‫‪Lecture 1‬‬

‫‪Internal Medicine‬‬

‫‪Cardiovascular‬‬

‫‪Introduction‬‬
‫‪Chest pain‬‬
‫‪Cardiac physical exam‬‬
‫‪Ischemic heart disease‬‬
‫‪Cardiac failure‬‬
‫© כל הזכויות שמורות לחברת שילוב ‪ -‬קורס הכנה‬
‫לבחינות הרישוי לרפואה בישראל בע"מ ‪ .2013‬אין‬
‫להעתיק או להפיץ את המצגות ואין לעשות כל שימוש‬
‫במצגות שאינו פרטי ואישי‪.‬‬
 Approach to the patient with acute chest pain and chest
discomfort

Life threatening or not?

The 4 life threatening risk factors of chest pain which must be excluded:

1. Acute myocardial infarction

2. Pneumothorax
An important ddx of chest pain is
3. Cardiac tamponade esophageal rupture which causes
usually unilateral left pleural
4. Pulmonary embolism effusion. A widened mediastanum
and high amylase content of
pleural fluid results.

Tip! Bpp none. Exertion- yes.

To DD: history, physical exam, ECG .
History

1. Pain & Provocation: 95% is

substernal, worsen by stress, PE.
Alleviating factor: relieved by rest, nitro.

2. Quality of the pain: dull, sore, squeezing.

3. Radiation & Region: neck, jaw, arm(s), back

4. Severity (1-10), Same like other pain before?

5. Time & Temporal factors: 10-30 minutes,

 Physical exam

Jugular venous distension: > 7 cm above sternal angle

suggests right heart failure, pulmonary hypertension,
volume overload, tricuspid regurgitation or pericardial
disease.

Hepatojugular reflux: Fluid overload, impaired right

ventricle. If positive - the etiology is from the heart. If
negative, the edema is from a liver source.

Kussmaul’s sign: (increase in JVP with inspiration):

right ventricular infarction, post operative cardiac
tamponade, constrictive pericarditis, tricuspid
regurgitation.
 75 year old man with severe chest pain, that started abruptly.
Treated for hypertension, suffers also from PVD. BP 80/50. ECG
without sign of acute ischemia. CXR is shown.What is the m.p
diagnosis in this patient?

A. Pericardial effusion
B. Pneumothorax
C. Acute MI
D. Aortic dissection
E. Pulmonary embolism
 75 year old man with severe chest pain, that started abruptly.
Treated for hypertension, suffers also from PVD. BP 80/50. ECG
without sign of acute ischemia. CXR is shown.What is the m.p
diagnosis in this patient?

A. Pericardial effusion
B. Pneumothorax
C. Acute MI
D. Aortic dissection
E. Pulmonary embolism
A 54-year-old man presents to the emergency department with chest pain. He has
had three episodes of chest pain in the past 24 h with exertion. Each has lasted 20–
30 min and resolved with rest. His past medical history is significant for hypertension,
hyperlipidemia, asthma, and chronic obstructive pulmonary disease. He currently
smokes one pack/day of cigarettes. His family history is remarkable for early coronary
artery disease in a sibling. Home medications include chlorthalidone, simvastatin,
aspirin, albuterol, and home oxygen. In the emergency department, he becomes
chest pain–free after receiving three sublingual nitroglycerin tablets and IV heparin.
ECG shows 0.8-mm ST-segment depression in V5, V6, lead I and aVL. Cardiac
biomarkers are negative. An exercise stress test shows inducible ischemia. Which
aspects of this patient’s history add to the likelihood that he might have death,
myocardial infarction (MI), or urgent revascularization in the next 14 days?

A. Age
B. Aspirin usage
C. Beta-agonist usage
D. Diuretic usage
A 54-year-old man presents to the emergency department with chest pain. He has
had three episodes of chest pain in the past 24 h with exertion. Each has lasted 20–
30 min and resolved with rest. His past medical history is significant for hypertension,
hyperlipidemia, asthma, and chronic obstructive pulmonary disease. He currently
smokes one pack/day of cigarettes. His family history is remarkable for early
coronary artery disease in a sibling. Home medications include chlorthalidone,
simvastatin, aspirin, albuterol, and home oxygen. In the emergency department, he
becomes chest pain–free after receiving three sublingual nitroglycerin tablets and IV
heparin. ECG shows 0.8-mm ST-segment depression in V5, V6, lead I and aVL. Cardiac
biomarkers are negative. An exercise stress test shows inducible ischemia. Which
aspects of this patient’s history add to the likelihood that he might have death,
myocardial infarction (MI), or urgent revascularization in the next 14 days?

