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Valvular heart disease
Mitral stenosis
Mitral regurgitation
Mitral valve prolapse
Aortic stenosis
Aortic regurgitation
Tricuspid stenosis
Tricuspid regurgitation
Pulmonary stenosis
Pulmonary regurgitation
Content
Congenital heart disease
Ventricular septal defect
Atrial septal defect
Patent ductus arteriosus
Coarctation of aorta
Cyanotic congenital heart disease
Fallots tetralogy
Transposition of great arteries (TGA)
Cardiac catheterization
now seldom required and is only used if coexisting cardiac problems (e.g. mitral regurgitation or
coronary artery disease) are suspected.
The typical findings in mitral stenosis are a diastolic pressure that is higher in the left atrium than in
the left ventricle.
This gradient of pressure is usually proportional to the degree of the stenosis.
Electrocardiogram
left atrial delay (bifid P waves) and
left ventricular hypertrophy as manifested by tall R waves in the left lateral leads (e.g. leads I and
V6) and deep S waves in the right-sided precordial leads, (e.g. leads V1 and V2).
(Note that SV1 plus RV5 or RV6 > 35 mm indicates left ventricular hypertrophy.)
Left ventricular hypertrophy occurs in about 50% of patients with mitral regurgitation.
Atrial fibrillation may be present.
Precordial palpation
The apex beat is not usually displaced because hypertrophy (as opposed to dilatation) does
not produce noticeable cardiomegaly.
However, the pulsation is sustained and obvious.
A double impulse is sometimes felt because the fourth heart sound or atrial contraction
(kick) may be palpable.
A systolic thrill may be felt in the aortic area.
soft or inaudible aortic second heart sound when the aortic valve becomes
immobile
reversed splitting of the second heart sound (splitting on expiration)
prominent fourth heart sound, which is caused by atrial contraction, is
heard unless coexisting mitral stenosis prevents this.
Electrocardiogram
The ECG appearances are those of left ventricular hypertrophy due to volume overload tall R
waves and deeply inverted T waves in the left-sided chest leads, and deep S waves in the rightsided leads.
Normally, sinus rhythm is present.
Tricuspid stenosis
Pathophysiology
Tricuspid valve stenosis results in a reduced cardiac output, which is restored towards normal
when the right atrial pressure increases.
The resulting systemic venous congestion produces hepatomegaly, ascites and dependent oedema.
Symptoms
Usually, patients with tricuspid stenosis complain of symptoms due to associated left-sided
rheumatic valve lesions.
The abdominal pain (due to hepatomegaly) and swelling (due to ascites), and peripheral oedema
that occur are relatively severe when compared with the degree of dyspnoea.
Tricuspid stenosis
Signs
If the patient remains in sinus rhythm, which is unusual, there is a prominent
jugular venous a wave.
This pre-systolic pulsation may also be felt over the liver.
There is usually a rumbling mid-diastolic murmur, which is heard best at the
lower left sternal edge and is louder on inspiration.
It may be missed because of the murmur of coexisting mitral stenosis.
A tricuspid opening snap may occasionally be heard.
Hepatomegaly, abdominal ascites and dependent oedema may be present.
Tricuspid regurgitation
Symptoms and signs
The valvular regurgitation gives rise to high right atrial and systemic venous
pressure.
Patients may complain of the symptoms of right heart failure.
Physical signs include a large jugular venous cv wave and a palpable liver that
pulsates in systole.
Usually a right ventricular impulse may be felt at the left sternal edge, and
there is a blowing pan systolic murmur, best heard on inspiration at the lower
left sternal edge.
Atrial fibrillation is common.
Electrocardiogram
The ECG demonstrates both right atrial and right ventricular hypertrophy, although it may sometimes
be normal even in severe pulmonary stenosis.
Echocardiogram
Doppler is the investigation of choice.
Cardiac catheterization
The passage of a catheter through the right heart allows the level and degree of the stenosis to be
established by measuring the systolic pressure gradient.
Pulmonary regurgitation
This is the most common acquired lesion of the pulmonary
valve.
It results from dilatation of the pulmonary valve ring, which
occurs with pulmonary hypertension.
It is characterized by a decrescendo diastolic murmur, beginning
with the pulmonary component of the second sound, that is
difficult to distinguish from the murmur of aortic regurgitation.
Pulmonary regurgitation usually causes no symptoms and
treatment is rarely necessary.
VSD : Investigations
A small VSD produces no abnormal X-ray or ECG findings.
Chest X-ray
prominent pulmonary artery owing to increased pulmonary blood flow in larger defects.
