Pathophysiology Review - part 3 pdf

CHAPTER 6 ✚ Cardiovascular System 167
ț Medications not helpful.
ț Removal of blood at regular intervals: reduces amount of stored iron
in clients with iron overload.
ț Heart transplant.
What can harm my client?
ț Infection.
ț Malnutrition.
ț Fall/injury.
ț Depression.
If I were your teacher, I would test you on . . .
ț Causes and why.
ț Signs and symptoms and why.
ț Cardiac physical assessment.
ț Diagnostic tests.
ț Nursing actions to increase oxygenation.
ț End-of-life care.
Hypertrophic cardiomyopathy: what causes it and why
See Figure 6-2 and Tables 6-10 and 6-11.
Table 6-10
Causes Why
Uncontrolled hypertension Uncontrolled hypertension causes the ventricles and septum muscle to become hypertrophic.
This causes the actual chambers of the heart to become very small and little volume ejects
out of the heart, decreasing cardiac output. Less forward flow leads to backward flow
Inherited gene The inherited gene affects the cells of the myocardium (sarcomeres) so that there is
hypertrophy and asymmetry of the left ventricle
Acromegaly Excessive growth of the heart muscle due to overproduction of growth hormone
Source: Created by author from References #3, #4, #5, #6, #9, and #10.
Enlarged
heart muscle
Right

ventricle
AB
Left
ventricle
ǡ Figure 6-2. A. Normal heart.
B. Hypertrophic cardiomyopathy.
168 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
Hypertrophic cardiomyopathy: signs and
symptoms and why
Table 6-11
Signs and symptoms Why
ț Fatigue; weakness
ț Late signs include signs
and symptoms of left-sided
heart failure such as
nocturnal dyspnea, S3,
pink frothy sputum, cough,
crackles, orthopnea,
tachycardia, restlessness,
shortness of breath
Arrhythmias; chest pain Especially seen with inherited HCM. As the
heart hypertrophies, there is increased oxy-
gen demand. When demand exceeds supply,
myocardial ischemia occurs, leading to
arrhythmias
A second contributing factor is that the size of
the ventricle itself impedes coronary perfusion.
The stiff large muscle mass creates resistance
to coronary perfusion during diastole
Palpitations The client can sense the arrhythmias as

palpitations
Faintness; dizziness Decrease in cardiac output; decreased
perfusion to the brain
Sudden cardiac death (SCD) Lethal arrhythmias leading to death
Source: Created by author from References #4, #5, #6, #9, and #10.
The left ventricle becomes a large stiff
muscle mass. This leaves very little room to
fill the left ventricle with volume. As a result,
cardiac output drops. Less ventricular filling
and less forward flow results in fluid backing
up into lungs. As cardiac output drops, oxygen
delivery is decreased
Quickie tests and treatments
Tests:
ț Chest x-ray: shows mild to moderate increase in heart size.
ț Thallium scan: reveals myocardial perfusion defects.
ț ECHO: shows left ventricular hypertrophy and thick intraventricular
septum.
ț Cardiac catheterization: measures pressures in the heart chambers if
surgery is being considered.
ț EKG: shows left ventricular hypertrophy; ventricular and atrial
arrhythmias.
Treatments:
ț Beta-adrenergic blockers: slow heart rate, reduce myocardial oxygen
demands, increase ventricular filling by relaxing obstructing muscle.
ț Calcium-channel blockers: increase ventricular filling by relaxing
obstructing muscle.
ț Antiarrhythmic drugs: reduce arrhythmias.
Coronary artery circulation occurs
during diastole when the ventricles

relax. This slows heart rate and
increases diastolic time, giving the
heart muscle more time for oxygen
delivery.
CHAPTER 6 ✚ Cardiovascular System 169
ț Cardioversion: treats atrial fibrillation.
ț Anticoagulants: reduce risk of systemic embolism with atrial
fibrillation.
ț Implantable cardioverter-defibrillator (ICD): treats ventricular
arrhythmias.
ț Ventricular myotomy or myectomy (resection of hypertrophied septum):
eases outflow obstruction and relieves symptoms.
ț Heart transplant: replaces malfunctioning heart.
What will harm my client?
ț Not taking antibiotics prior to dental or surgical procedures to reduce
risk of infective endocarditis.
ț Pulmonary edema.
ț Lethal arrhythmias: ventricular tachycardia and ventricular fibrillation.
If I were your teacher, I would test you on . . .
ț Factors that cause hypertension to lead to heart failure.
ț Medications that decrease workload on heart.
ț Signs and symptoms of fluid volume excess.
ț Effective client coping strategies.
ț Medications that are contraindicated.
ț Pre- and postop care.
ț Causes and why.
ț Signs and symptoms and why.
ț Safety precautions.
Dilated cardiomyopathy: what causes it and why
See Figure 6-3, Tables 6-12 and 6-13.

Enlarged left and
right ventricles
AB
ǡ Figure 6-3. A. Normal heart.
B. Dilated cardiomyopathy.
If you are on a beta-blocker, you
will stay cool as a cucumber (or
your vegetable of choice) if you
come home one night and there is
a man in a mask waiting for you in
your bedroom. Why? Because
beta-blockers won’t let you release
epinephrine and norepinephrine,
so you will just kindly say, “Do I
know you?”
Many medications commonly used
to treat heart failure may not help
because they may decrease cardiac
output even further.
170 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
Dilated cardiomyopathy: signs and symptoms and why
Table 6-12
Causes Why
Chemotherapy Toxic effects of the drugs on the myocardial
cells dilate the ventricles and they cannot
contract properly. Cardiac output decreases.
Signs and symptoms of heart failure are
observed
Alcohol and drugs Direct toxic effects of alcohol on the
myocytes (heart cells)

