It is clinically useful to divide heart failure into the syndromes of right, left and biventricular (congestive) cardiac failure, but it is rare for any part of the heart to fail in isolation.
Right heart failure
This syndrome occurs in association with:
• Chronic lung disease (cor pulmonale)
• Pulmonary embolism or pulmonary hypertension
• Tricuspid valve disease
• Pulmonary valve disease
• Left-to-right shunts, e.g. atrial or ventricular septal defects
• Isolated right ventricular cardiomyopathy
• Mitral valve disease with pulmonary hypertension
The most frequent cause of right heart failure is secondary to left heart failure.
SYMPTOMS include fatigue, breathlessness, anorexia and nausea and relate to distension and fluid accumulation in areas drained by the systemic veins.
PHYSICAL SIGNS are usually more prominent than the symptoms, with:
• Jugular venous distension (± v waves of tricuspid regurgitation)
• Tender smooth hepatic enlargement
• Dependent pitting oedema
• Development of free abdominal fluid (ascites)
• Pleural transudates (commonly right-sided)
Dilatation of the right ventricle produces cardiomegaly and may give rise to functional tricuspid regurgitation. Tachycardia and a right ventricular third heart sound are usual.
Left heart failure
• Ischaemic heart disease (commonest)
• Systemic hypertension (chronic or ‘malignant’)
• Mitral and aortic valve disease
Mitral stenosis causes left atrial hypertension and signs of left heart failure but does not itself cause failure of the left ventricle.
SYMPTOMS are predominantly fatigue, dyspnoea, orthopnoea and paroxysmal dyspnoea.
PHYSICAL SIGNS are few and not prominent until a late stage or if the ventricular failure is acute. Cardiomegaly is demonstrable with a displaced and often sustained apical impulse. Auscultation reveals a left ventricular third or fourth heart sound that, with tachycardia, is described as a gallop rhythm. Dilatation of the mitral annulus results in functional mitral regurgitation. Crackles are heard at the lung bases. In severe left heart failure the patient has pulmonary oedema. In this circumstance a chest X-ray is the most useful investigation. Rarely the cause of left ventricular failure is apparent, e.g. ventricular aneurysm at the site of previous infarction.
Biventricular failure (congestive)
This term is used variously but is best restricted to cases where right heart failure is a result of pre-existing left heart failure. The physical signs are thus a combination of the above syndromes cute heart failure Acute failure of the heart most commonly occurs in the setting of acute myocardial infarction when there is extensive loss of ventricular muscle. The condition may also occur with rupture of the interventricular septum producing a ventricular septal defect, or due to acute valvular regurgitation. Common examples of valvular regurgitation are papillary or chordal rupture producing mitral regurgitation or sudden aortic valve regurgitation in infective endocarditis. Other causes of acute heart failure include obstruction of the circulation due to acute pulmonary embolus and cardiac tamponade. In each case ~evere Cardilw failure can occur with a relatively normal heart size.
High-output heart failure
The heart may not be able to meet the demands placed on it in conditions such as anaemia, thyrotoxicosis, beriberi and Gram-negative septicaemia. This form of heart failure presents in much the same manner as low-output states but is associated with tachycardia and a gallop rhythm. Patients are often warm with distended superficial veins. Unlike low-output failure the oxygen content of systemic venous blood is high owing to the delivery of large amounts of arterial blood to non-metabolizing tissues.
Factors aggravating or precipitating heart failure
Any factor that increases myocardial work may aggravate existing heart failure or initiate failure. These factors must be carefully considered in patients who present with heart failure. The most common are arrhythmias, anaemia, thyrotoxicosis, pregnancy, infective endocarditis, pulmonary infection or adjustment of heart failure therapy.
The diagnosis ‘heart failure’ is inadequate and a cause should be determined. In many cases the cause will be evident from the clinical history and examination. Investigations are determined by the suspected cause of heart failure and include the following.
CHEST X-RAy/ECG for cardiac size and evidence of ischaemia or hypertension
ECHOCARDIOGRAPHY for valvular disease and assessment of left ventricular function
BLOOD ·TESTS: full blood count, liver biochemistry, urea and electrolytes
CARDIAC ENZYMES IN ACUTE heart failure to diagnose myocardial infarction
CARDIAC CATHETERIZATION, FunctionaIJprognostic
EXERCISE TESTING and a 6 min exercise wal
ESTI G A.’D STRESS RADIONUCLIDE ANGIOGRAPHY (MUGA)-ejection fraction, regional wall motion abnormality
24-48-HoUR AMBULATORY ECG MONITORING-if arrhythmia suspected
Treatment of heart failure
Treatment of chronic heart failure is aimed at relieving symptoms, retarding disease progression and improving survival. The management of heart failure requires that any factor aggravating the failure should be identified and treated. Similarly the cause of heart failure must be elucidated and where possible corrected. Nursing care of the mouth and pressure areas is necessary and patients should be nursed in a comfortable upright position.
