Angelina A Joho

MSc in Critical Care and Trauma.

 By the end of this presentation, students
should be able to Describe;
 the valvular heart disease
 Anatomy of the heart
 Epidemiology of valvular heart disease
 Types of valvular heart disease
 Causes of valvaular heart disease
 Path physiology of valvular heart disease
 Clinical manifestation
 Investigations
 Treatment of heart failure
 Valvular heart disease describes structure and/or
functional abnormalities of single or multiple cardiac
valves.
 The result is alteration in blood flow across the valve.
 The heart contains two antrioventricular
valves, the mitral and the tricuspid, and two
semilunar valves, the aortic and the pulmonic,
which are located in four strategic location to
control unidirectional blood flow.
 If structural changes occur as a result of
disease, this functional is disrupted.
 The exact incidence of valvular heart disease is
unknown.
 Some have suggested that more than 5 million people

have some form (moderate to severe) of valvular

regurgitation,.
 There has been as much as fourfold increase in hospital

discharge diagnoses of aortic and mitral regurgitation in

the last 20yrs.
 In 2003 an estimated 95,000 heart valve surgical

procedures were performed, the most frequent being

aortic valve surgery, followed by surgery on the mitral
valve, pulmonic valve, and triscupid valve.
 Disease processes of heart valves will cause
either a stenotic or an insufficiency
(regurgitation incompetence)
 The stenotic valve has a narrowed orifice and
does not open properly, that creates a partial
obstruction to blood flow, resulting in
increasing pressure behind the valve and
decreasing forward blood flow.
 Purestenosis will block the flow of blood
from one heart chamber (atrium to ventricle)
or may prevent adequate ejection of the blood
from the ventricle into the circulation
(pulmonary or peripheral)
 Insufficiency indicates the valve is leaking
allowing blood to leak back (or regurgitate)
into the previous heart chamber.
 Frequently pt with valvular heart disease will

have a combination of stenosis and

regurgitation involving one or more valves.
 The most common diseases that cause
valvular heart disease are the rheumatic fever
and bacterial endocarditis.
 Rheumatic fever is an autoimmune disease
 Occur as the result of a group A hemolytic

streptococci
 Protein from rheumatogenic strains share certain

epitopes with cardiac myosin and sarcolemmal

membrane protein.
 Antibodies produced in the host against these

epitopes of streptococci cross- react with cardiac

tissues resulting in an inflammatory response in
pericardium, myocardium and endocardium.
 Aortic stenosis causes left venricular outflow
tract obstruction at the supravalvular, valvular,
or subvalvular level.
 Valvular aortic stenosis is the most common

lesion.
 Aortic stenosis can be congenital or secondary

to rheumatic inflammation or calcification .

 Aortic stenosis is observed during systole when
blood is being ejected from the ventricle to the
aorta across a narrowed aortic valve.
 It is hemodynamic abnormality caused by an
obstruction to the left ventricle outflow tract ,
causing a high pressure gradient btn the left
ventricle and aorta during systolic ejection.
 Because of the increase in left ventricular
pressure over a period of time , the cardiac work
load increased,
 Leading to a progressive ventricular
hypertrophy, increase in myocardial oxygen
demands. These compensatory mechanisms
generally permit cardiac output and stroke
volume to be maintained at rest but fail during
exercise.
 The normal aortic valve has a cross-sectional

area of 2.5 to 3.5cm², severe aortic stenosis is

when the cross-sectional area of 0.5 to 0.7cm²
 There is a prolonged latent period before the
symptoms and signs of aortic stenosis are
developed.
 Most patient do not show symptoms until their

forties or fifties, these are not produced until

the valve orifice has been narrowed to
approximately 1/3 normal.
 The cardinal signs; angina pectoris, syncope, or

exertional dyspnea.
 During late stages of the disease patient show
fatigability, peripheral cyanosis, orthopnea,
paroxysmal nocturnal dyspnea, pulmonary
edema.
 Sudden death associated with the disease is

about 20%
 Patient average life expectance after appearing

of angina pectoris or syncope is 3-4

years(untreated patients)
 Low- pitched, harsh murmur is best heard in
the aortic region (the second intercostal space
to the right of the sternum), and it is generally
transmitted up to the neck and carotid vessels.
 It begins shortly after the first heart sound ,

increasing in intensity toward the middle of

the ejection period and decreasing until aortic
valve closure.
 A systolic thrill is generally present at the base
of the heart.
 The jugular pulse is normal, cardiac rhythm is

usually regular.
 In advancing stages, left ventricular systole may

became so delayed that aortic valve closure

comes after pulmonic valve closure.
 This is known as paradoxical splitting of the

second heart sound.

