ValvularHeart Diseases
Pathophysiology
VALVULAR HEART DISEASES
- Refers to alteration in the structure of
the valve that either impedes the blood
flow or permits regurgitation
- Aortic and mitral valves are more often
affected than do pulmonic and tricuspid
valves
- Categories:
- Stenosis
- Insufficiency (Incompetence)
Etiology and Risk Factors:
• Myocardial
Ischemia/Atherosclerosis
• Inflammation of the
Endocardium
• Congenital Abnormalities of the
Heart
MITRAL VALVE DISEASE
1. Mitral Stenosis – narrowing of the
mitral valve that interferes with left
ventricular filling and produces
pulmonary hypertension and right
ventricular failure. It is often caused by
rheumatic endocarditis.
Effects:
• Reduced flow into left ventricle
• Left atrial hypertrophy
• Pulmonary hypertension
• Right ventricular hypertrophy
and failure
Narrowing of mitral valve
Left atrium has great difficulty moving blood
into the ventricle because of the increased
resistance of the narrowed orifice
it dilates and hypertrophies due to increased
blood volume.
Since there is no valve to protect the pulmonary
veins from the backward flow of blood from the
atrium, the pulmonary circulation becomes
congested.
As a result, the right ventricle must contract
against an abnormally high pulmonary arterial
pressure and is subjected to excessive strain.
Eventually, the right ventricle fails.
Signs and Symptoms
• Dyspnea on exertion as a result of
pulmonary venous hypertension.
• Progressive fatigue due to low cardiac
output.
• Hemoptysis
• Cough
• Repeated respiratory infections
Assessment & Diagnostic Findings
• The pulse is weak and often irregular
because of atrial fibrillation.
• A low-pitched, rumbling diastolic
murmur is heard at the apex.
 Assessment and Diagnostic Findings

Medical Management • A systolic murmur is heard as a high-

• Prophylactic antibiotics to prevent the
recurrence of infections.
• Anticoagulants such as warfarin
(Coumadin) to decrease the risk of
thrombus formation at the atrium.
Make sure to check Prothrombin Time
(PT) and Partial Thromboplastin Time
(PTT) before giving the drug.
pitched, blowing sound at the apex.
• The pulse may be regular and of good
volume, or it may be irregular as a
result of extrasystolic beats or atrial
fibrillation.
• Echocardiography is used to diagnose
and monitor the progression of mitral
regurgitation.

• PT – 10-12 seconds

• PTT – 30-45 seconds Medical Management

• Valvuloplasty – repair of the valve
through surgery
• Same with CHF.
• Surgical intervention consists of mitral
valve replacement or valvuloplasty (ie,
surgical repair of the heart valve).

2. Mitral Valve Prolapse – one or both

of the valve leaflets bulge into the left
atrium during ventricular contractions

2. Mitral Insufficiency – leaking or

regurgitation of blood back into the left atrium
leading to pulmonary hypertension and right
ventricular failure

Effects:

• Left atrial dilation and hypertrophy

• Pulmonary hypertension
• Right ventricular hypertrophy

Signs and Symptoms

• Usually asymptomatic, but acute mitral
regurgitation brought about by MI
usually manifests as sever CHF.

• Dyspnea, fatigue, and weakness are

common.

• Palpitations, SOB, and cough from

pulmonary congestion may occur.