Reduction of physical activity
Bed rest reduces the demands of the heart and is useful for a few days. Migration of fluid from the interstitium promotes a diuresis, reducing heart failure. Prolonged bed rest may, however, lead to development of deep vein thrombosis; this can be avoided by daily leg exercises, low-dose subcutaneous heparin and elastic support stockings.
Large meals should be avoided and if necessary weight reduction instituted. Salt restriction is important and foods rich in salt or added salt in cooking and at the table should be avoided. A low-sodium diet is unpalatable and of questionable value. Alcohol has a negatively inotropic effect and patients should abstain.
The pharmacological management of heart failure relies on the following categories of drugs: diuretics, vasodilators, positive inotropic agents including digitalis glycosides, and antiarrhythmic agents.
These act by promoting the renal excretion of salt and water by blocking tubular reabsorption of sodium and chlo ride. The resulting loss of fluid reduces ventricular filling pressures (pre-load) and produce consistent haemodynamic and symptomatic benefits in patients with heart failure and rapidly relieve dyspnoea and peripheral oedema. The intravenous administration of loop diuretics such as frusemide relieves pulmonary oedema rapidly by means of arteriolar vasodilatation reducing after-load, an action that is independent of its diuretic effect. Diuretics act in different ways.
Loop DIURETICS such as frusemide and bumetanide act by reducing sodium and chloride reabsorption in the ascending limb of the loop of Henle. They cause a brisk and generally short-lived diuresis as the concentrating power of the kidney is reduced. These agents also produce marked potassium loss and promote hyperuricaemia.
THIAZIDE DIURETICS such as bendrofluazide have a mild diuretic effect and act on the distal convoluted tubule, reducing sodium reabsorption. Potassium excretion is enhanced. Metolazone is a powerful thiazide producing profound diuresis acting synergistically with loop diuretics. This combination is useful in treating severe and resistant heart failure.
POTASSIUM-SPARING DIURETICS. Spironolactone is a specific competitive antagonist to aldosterone, producing a weak diuresis but with a potassium-sparing action. Amiloride and triamterene act at the distal tubule preventing potassium secretion in exchange for sodium.
These drugs are weak diuretics but are useful in combination with more powerful loop diuretics. They should be avoided in the presence of renal failure. Although heart failure symptoms are improved by diuretic treatment alone, they do not provide any survival benefit. In addition, their use may be complicated by over-diuresis, electrolyte depletion (potassium and magnesium) which may predispose to the development of lethal ventricular arrhythmias, hyperkalaemia (potassium-sparing diuretics) and other metabolic disturbances (hyperuricaemia and dyslipidaemia).
Diuretics and sodium restriction serve to activate the renin-angiotensin system, promoting formation of angiotensin (a potent vasoconstrictor) and an increase in afterload. A variety of other neural and hormonal reactions also serve to increase pre-load and after-load. These compensatory mechanisms are initially beneficial in maintaining blood pressure and redistributing blood flow, but in the later stages of heart failure they are deleterious and reduce cardiac output. The high venous pressures found in heart failure are also related to the activation of the sympathetic nervous system and the presence of circulating vasoconstrictors, thus shifting the Starling curve to the right.
Several large controlled trials, e.g. CONSENSUS an OL VD, have established the benefit of vasodilator therapy in heart failure. The trials have shown that in addition to producing considerable symptomatic improvement in patients with symptomatic heart failure, vasodilators markedly improve prognosis and limit the development of progressive heart failure. Whether there are significant Clinical differences between treatment with different angiotensin-converting enzyme (ACE) inhibitors or between ACE inhibitors and combined nitrate/hydralazine treatment remains uncertain. The recent SAVE study has confirmed the benefit of ACE inhibitor therapy in patients with asymptomatic heart failure following myocardial infarction in whom the development of overt heart failure was reduced by this treatment.
ARTERIOLAR VASODILATORS. Drugs such as a-adrenergic blockers (e.g. prazosin) and direct smooth-muscle relaxants (e.g. hydralazine) are potent arteriolar vasodilators. Calcium antagonists , e.g. nifedipine, are also used and reduce afterload. The reduction in after-load causes an increase in cardiac output. Any tendency to hypotension is usually offset by the increased output.
VE ODILATORS . Short- and long-acting nitrates (e.g. glyceryl trinitrate and isosorbide mononitrate) act by reducing pre-load and lowering venous pressure with resulting reduction in pulmonary and dependent oedema. Reduction of filling pressure does not significantly enhance cardiac output because the heart is operating on the flat portion of the ventricular filling curve. With chronic use, tolerance develops with loss of efficacy and consequent worsening of heart failure.
ANGIOTENSIN-CONVERTI G ENZYME INHIBITORS. ACE inhibitors lower systemic vascular resistance, venous pressure and reduce levels of circulating catecholarnines, thus improving myocardial performance. The beneficial haemodynamic effect of these drugs appears to be independent of their inhibition of ACE as they are equally effective when plasma renin activity is normal.