 An atrial gallop s₄ may be audible at the apex,
signifying the presence of left ventricular
hypertrophy
Investigations
 ECG reveals left ventricular hypertrophy
 Chest x-ray may show enlargement of the left

ventricles and in advanced cases, pulmonary

congestion.
 Chest x-ray and echocardiogram may reveal

valvular calcification.
A cardiac catheterization is performed to
determine the pressure gradient between the
left ventricle and the aorta in order to estimate
the severity of the stenosis.
 Coronary angiography is generally performed

on patients who have anginal symptoms and

on all patients over age 40 regardless of
symptoms
 Management of the patient depends on the
degree of stenosis and cardiac hypertrophy.
 Patient with associated cardiac failure is treated

with digitalis, glycosides, a low –sodium diet,

diuretics and reduction of activities.
 Surgical replacement of the aortic valve.
 Etiology
 Approximately 75% of all patients suffering
from aortic regurgitation are men.
 The common cause of aortic regurgitation is

the Rheumatic fever.

 It may be also congenital in origin
 Infective endocarditis (active or healed)
 Pharmacological agents
 Aortic regurgitation is observed during diastole
when the aortic valve is closed. Because the aortic
valve is incompetence, blood is ejected forward in
the aorta, but it also leaks back through the closed
aortic valve into the left ventricle
There is an increase in the total stroke volume ejected
by the left ventricle.
 Over time the end diastolic volume of left ventricle

increases and myocardial fibers stretch to

accommodate the extra fluid.
 The compensatory dilatation permits the left
ventricle to increase its stroke volume and maintain
CO. Ventricular dilatation and hypertrophy
eventually cease to compensate aortic
incompetence.
 In advanced stages of illness there will be; left

ventricular failure, lowering cardiac output, and rise

pressure in left atrial, pulmonary capillary and right
ventricle.( heart failure develops)
 Coronary perfusion may be impaired due to reduced

diastolic perfusion pressure, thus may result in

 Coronary blood flow is affected by two major
factors;
1. Decreased diastolic coronary aortic pressure
due to low diastolic aortic pressure.
2. Increased left ventricular oxygen demands
due increased mass and wall stress
 A person with aortic regurgitation may be
asymptomatic for long time.
 The earliest symptom may be palpitation produced by

the forceful contractions of a dilated left ventricle

 Sinus tachycardia
 Exertional dyspnea most likely due to an eleveted left

ventricular end –diastoly pressure with exercise.

 A ngina may occur, even in the absence of

atherosclerotic coronary artery disease, because of a

decreased myocardial oxygen demand
 S, and decreased ratio of coronary artery size and to

myocardial mass.
 Patient may present with signs of heart failure,
including dsypnea at rest, paroxysmal
nocturnal dyspnea, and orthopnea.
 Syncope and sudden death although rare may

occur in aortic regurgitation patients, even in

absence of prior symptoms.
 The carotid pulse is typically bounding, with
more rapid
 The classical peripheral signs of aortic

regurgitation are seen only with severe

disease:
 waterhammer pulse
 Quincke’s sign
capillary pulsation in the nail beds
 De Musset’s sign (heard bob)

head nodding with each heart beat

 Duroziez’s sign (if found, it is a sign of severe

aortic regurgitation
a to-and-fro murmur heard when the femoral artery
is auscultated with pressure applied distally
 Pistol shot femorals

a sharp bang heard on auscultation over the femoral

arteries in time with each heart beat.
 Chest X-ray
The chest X-ray features are those of left ventricular
enlargement and possibly of dilatation of the ascending aorta.
 Electrocardiogram

left ventricular hypertrophy due to ‘volume overload’ – tall R

waves and deeply inverted T waves. Normally, sinus rhythm
is present.
 Echocardiogram

demonstrates vigorous cardiac contraction and a dilated left

ventricle. The aortic root may also be enlarged.

 .
 Cardiac catheterization
During cardiac catheterization, injection of
contrast medium into the aorta (aortography) will
outline aortic valvular abnormalities and allow
assessment of the degree of regurgitatio n
 The underlying must be treated (e.g. Syphilitic
aortitis or infective endocarditis) antibiotic
therapy.
 If pt has S &S of volume overload, vasodilators

such as Calcium-channel blocking agent eg

nifedipine and ACE-Inhibitors eg captopril,
seem to have beneficial effects.
 If the regurgitation is severe, pt should be

managed as in severe heart failure.

 Thetreatment of aortic regurgitation usually
requires aortic valve replacement but the
timing of surgery is critical

 Both mechanical prostheses and tissue valves

are used.
 Almost all mitral stenosis is due to rheumatic heart disease.
 At least 50% of sufferers have a history of rheumatic fever
 The mitral valve is affected in over 90% of those with

rheumatic valvular heart disease.

 Rheumatic mitral stenosis is much more common in women.
 The pathological process results after some years in valve

thickening, cusp fusion, calcium deposition, a narrowed

(stenotic) valve orifice and progressive immobility of the
valve cusps.
 Mitral stenosis is caused most commonly by
o acute rheumatic fever or
o bacterial endocarditis.
 Theforward flow from left atrium to the left
ventricle decreases, cardiac output falls, creating
a decrease in systemic perfusion.

