Heart failure is a pathophysiological state in which an abnormality of cardiac function results in failure of the heart to pump and maintain adequate blood supply for the metabolic requirements of the body.
Not all patients with congestive cardiac failure have myocardial failure. Heart failure may occur because the normal heart is faced with an excessive load that exceeds compensatory mechanisms or because ventricular filling is impaired. Conversely, myocardial failure (in the early stages) may be present without overt congestive heart failure, the latter only occurs once myocardial dysfunction is far advanced and compensatory mechanisms, including chamber dilatation, vasoconstriction, and fluid retention, come into play.
Magnitude of the Problem:
Congestive cardiac failure is a common ailment with a variety of causes. An estimated 3.5 to 4 million Americans have chronic congestive cardiac failure. Data from the Framingham study suggest that the incidence (i.e. the number of new cases per year) averages 3.7 per 1000 few men and 2.5 per 1000 for women. The incidence of cardiac failure more than doubles for each decade of life from 45 to 75 years.
Pathophysiology of Congestive Cardiac Failure:
It is convenient to consider separately the consequences of impaired function of the left and the right sides of the heart. Left sided failure is characterised by a reduction in effective left ventricular output for a given pulmonary venous or left atrial pressure, or conversely, an increase in the left atrial pressure needed to sustain a given cardiac output.
An acute increase in left atrial pressure may cause pulmonary congestion or pulmonary oedema but with more gradual increase in left atrial pressure there tends to be, reflex pulmonary vaso-constriction which protects the patient from pulmonary oedema at the cost of increasing pulmonary hypertension.
In right-sided cardiac failure there is similarly a reduction of right ventricular output for a given right atrial pressure or a need for an increased right atrial pressure to maintain a given output. The increased right atrial pressure is manifested as an increase in Jugular venous pressure and as hepatic engorgement.
In both left and right sided cardiac failure the body attempts to compensate for the drop in cardiac output by activation of the sympathetic nervous system, causing tachycardia and vasoconstriction, and retention of salt and water by the kidneys. Fluid retention is accompanied by the development of oedema, in pure left sided failure this is principally pulmonary.
In right sided failure or in a combination of right and left sided failure, most of the oedema is peripheral. It affects the ankles in ambulant patients and the thighs or sacrum in bed ridden patients. Considerable quantities of peripheral oedema may accumulate without causing distress. Massive accumulation of fluid may cause ascites or pleural effusion.
Left Heart Failure:
Causes:
(1) Primary disease of the left ventricle such as myocardial infarction, cardiomyopathy and myocarditis.
(2) Systolic overload of the left ventricle from systemic hypertension, aortic stenosis and hypertrophic obstructive cardiomyopathy.
(3) Diastolic overload of left ventricle from mitral and aortic incompetence, ventricular septal defect and persistent ductus arteriosus.
(4) Restriction of the left ventricle due to localised constrictive pericarditis externally and endomyocardial fibrosis internally.
(5) Left atrial failure from mitral stenosis.
Symptoms:
The earliest symptom is dyspnoea on effort. Eventually dyspnoea occurs at rest and the patient is distressed if he lies flat i.e. orthopnoea. Finally paroxysmal cardiac dyspnoea appears, usually nocturnal, and is commonly associated with bronchospasm i.e. cardiac asthma. It is not clear why these attacks are more common at night.
Acute pulmonary oedema results in severe dyspnoea, sweating, and cough associated with copious, frothy sputum, occasionally pink. Infection is apt to occur and frequently precipitates failure. Occasionally paroxysmal cough on effort is a symptom of left heart failure.
Haemoptysis may be due to pulmonary infection or congestion, but if severe a pulmonary infarct should be suspected. Profuse sweating is an early characteristic of left sided failure. The reduction in forward flow may give rise to fatigue and reduction in renal flow may produce diurnal oliguria with nocturnal diuresis.
Signs:
The signs of left heart failure are few and chronic left ventricular failure is the commonest missed cardiac diagnosis.
(1) Left ventricular hypertrophy.
(2) Triple rhythm — If it is presystolic it is less ominous, being usually associated with systolic overload of the left ventricle. Protodiastolic triple rhythm, due to exaggeration of the third heart sound, is common in the diastolic ventricular overload of advanced heart failure and is therefore more ominous. Tachycardia is always well marked.
(3) Basal rales are present with often expiratory wheezing. In acute pulmonary oedema medium to loud bubbling rales are heard all over the lungs.
(4) Pulsus alternans (alternate large and small pulse) which usually needs a sphygmomanometer for its detection implies that the heart is labouring.
(5) Cheyne-stokes respiration — A periodic form of breathing characterised by waxing and waning of the depth of respirations and regularly recurring periods of apnoea may occur.
(6) Signs of causative disease — e.g. hypertension.
