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Back to Cardiovascular Diseases

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).

Isosorbide dinitrate ? hydralazine:

The combination of these two drugs also improves survival. They are given as a 2nd line in patients who do not tolerate ACE inhibitors.

Diuretics

If congested diuretics are beneficial.

Digoxin

If uncontrolled by above or concomitant supraventricular arrhythmias.
other inotropics.

Dose:

0.25mg daily maintenance dose to be monitored by serum levels. It is reduced in the elderly and in individuals with short stature and those with renal insufficiency.

If the patients is hypotensive

Sympathomimetic amines and amrinone (see below).

Refractory heart failure

When the response to ordinary treatment is inadequate, heart failure is considered to be refractory. Before assuming that this condition simply reflects advanced, perhaps preterminal, myocardial depression, careful consideration must be given to several possibilities: (1) an underlying and overlooked cause of the heart disease that may be amenable to specific surgical or medical therapy, such as silent aortic or mitral stenosis, constrictive pericarditis, infective endocarditis, hypertension, or thyrotoxicosis, (2) one or a combination of the precipitating causes of heart failure, such as pulmonary or urinary tract infection, recurrent pulmonary emboli, arterial hypoxemia, anemia, or arrhythmia, and (3) complications of overly vigorous therapy, such as digitalis intoxication, hypovolemia, or electrolyte imbalance.

The combination of an intravenously administered vasodilator, such as sodium nitroprusside, along with a potent sympathomimetic amine, such as dopamine or dobutamine, often results in an additive effect, raising cardiac output and lowering filling pressure. Intravenous amrinone, sometimes accompanied by the administration of a converting enzyme inhibitor, also may be useful in patients with refractory heart failure.

Sympathomimetic amines

Dopamine, the naturally occurring immediate precursor of norepinephrine, has a combination of actions which makes it particularly useful in the treatment of a variety of hypotensive states and congestive heart failure. At very low doses, i.e., 1 to 2 (ug/kg)/min, it dilates renal and mesenteric blood vessels through stimulation of specific dopaminergic receptors, thereby augmenting renal and mesenteric blood flow and sodium excretion. In the range of 2 to 10 (ug/kg)/min, dopamine stimulates myocardial beta receptors but induces relatively little tachycardia, while at higher doses it also stimulates alpha-adrenergic receptors and elevates arterial pressure.

Dobutamine is a synthetic catecholamine which acts on beta1, beta2, and alpha receptors. It exerts a potent inotropic action, has only a modest cardioaccelerating effect, and lowers peripheral vascular resistance, but since it simultaneously raises cardiac output, it has little effect on systemic arterial pressure. Dobutamine, given in continuous infusions of 2.5 to 10 (ug/kg)/min, is useful in the treatment of acute heart failure without hypotension. Like the other sympathomimetic amines, it may be particularly valuable in the management of patients requiring relatively short-term inotropic support--up to 1 week--in conditions which are reversible, such as the cardiac depression which sometimes follows open-heart surgery, or in patients with acute heart failure who are being prepared for operation. Adverse effects include sinus tachycardia, tachyarrhythmias, and hypertension.

A major problem with all sympathomimetics is the loss of responsiveness, apparently due to "downregulation" of adrenergic receptors, which becomes evident within 8 h of continuous administration. This problem may be managed by intermittent therapy.

Cardiac transplantation: improved survival from 50% for 1yr to 50% 5yrs.

Diastolic heart failure

Diuretics if congested
Ca++  channel blockers in some cases
NO ROLE for digoxin.

The rapid relief of acute myocardial ischemia is often effective when diastolic dysfunction is secondary to this condition. The reduction in heart rate caused by beta-blockers has several beneficial on diastolic function, including a prolongation of the filling period and an amelioration of ischemia. calcium channel blockers, especially Verapamil, have been shown to accelerate ventricular relaxation in patients with hypertrophic cardiomyopathy and have been reported to be useful in the treatment of diastolic dysfunction characteristic of this condition. Other beneficial mechanisms are reduction in heart rate, control of hypertension, reduced microvascular ischemia and oxygen demand, amelioration of intracellular calcium overload and regression of left ventricular hypertrophy.

Ventricular filling pressure and secondary venous congestion may be reduced by restriction of sodium intake and the administration of diuretics and venodilators. Even in the absence of ischemia, nitrates, by reducing preload, are useful in managing diastolic dysfunction and in the treatment and prevention of consequent severe pulmonary congestion. Nitroglycerin may be administered intravenously or sublingually in emergency situations, and long acting nitrates, such as isosorbide dinitrate, are often effective in the long term. In the long term, however, excessive preload reduction should be avoided because these patients often require higher-than-normal filling pressures to maintain an adequate stoke volume.

The maintenance of heart rhythm and rate is of critical importance. Tachycardia, whatever the underlying mechanism, must be controlled, thereby increasing the fraction of each cardiac cycle available for ventricular filling. Maintenance of sinus rhythm with synchronized atrioventricular sequential pacing may be crucial in permitting atrial augmentation of ventricular filling. Digoxin and other inotropic agents have no established place in these patients with relatively well preserved ejection fraction, and could, in principle, have an adverse effect in this group. Exercise training induces significant improvement in exercise capacity in patients with dilated cardiomyopathy and a pattern of abnormal left ventricular relaxation. Finally, it has been shown that endogenous nitric oxide released from the coronary microcirculation selectively enhances left ventricular relaxation in the isolated ejecting guinea pig heart. These findings may lead to a new therapeutic approach to diastolic heart failure, with treatments aimed at the coronary microcirculation.

The American College of Cardiology / American Heart Association task force divides pharmacologic treatment into three classifications for the management of diastolic HF : Class I refers to drugs that are always indicated, such as diuretics and nitrates, and drugs suppressing atrioventricular conduction and anticoagulation if atrial fibrillation is present. Class II agents are " acceptable "; however, their efficacy is uncertain. These include calcium channel blockers, beta-blockers, ACE inhibitors and anticoagulation in patients with intracardiac thrombus. Class III drugs are not indicated and include drugs with positive inotropic effects.

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