Coronary heart disease Decreased oxygen delivery to the heart
muscle leads to pump failure. The heart
muscle dies and is replaced by scar tissue.
The uninjured heart muscle stretches and
thickens to compensate for the lost pumping
action
Valvular heart disease Increased volume or increased resistance
to outflow in the chamber of the heart
over time distends the chambers and the
muscle becomes stretched, thinned, and
weakened
Viral or bacterial infections Inflammation of the heart muscle; heart
muscle weakens; the heart stretches to
compensate, resulting in heart failure
Hypertension Ventricles and septum muscle hypertrophy,
causing the actual chambers of the heart
to become very small and little volume
ejects out of the heart, decreasing cardiac
output. Less forward flow leads to
backward flow
Source: Created by author from References #3, #4, #5, #6, #9, and #10.
Table 6-13
Signs and symptoms Why
Shortness of breath, orthopnea, Left-sided heart failure: ineffective left
dyspnea on exertion, paroxysmal ventricular contractility; reduced pumping
nocturnal dyspnea, fatigue, ability; decreased cardiac output to body;
generalized weakness, dry blood backs up into the left atrium
cough at night and lungs
Peripheral edema, hepatomegaly, Right-sided heart failure: ineffective right
jugular vein distension, ventricular contractility; reduced pumping

weight gain ability; decreased cardiac output to lungs;
blood backs up into right atrium and
peripheral circulation
(Continued)
CHAPTER 6 ✚ Cardiovascular System 171
Quickie tests and treatments
Tests:
ț Angiography: rules out ischemic heart disease.
ț Chest X-ray: shows moderate to marked cardiomegaly and pulmonary
edema.
ț Echocardiography: may reveal ventricular thrombi; degree of left
ventricular dilation and dysfunction.
ț Gallium scan: identifies clients with dilated cardiomyopathy and
myocarditis.
ț Cardiac catheterization: shows left ventricular dilation and
dysfunction, ventricular filling pressures, and diminished cardiac
output.
ț Endomyocardial biopsy: determines underlying disorder.
ț Electrocardiography: rules out ischemic heart disease.
Treatments:
ț Oxygen therapy.
ț ACE inhibitors: reduce afterload through vasodilation.
ț Diuretics: reduce fluid retention.
ț Beta-adrenergic blockers: treat heart failure.
ț Antiarrhythmics: control arrhythmias.
ț Pacemaker: corrects arrhythmias.
ț Coronary artery bypass graft (CABG) surgery: manages dilated
cardiomyopathy from ischemia.
ț Valvular repair or replacement: manages dilated cardiomyopathy from
valve dysfunction.

ț Heart transplant: replaces damaged heart.
ț Lifestyle modifications (smoking cessation; low-fat, low-sodium diet;
physical activity; abstinence from alcohol/illicit drugs): reduces
symptoms and improves quality of life.
Table 6-13. (Continued )
Signs and symptoms Why
Peripheral cyanosis, tachycardia Low cardiac output
Murmur Leaking heart valves
Arrhythmia Stretching of the heart muscle leads to
abnormal heart rhythms
Chest pain; palpitations Arrhythmias may be felt as pain or
palpitations
Syncope Decreased cardiac output
Source: Created by author from References #4, #5, #6, #9, and #10.
172 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
What can harm my client?
ț Pulmonary edema.
ț Lethal arrhythmias.
ț Malnutrition.
ț Infection.
If I were your teacher, I would test you on . . .
ț Causes and why.
ț Signs and symptoms and why.
ț Diagnostic tests.
ț Medications, proper administration, and possible side effects.
ț Client teaching of lifestyle modifications.
ț Client care of a pacemaker.
ț Complete cardiorespiratory assessment.
ț Oxygen safety.
✚ Valvular heart disease

Valvular heart disease can affect any of the valves in the heart.
Diseased valves may have an
altered structure, which
changes the blood flow.
Disorders of the endo-
cardium, the innermost
lining of the heart and
valves, damage heart valves.
Valvular heart diseases
include:
ț Mitral stenosis.
ț Mitral regurgitation.
ț Mitral valve prolapse.
ț Aortic stenosis.
ț Aortic regurgitation.
See Table 6-14 for val-
vular heart disease at a
glance.
173
Table 6-14. Valvular Heart Disease at a Glance
Signs and symptoms Quickie tests What can harm If I were your teacher,
Type What is it? Causes and why and why and treatments my client? I would test you on . . .
Mitral Stenosis
Mitral stenosis is
narrowing of the
mitral valve. The left
atrium meets resist-
ance as it attempts
to move blood for-
ward into left ven-

tricle. Eventually the
left atrium dilates
and contractility
decreases. Forward
flow is decreased
and fluid backs up
into lungs. Increased
volume in the lungs
increases pressure
in lungs.
Remember: more
volume, more pres-
sure. Pulmonary
hypertension in turn
can lead to right-
sided heart failure
ț Acute rheumatic
fever or infective
endocarditis
causes inflamed
tissues. When
they heal, there
is scarring and
thickening. This
narrows the
valves
ț Congenital abnor-
mality causes the
valve to thicken
by fibrosis and

calcification,
obstructing blood
flow
ț Myxoma (non-
cancerous tumor
in left atrium)
obstructs the
blood flow
through the mitral
valve
ț Blood clot reduces
blood flow
through the mitral
valve
ț Adverse effect of
fenfluramine and
phentermine diet
drug combination
causes the valve
to thicken by
fibrosis and
calcification
ț Exertional dyspnea:
the narrowed mitral
valve decreases
filling into the ven-
tricles. Decreased
volume in ventricle
decreases SV and
CO. Supply does not

meet demand,
causing exertional
dyspnea. The mitral
valve is narrowed,
causing backward
flow of volume
from the left atrium
into the lungs,
resulting in exer-
tional dyspnea
ț Orthopnea: fluid
accumulates in the
lungs and the client
sits up to breathe
better
ț Nocturnal dyspnea:
when lying down,
all the blood that
pools in the
extremities during
the day returns to
the heart. This
causes more fluid
in the lungs
ț Atrial fibrillation:
the enlarged left
atrium interferes
Tests
ț Echocardiography:
shows blood

passing through
narrowed valve
opening
ț Electrocardiography
(EKG): reveals left
atrial enlargement,
right ventricular
hypertrophy, atrial
fibrillation
ț Chest x-ray: shows
left atrial and ven-
trical enlargement,
mitral valve
calcification
ț Cardiac catheteriza-
tion: to determine
location and extent
of blockage
Treatments
ț Prevention of
rheumatic fever
ț Digoxin, low-
sodium diet,
diuretics, vasodila-
tors, ACE inhibitors:
treat left-sided
heart failure
ț Oxygen: increases
oxygenation
ț Embolitic stroke

