Cardiac Nursing

Applied Anatomy And Physiology:

 hollow muscular behind the sternum and between the lungs

 has heart wall has 3 layers:

 Endocardium – thin lining, covers valves

 Myocardium – muscular layer
 Epicardium – thin covering(mesothelium)
 Pericardium – invaginated sac
 Visceral – attached to the exterior of myocardium
 Parietal – attached to the great vessels and diaphragm

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 separated into 2 pumps:
 right heart – pumps blood through the lungs
 left heart – pumps blood through the peripheral organs
 chambers of the heart
 atrium – weak pump and blood reservoir
 ventricle – main force that propels blood to pulmonary
and peripheral circulation
 Blood Supply

 Arteries
 Coronary artery – 1st branch of aorta
• Right Coronary
o SA nodal Branch – supplies SA node
o Right marginal Branch – supplies the
right border of the heart
o AV nodal branch – supplies the AV node
o Posterior interventricular artery –
supplies both ventricles
• Left Coronary
o Circumflex branch – supplies SA node in
40 % of people
o Left marginal – supplies the left ventricle
o Anterior interventricular branch aka Left
anterior descending(LAD)–supplies both
ventricles and interventricular septum

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 o Lateral branch – terminates in ant
surface of the heart
 Veins
 Coronary sinus – main vein of the heart
 Ant interventricular vein or Great Cardiac vein –
main tributary of the coronary sinus
 Post interventricular vein or Middle cardiac vein
 Small Cardiac vein
 Left Posterior ventricular vein
 Left Marginal Vein
 Oblique vein – remnant of SVC, small unsignificant
 Smallest cardiac veins- valveless
 Action Potential
Resting Membrane Potentials
 -85 to -95 mV – cardiac muscle
 -90 to -100 mV – Purkinje fibers
 Circulation

 Blood from head and UE; Trunk and LE

 Superior Vena Cava: Inferior Vena Cava
 Right Atrium
 Tricuspid Valve
 Right Ventricle
 Pulmonary Valve
 Pulmonary Artery
 Lungs
 Pulmonary Vein
 Left Atrium

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  Mitral Valve
 Left Ventricle
 Aortic valve
 Aorta
 Myocardial cell
 Intercalated disks
 Cell membranes that separates individual cells from
each other
 Two Groups of Myocardial Cells
 Cells specialized for impulse generation and
conduction
• Automatic cells
• Found in SA, AV nodes and Purkinje
system(transitional cells)
 Cells specialized for contraction
• Non Automatic Cells

 Specialized Cardiac Cells

 Nodal tissues
 SA Node( Sino-atrial, Keith and Flack)
• Primary Pacemaker
• Between SVC and RA
• Vagal and symphatetic innervation
• Sinus Rhythms
 AV Node( Atrioventricular , Kent and Tawara)
• At the right atrium

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 • 3 zones
o AN Zone(atrionodal)
o N Zone (nodal)
o NH zone (nodal –HIS)

 Internodal and Interatrial Pathways

 Connects SA and AV Node
 Ant. Internodal(bachman) tract
 Middle Internodal(wenkebach) tract
 Posterior internodal(Thorel) tract
 Bundle of His/ Purkinje Fibers
 Provides for ventricular conduction system
 Fastest conduction among cardiac tissues
 Right bundle
 Left Bundle
• Septal branches and 2 fascicles

 Mechanism of Contraction of Contractile Cardiac Muscle Fibers

1. Na+ influx from extracellular space, causes positive

feedback opening of voltage-gated Na+ channels;
membrane potential quickly depolarizes (-90 to +30 mV);
Na+ channels close within 3 ms of opening.

2. Depolarization causes release of Ca++ from sarcoplasmic

reticulum (as in skeletal muscle), allowing sliding actin
and myosin to proceed.

3. Depolarization ALSO causes opening of slow Ca++

channels on the membrane (special to cardiac muscle),
further increasing Ca++ influx and activation of filaments.
This causes more prolonged depolarization than in
skeletal muscle, resulting in a plateau action potential,
rather than a "spiked" action potential (as in skeletal
muscle cells).

 Differences Between Skeletal & Cardiac MUSCLE Contraction

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1. All-or-None Law - Gap junctions allow all cardiac muscle cells
to be linked electrochemically, so that activation of a small
group of cells spreads like a wave throughout the entire heart.
This is essential for "synchronistic" contraction of the heart as
opposed to skeletal muscle.