 Blood backed up behind the stenotic valve causes

left atrial dilatation and increased left atrial
pressure.
 This is reflected backward into pulmonary

circulation, and with prolonged high pressures,

fluid moves from pulmonary capillaries into
interstitial space and eventually the alveoli.
 Pulmonary hypertension leads to right
ventricular hypertrophy, dilatation and failure.
Right ventricular dilatation results in tricuspid
regurgitation.
 Progressively severe dyspnoea develops.
 Hemoptysis - A cough productive of blood-tinged,

frothy sputum is quite common, and occasionally

frank haemoptysis may occur.(pulmonary apoplexy)
 weakness, fatigue and abdominal or lower limb

swelling.
 Palpitations due to enlarge L atrium –Atrial fib
 Atrial fibrillation may result in systemic emboli,

most commonly to the cerebral vessels

 On physical examination pt may be found to
have peripheral cyanotic and a classic malar
flush
 If right heart failure develops, there is distension

of the jugular veins.

 Chest pain,15% of pts with mitral stenosis,

experince chest discomfort that is

indistinguishable from angina pectoris.
 Symptomatic patients are treated medically
with avoidance of strenuous activity,
restriction of sodium intake, and diuretics.
 Glycosides indicated to control ventricular rate

in patients with rapid atrial fibrillation.

 Surgery is recommended for patients who are

symptomatic.
 There are 3 major surgical procedure to
correct mitral stenosis; closed
commissurotomy, open commissurotomy and
mitral valve replacement.
 The most common is valve replacement.
 Mitral valve regurgitation, also known as
mitral regurgitation, is a condition in which
the mitral valve leaflets do not seal tightly.
This valvular defect allows blood to flow
backward in your heart and is often referred to
as a leaking heart valve.
 Mitral regurgitation is observed during ventricular
systole, when the mitral valve is closed and the
ventricle is ejecting blood to the aorta.
 Due to its incompetent, blood is ejected not only

forward to the aorta , but also backward to the left

atrium.
 The left ventricle attempts to compensate for the

regurgitant blood flow by emptying more

completely during systole to maintain Cardiac
output.
 Progressively, the left ventricle dilates,
producing a rise in left ventricular end diastolic
pressure.
 The regurgitant blood produces a rise in left

atrial pressure and enlargement of the left

atrium.
 Left atrial hypertension may eventuaaly the

cause of increased pulmonary vascular

resistance and right -heart failure.
 Weakness and fatique
 Exertional dyspnea
 Palpitation
 Severe symptoms precipitated by left
ventricular failure, with consequent low output
and pulmonary congestion.
 Chest radiograph- left atrial and left ventricular
enlargement, variable pulmonary congestion.
 ECG – P mitrale, left ventricular hypertrophy,

atrial fibrillation
 Auscultation- murmur throughout systole
 Catheterization – opacification of left atrium,

during left ventricular injection, V waves,

increased left atrial and left ventricular pressures.
 Variable elevations of pulmonary pressures.
 potential problems might pt have related to Valvular
Heart Disease
1.decreased cardiac out put r/t alterations in preload, in
afterloard, in contractility, in heart rate.
2. alteration in comfort r/t cardiopulmonary dysfunction
3. knowledge deficit r/t lack of previous exposure to
information
4. potential for infection r/t...
5. Ineffective breathing pattern r/t
7.
 Assist the patient in bathing, if necessary.
 Offer diversional activities that are physically

undemanding.
 Alternate periods of rest to prevent extreme

fatigue and dyspnea.

 To reduce anxiety, allow the patient to

express his concerns about the effects of

activity restrictions on his resposibilities and
routine.
 Place the patient in an upright position to

relieve dyspnea.
 Administer oxygen as needed to prevent

tissue hypoxia.
 Keep the patient in a low sodium diet.
 Allow the patient to express his fears and
concerns about the disorder, it’s impact on
his life, and any impending surgery.
 Monitor the patient’s vital signs, weight, and

intake and output for signs of fluid overload.

 Evaluate patient’s activity tolerance and

degree of fatigue.
 Monitor the patient for chest pain that may

indicate cardiac ischemia.

 Regularly assess the patient’s

cardiopulmonary function.
 Observe the patient for complications and

adverse reactions to drug therapy.

 Karen K. Carlson, (2009),Critical Care
Nursing, p 322-345
 Barbara Montgomery Dossey, P 452-467
 Morton,P.G, et al. (1994), Critical Care

Nursing A HOLISTIC Approach, 8th edition,p

451-455.
 Urden L.D, et al (2008),Priorities in Critical

Care Nursing 5th edition p 210-213.

 Internet .