These drugs should be carefully introduced to patients with heart failure because of the risk of first-dose hypotension. This is a particular risk in patients who are receiving large doses of diuretics and in the presence of hyponatraemia «130 mmol litre “). In such cases a test dose of ACE inhibitor should be commenced and the preceding diuretic doses omitted. Some of these agents are prodrugs (e.g. enalapril) and require conversion to the active metabolite (enalaprilat) by liver enzymes; these drugs have a delayed onset of action and first-dose hypotension may not occur for several hours. Prod rugs are best avoided if heart failure results in significantly altered hepatic function. Serious hypotension may result in acute renal failure. Concomitant potassium-sparing diuretics should be discontinued, as ACE inhibitors tend to promote potassium retention.
Recently, several orally active positive inotropic drugs have become available, supplementing digoxin and those currently available for intravenous use. They can be classified as follows:
• Digitalis glycosides
• f3-Adrenergic agonists
• Phosphodiesterase inhibitors
Efficacy of these agents is variable and must be judged both in terms of objective and symptomatic improvement on an individual patient basis. DIGITALIS GLYCOSIDES. Digitalis glycosides are no longer extensively used in the management of heart fail ure, although they remain effective positive inotropic agents. Digoxin usage is of particular benefit in congestive heart failure associated with atrial fibrillation when the rapid ventricular response is effectively controlled. Studies have suggested that digoxin may also be beneficial in patients with heart failure and sinus rhythm. The withdrawal of digoxin in these patients is associated with clinical deterioration and increased hospitalization. Further studies are currently underway to determine if digoxin provides useful adjunctive therapy in conjunction with ACE inhibitors. Digoxin is the most common glycoside in use with a half-life of approximately 36 hours. It is highly protein-bound, making it liable to drug interaction. Ninety per cent is excreted unchanged in the urine, causing accumulation in renal failure. Digoxin acts as a positive inotrope by competitive inhibition of Na+,K+ ATPase, producing high intracellular levels of sodium. The intracellular sodium is exchanged for extracellular calcium. High intracellular levels of calcium ions allow increased binding of the contractile proteins actin and myosin, enhancing the force of cardiac contractility. Digoxin is usually administered orally (1 mg loading and 0.125-0.25 mg daily). In elderly patients and in patients with impaired renal function digoxin may accumulate, resulting in serious toxicity. Careful titration of the dose is important with monitoring of trough serum levels (1.3-2.6 nmollitre -I) and avoidance of hypokalaemia. Patients with hypothyroidism are particularly sensitive to digitalis glycosides. In patients with fluctuating renal function the administration of the liver-metabolized digitoxin may be preferable.
With improvement in formulation, digoxin toxicity has become less problematic but is prone to occur in the elderly and in patients with renal impairment. The most common features of digoxin toxicity are:
• Anorexia, nausea, altered vision
• Arrhythmia, e.g. ventricular premature beats especially bigeminy, ventricular tachycardia and AV block
• Digoxin levels >2.5 ng ml-1.
Digoxin toxicity is treated by discontinuing the drug, restoration of serum potassium levels and management of arrhythmias. Digoxin antibodies (Fab fragments) are a specific antidote that are useful for life-threatening toxicity.
f3-ADRENERGIC AGONISTS. Dopamine and dobutamine are adrenergic agonists but are only effective intravenously. Dobutamine is a selective agonist of the f31- receptor, increasing intracellular cyclic AMP, which in turn increases calcium availability for the contractile process. Dopamine is a less potent inotrope than dobutamine but because of its unselective action on the adrenergic system it also improves renal perfusion. Xamoterol is a f3-blocking drug with high intrinsic sympathomimetic activity (ISA) and is effective in improving cardiac performance. Xamoterol competes competitively with endogenous catecholamines at the f31-receptor. At states of low sympathetic tone (rest) this produces a positive inotropic effect together with lowering of filling pressures.
At states of high sympathetic tone (e.g. exercise), xarnoterol produces a f3-blocking effect, blunting the chronotropic response. In mild to moderate heart failure xamoterol (200 mg twice daily) is as effective as intravenous dobutamine in improving cardiac performance. Chronic high levels of circulating catecholamines in severe heart failure may lead to down-regulation of the f3-receptors;
the administration of xamoterol to these patients may precipitate acute heart failure.
PHOSPHODIESTERASE INHIBITORS. Amrinone, milrinone and enoximone are in a class of so-called ‘inodilator’ drugs that act by inhibiting phosphodiesterase, thus preventing breakdown of cyclic AMP. Accumulation of cAMP produces an increase in contractility and also peripheral vasodilatation. The Starling curve is shifted upwards. Although these agents are effective in improving myocardial performance acutely, there is evidence that they have a deleterious effect on myocardial cells when administered in the long term with an increased mortality. They are not often used.