2. Automicity (Autorhythmicity) - some cardiac muscle cells are

"self-excitable" allowing for rhythmic waves of contraction to
adjacent cells throughout the heart. Skeletal muscle cells must
be stimulated by independent motor neurons as part of a motor
unit.

3. Length of Absolute Refractory Period - The absolute refractory

period of cardiac muscle cells is much longer than skeletal
muscle cells (250 ms vs. 2-3 ms), preventing wave summation
and tetanic contractions which would cause the heart to stop
pumping rhythmically.

 Internal Conduction (Stimulation) System of the Heart

A. General Properties of Conduction

1. heart can beat rhythmically without nervous input

2. nodal system (cardiac conduction system) - special
autorhythmic cells of heart that initiate impulses for
wave-like contraction of entire heart (no nervous
stimulation needed for these)
3. gap junctions - electrically couple all cardiac muscle
cells so that depolarization sweeps across heart in
sequential fashion from atria to ventricles

B. "Pacemaker" Features of Autorhythmic Cells

1. pacemaker potentials - "autorhythmic cells" of heart

muscle create action potentials in rhythmic fashion;
this is due to unstable resting potentials which
slowly drift back toward threshold voltage after
repolarization from a previous cycle.

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  Theoretical Mechanism of Pacemaker Potential:

a. K+ leak channels allow K+ OUT of the cell more slowly than in

skeletal muscle
b. Na+ slowly leaks into cell, causing membrane potential to slowly
drift up to the threshold to trigger Ca++ influx from outside (-40
mV)
c. when threshold for voltage-gated Ca++ channels is reached (-40
mV), fast calcium channels open, permitting explosive entry of
Ca++ from of the cell, causing sharp rise in level of
depolarization
d. when peak depolarization is achieved, voltage-gated K+
channels open, causing repolarization to the "unstable resting
potential"
e. cycle begins again at step a.

C. Anatomical Sequence of Excitation of the Heart

1. Autorhythmic Cell Location & Order of Impulses
 (right atrium)
 sinoatrial node (SA)
 (right AV valve)
 atrioventricular node (AV)
 atrioventricular bundle (bundle of His)
 right & left bundle of His branches
 Purkinje fibers of ventricular walls

(from SA through complete heart contraction = 220 ms = 0.22 s)

a. sinoatrial node (SA node) "the pacemaker" - has the fastest

autorhythmic rate (70-80 per minute), and sets the pace for the
entire heart; this rhythm is called the sinus rhythm; located in
right atrial wall, just inferior to the superior vena cava

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b. atrioventricular node (AV node) - impulses pass from SA via
gap junctions in about 40 ms.; impulses are delayed about 100
ms to allow completion of the contraction of both atria; located
just above tricuspid valve (between right atrium & ventricle)

c. atrioventricular bundle (bundle of His) - in the interATRIAL

septum (connects L and R atria)

d. L and R bundle of His branches - within the

interVENTRICULAR septum (between L and R ventricles)

e. Purkinje fibers - within the lateral walls of both the L and R

ventricles; since left ventricle much larger, Purkinjes more
elaborate here; Purkinje fibers innervate “papillary muscles”
before ventricle walls so AV can valves prevent backflow

 External Innervation Regulating Heart Function

1. heart can beat without external innervation

2. external innervation is from AUTONOMIC SYSTEM

Parasympathetic
 (acetylcholine)
 DECREASES rate of contractions
 cardioinhibitory center (medulla)
 vagus nerve (cranial X)
 heart

Sympathetic
 (norepinephrine)
 INCREASES rate of contractions
 cardioacceleratory center (medulla)
 lateral horn of spinal cord to preganglionics Tl-T5
 postganlionics cervical/thoracic ganglia
 heart