ț Heart failure
ț Infection, espe-
cially with valve
replacement
surgery
ț Pulmonary
embolism
ț Causes and why
ț Signs and symptoms
and why
ț Medication administra-
tion, monitoring, and
possible side effects
ț Diagnostic tests
ț Proper cardiorespiratory
assessment
ț Patient comfort
techniques
ț Pre- and postop
nursing care
ț Patient teaching
regarding infection,
prophylactic antibiotics,
and lifestyle
modifications
(Continued)
174
Table 6-14. Valvular Heart Disease at a Glance (Continued )
Signs and symptoms Quickie tests What can harm If I were your teacher,
Type What is it? Causes and why and why and treatments my client? I would test you on . . .

with normal con-
duction pathways.
The atrium no
longer contracts or
contributes to left
ventricular volume
as before. Loss of
atrial contraction
decreases CO even
more
ț Diastolic murmur:
turbulent flow
occurs at the nar-
rowed valve.
Murmur is heard
after S2. You will
hear lub (S1) dub
(S2), whoosh . . .
lub dub, whoosh
ț JVD, hepatomegaly,
peripheral edema,
weight gain,
ascites, epigastric
discomfort, tachy-
cardia, crackles, pul-
monary edema:
fluid in the lungs
causes increased
pressures in the
lungs—pulmonary

hypertension.
Pulmonary hyper-
tension leads to
right sided heart
failure. These signs
ț Anticoagulants:
prevent thrombus
formation around
diseased or
replaced valves
ț Prophylactic antibi-
otics before and
after surgery and
dental care: pre-
vent endocarditis
ț Nitrates: relieve
angina
ț Beta-adrenergic
blockers or digoxin:
slow ventricular
rate in atrial
fibrillation/flutter
ț Cardioversion: con-
verts atrial fibrilla-
tion to sinus
rhythm
ț Balloon valvulo-
plasty: enlarges
orifice of stenotic
mitral valve

ț Prosthetic valve:
replaces damaged
valve that can’t be
repaired
175
Mitral
Insufficiency/
Regurgitation
The mitral valve
does not close
properly during ven-
tricular systole,
causing backward
flow of blood during
systole. This back-
ward flow can cause
heart failure
ț Infective endo-
carditis or
rheumatic heart
disease causes
inflammation and
damages the
valve
ț Coronary artery
disease: ischemia
and/or necrosis
of the heart
muscle can cause
damage to the

supporting struc-
tures of the mitral
valve, impeding
proper closure of
the valve
ț Aging: over time,
degenerative
changes can
weaken the valve
and symptoms are
related to right-
sided heart failure
ț Peripheral and
facial cyanosis:
hypoxemia
ț Hemoptysis: high
pressure causes a
vein or capillaries in
the lungs to burst
ț Fatigue; weakness:
during ventricular
systole, blood backs
up into left atrium.
The left side of the
heart, both the
atrium and ventri-
cles, hypertrophy
and dilate. Cardiac
output decreases.
There is an imbal-

ance between sup-
ply and demand,
causing fatigue in
the client
ț Pansystolic murmur:
murmur heard
through all of sys-
tole as blood backs
up into left atrium.
If S1 and S2 are
audible, the murmur
will be heard
between these
two sounds: lub,
“whoosh,” dub
ț Angina: decreased
coronary artery
circulation
Tests
ț Auscultation:
presence of heart
murmur
ț Electrocardiography
(EKG): shows left
ventricle
enlargement
ț Chest x-ray: shows
left ventricle
enlargement; fluid
accumulation in

the lungs
ț Echocardiography:
shows the faulty
valve and amount
of blood leaking
Treatment
ț Anticoagulants:
prevent clots
ț ACE inhibitors: treat
mild heart failure
ț Valvuloplasty: repairs
the faulty valve
ț Valve replacement:
with a prosthetic
valve
ț Severe pulmonary
edema
ț Embolitic stroke
ț Heart failure
ț Infection, espe-
cially with valve
replacement
surgery
ț Pulmonary
embolism
ț Causes and why
ț Signs and symptoms
and why
ț Pre- and postop care
ț Proper cardiorespira-

tory assessment
ț Diagnostic tests
ț Patient teaching
regarding infection and
valve replacement
surgery
ț Medication administra-
tion, monitoring, and
side effects
ț Signs, symptoms, and
management of
thrombosis and pul-
monary embolism
(Continued)
176
Table 6-14. Valvular Heart Disease at a Glance (Continued )
Signs and symptoms Quickie tests What can harm If I were your teacher,
Type What is it? Causes and why and why and treatments my client? I would test you on . . .
The valve cusps
bulge into the left
atrium when the
left ventricle con-
tracts, allowing
leakage of small
amount of blood
into the atrium
ț Connective tissue
disorders (systemic
lupus erythe-
matosus, Marfan’s

syndrome): the
chordae tendineae
can become elon-
gated, which
allows the mitral
valve leaflets to
open backward
into the atrium
during systole.
Remember:
backflow equals
heart failure
ț Congenital heart
disease: auto-
somal dominant
ț Palpitations: heart-
beats are more
forceful because the
left ventricle has to
pump more blood
to compensate for
the leakage back
into the left atrium
ț Late signs include
signs and symp-
toms of left-sided
heart failure: noc-
turnal dyspnea; S3;
pink, frothy sputum;
cough; crackles;