Right Heart Failure:
Causes:
(1) Systolic overload of right ventricle due to pulmonary hypertension of whatever cause. Congestive heart failure is most commonly secondary to left heart failure. The next most common cause is chronic cor pulmonale.
(2) Systolic overload of the right ventricle due to obstruction of the right ventricular cavity given rise to pure right ventricular failure e.g. pulmonary valvular and infundibular stenosis.
(3) Diastolic overload of the right ventricle. Atrial septal defect is relatively common. But tricuspid incompetence and pulmonary incompetence are rare as causes and almost invariably secondary to other lesions.
(4) Restriction of the right ventricle—localised constrictive pericarditis on the outside of the ventricle and endomyocardial fibrosis on the inside, can both lead to right ventricular failure.
(5) Right atrial failure rarely follows tricuspid stenosis and a right atrial tumour.
Symptoms:
These are due mainly due to congestion. Pain may be experienced over right hypochondrium, commonly aggravated on exertion — so called hepatic angina. The patient may notice that his liver is tender and his abdomen has become distended. Jaundice may appear when cirrhosis develops. Congestion of the gut results in anorexia and sometimes vomiting.
Oedema is not an early or reliable sign of heart failure. It may be minimal with a high venous pressure and may be massive when the venous pressure not very high. Dyspnoea is usually present even in the absence of pulmonary congestion. The low cardiac output gives rise to fatigue, sluggish mental state and oliguria.
Signs:
(1) Raised venous pressure is invariable and is best seen in the neck. Pressure on the liver will produce elevation of the jugular venous pressure, the hepatojugular reflex.
(2) Hepatomegaly is present and in tricuspid incompetence systolic pulsation over liver may be appreciated.
(3) Oedema: the erect position favours collection of fluid in feet, ankles, lower parts of legs, whereas recumbent position favours accumulation of fluid in sacral region. If oedema is severe it may be associated with ascites, hydrothorax and hydropericardium.
(4) Peripheral cyanosis may be due to slow peripheral circulation.
(5) Signs of right ventricular or combined ventricular enlargement are present and triple rhythm is common. Tachycardia is always present.
A right ventricular protodiastolic triple rhythm carries a more serious prognosis than atrial gallop. A murmur of tricuspid incompetence, usually functional is common too.
Investigation of Heart Failure:
(1) Skiagram Chest:
The silhouette of the heart will vary with the cause of the heart diseases, prominence of upper lobe veins and hilar congestion an early sign of left ventricular failure. Opacities feed to spread in a butterfly manner from the hila. In acute pulmonary oedema with more extensive oedema diffuse mottling of lungs will be seen.
(2) ECG:
Will show changes hypertrophy, infarction, strain pattern?
(3) Non-Invasive Methods:
(a) Measurement of the systolic time interval by using simultaneous records of the ECG, Phonocardiogram and carotid tracing for evaluation of left ventricular function.
(b) Apex cardiography will demonstrate various types of triple rhythm and other abnormal features.
(c) Echocardiography besides evaluation of left ventricular function (ejection fraction) helps in diagnosis of basic problem e.g. cardiomyopathy of various types, valvular heart disease and L.V. aneurysm.
(d) Radionuclide studies — multiple gated acquisition study (MUGA) using Technetium 99 helps in seeing the anatomy and function of the heart and in particular the assessment of left ventricular function and dyskinetic movement.
Clinical Approach to Management of Congestive Cardiac Failure:
Three general principles apply to the treatment of heart failure:
(1) Removal of the underlying cause.
(2) Removal of the precipitating cause.
(3) Control of the congestive heart failure state.
(4) Be sure that bronchial asthma is excluded. L.V.F. may be diagnosed by mistake when patient has bronchial asthma.
(1) Removal of the underlying cause:
Every patient who presents with congestive cardiac failure should be suspected of having a treatable underlying condition until proven otherwise. Practically, this entails search for a surgically correctable structural abnormality (e.g., congenital cardiac malformation, acquired valvular lesion, localised large ventricular aneurysm) or a medically treatable condition (e.g., infective endocarditis, rheumatic activity and hypertension).
(2) Removal of the precipitating cause:
The recognition, prompt treatment and, if possible, prevention of precipitating factors that produce or exacerbate heart failure are critical to successful management of congestive cardiac failure.
Common precipitating factors include:
(1) Inappropriate reduction of therapy or dietary excesses of sodium.
(2) Tachy or bradyarrythmias.
(3) Systemic infection.
(4) Pulmonary embolism.
(5) High-output states (anaemia, pregnancy, and thyrotoxicosis).
(6) Administration of cardiac depressant drugs (Beta-adrenergic blocking agents, verapamil, disopyramide).
(7) Development of an unrelated illness (e.g., renal failure, hepatic failure, prostatic obstruction).
(8) Injudicious fluid administration.