The Normal Cardiac Cycle

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 A. General Concepts

1. systole - period of chamber contraction

2. diastole - period of chamber relaxation
3. cardiac cycle - all events of systole and diastole
during one heart flow cycle
B. Events of Cardiac Cycle
1. mid-to-late ventricular diastole: ventricles filled
 the AV valves are open
 pressure: LOW in chambers; HIGH in aorta/pulmonary trunk
 aortic/pulmonary semilunar valves CLOSED
 blood flows from vena cavas/pulmonary vein INTO atria
 blood flows through AV valves INTO ventricles (70%)
 atrial systole propels more blood > ventricles (30%)
 atrial diastole returns through end of cycle
2. ventricular systole: blood ejected from heart
 filled ventricles begin to contract, AV valves CLOSE
 isovolumetric contraction phase - ventricles CLOSED
 contraction of closed ventricles increases pressure
 ventricular ejection phase - blood forced out
 semilunar valves open, blood -> aorta & pulmonary trunk

3. isovolumetric relaxation: early ventricular diastole

 ventricles relax, ventricular pressure becomes LOW

 semilunar valves close, aorta & pulmonary trunk backflow
 dicrotic notch - brief increase in aortic pressure

TOTAL CARDIAC CYCLE TIME = 0.8 second

(normal 70 beats/minute)

atrial systole (contraction) = 0.1 second

ventricular systole (contraction) = 0.3 second
quiescent period (relaxation) = 0.4 second

Heart Sounds: Stethoscope Listening

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 A. Overview of Heart Sounds

1. lub-dub, - , lub, dub, -

2. lub - closure of AV valves, onset of ventricular
systole
3. dub - closure of semilunar valves, onset of diastole
4. Pause - quiescent period of cardiac cycle
5. Tricuspid valve (lub) - RT 5th intercostal, medial
6. Mitral valve (lub) - LT 5th intercostal, lateral
7. Aortic semilunar valve (dub) - RT 2nd intercostal
8. Pulmonary semilunar valve (dub) - LT 2nd
intercostals

1. S1- due to closure of the AV valves

2. S2- due to the closure of the semi-lunar valves
3. S3- due to increased ventricular filling
4. S4- due to forceful atrial contraction

B. Heart Murmurs

1. murmur - sounds other than the typical "lub-dub"; typically

caused by disruptions in flow
2. incompetent valve - swishing sound just AFTER the
normal "lub" or "dub"; valve does not completely close,
some regurgitation of blood
3. stenotic valve - high pitched swishing sound when blood
should be flowing through valve; narrowing of outlet in the
open state

Cardiac Output - Blood Pumping of the Heart

A. General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute

 CO (ml/min) = HR (beats/min) X SV (ml/beat)
 normal CO = 75 beats/minX 70 ml/beat = 5.25 L/min
2. Stroke Volume (SV) - ventricle blood pumped per beat
3. Heart Rate (HR) - cardiac cycles per minute
 Normal range is 60-100 beats per minute
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  Tachycardia is greater than 100 bpm
 Bradycardia is less than 60 bpm
 Sympathetic system INCREASES HR
 Parasympathetic system (Vagus) DECREASES HR
4. Blood pressure - Cardiac output X peripheral resistance
 Control is neural (central and peripheral) and hormonal
 Baroreceptors in the carotid and aorta
 Hormones- ADH, aldosterone, epinephrine can increase BP;
ANF can decrease BP
B. Regulation of Stroke Volume (SV)

1. end diastolic volume (EDV) - total blood collected in

ventricle at end of diastole; determined by length of
diastole and venous pressure (~ 120 ml)
2. end systolic volume (ESV) - blood left over in
ventricle at end of contraction (not pumped out);
determined by force of ventricle contraction and
arterial blood pressure (~50 ml)

SV (ml/beat) =EDV (ml/beat) - ESV (ml/beat)

normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat

3. Frank-Starling Law of the Heart - critical factor for

stroke volume is "degree of stretch of cardiac
muscle cells"; more stretch = more contraction
force

a. increased EDV = more contraction force

i. slow heart rate = more time to fill

ii. exercise = more venous blood return

C. Regulation of Heart Rate (Autonomic, Chemical, Other)

1. Autonomic Regulation of Heart Rate (HR)

a. sympathetic - NOREPINEPHRINE (NE)

increases heart rate (maintains stroke volume
which leads to increased Cardiac Output)

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 b. parasympathetic - ACETYLCHOLINE (ACh)
decreases heart rate
c. vagal tone - parasympathetic inhibition of
inherent rate of SA node, allowing normal HR
d. baroreceptors, pressoreceptors - monitor
changes in blood pressure and allow reflex
activity with the autonomic nervous system