orthopnea; tachy-
cardia; restlessness
ț Fatigue; weakness:
during ventricular
systole, blood backs
up into left atrium.
The left side of
heart, both the
atrium and ventri-
cles, hypertrophy
and dilate. Cardiac
output decreases.
There is an imbal-
ance between sup-
ply and demand,
causing fatigue in
the client
ț Angina: decreased
coronary artery
circulation
ț Prophylactic anti-
biotics before and
after surgery and
dental care: prevent
endocarditis
ț Nitrates: relieve
angina
Tests
ț Auscultation:
reveals clicking

sound; murmur
when left ventricle
contracts
ț Echocardiography:
shows the prolapse
and determines
the severity of
regurgitation if
present
ț Electrocardiography
(EKG): may reveal
atrial or ventricular
arrhythmia
ț Holter monitor for
24 hours: may
show arrhythmia
ț Arrhythmias
ț Infective
endocarditis
ț Mitral insuffi-
ciency from
chordal rupture
Mitral Valve
Prolapse
ț Causes and why
ț Signs and symptoms
and why
ț Medication administra-
tion, monitoring, and
side effects

ț Proper cardiorespira-
tory assessment
ț Assessment and treat-
ment of infection
ț Patient education
regarding rest periods,
signs of possible
depression, safety
measures
ț Antibiotics before sur-
gical, dental, medical
procedures and why?
To prevent infection of
the heart valve
177
Aortic Stenosis
Narrowing of the
aortic valve opening
that increases resist-
ance to blood flow
from the left ventricle
to the aorta. The left
ventricle hyper-
trophies and
weakens, leading to
left-sided heart failure
inheritance seen
in young women
ț Acquired heart
disease (coronary

artery disease
[CAD], rheumatic
heart disease):
causes valve
bulge due to
inflammation
ț Age: degenerative
changes causing
scarring and
calcium accumu-
lation in the valve
cusps
ț Rheumatic fever:
causes inflamma-
tion of the cusps
that leads to
ț Palpitations: heart-
beats are more
forceful because
the left ventricle
has to pump more
blood to compen-
sate for the leakage
back into the left
atrium
ț Migraine headaches:
decreased cardiac
output; not enough
blood to the brain
ț Dizziness: decreased

cardiac output; not
enough blood to
the brain
ț Orthostatic
hypotension:
decreased cardiac
output; blood flow
not able to rapidly
adjust to client
position changes
ț Mid-to-late systolic
click; late systolic
murmur: blood
backing up into left
atrium
ț Exertional dyspnea:
decreased blood
supply to the
enlarged heart leads
to decreased CO
ț Angina: decreased
blood supply to the
enlarged heart is
inadequate
Treatments
ț Decreased caffeine,
alcohol, tobacco,
stimulant intake:
decreases
palpitations

ț Fluid intake: main-
tains hydration
ț Beta-blocker: slows
heart rate; reduces
palpitations
ț Antibiotics before
surgical, dental,
medical procedures:
prevention against
bacterial infection
of heart valve
ț Anticoagulants:
prevent thrombus
formation
ț Antiarrhythmics:
prevent
arrhythmias
Tests
ț Chest x-ray: shows
valvular calcifica-
tion, left ventricle
enlargement,
pulmonary vein
congestion
ț Echocardiography:
shows decreased
ț Left-sided heart
failure
ț Right-sided heart
failure

ț Infective
endocarditis
ț Cardiac arrhyth-
mias, especially
atrial fibrillation
ț Causes and why
ț Signs and symptoms
and why
ț Medication administra-
tion, monitoring, and
side effects
ț Proper cardiorespira-
tory assessment
(Continued)
178
Table 6-14. Valvular Heart Disease at a Glance (Continued )
Signs and symptoms Quickie tests What can harm If I were your teacher,
Type What is it? Causes and why and why and treatments my client? I would test you on . . .
scarring; usually
accompanied by
mitral stenosis
and leakage
ț Birth defect: valve
with two cusps
instead of usual
three; valve with
abnormal funnel
shape; calcium
accumulates,
causing the valve

to become stiff
and narrow
ț Atherosclerosis:
lipids can increase
calcium accumu-
lation of the
valves
ț Syncope: sudden
drop in blood
pressure because
the arteries in the
skeletal muscles
dilate during exer-
cise to receive more
oxygen-rich blood,
but the narrowed
valve opening pre-
vents the left ven-
tricle from pumping
enough blood to
compensate
ț Pulmonary
congestion: left-
sided heart failure
ț Harsh, rasping,
crescendo-
decrescendo systolic
murmur: forced
blood flow across
stenotic valve

valve area, increased
left ventricular wall
thickness
ț Cardiac catheteriza-
tion: increased
pressure across aortic
valve; increased left
ventricular pressures;
presence of coronary
artery disease
Treatments
ț Low-sodium, low-fat,
low-cholesterol diet:
treats left-sided heart
failure
ț Diuretics: treat left-
sided heart failure
ț Periodic noninvasive
evaluation: monitors
severity of valve
narrowing
ț Cardiac glycosides:
control atrial
fibrillation
ț Antibiotics before
medical, dental,
surgical procedures:
prevent endocarditis
ț Percutaneous balloon
aortic valvuloplasty:

reduces degree of
stenosis
ț Aortic valve
replacement: replaces
diseased valve
ț Assessment and
treatment of infection
ț Patient education
regarding diet
modifications
ț Recognition of heart
murmurs and
arrhythmias
ț Antibiotics before
surgical, dental,
medical procedures
and why?
179
Leakage of the
aortic valve. Each
time the left
ventricle relaxes,
blood leaks back
into it. (Atria are
contracting while
ventricles are
relaxing)
ț Bacterial
endocarditis,
rheumatic fever:

inflammatory
process damages
the endocardial
cells, making
the valves
dysfunctional
ț Connective
tissue diseases
(Marfan’s
syndrome):
direct damage
of the heart
valves can occur,
causing valvular
regurgitation or
valvular stenosis
ț Left-sided heart
failure such as
nocturnal dyspnea,
S3, pink frothy
sputum, cough,
crackles, orthopnea,
tachycardia,
restlessness: In
aortic regurgitation
volume is backing
up through the
aortic valve during
diastole. In an
attempt to maintain

cardiac output and
manage the extra
volume, the left
ventricle hyper-
trophies. Over time,
though, the left
ventricle fails,
resulting in left-
sided heart failure
ț Diastolic murmur:
blood is backing up
into left ventricle
from aorta during
diastole. You will
hear S1, S2, then
the murmur, e.g.,
lub, dub, whoosh
Tests
ț Chest x-ray: may show left
ventricular enlargement and
pulmonary vein congestion
ț Echocardiography: shows
left ventricular enlargement,
thickening of the valve cusps,
prolapse of the valve, and
vegetations (accumulation
of debris blood, etc.)
ț Electrocardiography: shows
sinus tachycardia, left
ventricular hypertrophy