Control of congestive failure state:
(1) Increase myocardial contractility and increase cardiac output.
(2) Decrease congestion by reducing preload.
(3) Decrease after load and increase cardiac output.
(4) Decrease workload by agents which alter preload and after load.
It is more convenient however to discuss the treatment of chronic cardiac failure under three principal classes of therapeutic agents, which may be employed: digoxin, diuretics, and vasodilator drugs.
Digoxin:
For over 200 years, the place of cardiac glycosides in the treatment of congestive heart failure is secured. Digitalis has direct action on the myocardium. It improves the contractility of a failing heart. By its action on the AV node it slows the heart rate. The other effects, e.g., lowering of venous pressure, relief of hepatic congestion and increase of urinary output are indirect effects.
While it appears that some-patients with heart failure do not require digitalis when they have normal sinus rhythm, the majority do benefit by chronic digitalis therapy. In fact the majority of patients with heart failure should receive digitalis. A good response often occurs in patients with hypertensive heart disease, valvular heart disease, heart failure due to ischaemic heart disease and congenital heart disease with left to right shunt. A less satisfactory response may be noted in patients whose heart failure is due to acute myocardial infarction, chronic cor pulmonale, myocarditis, chronic constrictive pericarditis.
Digoxin should be given orally unless the clinical situation demands more rapid action. The usual oral loading dose for adults and children over 10 years of age is 1.0 mg. The usual oral maintenance dose is 0.25 mg each day, six days in a week. Smaller doses may be effective for elderly patients.
When the clinical situation does not demand speed, it may be preferable to start therapy with an average maintenance daily dose. This gradual method achieves an adequate steady-state: plateau in about 6 to 7 days. The maximum speed which may be obtained by oral dose is accomplished by giving 0.5 mg followed by 0.25 to 0.5 mg every 6 to 8 hours until the average total loading dose is given.
If greater speed is demanded then digoxin may be given intravenously. If no digitalis preparation has been given in last 2 to 3 weeks, an initial dose of 0.25 to 0.5 mg may be given intravenously. The action starts within 15 to 30 mins and reaches its peak in one to 5 hours.
Digitalis Toxicity:
Anorexia, nausea, vomiting, slurring of vision and all types of cardiac arrhythmias are present, but multiple ventricular premature contraction, paroxysmal atrial tachycardia with A-V block, A-V dissociation, A-V block, paroxysmal ventricular tachycardia are common.
Treatment: Stop the drug, correction of hypokalemia and if required give phenytoin 100 mg intravenous which can be repeated if necessary.
Other drugs which increase myocardial contractility:
Certain sympathomimetic amines (ephedrine, dopamine, dobutamine) increase contractility and may be helpful in certain acute situations but are not recommended for long term use.
Bipyridine agents are new drugs that increase cardiac contractility and cause arterial vasodilatation. Amrinone, the first bipyridine group of drug was not clinically useful for long time due to toxicity (thrombocytopenia).
Milrinone is a very potent bipyridine derivative and has got both inotrophic and afterload reducing properties. The drug appears promising and merits further study.
Diuretics:
Diuretics form the corner stone of management of congestive heart failure and the main effects are:
(1) Reduction in oedema both pulmonary and peripheral.
(2) Reduction in blood and plasma volume. This reduces right and left ventricular preload, lower jugular and pulmonary venous pressure.
(3) There is also reduction in left ventricular afterload as a result of peripheral arteriolar dilatation.
Commonly used diuretics have been classified in three groups:
1. High potency loop diuretics.
2. Medium potency thiazide diuretics.
3. Low potency potassium sparing diuretics.
1. Loop Diuretics (High Potency Loop Diuretics):
Major action is on the ascending loop of Henle. (a) Furosemide average single dose is 40 mg oral or I. V. (b) Ethacrynic acid 50 mg oral once or twice a day, (c) Bumetanide 1 mg O.D. or BD.
2. Benzothiazine Compounds (Medium Potency Thiazide Diuretics):
Site of action is on the cortical diluting segment of loop of Henle and at the beginning of distal convoluted tubule where they interfere with active reabsorption of sodium ions.
Thiazide—Daily Dose:
(i) Hydrochlorothiazide 50 mg.
(ii) Polythiazic/e 2 mg.
(iii) Hydroflumethiazide 100 mg.
(iv) Chlorthalidone 50 mg twice weekly.
3. Low Efficacy Diuretics (Potassium Sparing Diuretics):
(i) Aldosterone antagonists — Spironolactone useful in patients resistant with thiazide groups. Its important clinical effect is the reduction of renal excretion of potassium which it shares with low potency diuretics. It should not be given with potassium supplement. Dose – 25 mg QDS.
(ii) Triamterene best used in combination with thiazide because it not only potentiates the sodium loosing effect of thiazide but also reduces potassium loss.