2. Hormonal and Chemical Regulation of Heart Rate (HR)

a. epinephrine - hormone released by adrenal medulla

during stress; increases heart rate
b. thyroxine - hormone released by thyroid; increases heart
rate in large quantities; amplifies effect of epinephrine
c. Ca++, K+, and Na+ levels very important;

* hyperkalemia - increased K+ level; KCl used to

stop heart on lethal injection
* hypokalemia - lower K+ levels; leads to
abnormal heart rate rhythms
* hypocalcemia - depresses heart function
* hypercalcemia - increases contraction phase
* hypernatremia - HIGH Na+ concentration; can
block Na+ transport & muscle contraction

3. Other Factors Effecting Heart Rate (HR)

a. normal heart rate - fetus 140 - 160 beats/minute

female 72 - 80 beats/minute
male 64 - 72 beats/minute

b. exercise - lowers resting heart rate (40-60)

c. heat - increases heart rate significantly
d. cold - decreases heart rate significantly
e. tachycardia - HIGHER than normal resting heart
rate (over 100); may lead to fibrillation
f. bradycardia - LOWER than normal resting heart
rate (below 60); parasympathetic drug side effects;
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 physical conditioning; sign of pathology in non-healthy
patient

Assessment

Diagnostic Tests:

Laboratory Test Rationale

1. To assist in diagnosing MI
2. To identify abnormalities
3. To assess inflammation
4. To determine baseline value
5. To monitor serum level of medications
6. To assess the effects of medications

LABORATORY PROCEDURES

CARDIAC Proteins and enzymes

1. CK- MB ( creatine kinase)
 Elevates in MI within 4 hours, peaks in 18 hours and
then declines till 3 days
 Normal value is 0-7 U/L
2. Lactic Dehydrogenase (LDH)
 Elevates in MI in 24 hours, peaks in 48-72 hours
 Normally LDH1 is greater than LDH2
 Lactic Dehydrogenase (LDH)
 MI- LDH2 greater than LDH1 (flipped LDH pattern)
 Normal value is 70-200 IU/L
3. Myoglobin
 Rises within 1-3 hours
 Peaks in 4-12 hours

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  Returns to normal in a day
 Not used alone
 Muscular and RENAL disease can have elevated
myoglobin
4. Troponin I and T
 Troponin I is usually utilized for MI
 Elevates within 3-4 hours, peaks in 4-24 hours and
persists for 7 days to 3 weeks!
 Normal value for Troponin I is less than 0.6 ng/mL
 REMEMBER to AVOID IM injections before obtaining
blood sample!
 Early and late diagnosis can be made!
5. SERUM LIPIDS
 Lipid profile measures the serum cholesterol,
triglycerides and lipoprotein levels
 Cholesterol= 200 mg/dL
 Triglycerides- 40- 150 mg/dL
 LDH- 130 mg/dL
 HDL- 30-70- mg/dL
 NPO post midnight (usually 12 hours)

ELECTROCARDIOGRAM (ECG)

 A non-invasive procedure that evaluates the electrical

activity of the heart

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 A. Deflection Waves of ECG
1. P wave - initial wave, demonstrates the depolarization from
SA Node through both ATRIA; the ATRIA contract about 0.1 s after
start of P Wave
2. QRS complex - next series of deflections, demonstrates the
depolarization of AV node through both ventricles; the ventricles
contract throughout the period of the QRS complex, with a short
delay after the end of atrial contraction; repolarization of atria also
obscured

3. T Wave - repolarization of the ventricles (0.16 s)

4. PR (PQ) Interval - time period from beginning of atrial

contraction to beginning of ventricular contraction (0.16 s)

5. QT Interval the time of ventricular contraction (about 0.36 s);

from beginning of ventricular depolarization to end of repolarization

 Electrodes and wires are attached to the patient

Holter Monitoring

 A non-invasive test in which the

client wears a Holter monitor
and an ECG tracing recorded

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 continuously over a period of
24 hours
 Instruct the client to resume
normal activities and maintain a
diary of activities and any
symptoms that may develop

ECHOCARDIOGRAM

 Non-invasive test that studies the

structural and functional changes of
the heart with the use of ultrasound
 No special preparation is needed

