INVESTIGATION Medical Assignment Help

Chest X-ray

The chest X-ray usually reveals a relatively small heart with a prominent, dilated, ascending aorta. This occurs because turbulent blood flow above the stenosed aortic valve produces so-called ‘poststenotic dilatation’. The aortic valve may be calcified. When heart failure occurs, the CTR increases.

ECG

The ECG shows left ventricular hypertrophy and left atrial delay. A left ventricular ‘strain’ pattern due to ‘pressure overload’ (depressed ST segments and T wave inversion in leads orientated towards the left ventricle, i.e. leads I, AVL, Vs and V6) is common when the disease is severe. Usually, sinus rhythm is present, but ventricular arrhythmias may be recorded.

Echocardiogram

The echocardiogram readily demonstrates the thickened, calcified and immobile aortic valve cusps. Left ventricular hypertrophy may also be seen. The gradient across the valve can be estimated by CW Doppler.

Cardiac catheterization

Cardiac catheterization is used to document the systolic pressure difference (gradient) between the aorta and the left ventricle. A gradient of 50 mmHg or more is usually sufficient to advise surgery. A trivial degree of aortic regurgitation that is undetectable clinically is often demonstrated by contrast aortography. Coronary angiography is important before recommending surgery.

ECG and pressure

ECG and pressure

TREATMENT

Patients with aortic stenosis should not overly exert themselves, and in particular they should not compete in strenuous physical games. Angina is best treated with f3- blockade because vasodilators such as glyceryl trinitrate or isosorbide dinitrate may aggravate exertional syncope. Antibiotic prophylaxis against infective endocarditis is essential.

Irrespective of symptoms, aortic valve replacement with a prosthetic or tissue valve is recommended when aortic stenosis is severe. Cardiopulmonary bypass is necessary to achieve this. Provided that the valve is not severely deformed or heavily calcified, critical aortic stenosis in childhood or adolescence can be treated by valvotomy (performed under direct vision by the surgeon or by balloon dilatation using X-ray visualization). This produces temporary relief from the obstruction. Aortic valve replacement will usually be needed a few years later. Balloon dilatation (valvuloplasty) has been tried in adults, especially in the elderly, as an alternative to surgery. Generally results are poor and such treatment is reserved for patients unfit for surgery or as a ‘bridge’ to
surgery (i.e. to improve them for surgery).

AORTIC REGURGITATION

The most common causes of aortic regurgitation are rheumatic fever and infective endocarditis complicating a previously damaged valve. This can be a congenitally abnormal valve (e.g. a bicuspid valve) or one damaged by rheumatic fever. There are numerous other causes and associations. The majority of patients with aortic regurgitation are men (75%), but rheumatic aortic regurgitation occurs more commonly in women.

PATHOPHYSIOLOGY

Aortic regurgitation is reflux of blood from the aorta through the aortic valve into the left ventricle during diastole. If net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase, and consequently the left ventricular size must enlarge. Because of the aortic run-off during diastole, diastolic blood pressure falls and coronary perfusion is decreased. In addition, the larger left ventricular size is mechanically less efficient so that the demand for oxygen is greater and cardiac ischaemia develops.

Causes and associations of aortic regurgitation.

Causes and associations of aortic regurgitation.

SYMPTOMS

In aortic regurgitation significant symptoms occur late and do not develop until left ventricular failure occurs. As with mitral regurgitation, a common symptom is ‘pounding of the heart’ because of the increased left ventricular size and its vigorous pulsation. Angina pectoris is a frequent complaint. Varying grades of dyspnoea occur depending on the extent of left ventricular dilatation and dysfunction. Arrhythmias are relatively uncommon.

SIGNS

The signs of aortic regurgitation are many and are due to the hyperdynamic circulation, reflux of blood into the left ventricle and the increased left ventricular size. The pulse is bounding or collapsing. The following signs, which are rare, also indicate a hyperdynamic circulation:
QUINCKE’S sIGN-capillary pulsation in the nail beds DE MUSSET’S SIGN-head nodding with each heart beat
DUROZIER’S SIGN-systolic bruit over the femoral arteries when the stethoscope is lightly applied
PISTOL SHOT FEMORALs-a sharp bang heard on auscultation over the femoral arteries in time with each heart beat.
The apex beat is displaced laterally and downwards and is thrusting in quality. On auscultation there is a high-pitched diastolic murmur running from the aortic component of the second heart sound.
It is loudest in early diastole and is heard best at the lower left sternal edge or the cardiac apex .

INVESTIGATION

Chest X-ray

The chest X-ray features are those of left ventricular enlargement and possibly of dilatation of the ascending aorta. The ascending aortic wall may be calcified in syphilis and the aortic valve may be calcified if valvular disease is responsible for the regurgitation.

ECG

The ECG appearances are those of left ventricular hypertrophy due to ‘volume overload’, i.e. tall R waves and deeply inverted T waves in the left-sided chest leads, and deep S waves in the right-sided leads. Normally, sinus rhythm is present.

Echocardiogram

The echocardiogram demonstrates vigorous cardiac contraction and a dilated left ventricle. The aortic root may also be enlarged. Diastolic fluttering of the mitral leaflets or septum occurs in severe aortic regurgitation (producing the Austin Flint murmur. The regurgitant jet can be detected by CW Doppler.

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 regurgitation.

TREATMENT

The underlying cause of aortic regurgitation (e.g. syphilitic aortitis or infective endocarditis) may require specific treatment. The treatment of aortic regurgitation usually requires aortic valve replacement but the timing of surgery is important.
Because symptoms do not develop until the myocardium fails and because the myocardium does not recover fully after surgery, it is important to operate before significant symptoms occur. The timing of the operation is best determined according to haemodynamic, echocardiographic or nuclear angiographic criteria. Both mechanical prostheses and tissue valves are used. Tissue valves are preferred in the elderly and when anticoagulants must be avoided, but are contraindicated in children and young adults because of the rapid calcification and degeneration of the valves.
Antibiotic prophylaxis against infective endocarditis is necessary even if a prosthetic valve replacement has been performed.

TRICUSPID STENOSIS

This uncommon valve lesion, which is seen much more often in women than in men, is usually due to rheumatic heart disease and is frequently associated with mitral and/or aortic valve disease. Tricuspid stenosis is also seen in the Carcinoid syndrome.

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 the 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.

SIGNS

If the patient remains in sinus rhythm, which is unusual, there is a prominent jugular venous a wave. This presystolic 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.

INVESTIGATION

Chest X-rayOn the chest X-ray there may be a prominent right atrial bulge.

ECG

The enlarged right atrium may be manifest on the ECG by peaked, tall P waves (2:3 mm) in lead 2.

Echocardiogram

The echocardiogram may show a thickened and immobile tricuspid valve, but this is not so clearly seen as an abnormal mitral valve.

Cardiac catheterization

This demonstrates a diastolic pressure gradient between the right atrium and the right ventricle. Contrast injection will demonstrate a large right atrium.

TREATMENT

Medical management consists of diuretic therapy and salt restriction. Tricuspid valvotomy is occasionally possible, but tricuspid valve replacement is often necessary. Other valves usually also need replacement because tricuspid valve stenosis is rarely an isolated lesion.

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