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

 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
2

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

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

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.
2.

3.

B.

heart can beat rhythmically without nervous input

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)
gap junctions - electrically couple all cardiac muscle
cells so that depolarization sweeps across heart in
sequential fashion from atria to ventricles

"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.

 Theoretical Mechanism of Pacemaker Potential:

K+ leak channels allow K+ OUT of the cell more slowly than in
skeletal muscle
Na+ slowly leaks into cell, causing membrane potential to slowly
drift up to the threshold to trigger Ca++ influx from outside (-40
mV)
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
when peak depolarization is achieved, voltage-gated K+
channels open, causing repolarization to the "unstable resting
potential"
cycle begins again at step a.

a.
b.
c.

d.
e.

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.
2.

heart can beat without external innervation

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

A.

General Concepts
1.
2.
3.

B.

systole - period of chamber contraction

diastole - period of chamber relaxation
cardiac cycle - all events of systole and diastole
during one heart flow cycle
Events of Cardiac Cycle
1.

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.

mid-to-late ventricular diastole: ventricles filled

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
(normal 70 beats/minute)

0.8 second

atrial systole (contraction)

ventricular systole (contraction)
quiescent period (relaxation)

=
=

0.1 second
0.3 second
=
0.4 second

Heart Sounds: Stethoscope Listening

9

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

2.
3.

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.
2.

end diastolic volume (EDV) - total blood collected in

ventricle at end of diastole; determined by length of
diastole and venous pressure (~ 120 ml)
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
=
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.
ii.

C.

70 ml/beat

slow heart rate = more time to fill

exercise = more venous blood return

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.
c.
d.

parasympathetic - ACETYLCHOLINE (ACh)

decreases heart rate
vagal tone - parasympathetic inhibition of
inherent rate of SA node, allowing normal HR
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.
b.
c.

epinephrine - hormone released by adrenal medulla

during stress; increases heart rate
thyroxine - hormone released by thyroid; increases heart
rate in large quantities; amplifies effect of epinephrine
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.
c.
d.
e.

exercise - lowers resting heart rate (40-60)

heat - increases heart rate significantly
cold - decreases heart rate significantly
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
14

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

15

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
16

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-Fowlers
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 clients 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
18

 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:
21

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
22

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
23

 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
24

thyroid cancer
Right sided HF
Predisposing factors
1. Tricuspid v stenosis
2. Pulm edema
3. COPD
B. S/S
1. Jugular vein distention
2. Pitting edema
3. Ascites
4. Wt gain
5. Hepatosplenomegaly

4. Pulm valve stenosis

5. left sided heart failure
6.
7.
8.
9.

Jaundice
Pruritus
Anorexia, gen body malaise
Esophageal varices

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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