Stress Test
 A non-invasive test that studies the heart during activity and
detects and evaluates CAD
 Exercise test, pharmacologic test and emotional test
 Treadmill testing is the most commonly used stress test
 Used to determine CAD, Chest pain causes, drug effects
and dysrhythmias in exercise
 Pre-test: consent may be required, adequate rest , eat a light
meal or fast for 4 hours and avoid smoking, alcohol and
caffeine
 Post-test: instruct client to notify the physician if any chest
pain, dizziness or shortness of breath . Instruct client to
avoid taking a hot shower for 10-12 hours after the test
Pharmacological stress test
 Use of dipyridamole
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  Maximally dilates coronary artery
 Side-effect: flushing of face
 Pre-test: 4 hours fasting, avoid alcohol, caffeine
 Post test: report symptoms of chest pain
Cardiac Catheterization
 Insertion of a catheter into the heart and surrounding vessels
 Determines the structure and performance of the heart
valves and surrounding vessels
 Used to diagnose CAD, assess coronary atery patency and
determine extent of atherosclerosis
 Pretest: Ensure Consent, assess for allergy to seafood and
iodine, NPO, document weight and height, baseline VS,
blood tests and document the peripheral pulses
 Pretest: Fast for 8-12 hours, teachings, medications to allay
anxiety
 Intra-test: inform patient of a fluttery feeling as the catheter
passes through the heart; inform the patient that a feeling of
warmth and metallic taste may occur when dye is
administered
 Post-test: Monitor VS and cardiac rhythm
 Monitor peripheral pulses, color and warmth and sensation
of the extremity distal to insertion site
 Maintain sandbag to the insertion site if required to maintain
pressure
 Monitor for bleeding and hematoma formation

Central Venous Pressure(CVP)

 Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O

 Elevated CVP indicates increase in blood volume, excessive
IVF or heart/renal failure
 Low CVP may indicated hypovolemia, hemorrhage and
severe vasodilatation

Measuring CVP
1. Position the client supine with bed elevated at 45 degrees
2. Position the zero point of the CVP line at the level of the right
atrium. Usually this is at the MAL, 4th ICS

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3. Instruct the client to be relaxed and avoid coughing and straining.

CARDIAC IMPLEMENTATION

1. Assess the cardio-pulmonary status

 VS, BP, Cardiac assessment
2. Enhance cardiac output
 Establish IV line to administer fluids
3. Promote gas exchange
 Administer O2
 Position client in semi-Fowler’s
 Encourage coughing and deep breathing exercises
4. Increase client activity tolerance
 Balance rest and activity periods
 Assist in daily activities
5. Promote client comfort
 Assess the client’s description of pain and chest discomfort
 Administer medication as prescribed
6. Promote adequate sleep
7. Prevent infection
 Monitor skin integrity of lower extremities
 Assess skin site for edema, redness and warmth
 Monitor for fever
 Change position frequently
8. Minimize patient anxiety
 Encourage verbalization of feelings, fears and concerns

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  Answer client questions. Provide information about
procedures and medications

Imbalance of Cardiac Output & Heart Pathologies

1. congestive heart failure - heart cannot pump sufficiently to meet

needs of the body

a. coronary atherosclerosis - leads to gradual occlusion of heart

vessels, reducing oxygen nutrient supply to cardiac muscle
cells; (fat & salt diet, smoking, stress)
b. high blood pressure - when aortic pressure gets too large, left
ventricle cannot pump properly, increasing ESV, and lowering
SV
c. myocardial infarct (MI) - "heart cell death" due to numerous
factors, including coronary artery occlusion
d. pulmonary congestion - failure of LEFT heart; leads to buildup of
blood in the lungs
e. peripheral congestion - failure of RIGHT heart; pools in body,
leading to edema (fluid buildup in areas such as feet, ankles,
fingers)

Angina Pectoris

 Chest pain resulting from coronary atherosclerosis or

myocardial ischemia

Clinical Syndromes:

Three Common Types of ANGINA

1. STABLE ANGINA
 The typical angina that occurs during exertion, relieved by rest
and drugs and the severity does not change
2. Unstable angina
 Occurs unpredictably during exertion and emotion, severity
increases with time and pain may not be relieved by rest and
drug
3. Variant angina, Prinzmetal angina
 results from coronary artery VASOSPASMS, may occur at rest