ț Cardiac catheterization:
shows coronary artery
disease
Treatments
ț Oxygen: increases
oxygenation
ț Vasodilators: reduce systolic
load and regurgitant volume
Valve replacement with
prosthetic valve: removes
diseased aortic valve
ț Low-sodium diet: treats
left-sided heart failure
ț Diuretics: treat left-sided
heart failure
ț Prophylactic antibiotics
before and after surgery,
medical, dental care:
prevent endocarditis
ț Nitroglycerin: relieves
angina
ț Left-sided heart
failure
ț Pulmonary
edema
ț Myocardial
ischemia
ț Pre- and postop
care
ț Proper cardio-

respiratory
assessment
ț Diagnostic tests
ț Patient teaching
regarding infection
and valve
replacement
surgery
ț Medication
administration,
monitoring, and
side effects
ț Signs, symptoms,
and management
of left-sided heart
failure, pulmonary
edema, MI
ț Antibiotics before
surgical, dental,
medical procedures
and why?
Source: Created by author from References #4, #5, #6, #11, and #12.
Aortic
Insufficiency/
Regurgitation
180 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
✚ Infectious cardiac disease
Infectious cardiac disease is a general term used to describe an infectious
disease process of the endocardium or lining of the heart. The mitral valve
is often the site affected by the infection. Microorganisms, such as bacteria

or fungi, enter the blood and colonize on heart valves. This colonization
makes the site extremely resistant to antibiotic treatment. An older term—
bacterial endocarditis—is no longer used, as it is now known there is also a
thrombotic component to the problem. The presence of the thrombus on
the valve, though, increases the likelihood of infection developing.
Infectious cardiac diseases include:
ț Infective endocarditis.
ț Pericarditis.
Infective endocarditis: what is it?
Infective endocarditis is an infection of the endocardium, heart valves, or
cardiac prosthesis (Tables 6-15 and 6-16).
Infective endocarditis: what causes it and why
Table 6-15
Causes Why
Bacteria: streptococci, Bacteria like to attack two organs: the kidneys
staphylococci, fungi and heart. When they attack the heart, they
attack the valves. Once the microorganisms
begin to proliferate on the valve, they can
form what’s called “vegetation” or purulent
stuff attached to the heart valve. Fungi can
proliferate on heart valves just like bacteria
Prosthetic valves Bacteria easily stick to the foreign device
Long-term indwelling Clients with catheters—central lines, Foleys—
catheters that remain in place for extended time periods
are at risk for developing an infection. This
can lead to an infection in the heart valve
Recent cardiac surgery Contamination of the area during surgery
Rheumatic heart disease; Deposit of immune complex on the heart valve;
Systemic lupus erythematosus calcification of the heart valve, making it stiff
Congenital heart defects Malformed heart valves are more susceptible

to colonization
Valvular dysfunction Turbulent flow causes damage to the
endothelial lining and can lead to a thrombus
formation
IV drug abuse IV drug abusers who do not follow aseptic
technique can “inject” bacteria into the blood.
Injection of bacteria into a vein follows the
normal blood flow and returns to the right side
of the heart. The first valve for the bacteria to
attack is the tricuspid valve. This is why IV drug
abusers develop tricuspid valve problems
Source: Created by author from References #4 to #6.
Before you run off and get that
tongue ring, be sure to check for
the infections that can occur
(like mediastinitis) from all that
bacteria draining down around
your heart. Okay?
Anytime a client has a foreign
(nonself) device in his body, a
greater risk exists for developing
an infection.
CHAPTER 6 ✚ Cardiovascular System 181
Infective endocarditis: signs and symptoms and why
Chronic mitral regurgitation is not
life threatening; however, it is a
medical emergency when a myo-
cardial infarction causes abrupt rup-
ture of the supporting structures of
the valve. Your client will suddenly

develop severe pulmonary edema,
which is life threatening.
Table 6-16
Signs and symptoms Why
Fever Normal response to infection. Some bacteria and fungi cannot
survive in an environment with an elevated temperature
Splenomegaly: the spleen is an important The spleen is working overtime to protect immunity; this
immune system organ causes hypertrophy
Petechia Tiny spots caused by hemorrhaging under the skin. The
microemboli and septic emboli can shower any organ, including
the skin, leading to clotting followed by bleeding
Hematuriae Microemboli and septic emboli can shower any organ, especially
the glomeruli, leading to clotting followed by bleeding
Cardiac murmurs Vegetation on the valve prevents the valve from closing
properly, resulting in a murmur
Pleuritic pain Microemboli and septic emboli can shower any organ including
the lungs. The inflammatory response kicks in. Tissue edema
occurs and places pressure on nerve endings. This pleuritic pain
may be present during inspiration or expiration
Fatigue; weakness Vegetation on the mitral valve prevents proper closure of the
valve, causing backward flow during systole, which eventually
leads to heart failure. This causes fatigue and weakness
Late signs include signs and symptoms of left-sided Infection and/or clot formation on the mitral or aortic valves
heart failure: nocturnal dyspnea; S3; pink, frothy can lead to left-sided heart failure
sputum; cough; crackles; orthopnea; tachycardia;
restlessness; JVD; hepatomegaly; ascites; peripheral
edema; pulmonary edema
Source: Created by author from References #4 to #6.
Quickie tests and treatments
Tests:

ț Blood cultures: determine causative organism.
ț White blood cell with differential count: elevated.
ț Complete blood count and anemia panel: positive for anemia in
infective endocarditis.
ț Erythrocyte sedimentation rate: elevated.
ț Creatinine level: elevated.
ț Urinalysis: proteinuria, hematuria.
ț Echocardiography: shows valvular damage.
ț Electrocardiogram: atrial fibrillation.
Treatments:
ț Antibiotics: given for 2 to 6 weeks IV in high doses.
ț Surgery: repair or replace damaged valve and remove vegetations.
182 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
What can harm my client?
ț Microemboli or septic emboli traveling to other organs.
ț Stroke.
ț Heart failure.
ț Infection.
ț Valve stenosis or regurgitation.
ț Myocardial erosion.
If I were your teacher, I would test you on . . .
ț Causes and why.
ț Signs and symptoms and why.
ț Monitoring for IV complications.
ț Laboratory values.
ț Pre- and postop care.
ț Cardiovascular assessment.
ț Monitoring renal status.
ț Patient education regarding when to notify the doctor.
ț Identify the location to listen for tricuspid, mitral, and aortic

murmurs.
Acute pericarditis: what is it?
Acute pericarditis is an inflammation of the sac surrounding the
heart (Fig. 6-4, Tables 6-17 and 6-18). The area becomes roughened
and scarred. Exudates develop and pericardial effusions are
possible.
Sternum
Heart
Pericardium
Inflamed
pericardium
(pericarditis)
Ǡ Figure 6-4. Pericarditis.
Clients who have mechanical valves
are at risk for developing clots on
their valves, because like bacteria,
platelets like to “stick” to foreign
bodies and form clots. These clients
will be placed on anticoagulants.
Clients with biological valves do
not require anticoagulation therapy
because the natural valve does
not increase platelet aggregation.
CHAPTER 6 ✚ Cardiovascular System 183
Acute pericarditis: what causes it and why
Table 6-18
Signs and symptoms Why
Pericardial friction rub (scratchy, Inflammation of the inner- and outermost
grating-like sound heard in lining of the pericardial sac causes scarring
systole and diastole) and roughening. The scraping together of

the inner- and outermost layers produces
a sound called a friction rub. It can best be
heard at the apex of the heart
Dysphagia (difficulty swallowing) The fluid around the heart can place
pressure on the nerve endings supplying
the esophagus
Chest pain: worsens with Inflammatory process stimulates the pain
inspiration and decreases when receptors in the heart. Leaning forward
the client leans forward; can takes some of the pressure off the pleural
radiate to neck, shoulders, chest, tissue
and arms
Source: Created by author from References #4 to #6.
Acute pericarditis: signs and symptoms and why
Table 6-17
Causes Why
Myocardial infarction The normal response to injury is to activate
the inflammatory response. Once activated,
inflammatory mediators migrate to the injured
area. Chemical mediators such as histamine,
prostaglandins, bradykinins, and serotonin cause
vasodilation and increased capillary permeability.
Increases in capillary permeability allow fluid
and protein to leak into the surrounding tissue.
Exudates of dead tissue, proteins, RBCs, and fluid
may be purulent if infective and collect in the
area. The inner and outermost linings become
roughened and scarred
Radiation Damage from radiation causes activation of
the inflammatory response (see above)
Bacterial, fungal, The body attempts to “mount” an attack on

or viral infections the invading organisms. Immune response
kicks in by activating B- and T-cell lymphocytes.
The inflammatory response occurs, causing
leakage of fluid into the pericardial sac
Autoimmune disorders: Activation of the inflammatory response
rheumatoid arthritis, causes increased capillary permeability. Fluid
systemic lupus accumulates in the pericardial sac
erythematosus (SLE)
Previous trauma Trauma and surgery activate the inflammatory
or cardiac surgery response. This can result in the accumulation
of fluid in the pericardial sac
Source: Created by author from References #4 to #6.
184 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
Chronic pericarditis: what is it?
Chronic pericarditis (Tables 6-19 and 6-20) is the result of continued
irritation to the pericardial lining. The lining becomes thickened and
stiff and the client may develop restrictive pericarditis.
Chronic pericarditis: what causes it and why
Table 6-19
Causes Why
Uremia Chronic presence of high urea levels in the blood
causes irritation and inflammation to the peri-
cardial lining. Chronic inflammation leads to thick-
ening of the pericardial lining, causing stiffness
Autoimmune diseases: Chronic irritation sets the inflammatory response
SLE, rheumatoid arthritis into motion (see above)
Source: Created by author from References #4 to #6.
Table 6-20
Signs and symptoms Why
Weakness The heart chambers can no longer fill

or contract effectively because they are
being “squeezed” by the pericardial sac.
This leads to a decrease in cardiac output,
with less oxygen and nutrient delivery to
the cells
Signs and symptoms of right-sided The heart is being “squeezed” and the
heart failure: edema, right side of the heart cannot fill well.
hepatomegaly, ascites, JVD This results in signs and symptoms of
right-sided heart failure
Source: Created by author from References #4 to #6.
Chronic pericarditis: signs and symptoms and why
Quickie tests and treatments
Tests:
ț White blood cell count: elevated.
ț Erythrocyte sedimentation rate: elevated.
ț Serum creatinine: elevated.
ț Pericardial fluid culture: identifies causative organism in bacterial or
fungal pericarditis.
ț Blood urea nitrogen: elevated.
ț Echocardiography: shows pericardial effusion.
ț Electrocardiography: shows elevated ST segment.
Treatments:
ț Bed rest as long as fever and pain persist: reduces metabolic needs.
ț NSAIDs: relieves pain and reduces inflammation.
CHAPTER 6 ✚ Cardiovascular System 185
ț Corticosteroids: if NSAIDs are ineffective and no infection exists.
ț Antibacterial, antifungal, antiviral therapy: if infectious cause.
ț Pericardiocentesis: removes excess fluid from pericardial space.
ț Partial pericardiectomy: creates window that allows fluid to drain into
pleural space (chronic pericarditis).

