Systolic heart failure

Systolic heart failure

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Heart failure

Definition

The heart cannot produce enough blood flow to satisfy the body�s needs or can do so only with difficulty.

Aetiology

Heart dysfunction may be either systolic or diastolic.

Systolic dysfunction: systole is the act of contraction by  the heart and is governed by 2 cardiac properties (1) contractility (the ability of the muscle to contract) and (2) afterload (the force against which the heart is pumping).

     Decreased contractility: myocardial infarction, valvular heart disease, hypertension, cardiomyopathy.

     Increased afterload such as hypertension, aortic valve stenosis.

Diastolic dysfunction: diastole is the phase of relaxation of the heart muscles after pumping and is governed by active and passive properties. Active relaxation occurs early in diastole when Ca++ is pumped outside the myocardium. It is active because it utilizes energy and is impaired by ischemia. Passive relaxation occurs when the mitral and tricuspid valves open thus letting the blood pooled in the atria enter the ventricles. It is impaired by increased stiffness of the ventricles as occurs in concentric hypertrophy and in infiltrative diseases of the heart.

Clinical suspicion

Heart failure is suspected by clinical presentation. Symptoms include shortness of breath on effort, palpitations, syncope, cough, swelling of the legs. Radiographic evidence of large heart size and pulmonary vasculature redistribution strengthens the suspicion.

Diagnosis

The diagnosis should be confirmed by echocardiography, radionuclide ventriculography, or cardiac catheterization with left ventriculography.

Treatment

The ideal treatment would be to remove the cause, if not then attempt at removing the precipitating cause however most of the time this is not possible.



   
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Systolic heart failure

General strategy of management if patient's blood pressure >90/60

Vasodilators

These dilate the vessels in the body.

Angiotensin - converting enzyme inhibitors (ACE inhibitors)

1st line therapy for the entire spectrum of congestive heart failure, whether asymptomatic or severe; unless contraindicated.

Rationale: heart failure is accompanied by compensation mechanisms one of which is vasoconstriction. This increases venous return and arterial tone which maintains blood pressure and perfusion. However, it also increases impedance to ventricular ejection (afterload). This results in a vicious cycle in which decreased stroke volume results in more intense vasoconstriction which further decreases stroke volume. Hence vasodilator therapy breaks the cycle. vasodilator therapy was the only therapy in congestive heart failure found to prolong survival associated with improved quality of life.

Contraindications: not given in patients with predominant diastolic failure or with those in which heart failure results from aortic stenosis / mitral stenosis. Not given in patients with impaired renal function or with bilateral renal artery stenosis. Do not give concomitant potassium sparing diuretic with angiotensin converting enzyme and monitor blood pressure carefully when initially instituted in combination with a diuretic.

ACE inhibition should be started 72 h after any acute myocardial infarction with symptoms or echocardiographic evidence of systolic dysfunction.

ACE inhibition should not be started within the first 24 h of an acute myocardial infarction.

Dose and type: start with small doses (1/4 to 1/2 a tablet) of ACE inhibitors and give in sitting position to avoid first dose hypotension. Gradually titrate the dose every other dosing schedule to reach 3 tablets daily (maximum dose is 50mg tds).