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ASSESSMENT FINDINGS:
 Chest pain- ANGINA
 The most characteristic symptom
 PAIN is described as mild to severe retrosternal pain,
squeezing, tightness or burning sensation
 Radiates to the jaw and left arm
 Precipitated by Exercise, Eating heavy meals, Emotions like
excitement and anxiety and Extremes of temperature
 Relieved by REST and Nitroglycerin
 Diaphoresis
 Nausea and vomiting
 Cold clammy skin
 Sense of apprehension and doom
 Dizziness and syncope

LABORATORY FINDINGS
 ECG may show normal tracing if patient is pain-free. Ischemic
changes may show ST depression and T wave inversion
 Cardiac catheterization
 Provides the MOST DEFINITIVE source of diagnosis by
showing the presence of the atherosclerotic lesions
NURSING MANAGEMENT

 Administer prescribed medications

 Nitrates- to dilate the coronary arteries
 Aspirin- to prevent thrombus formation
 Beta-blockers- to reduce BP and HR
 Calcium-channel blockers- to dilate coronary artery and reduce
vasospasm
 Teach the patient management of anginal attacks
 Advise patient to stop all activities
 Put one nitroglycerin tablet under the tongue
 Wait for 5 minutes
 If not relieved, take another tablet and wait for 5 minutes
 Another tablet can be taken (third tablet)
 If unrelieved after THREE tablets seek medical attention
 Obtain a 12-lead ECG

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  Promote myocardial perfusion
 Instruct patient to maintain bed rest
 Administer O2 @ 3 lpm
 Advise to avoid valsalva maneuvers
 Provide laxatives or high fiber diet to lessen constipation
 Encourage to avoid increased physical activities
 Assist in possible treatment modalities
o PTCA- percutaneous transluminal coronary angioplasty
 To compress the plaque against the vessel wall,
increasing the arterial lumen
o CABG- coronary artery bypass graft
 To improve the blood flow to the myocardial tissue
 Provide information to family members to minimize anxiety and
promote family cooperation
 Assist client to identify risk factors that can be modified
 Refer patient to proper agencies

Myocardial Infarction
 terminal stage of coronary art dse resulting from permanent
mal-occlussion, necrosis and scarring
types of MI:
1. Transmural
 most dangerous form of MI characterized by occlussion of right
and left coronary art.
2. Subendocardial
 critical period of MI: 24-48 hours - arrythmias, PVC (lidocaine
as ordered)
S/S:
a. Pain: sharp, excruciating visceral pain
 substernal: radiates to back, arms, shoulder, axilla, jaw and
abdominal ms
 not usually received by rest
b. Dyspnea
c. Hyperthermia
d. Mild restlessness or apprehension
e. Initial inc in bld pressure
f. Occasional findings:

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  Rales or crackles upon auscultation
 Pericardial friction rub
 Split S1 and S2
 Atrial gallop (S4)

Dx procedures
1. Cardiac enzymes
 CPK-MB
 Lactic dehydrogenase
 SGPT (ALT)
 SGOT (AST)
2. Troponin test: inc
3. ECG tracing reveals:
 ST segment elevation
 Widening of QRS complex
 Arrythmia in MI: PVCs
4. Serum uric acid and cholesterol: inc
5. CBC: inc in WBC count

Nursing Management:
1. Administer meds as ordered
a. Narcotic analgesic: morphine sulfate - induce vasodilation, reduce
levels of anxiety
 side effect: resp depression: antidote - Naloxone
Naloxone toxicity: - tremor
2. Administer O2 inhalation as ordered
3. Enforce complete bedrest
a. Bedside commode
 dec myocardial O2 demand
4. Instruct client to avoid vasalva manuever
5. semi-fowler's pos'n
6. General liquid -> soft diet
7. Avoid foods rich in caffeine, sodium and saturated fats
8. Monitor VS, I and O
9. Administer meds as ordered:
a. Vasodilators
 nitroglycerin
 isosorbide dinitrate
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b. Anti-arrhythmic agents
 xylocaine
c. Beta blockers
 propanolol
d. ACE-inhibitors
 captopril, enalopril
e. Thrombolytic/fibrinolytic agents
 streptokinase
 urokinase
 TPAF (tissue plasminogen activating factor): monitor bleeding
time
f. Anticoagulants
 heparin and coumadin simultaneously: late effect of coumadin -
3 days
 heparin: monitor PTT (partial thromboplastin time)
 heparin antidote: protamine sulfate
 coumadine antidote: vit K
g. Antiplatelet
 anti thrombotic property
10. Assist in surgical procedure
 coronary art by pass
 PTCA
11. Provide client health teaching concerning:
a. Avoidance of precipitating factors
b. Dietary restrictions
c. Prevention of Complications
 arrhythmia: PVCs
 shock: cardiogenic - oliguria as late sign
 congestive heart failure
 thrombophlebitis
 CVA
 Dressler's Syndrome: post MI syndrome - resistance to
pharmacologocal agents: administer 450,000 units of
streptokinase as ordered
d. Instruct client re resumption of ADL
 sexual intercourse: 3-6 weeks post carrdiac rehab
 sex before meals
 assume a non wt-bearing position