ț Total pericardiectomy: permits adequate filling and contraction of
heart.
What can harm my client?
ț Cardiac tamponade.
ț Pericardial effusion.
ț Infection.
If I were your teacher, I would test you on . . .
ț Monitoring for drop in cardiac output.
ț Causes and why.
ț Signs and symptoms and why.
ț Pre- and postop care.
ț Infection control.
ț Patient education regarding deep breathing and coughing exercises;
scheduled rest periods.
ț Identification of heart rhythm and sounds.
ț Monitoring hemodynamic status.
✚ Cardiac tamponade
What is it?
Cardiac tamponade (Fig. 6-5, Tables 6-21 and 6-22) is caused by accu-
mulation of fluid or blood between the two layers of the pericardium. It
is the most serious complication of pericarditis.
Sternum
Heart
Pericardium
Fluid inside the pericardium
(cardiac tamponade)
ǡ Figure 6-5. Cardiac tamponade.
186 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
What causes it and why
Table 6-21

Causes Why
Trauma to the chest Cardiac contusion may occur. (Bruising of the heart
muscle.) Blood and fluid leak into the pericardial sac
Myocardial infarction Inflammation at the site of the infarction leads to
increased capillary permeability. Fluid can leak into
the pericardial sac resulting in a tamponade
Cardiac bypass surgery Normally blood and fluid accumulate around the
heart after heart surgery. Sometimes, though,
one of the sutures to a graft may burst. This
may cause sudden accumulation of blood in the
mediastinum, resulting in a cardiac tamponade
Source: Created by author from References #4 to #6.
Signs and symptoms and why
Table 6-22
Signs and symptoms Why
Jugular vein distension (JVD) Heart is “squeezed” so blood cannot fill
heart. Instead blood backs up into venous
system, causing distension of jugular vein
Drop in blood pressure The heart squeezes → CO drops →
decreased forward flow of volume.
Remember: less volume, less pressure
Muffled heart sounds Fluid accumulates around the heart
muffling heart sounds
Pulsus paradoxus Blood pressure drops more than 10 mm Hg
with inspiration. This is because with
inspiration there is even more pressure
“squeezing” down on heart
Change in level of consciousness Decreased head perfusion due to drop
(LOC) in CO
Increased HR Compensation for drop in CO

Edema Blood backing up into the venous system
Source: Created by author from References #4 to #6.
Quickie tests and treatments
Tests:
ț Chest x-ray: widened mediastinum due to blood accumulation.
ț Echocardiography: detects compression of the heart, variation in
blood flow in heart that occurs with breathing; shows fluid
accumulation.
ț Electrocardiography: fast, slow, or normal HR with no pulse.
CHAPTER 6 ✚ Cardiovascular System 187
Treatments:
ț Echocardiography: monitors fluid removal.
ț Pericardiocentesis: removes fluid from the pericardium.
ț Percutaneous balloon pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through the skin.
ț Subxiphoid limited pericardiotomy: drains fluid using a balloon-tipped
catheter inserted through a small incision in the chest.
ț Pericardiectomy: removal of the pericardium.
ț Sclerotheraphy: obliterates the pericardium by causing scar tissue
to form.
ț Oxygen therapy: increases oxygenation and tissue perfusion.
ț Intravascular volume expansion: increases blood volume and
oxygenation.
ț Inotropic agents: controls heart rate and decreases atrial fibrillation.
What can harm my client?
ț A sudden accumulation of fluid in the pericardial sac or mediastinum
is a medical emergency.
ț Cardiogenic shock.
ț Death.
If I were your teacher, I would test you on . . .

ț Assessment for cardiac output.
ț Clients at risk for cardiac tamponade.
ț Causes and why.
ț Signs and symptoms and why.
ț Pre- and postop care.
ț IV administration and complications.
ț Patient teaching regarding bed rest, when to notify the doctor, and
postop infection prevention.
✚ Arteriosclerosis
Arteriosclerosis—hardening of the arteries—is a term for several
diseases in which the wall of an artery becomes thicker and less elastic.
We’ll look at atherolsclerosis in detail and then quickly look at
arteriolosclerosis.
Atherosclerosis: what is it?
Atherosclerosis (Fig. 6-6, Tables 6-23 and 6-24) is a condition where patchy
deposits of fatty material develop in the walls of arteries, leading to reduced
or blocked blood flow.
EKG may have fast, slow, or normal
HR with NO pulse! That’s bad! The
heart is being squeezed so it cannot
pump normally. The conduction
system, however, remains intact.
This is known as pulseless electrical
activity.
188 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
Table 6-23
Causes Why
Repeated injury to the artery wall Immune system involvement or direct
toxicity allows materials to deposit on
the artery’s inner lining

High cholesterol High levels of cholesterol in the blood
injure the artery’s lining, causing an
inflammatory response, allowing choles-
terol and other fatty materials to deposit
Infection due to bacteria or virus Damages the lining of the artery’s wall,
encouraging deposits to form
Atheromas (patchy deposits Form where the arteries branch because
of fatty material) the artery’s wall is injured from constant
turbulent blood flow
Source: Created by author from Reference #13.
What causes it and why
Buildup of fatty
substances in the
wall of the artery
decreases the
size of the lumen
Ǡ Figure 6-6. Atherosclerosis.
RISK FACTORS There are many risk factors associated with atherosclerosis
including:
ț Smoking: decreases high-density lipoprotein (HDL), the good stuff,
and increases the bad stuff, low-density lipoprotein (LDL).
ț High cholesterol: risk of heart attack increases when the HDL and
LDL are out of whack.
ț High blood pressure: uncontrolled high blood pressure can lead to
heart attack or stroke.
ț Diabetes mellitus: the risk for developing atherosclerosis is 2 to 6 times
higher in diabetics because sugar deposits just like fat.
CHAPTER 6 ✚ Cardiovascular System 189
Quickie tests and treatments
Tests:

