUSES
(may opt for medical treatment temporarily before intervention) Large vessel vasculature
Acute (within 2 weeks) o Takayasu’s arteritis
Leak/rupture (hemothorax) o Giant cell arteritis
Uncontrolled HPN Rheumatic and HLA B27 associated Spondyloarthropathies
Uncontrolled or recurrent pain Behcet’s syndrome
Symptomatic aortic branch occlusion/avulsion (visceral, Antineutrophil cytoplasmic Antibodies (ANCA) associated
renal vessel occlusion, lower extremity ischemia) vasculitides

Cogan syndrome Duplex UTZ and echocardiography
Infection
o Syphilis TREATMENT
o TB
o Salmonella Glucocorticoids
Agent of choice but complete remission in 50% of cases
TAKAYASU’S ARTERITIS only
o Initial: prednisolone 4mg/KgW, dose reduction on
Granulomatous Vasculitis affecting the aorta and its branches with response
predilection for the aortic arch and its branches o Maintenance: low-dose (5mg/day)
Age <40 Methotrexate
Highest in Eastern Asia, Northern Germany Used in combination with glucocorticoids
nd rd
2 – 3 decade of life, 80-90% women 0.3 mg/ Kg, 1x/week + prednisolone
Cyclophosphamide
ETIOLOGY In fulminant cases
Supportive
Genetic ASA (Aspirin)
Associated with HLA Bw52 in eastern Asia, associated with BB (Beta blockers)
complement allotype C4A2 (board exam question!) Endovascular Tx, Percutaneous catheter, angiography, stent
Cellular Immune Reaction implantation (using these, conditions will just recur)
Activation of CD4 cells Vascular Surgery
Endocrine immune reactions
HISTOPATHOLOGY PROGNOSIS
Granulomatous polyarteritis 5-year survival 80-90% (high if diagnosed early)

Granuloma with multinucleic giant cells and lymphocytic Prognosis is poor f with AR, aneurysm, arterial HPN
infiltrates; fibrosis in the vessel wall; thrombi
CLASSIFICATION (ACR 1990) (no update)
CLINICAL FINDINGS
TAKE NOTE!
Movement dependent shoulder/arm pain (shoulder spasm) 1. Age < 40
Intermittent claudication in the arms and legs 2. Claudication in the extremities
Bilateral difference in BP up to 65% of the patients 3. Weakened pulse in one or both brachial arteries
Arterial HPN in 40-70% of cases (associated with RAS) 4. Systolic BP dfference between the arm >10 mmHg
Generalized symptoms often at the start of the disease 5. Flow murmur over the aorta or subclavian vein
Visual disturbance, amaurosis fugax w/ involvement of the carotid 6. Pathologic angiography findings
arteries
Cardiac symptoms: exertional dyspnea, angina, palpitations **3-6 criteria have to be met
Arthralgia and myalgia in 55% Sensitivity 90%
Specificity 98%
CLINICAL EXAM
OTHER TYPES
Stenotic murmurs over the large vessels especially aortic arch
branches Giant cell arteritis
Bilateral difference on BP on both arms and legs Rheumatic aortitis
Weakened pulse Idiopathic aortitis
Diastolic murmur over the aortic valve (AR) Infective aortitis
Cutaneous manifestations Chronic atherosclerotic occlusive disease
Pyoderma gangrenosum or erythema nodosum in 15% of Acute aortic Occlusion
pts
LABS & IMAGING
No specific lab
Angiography
Used to be the gold standard for the diagnosis and
assessment but does not provide info about inflammatory
activity
MRA
Demonstrate the quality of the arterial wall

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Medicine II

Coverage of Preliminary Examination:

- Electro- means electricity

Cardiac cycle – electrical events represented in the ECG. Since

Phase 0 - Rapid depolarization

Lead II – from R arm to L leg

Lead III – from L arm to L leg

Note: Right leg is for grounding electrode

EINTHOVEN TRIANGLE HYPOTHESIS

Unipolar Precordial Leads/ Chest Leads Landmarks:

Note: If you transpose this to Einthoven’s bipolar limb leads

ECG paper: Note:

Q wave without ST elevation = OLD INFARCT

Example: T wave inversion from V1, V2, V3 (Female, young, (-)

Right Ventricular Hypertrophy (RVH)

Example: Holosystolic murmur heard at the left lower parasternal

Left Ventricular Hypertrophy

Axis of this 12 lead ECG: Right Axis deviation

Wells PS, Anderson DR, Bormanis J, et al. Value of

Clinical Prediction Rules: Wells Clinical Criteria

Table 1: Clinical Model for Predicting the Pretest

CLINICAL ESTIMATE OF THE PROBABILITY OF DEEP

Wells Clinical Score Interpretation 1997

Wells Clinical Score Interpretation 2003

VENOUS DUPLEX SCAN

In patients who are considered clinically

TREATMENT RECOMMENDATIONS FOR DEEP VENOUS THROMBOSIS

Current Approach To Grades of Recommendations

Summary of Recommendations ACCP: Initial Anticoagulation of Acute DVT of the Leg

High sensitivity at the expense of lower specificity

Characteristics of new oral anticoagulants

Advantages with the new agents

Half life (9-17 hrs): OD/BID dosing for prophylaxis

VENOGRAPHY OR NON-INVASIVE STUDY OF THE

WHAT TO DO WITH THE IDIOPATHIC DVT? (RISK OF

POST THROMBOTIC SYNDROME

Use of Right Heart Catheterization

Clinical Classification of PH (Dana Point 2009)

WHO functional Classes of PAH

Class II patients with (PAH) resulting in slight limitation

Class III patients with (PAH) resulting in marked

Class IV patients with (PAH) with inability to carry out

What is the difference between PH and PAH?

Additional Risk Factors for Drugs and Toxins

Who develops risk for PAH? Other Risk Factors of PAH

Human Immunodeficiency Virus Infection (HIV)

How do we get an Accurate Diagnosis of PAH?

Symptoms at Time of Diagnosis of PAH

Common signs of PAH

Normal sinus rhythm, complete RBBB (Tall R), Biatrial

What is the most appropriate test to conduct to Rule

Is Echo a useful screening tool for PAH?

RVH or RA Enlargement in PAH (not LVH)

Echocardiographic Features of PAH

Your role in the Screening and diagnosis of PAH

Will the hemodynamics found on repeat RHC “match”

(Animation) Rheumatology appointment What is the most appropriate next step?

(Animation) Appointment with cardiologist #1

Be aware of the strengths and limitations of