AORTIC VALVE DISEASE
1. Aortic Stenosis – narrowing of the
orifice of the aortic valve which causes
a decrease in cardiac output and an
increase pressure in the left ventricle
Effects:
Assessment and Diagnostic Findings
• Increased blood volume in left
ventricle
• Left ventricular dilation and
hypertrophy
• Decreased cardiac output
Pathophysiology
There is progressive narrowing of the valve
orifice, usually over a period of several years to
several decades.
The left ventricle overcomes the obstruction to
circulation by contracting more slowly but with
greater energy than normal, forcibly squeezing
the blood through the very small orifice.
The obstruction to left ventricular outflow
increases pressure on the left ventricle, which
results in thickening of the muscle wall.
The heart muscle hypertrophies. When these
compensatory mechanisms of the heart begin
to fail, clinical signs and symptoms develop.
Medical Management
Signs and Symptoms
• Many patients with aortic stenosis are
asymptomatic.
• Patients usually first have exertional
dyspnea, caused by left ventricular
failure.
• Other signs are dizziness and syncope
because of reduced blood flow to the
brain.
• Angina pectoris is a frequent symptom
that results from the increased oxygen
demands of the hypertrophied left
ventricle, the decreased time in diastole
for myocardial perfusion, and the
decreased blood flow into the coronary
arteries.
• Blood pressure can be low but is usually
normal; there may be a low pulse
pressure (30 mm Hg or less) because of
diminished blood flow.
• Loud, rough systolic murmur may be
heard over the aortic area. The sound
to listen for is a systolic crescendo-
decrescendo murmur, which may
radiate into the carotid arteries and to
the apex of the left ventricle.
• The murmur is low-pitched, rough,
rasping, and vibrating. If the examiner
rests a hand over the base of the heart,
a vibration may be felt.
• The vibration is caused by turbulent
blood flow across the narrowed valve
orifice.
• Evidence of left ventricular hypertrophy
may be seen on a 12-lead ECG and
echocardiogram.
• Echocardiography is used to diagnose
and monitor the progression of aortic
stenosis.
• After the stenosis progresses to the
point that surgical intervention is
considered, left-sided heart
catheterization is necessary to measure
the severity of the valvular abnormality
and evaluate the coronary arteries.
• Antibiotic prophylaxis to prevent
endocarditis is essential for anyone with
aortic stenosis.
• Definitive treatment for aortic stenosis
is surgical replacement of the aortic
valve.
• Patients who are symptomatic and are
not surgical candidates may benefit
from one- or two-balloon percutaneous
valvuloplasty procedures
2. Aortic insufficiency– incomplete closure of
the aortic valve that causes backflow of blood
into the left ventricle from the aorta during
diastole.
Effects:
• Increased blood volume in left
ventricle
• Left ventricular dilation and
hypertrophy
• Decreased cardiac output
Pathophysiology
Blood from the aorta returns to the left
ventricle during diastole in addition to the
blood normally delivered by the left atrium.
The left ventricle dilates, trying to
accommodate the increased volume of blood.
It also hypertrophies, trying to increase muscle
strength to expel more blood with abovenormal
force—raising systolic blood pressure.
The arteries attempt to compensate for the
higher pressures by reflex vasodilation; the
peripheral arterioles relax, reducing peripheral
resistance and diastolic blood pressure.
Signs and Symptoms
• Asymptomatic in most patients.
• Some patients are aware of a forceful
heartbeat, especially in the head or
neck.
• There may be marked arterial
pulsations that are visible or palpable at
the carotid or temporal arteries.
• Exertional dyspnea and fatigue follow.
• Progressive signs and symptoms of left
ventricular failure include breathing
difficulties (eg, orthopnea, paroxysmal
nocturnal dyspnea), especially at night.
Assessment and Diagnostic Findings
• A diastolic murmur is heard as a high-
pitched, blowing sound at the third or
fourth intercostal space at the left
sternal border.
• The pulse pressure (ie, difference
between systolic and diastolic
pressures) is considerably widened in
patients with aortic regurgitation.
• One characteristic sign of the disease is
the water-hammer pulse, in which the
pulse strikes the palpating finger with a
quick, sharp stroke and then suddenly
collapses.
• Diagnosis may be confirmed by
echocardiogram, radionuclide imaging,
ECG, magnetic resonance imaging, and
cardiac catheterization.
Medical Management
• Before the patient undergoes invasive
or dental procedures, antibiotic
prophylaxis is needed to prevent
endocarditis.
• Heart failure and dysrhythmias are
treated.
• Aortic valvuloplasty or valve
replacement is the treatment of choice,
preferably performed before left
ventricular failure. Surgery is
recommended for any patient with left
ventricular hypertrophy, regardless of
the presence or absence of symptoms.
TRICUSPID VALVE DISEASE
1. Tricuspid Stenosis – narrowing of the
tricuspid valve that interferes with the
right ventricular filling and in increases
right atrial pressure
2. Tricuspid Insufficiency – leaking of
blood back into the right atrium from
the right ventricle
Effects:
• Decreased cardiac output
• Increased right atrial pressure
• Systemic Congestion
PULMONIC VALVE DISEASE • Increased RR, shallow
respiration
1. Pulmonic Stenosis – narrowing of the
orifice of the pulmonic valve which • Hemoptysis, pink-frothy
causes a decreased cardiac output and sputum
an increased pressure in right ventricle • Pulmonary crackles
2. Pulmonic Insufficiency – incomplete 3. Systemic Congestion
closure of the pulmonic valve that
causes backflow of blood into the right • Peripheral edema, cyanosis
ventricle from the pulmonary artery
• Jugular vein distention,
Effects: hepatojugular reflux