It is logical to combine diuretics from different classes if an increased action is desired, but it demands for monitoring of fluid or electrolyte imbalance.
Complications of Diuretic Therapy:
(1) Hypokalemia — High potency and-thiazide diuretics produce potassium depletion and is particularly serious since it may be responsible for increased sensitivity to digitalis. It can precipitate hepatic coma with patients having liver disease.
Management:
Potassium chloride in solution 1.5 g. TDS or slow release preparation (600 mg per tablet) 4-6 tablets daily. Fruit juice, bananas and salads are rich in potassium and may be enough if mild diuretics are used.
(2) Hypovolaemia may occur high potent diuretics.
(3) Hyponatraeipia seen in long standing congestive cardiac failure. Serum sodium may be less than 120 mEq/L.
Management:
To restrict diuretic therapy, limit fluid intake to one litre daily and unrestricted diet.
(4) Hyperglycemia, hyperuricemia, urinary retention in presence of prostatic obstruction are seen.
Vasodilators:
This is an important concept in the management of congestive cardiac failure. Venodilatation reduces central venous pressure and right ventricular output and slows the accumulation of pulmonary oedema, while arteriolar dilatation improves left ventricular function by reducing the afterload against which it has to work.
Isosorbide dinitrate (sorbitrate) is predominantly venodilator, hydralazine, nifedepine and salbutamol are predominantly arteriolar’ dilators. Prazosine dilates both arteries and veins. Captopril is a powerful vasodilator and also reduces aldosterone production. Captopril, because of its ability to inhibit the effects of renin, is particularly valuable in the management of severe chronic cardiac failure, where plasma renin level tends to be high.
Vasodilator therapy can be adjusted to the patient’s requirement, by using venodilator for relieving pulmonary congestion and arteriolar dilators to improve cardiac output. Choice of the therapy depends on patient’s tolerance. Side effects are headache, postural hypotension, sometimes increases peripheral oedema partly because fluid retention by the kidneys, higher doses of diuretics may be needed.
Dose:
Hydralazine — upto 200 mg daily better not exceeded.
Salbutamol — 4-8 mg TDS
Prazosine — 0.5 mg and gradually increase 10 mg TDS.
Captopril – 25-100 mg TDS
Sorbitrate — 10 to 20 mg 6 hourly.
Management of acute heart failure and acute pulmonary oedema:
(1) The majority of patients are more comfortable in the trunk up legs down position.
(2) 5 to 10 mg of morphine sulphate should be given intravenously, with close watch for respiratory depression.
(3) Oxygen should be given by mask or by intermittent positive pressure.
(4) Furosemide — 40 mg intravenously and may be repeated if necessary.
(5) It is important to reduce preload so as to decrease dyspnoea and pulmonary congestion. Sublingual nitroglycerine 0.4 to 1.2 mg may be given. Tourniquets have the advantage of being immediately reversible.
(6) If bronchospasm and wheezing are prominent, Aminophylline 250 mg diluted may be given intravenously slowly.
(7) When the patient is not receiving digitalis 0.5 to 0.75 mg digoxin may be given intravenously, followed by additional dose as indicated.
(8) Constant watches and monitor of vital parameters.
Do not make mistake in diagnosis between cardiac asthma and bronchial asthma.
Restriction of Physical Activity:
Rest depends on the severity of failure
(a) Complete rest (confine to bed-chair) for 3-4 weeks. Should move lower limbs from the beginning.
(b) Confine to the house, another 3-4 weeks.
(c) Discontinue full time work, there must be rest period during the day.
Restriction of Sodium Intake:
(a) In severe failure there should be low sodium diet and eliminate salt from cooking and at table (Na 0.2 to 1.0 gm a day).
(b) With improvement, eliminate salt in cooking and at table (Na 1.2 to 1.8 gm a day).
(c) Eliminate salt taken on the dining table (Na 1.6 to 2.8 gm a day).
Conclusion:
Medical therapy of congestive heart failure has improved markedly over the past few years. The wide variety of agents at our disposal has enabled us today to ensure better comfort although the effects on survival may be slight. The end-stage heart, however, like the end-stage kidney, liver disease is unlikely to respond dramatically to any therapy apart from organ replacement. Unfortunately, the resources available to support heart-transplantation, even in the wealthiest country in the world are limited.
It therefore seems appropriate that much greater attention should be directed towards the prevention and early detection of cardiac muscle dysfunction, before systemic decompensation ensues. This implies much greater attention to such antecedents as hypertension and coronary artery disease as well as other treatable causes of cardiac decompensation.
It also implies a much more precise understanding of the derangements that occur at a subcellular level in a variety of conditions that culminate in “heart failure”. Once the specific derangement is elucidated in a particular condition, it may be possible to direct more specific therapy to the problem that exists rather than to treat the consequences in an empirical manner. In this field, we are just beginning to scratch the surface.