A. Age
B. Aspirin usage
C. Beta-agonist usage
D. Diuretic usage
Patients with unstable angina/non-ST-segment elevation myocardial
infarction (UA/NSTEMI) exhibit a wide spectrum of risk of death, MI,
or urgent revascularization. Risk stratification tools such as the TIMI
risk score are useful for identifying patients who benefit from an early
invasive strategy and those who are best suited for a more
conservative approach. The TIMI risk score is composed of seven
independent risk factors: Age ≥65, three or more cardiovascular risk
factors, prior stenosis >50%, ST-segment deviation ≥0.5mm, two or
more anginal events in <24 h, aspirin usage in the past 7 days, and
elevated cardiac markers. Aspirin resistance can occur in 5–10% of
patients and is more common among those taking lower doses of
aspirin. Having unstable angina despite aspirin usage suggests
aspirin resistance. Use of a beta-agonist and a diuretic do not confer
an independent risk for death, MI, or need for urgent
revascularization.
‫‪TIMI SCORE‬‬ ‫לא לשכוח את ה‪-‬‬
 Diastolic murmurs Systolic murmurs

Aortic regurgitation: Early Aortic stenosis: systolic

decreshendo ejection murmur, radiation to
carotids

Mitral stenosis: mid to late Mitral regurgitation:

low pitched Holosystolic, radiation to
axilla
More about
valvulopathies
... next class
Mitral valve prolapse:
Midsystolic or late systolic
click
 Gallops www.youtube.com/watch?v=mVZFf0xaCQI

S4 S3

S4- not an acute S3- could be with an

situation acute presentation

Physiologic: normal
in young patients and
in pregnancy
Pathologic:
Hypertension, Pathologic: dilated
diastolic dysfunction, cardiomyopathy or
aortic stenosis, LVH mitral valve disease
 Edema
Peripheral Pulmonary
Cardiac: Cardiac:
Right heart failure, Left heart failure
constrictive (post-MI,
pericarditis, severe valvulopathy)
TR, peripheral
venous disease.

Extra-cardiac: Extra-cardiac:
hepatic disease, ARDS, PTX, PE
lymphedema, NS.
 Peripheral pulses
If increased: compensated aortic regurgitation,
coarctation, patent ductus arteriosus.

Pulsus paradoxus (decreased systolic pressure with

inspiration): pericardial tamponade, asthma, COPD,
tension pneumothorax, foreign body in airway.

Pulsus alterans (alternating weak and strong pulses):

cardiac tamponade, impaired left ventricular function.
Poor prognosis.

Pulsus parvus et tardus (weak and delayed): Aortic

stenosis.

Pulsus bisferiens: 2 strong systolic impulses. In aortic

regurgitation and IHSS.
Pulsus paradoxus can be described by which of the following
statements?
A. Pulsus paradoxus can be seen in patients with acute asthma
exacerbations in which the negative intra thoracic pressure
decreases afterload of the heart with a resultant increase in
systolic pressure during inspiration.
B. Pulsus paradoxus has not been described in patients with
superior vena cava syndrome.
C. Pulsus paradoxus describes the finding of diminished pulses
during inspiration, when the peripheral pulse is normally
augmented during inspiration.
D. A drop in systolic pressure during inspiration of
more than 5 mmHg indicates the presence of pulsus
Paradoxus.
E. Pulsus paradoxus occurs during cardiac tamponade when there
is an exaggeration of the normal decrease in the systolic blood
pressure during inspiration.
Pulsus paradoxus can be described by which of the following
statements?
A. Pulsus paradoxus can be seen in patients with acute asthma
exacerbations in which the negative intra thoracic pressure
decreases afterload of the heart with a resultant increase in
systolic pressure during inspiration.
B. Pulsus paradoxus has not been described in patients with
superior vena cava syndrome.
C. Pulsus paradoxus describes the finding of diminished pulses
during inspiration, when the peripheral pulse is normally
augmented during inspiration.
D. A drop in systolic pressure during inspiration of
more than 5 mmHg indicates the presence of pulsus
Paradoxus.
E. Pulsus paradoxus occurs during cardiac tamponade when
there is an exaggeration of the normal decrease in the systolic
blood pressure during inspiration.
During normal inspiration there is a small, less than 10mmHg
decrease in systolic pressure.

In several disease states, notably severe obstructive lung disease,

pericardial tamponade, and superior vena cava obstruction, an
accentuation of this normal finding can occur.