In Eisenmengers complex the radiological signs of pulmonary hypertension (i.e. pruned pulmonary arteries) can be seen.
Cardiomegaly occurs when a moderate or a large VSD is present.
ECG
shows features of both left and right ventricular hypertrophy.
CMR
is increasingly being used.
VSD :Treatment
Moderate and large VSDs should be surgically
repaired before the development of severe
pulmonary hypertension.
ASD : Investigations
Chest X-ray
ECG
usually shows some degree of right bundle branch block (because of dilatation of the right ventricle) and right
axis deviation.
Sometimes the ASD is part of a major developmental abnormality involving the ventricular septum and the
mitral and tricuspid valves. In this case there is left axis deviation on the ECG.
Echocardiogram
is usually abnormal if a significant defect is present. Indirect evidence includes right ventricular hypertrophy
and pulmonary arterial dilatation, and abnormal motion of the interventricular septum.
Subcostal views may demonstrate the ASD
Flow disturbance can be assessed by colour Doppler.
ASD :Treatment
A significant ASD (i.e. a pulmonary flow that is more than 50% increased when compared with systemic flow)
should be repaired before the age of 10 years or as soon as possible if first diagnosed in adulthood.
There is a dilemma with regard to whether less severe shunts should be closed when diagnosed in adulthood.
Anecdotal evidence suggests that the shunt might be progressive and that low-risk closure would be appropriate.
There is a good result from surgery with ostium secundum ASD unless pulmonary hypertension has developed.
Angiographic closure is now possible with significantly lower risk using a transcatheter clamshell device
A PFO discovered in a patient with an otherwise unexplained thrombotic stroke is now closed in this way to
prevent paradoxical thromboembolism.
In high-risk groups, e.g. deep-sea divers, such closures may be undertaken even though the patients are
asymptomatic.
Uncorrected ASDs do not require antibiotic prophylaxis for endocarditis.
If there is an accompanying valvular lesion, however, prophylaxis may be indicated.
PDA
Because aortic pressure exceeds pulmonary artery pressure throughout
the cardiac cycle, a persistent duct produces continuous aorta-topulmonary artery shunting.
This leads to an increased pulmonary venous return to the left heart
and an increased left ventricular volume load.
If the shunt is large, this results in severe left heart failure and
pulmonary hypertension.
One-third of individuals with an unrepaired ductus die from heart
failure, pulmonary hypertension or endocarditis by the age of 40; twothirds by the age of 60.
PDA : Investigations
The aorta and pulmonary arterial system are usually prominent on Xray, although a small ductus shows no abnormality.
There is both a left atrial abnormality and left ventricular hypertrophy
on the ECG.
With the development of Eisenmengers reaction, right ventricular
hypertrophy may be seen.
The echocardiogram shows a dilated left atrium and left ventricle.
Right heart changes are apparent in late disease.
CMR can be useful.
PDA : Treatment
Premature infants with a persistent duct are treated
medically with indometacin, which inhibits prostaglandin
production and stimulates duct closure.
In other cases the duct can be ligated surgically or
angiographically with very little risk.
Surgery should be performed as soon as possible and not
later than the age of 5 years.
Closure is inappropriate if pulmonary hypertension is severe.
Fallots tetralogy
Most children with cyanotic congenital
heart disease do not survive the
neonatal period.
Fallots is the most common cyanotic
anomaly in those who do survive and
is commonest amongst adults.
Transposition of the great vessels is
more common in the neonatal period
but is more likely to be fatal.
Fallots tetralogy consists of the four
features shown in Figure 13.96.
Fallots tetralogy
The level of the right ventricular outflow obstruction may
be subvalvular, valvular or supravalvular.
The most common obstruction is subvalvular, either alone
(50%) or in combinaion with valvular stenosis (25%).
This combination of lesions leads to a high right
ventricular pressure and right-to-left shunting of blood
through the VSD.
Thus the patient is centrally cyanosed.
TGA : Investigations
2-D Echocardiography can identify the
anatomical connections between the great vessels
and the cardiac chambers.
It can also detect an associated ASD, VSD or
PDA.
TGA: Treatment
The initial management in a cyanotic neonate with TGA is an atrial
septostomy (Rashkind procedure).
Balloon dilatation of the foramen ovale is performed to allow mixing
of atrial blood that maintains oxygen saturation of 5080% prior to
more definitive surgery.
Prostaglandins (E1) may be given initially to maintain a PDA.
The arterial switch operation is now performed in the first two weeks
of life the aorta is reconnected to the left ventricle; the pulmonary
artery is connected to the right ventricle; the coronary arteries are
connected to the aorta and any associated defects are repaired.