ț Blood pressure: monitors hypertension.
ț Lipid profile: cholesterol below 200 mg/dL is desired.
ț Coronary angiography: shows location and degree of coronary artery
stenosis or obstruction, circulation, and condition of the artery
beyond the narrowing.
ț Electrocardiography: evaluates damaged heart muscle and if there is
adequate blood supply.
ț Cardiac catheterization: confirms presence of hardening of arteries.
ț Intravascular ultrasound: views the inside walls of the arteries.
ț Nuclear imaging: dye shows area of blockage.
ț Exercise stress test: determines if angiography or coronary artery
bypass surgery (CABS) is needed.
ț Holter monitor: detects silent ischemia and angina.
ț Obesity: abdominal (truncal) obesity increases the risk for diabetes,
hypertension, and coronary artery disease (CAD).
ț Physical inactivity: leads to obesity, high blood pressure, and CAD.
ț High blood levels of homocysteine: homocysteine (an amino acid)
may directly injure the lining of the arteries, making the formation of
atheromas more likely.
Signs and symptoms and why
Table 6-24
Signs and symptoms Why
High blood pressure Atheromas grow, causing narrowing of the
arteries and calcium accumulation in the
arteries
Decreased peripheral pulses Decreased elasticity of the arteries and the
narrowed lumen contribute to decreased
peripheral circulation
Angina Arteries that supply the heart are narrowed
Leg cramps Narrowing of arteries in the legs

(intermittent claudication)
Stroke Blockage of the arteries supplying the brain
Heart attack Arteries supplying the heart are blocked
Kidney failure Arteries supplying one or both kidneys
become narrowed or blocked
Malignant hypertension Dangerously high blood pressure caused by
narrowing of the arteries
Source: Created by author from Reference #13.
190 MARLENE HURST ✚ Hurst Reviews: Pathophysiology Review
Treatements:
ț Lifestyle modifications: low-fat, low-sodium, high-fiber diet; decreased
alcohol intake; smoking cessation; weight loss program; exercise program.
ț Nitrates: decrease cardiac pain caused by angina by vasodilating the
coronary arteries, therefore supplying more blood to actual heart muscle.
ț Antihypertensives: lower blood pressure.
ț Anticoagulants: prevent blood clots.
ț Percutaneous transluminal coronary angioplasty (PTCA): balloon
compresses fatty plaque or blockage against vessel wall to widen
diameter of blood vessel and increase blood flow.
ț Balloon angioplasty with stenting: stent expands to the size of the
artery and holds it open.
ț Calcium-channel blockers: lower blood pressure.
ț Angiotensin-converting enzyme (ACE) inhibitors: widen bloods
vessels, lower blood pressure.
ț Beta-blockers: reduce blood pressure and improve circulation.
ț Antiplatelets: prevent platetelets from sticking together and
blocking vessels.
What can harm my client?
ț Stroke.
ț Heart attack.

ț Kidney failure.
ț Malignant hypertension.
ț Peripheral artery disease.
If I were your teacher, I would test you on . . .
ț Causes and why.
ț Signs and symptoms and why.
ț Medication administration, monitoring, and side effects.
ț Care of the patient during diagnostic procedures.
ț Patient safety measures.
ț Signs and symptoms and management of stroke, hypertension, heart
attack, and kidney failure.
ț Patient teaching regarding lifestyle modification, stress reduction,
recognition of dangerous signs and symptoms of illness.
ARTERIOLOSCLEROSIS AT A GLANCE
ț Hardening of the arterioles—small arteries.
ț The walls thicken, narrowing the arterioles.
ț Organs supplied by the affected arterioles do not receive enough blood.
This affects the kidneys.
ț Disorders occur mainly in people with high blood pressure or diabetes.
ț High blood pressure and diabetes stress the walls of the arterioles,
resulting in thickening.
CHAPTER 6 ✚ Cardiovascular System 191
✚ Hypertension
What is it?
Hypertension is abnormally high pressure in the arteries. Whatever the
etiology, the results are the same: hypertension is the result of peripheral
vasoconstriction. Vasoconstriction decreases blood flow to end organs
(Table 6-25).
What causes it and why
Table 6-25

Causes Why
Primary hypertension Etiology unknown. It is thought, though, that
there is a genetic predisposition. Gender plays
a role, and men are at greater risk than
women. Black males are at highest risk for the
illness. Diets high in sodium, glucose, and
heavy alcohol consumption are linked to
hypertension. Diabetes and obesity also play a
role. More recently, research indicates diets low
in potassium, magnesium, and calcium are
associated with hypertension
Secondary hypertension Related to underlying disease: pheochromo-
cytoma, hyperthyroidism, hyperaldosteronism,
Cushing’s syndrome, and renal disease
Pheochromocytoma Benign tumors in the adrenal medulla secrete
epinephrine and norepinephrine, leading to
hypertension
Hyperthyroidism Increase in thyroid hormone leads to increases
in heart rate and cardiac output, which
increases blood pressure
Hyperaldosteronism Too much aldosterone leads to increased
sodium and water. Remember, more volume,
more pressure
Cushing’s syndrome Too many of all the steroids including aldosterone,
which leads to increased sodium and water
Renal disease The high pressures eventually damage the
glomeruli (intrarenal failure). Now there is less
blood flow (perfusion) through the kidneys. The
kidneys try to fix the problem by activating
renin–angiotensin–aldosterone system. This

makes your client even more hypertensive and
causes more damage to the glomeruli. Left
untreated, this can progress to renal failure
Lifestyle: obesity, sedentary Can lead to hypertension in people who have
lifestyle, stress, smoking, an inherited tendency to develop the illness
excessive alcohol
consumption, increased
salt intake
Arteriosclerosis Fatty plaques collect on the artery walls,
narrowing them, and leading to increased
blood pressure
Source: Created by author from References #4 to #6.
Hypertension is the number one
cause of congestive heart failure.
A recommendation of attending
Happy Hour at least 3 to 4 times a
week is not good for treating athero-
sclerosis or arteriosclerosis. Sorry.