Indeed, in the most pronounced cases the peripheral pulse may

not be palpable during inspiration.
 ECG
Rate: normal is 60-100. Below is bradycardia above
tachycardia.

Rhythm: Look for sinus rhythm, irregular rhythms, junctional or

ventricular rhythms.

Axis: Normal signified by an upright QRS in lead II.

Intervals: Normal: PR between 120-200msec and QRS<100msec.

AV block: PR>200msec.
LBBB: QRS>120msec, no R wave in V1. Tall R waves in I, V5 and
V6.

Ischemia: Inverted T, poor R wave progression, St segment

changes.

Transmural infarct: Significant Q waves >40msec. St elevation. T

 Congestive heart failure

A clinical syndrome caused by the inability of the heart

to pump enough blood to maintain fluid and metabolic
homeostasis,

Risk factors are coronary disease, hypertension,

cardiomyopathy, valvular heart disease and diabetes.
Hypertension is the most common
risk factor for CHF.
Diabetes is the worst risk factor.
Correcting smoking, leads to the
fastest recovery from heart
disease.
.
 NYHA classification of CHF

I NO limitation of activity. No symptoms with normal

activity.

II Slight limitation of activity. Comfortable at rest or

with mild exertion.

III Marked limitation of activity. Comfortable only at

rest.

IV Confined to complete rest in bed or chair, as any

physical activity brings on discomfort.
Symptoms present at rest.
A 68-year-old man with a history of myocardial infarction
and congestive heart failure is comfortable at rest.
However, when walking to his car, he develops dyspnea,
fatigue, and sometimes palpitations. He must rest for
several minutes before these symptoms resolve. His New
York Heart Association classification is which of the
following?

A. Class I
B. Class II
C. Class III
D. Class IV
A 68-year-old man with a history of myocardial infarction
and congestive heart failure is comfortable at rest.
However, when walking to his car, he develops dyspnea,
fatigue, and sometimes palpitations. He must rest for
several minutes before these symptoms resolve. His New
York Heart Association classification is which of the
following?

A. Class I
B. Class II
C. Class III
D. Class IV
The NY Heart Association classification is a tool to define criteria
that describe the functional ability and clinical manifestations of
patients in heart failure. It is also used in patients with pulmonary
hypertension.
These criteria have been shown to have prognostic value with
worsening survival as class increases. They are also useful to
clinicians when reading studies to understand the entry and
exclusion criteria of large clinical trials.
Class I is used for patients with no limiting symptoms;
class II for patients with slight or mild limitation;
class III implies no symptoms at rest but dyspnea or angina or
palpitations with little exertion; patients are moderately limited;
class IV is severely limited, so that even minimal activity causes
symptoms.
Treatment guidelines also frequently base recommendations on
these clinical stages. This patient has symptoms with mild exertion
but is comfortable at rest; therefore he is NY Heart Association class
III.
Left sided CHF Right sided CHF
symptoms symptoms
Left sided s3/s4 gallop. Right sided s3/s4 gallop

Bilateral basilar rales. JVD

Pleural effusions. Hepatojugular reflex

Pulmonary edema. Peripheral edema

Orthopnea, paroxysmal Hepatomegaly, ascites

nocturnal dyspnea.
http://www.youtube.com/watch?v=EAd1tP0CL6Y
 Systolic dysfunction

When ejection fraction drops below 50%. Caused by inadequate left

ventricular contractilty or increased afterload.

History
Exertional dyspnea orthopnea rest dyspnea.

Chronic cough, fatigue, lower extremity edema, nocturia, Cheyne Strokes

respiration.

Diagnosis
S3/S4 gallop.

Cardiomegaly, cephalization of pulmonary vessels, pleural effusions,

vascular plumpness, prominent hila on CXR.

Decreased EF on echo.
 Acute Treatment

Correct underlying causes such as

arrythmias, myocardial ischemia,
drugs (CCBs, antiarrythmics,

NSAIDs), alcohol, thyroid and valvular

disease.

ACEi and if not tolerated ARBs.

B-blockers once the patient in

euvolemic (but not during
decompensation).

Acute pulmonary congestion treated

with LMNOP.
 Chronic treatment

Control co morbid conditions as diabetes, hypertension, obesity etc. Limit

diatery sodium and fluid intake.

B-blockers and ACEi help prevent neurohormonal remodeling of the

heart. They decrease mortality.

Daily ASA recommended.

Chronic diuretic therapy to treat overload.