• Decreased cardiac output • Ascites, Congestive

Hepatomegaly
• Increased right ventricular
pressure 4. Cardiac Manifestation

• Right ventricular dilation and • Murmurs (sound produced by

hypertrophy abnormal/turbulent blood flow)

• Systemic congestion • S3 heart sound (ventricular

gallop) – occurs after S2 when
• Narrowing of valve between right the mitral valve opens.
ventricle and pulmonary artery
• ECG changes
• Regurgitation of blood from the right
ventricle back into the right atrium • Angina pectoris

• Valve leaflet bulges into the left atrium Diagnostic Test

during systole
• Cardiac catheterization
• Reddish/Bluish discoloration of the
• X-ray
face
• Echocardiography
• (+) Corrigan’s pulse
• Electrocardiography
• (+) Mitral Click

• Decreased left ventricular filling and Management:

increased pressure in the left atrium Goals: Maintain a normal cardiac output;
• (+) Mitral Facies – rosy cheeks but the improve cardiac function and activity tolerance
rest of the face is cyanotic

Clinical Manifestation  Monitor the client’s hemodynamic

1. Decreased Cardiac Output status (i.e., vs q1-4 hours; auscultate
breathe and heart sounds; daily weight;
• Fatigue, weakness check for murmurs, edema)
• SOB, pallor  Oxygen therapy to improve oxygenation
and relieve respiratory distress
• Low BP
 Plan rest periods and limit visitors,
• Weak, irregular pulse; Water-
activity and noise
hammer pulse
 Administer the following medications as
ordered:
2. Pulmonary Congestion
 Digitalis (Digoxin) and other
• Orthopnea, Paroxysmal inotropic agents (Dopamine,
Nocturnal Dyspnea dobutamine)
  ACE inhibitors
 Diuretics
 Antibiotics
 Anticoagulants
 Monitor patient’s compliance/response
to medications
 Monitor F&E balance
 I&O
 Daily weight
 Lung sounds
 Presence of Edema
 Dietary modifications and
activity restrictions if indicated
 Educate patient in possible care
for valvular surgeries
 Monitor for complications such
as heart failure
SURGICAL MANAGEMENT
Candidates for surgery are those:
- Symptomatic clients
- Clients with progressive impairment of
cardiac function
- Gradual enlargement of the heart
1. VALVULOPLASTY – repair or
reconstruction of a cardiac valve
a. Commissurotomy
 Open Commissurotomy
 Closed Surgical
Commissurotomy
 Balloon Valvuloplasty
b. Annuloplasty – repair of the
valve annulus
c. Chordoplasty – repair of the
chordae tendinae
2. VALVE REPLACEMENT – replacement of a
diseased valve by a valve prosthesis
a. Mechanical Valves (e.g., Ball-
and-cage or Disk valve)
b. Tissue Valves
 Xenografts – tissue
valves from pigs or
cows are used
 Homografts/Allografts –
obtained from cadaver
tissue donations.
 Autografts - are
obtained by excising
the patient’s own
pulmonic valve and a
portion of the
pulmonary artery for
use as the aortic valve.
Nursing Management Post-Valvuloplasty
and Replacement
• Vital signs are assessed every 5 to 15
minutes and as needed until the patient
recovers from anesthesia or sedation
and then assessed every 2 to 4 hours
and as needed.
• Intravenous medications to increase or
decrease blood pressure and to treat
dysrhythmias or altered heart rates are
administered and their effects
monitored. The intravenous
medications are gradually decreased
until they are no longer required or the
patient takes needed medication by
another route (eg, oral, topical).
• Patient assessments are conducted
every 1 to 4 hours and as needed, with
particular attention to neurologic,
respiratory, and cardiovascular systems
• The nurse educates the patient about
long-term anticoagulant therapy,
explaining the need for frequent follow-
up appointments and blood laboratory
studies, and provides teaching about
any prescribed medication: the name of
the medication, dosage, its actions,
prescribed schedule, potential side
effects, and any drug-drug or drug-food
interactions.
• Patients with a mechanical valve
prosthesis require education to prevent
bacterial endocarditis with antibiotic
prophylaxis, which is prescribed before
all dental and surgical interventions.
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