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  importance of follow-up care

Congestive Heart Failure

 inability to pump blood toward systemic circulation

I. Left-sided heart failure

Pred. Factors
1. 90% mitral valve stenosis (RHD, aging): ASO titer (anti
streptolysin O) = > 300 Todd units
 complication of RHD ->  penicillin
CHF  aspirin
 steroids
2. IHD
3. Hypertension
4. MI
5. Aortic stenosis
Signs and symptoms:
1. Pulmonary edema and congestion
2. Paroxysmal nocturnal dyspnea (PND)
3. Orthopnea: place client in high Fowler's pos'n
4. Productive cough with bld tinge sputum
5. Frothy salivation
6. Cyanosis
7. Rales or crackles
8. Bronchial wheezing
9. Pulsus alternans
10. Anorexia, gen body malaise
11. Point of max impulse displaced laterally
 PMI 4th-5th ICS mid clavicular line
12. S3 (ventricular gallop)

Dx procedures
1. Chestx-ray:cardiomegaly
2. Angiography, echocardiography: site and extent of mal occlusion
3. ABG: pCO2 inc, pO2 dec -> resp acidosis, hypoxemia
4. PAP (pulmonary art pressure), pulmonary capillary wedge
pressure (PCWP): inc
 Swan Ganz catheterization: done at bedside
 tracheostomy: bedside, done in O.R if pt has laryngeal or

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 thyroid cancer

Right sided HF

Predisposing factors
1. Tricuspid v stenosis 4. Pulm valve stenosis
2. Pulm edema 5. left sided heart failure
3. COPD
B. S/S
1. Jugular vein distention 6. Jaundice
2. Pitting edema 7. Pruritus
3. Ascites 8. Anorexia, gen body malaise
4. Wt gain 9. Esophageal varices
5. Hepatosplenomegaly

Dx procedure
1. Chest x-ray: cardiomegaly
2. Echocardiogram: enlarged heart chamber
3. Central venous pressure: measures right atrium pressure
- N = 4-10 cm of H2O
- if CVP is dec -> hypovolemia -> fluid challenge
- if CVP is inc -> hypervolemia
- trendelenberg pos'n: CVP catheter insertion

4. Liver enzymes: inc

A. SGPT (ALT)
B. SGOT (AST)

Nursing Mgt
1. Administer meds as ordered
A. Cardiac glycoside (Digoxin - lanoxin): monitor heart rate before
admin > 60
 digitalis toxicity: digibind (antidote)
B. Bronchodilator
 aminophylline (theophylline)
 toxicity: tachycardia, tremors
C. Narcotic analgesic
 morphine sulfate
D. Loop diuretics

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  Lasix (furosemide): 6 hrs max effect, onset 15 mins
E. Vasodilators
 ISDN
F. Anti arrhythmic agents
 lidocaine
 bretylium
2. Restrict fluids
3. VS, I and O, breath sounds
4. Weigh pt daily, assess for pitting edema
5. Measure abdominal girth -> notify physician
6. O2 inhalation: 3-4 liters/min via nasal cannula - high inflow
7. High Fowler's position
8. Bloodless phlebotomy: rotating tournique - 3 tournique rotated
clockwise every 15 mins to dec venous return
9. Health teaching
A. Dietary modification: low Na, saturated fats, caffeine
B. Prevent complications
 Arrhythmia
 MI
 Thrombophlebitis
 Cor pulmonale
C. Follow-up care

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