Low dose spironolactone decreases mortality when given with ACEi.

Anticoagulate those with AF or previous embolic events.

For those unresponsive to therapy consider left ventricular assist device

or cardiac transplantation.
 Diastolic dysfunction

The ventricle has either impaired active relaxation secondary to

ischemia, aging or hypertrophy or impaired passive filling due to
scarring fromk previous MI or restrictive cardiomtyopathy.

History: it’s associated with stable and unstable angina, shortness

of breath, dyspnea on exertion, arrythmias, Mi, heart failre and
sudden death.

Treatment:
Diuretics are first line.
Rate and blood pressure are maintained by B-blockers, ACEi,
ARBs or CCBs.
Digoxin is NOT useful in these patients.
A 42-year-old male from El Salvador complains of several
months of dyspnea on exertion. Physical examination
reveals an elevated jugular venous pressure, clear lungs,
a third heart sound, a pulsatile liver, ascites, and
dependent edema. Chest radiography reveals no
cardiomegaly and clear lung fields. An echocardiogram
demonstrates normal to mildly decreased left ventricular
systolic function. The initial diagnostic workup should
include all the following except?

A. computed tomography of the chest

B. coronary angiogram
C. fat pad biopsy
D. iron studies
E. tuberculin skin test
A 42-year-old male from El Salvador complains of several
months of dyspnea on exertion. Physical examination
reveals an elevated jugular venous pressure, clear lungs,
a third heart sound, a pulsatile liver, ascites, and
dependent edema. Chest radiography reveals no
cardiomegaly and clear lung fields. An echocardiogram
demonstrates normal to mildly decreased left
ventricular systolic function. The initial diagnostic
workup should include all the following except?

A. computed tomography of the chest

B. coronary angiogram
C. fat pad biopsy
D. iron studies
E. tuberculin skin test
This patient presents with classic findings of right-sided heart failure. The
differential diagnosis includes pulmonary vascular disease,restrictive
cardiomyopathy, constrictive pericarditis, cor pulmonale, and any cause of
longstanding left-sided heart failure.
A CT or MRI of the chest would assess for pericarial calcifications or
parenchymal lung disease not visualized on radiography.
Iron studies are a component of the evaluation for hemochromatosis, and
fat pad biopsy is a component of the evaluation for amyloidosis, both of
which may cause restrictive cardiomyopathy.
The tuberculin test is useful for ascertaining the presence of prior infection
with Mycobacterium tuberculosis, which is associated with the
development of constrictive pericarditis.
A coronary angiogram would not be helpful in a young patient with no
physical signs or echocardiographic findings of left-sided heart failure.
 Coronary syndromes

Unstable angina / NSTEMI

Unstable angina describes chest pain which is
new in onset, is accelerating, is less
responsive to medication (nitrates) and occurs
at rest.
It signals the presence of a possible impending
infarction.

NSTEMI indicates myocardial necrosis marked

by elevation of troponin I, troponin T or CK-MB.
Diagnosis

Is made by the TIMI score (thrombolysis in myocardial infarction study)

criteria to determine the likelihood of adverse cardiac events.
Unstable angina is not associated with elevated cardiac markers, but ST
changes may be seen of ECG.

Treatment
Acute treatment of symptomes is similar as in stable angina (O2, nitrates,
morphine, diuretics, ACEi, aspirin).
In addition, clopidogrel, heparin or enoxaprin should also be considered.
Patients who are refractory to medical therapy should be given heparin
and schedued for PCI or CABG.
Clopidogrel should be perscribed
for 30 days in case of bare metal
stents and 1 year in case of a drug
eluting stent implantation following
a PCI.
 STEMI

ST segment elevations and cardiac enzyme release secondary to

prolonged cardiac ischemia and necrosis.

History

Acute onset substernal chest pain described as pressing or tight.

Associated symptoms may include diaphoresis, shortness of
breath, light headedness, anxiety, nausea/vomiting and syncope.

Physical exam may reveal arrythmias, new mitral regurgitation

(ruptured pappilary muscle), hypotension (cardiogenic shock) and
evidence of new CHF (rales, perpheral edema, S3 gallop).

The best predictor of survival is left ventricular EF.

Left ventricular infarctions can
present with hypotension and
pulmonary edema. Right infarctions
can present with clear lung fields and
JVP. Right infarctions are managed by
an IV bolus of normal saline and to
stop nitro glycerin (Viagra!)
Cardiac enzymes

Troponins are most sensitive . CK-MB more specific. Both can

take up to six hours after the onset of chest pain.

CK-MB is the marker of chioce for re-infarction since troponin

stays high for as 5 days.
A 61-year-old woman with a history of diabetes and
hypertension is brought to the ED by her daughter. The patient
states she started feeling short of breath approximately 12
hours ago and then noticed a tingling sensation in the middle
of her chest and became diaphoretic. An ECG reveals ST-
depression in leads II, III, and aVF. You believe the patient had
a non-ST elevation MI. Which of the following cardiac markers
begins to rise within 3–6 hours of chest pain onset, peaks at
12–24 hours, and returns to baseline in 7–10 days?

a.Myoglobin
b.Creatinine kinase (CK)
c.Creatinine kinase-MB (CK-MB)
d.Troponin
e.Lactic dehydrogenase (LDH)
A 61-year-old woman with a history of diabetes and
hypertension is brought to the ED by her daughter. The patient
states she started feeling short of breath approximately 12
hours ago and then noticed a tingling sensation in the middle
of her chest and became diaphoretic. An ECG reveals ST-
depression in leads II, III, and aVF. You believe the patient had
a non-ST elevation MI. Which of the following cardiac markers
begins to rise within 3–6 hours of chest pain onset, peaks at
12–24 hours, and returns to baseline in 7–10 days?

a.Myoglobin
b.Creatinine kinase (CK)
c.Creatinine kinase-MB (CK-MB)
d.Troponin
e.Lactic dehydrogenase (LDH)
A 61-year-old woman with a history of diabetes and hypertension is brought to the ED by her daughter. The patient states she
started feeling short of breath approximately 12 hours ago and then noticed a tingling sensation in the middle of her chest and
became diaphoretic. An ECG reveals ST-depression in leads II, III, and aVF. You believe the patient had a non-ST elevation
MI. Which of the following cardiac markers begins to rise within 3–6 hours of chest pain onset, peaks at 12–24 hours, and
returns to baseline in 7–10 days?
a.Myoglobin -found in both skeletal and cardiac muscle and released into the
bloodstream when there is muscle cell death. It tends to rise within 1–2 hours of
injury, peaks in 4–6 hours, and returns to base- line in 24 hours.
b.Creatinine kinase (CK)-found in skeletal and cardiac muscle. Following AMI,
increases in serum CK are detectable within 3–8 hours with a peak at 12–24 hours
after injury, and normalizes within 3–4 days.
c.Creatinine kinase-MB (CK-MB)-isoenzyme found in cardiac muscle and
released into the bloodstream upon cell death. It rises 4–6 hours after AMI, peaks
in 12–36 hours, and returns to normal within 3–4 days.
d.Troponin -Serum cardiac markers are used to confirm or exclude myocardial
cell death, and are considered the gold standard for the diagnosis of MI. There
are many markers currently used; the most sensitive and specific markers are
troponin I and T. A rise in these levels, as seen on the next page, is diagnostic for
an AMI. Troponin levels rise within 3–6 hours of chest pain onset, peak at 12–24
hours, and remain elevated for 7–10 days.
e.Lactic dehydrogenase (LDH) -Lactic dehydrogenase is an
enzyme found in muscle and rises 12 hours after AMI, peaks at
24–48 hours, and returns to normal at 10–14 days.
The most common cause of death in a
pateint with MI is complex ventricular
arrythmia. The acute ischemia leads to
areas of partial block reentry arrythmia.
VF is the most common arrythmia.
Treatment

Six key medications should be considered

ASA, B-blockers, clopidogrel, morphine, nitrates and O2.
If the pateint is in heart failure or cardiogenic shock fo not give B-blockers,
instead, give ACEi, provided the patient is not hypotensive.

Emergent angiography or PCI should be performed, if possible.

If the pateint presents within 3 hours, PCI can not be performed within 90
minutes and there are no contraindications for thrombolysis, tPA,
streptokinase or reteplase may be used.

In the setting of 3 vessel disease, left main coronary artery disease or

diffuse disease with good target vessels, PCI should be attempted
immediatley.

Long term treatment includes ASA, ACEi, B-blockers, high dose statins
and clopidogrel.
Complications

1st day
Heart failure, Reinfarction

2nd -4th days

Arrythmia, Pericarditis

5th-10th days
Left ventricular wall rupture (acute pericardial
tamponade causing electrical alterans, PEA). Pappilary
muscle rupture causing mitral regirgitation.

Weeks to months
Ventricular aneursm,Dressler’s syndrome (pericarditis
with fever, leukocytosis and pleural effusion).