Heart failure
Prof. Oday AlsalihiHeart failure describes the clinical syndrome that develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filling pressure.
In mild to moderate forms of heart failure, symptoms occur only when the metabolic demand increases during exercise or some other form of stress. In severe heart failure, symptoms may be present at rest.
In clinical practice, heart failure may be diagnosed when a patient with significant heart disease develops the signs or symptoms of a low cardiac output, pulmonary congestion or systemic venous congestion at rest or on exercise
Pathophysiology :
Heart failure occurs when cardiac output fails to meet the demands of the circulation. Cardiac output is determined by preload (the volume and pressure of blood in the ventricles at the end of diastole), afterload (the volume and pressure of blood in the ventricles during systole) and myocardial contractility, forming the basis of Starling’s Law.
Classification of heart failure
Most common classification for heart failure are
Left side HF
Right side HFBiventricular HR
Left heart failure:
In this type , the left ventricle fail to pump adequate blood amount according to body requirement , so the ventricle will fail also to pull out all the blood in LA resulting in increase LA pressure that will be transmitted back ward to pulmonary artery and cause lung congestionIf left heart failure occurs suddenly – for example, as the result of an acute MI – the rapid increase in left atrial pressure causes pulmonary oedema.
If the rise in atrial pressure is more gradual, as occurs with mitral stenosis, there is reflex pulmonary vasoconstriction, which protects the patient from pulmonary oedema.
However, the resulting increase in pulmonary vascular resistance causes pulmonary hypertension, which in turn impairs right ventricular function
Right heart failure
This is characterized by a reduction in right ventricular output and an increase in right atrial and systemic venous pressure.
The most common causes are chronic lung disease, pulmonary embolism and pulmonary valvular stenosis.
The term ‘cor pulmonale’ is used to describe right heart failure that is secondary to chronic lung disease.
Biventricular heart failure
In biventricular failure, both sides of the heart are affected. This may occur because the disease process, such as dilated cardiomyopathy or ischemic heart disease, affects both ventricles or because disease of the left heart leads to chronic elevation of the left atrial pressure, pulmonary hypertension and right heart failure.Prognosis of heart failrue ;
Although the outlook depends, to some extent, on the underlying cause of the problem, untreated heart failure generally carries a poor prognosis; approximately 50% of patients with severe heart failure due to left ventricular dysfunction will die within 2 years because of either pump failure or malignant ventricular arrhythmias.The most common causes are coronary artery disease and myocardial infarction but almost all forms of heart disease can lead to heart failure
Mechanisms of hear failure
Ventricular dysfunction
Ventricular dysfunction is the most common cause of heart failure. This can occur because of impaired systolic contraction due to myocardial disease, or diastolic dysfunction where there is abnormal ventricular relaxation due to a stiff, non-compliant ventricle : This is most commonly found in patients with left ventricular hypertrophy. Systolic dysfunction and diastolic dysfunction often coexist, particularly in patients with coronary artery disease.
Ventricular dysfunction reduces cardiac output, which, in turn, activates the sympathetic nervous system (*SNS) and renin angiotensin aldosterone system (*RAAS). Under normal circumstances, activation of the SNS and RAAS supports cardiac function but, in the setting of impaired ventricular function, the consequences are negative and lead to an increase in both afterload and preload.
Activation of the RAAS causes vasoconstriction and sodium and water retention. This is primarily mediated by angiotensin II, a potent constrictor of arterioles, in both the kidney and the systemic circulation.
Activation of the SNS also occurs and can initially sustain cardiac output through increased myocardial contractility and heart rate. Prolonged sympathetic stimulation has negative effects, however, causing cardiac myocyte apoptosis, cardiac hypertrophy and focal myocardial necrosis.
Sympathetic stimulation also contributes to vasoconstriction and predisposes to arrhythmias. Sodium and water retention is further enhanced by the release of *aldosterone, *endothelin-1 (a potent vasoconstrictor peptide with marked effects on the renal vasculature) and in severe heart failure,* vasopressin (antidiuretic hormone, ADH).
Natriuretic peptides are released from the atria in response to atrial dilatation and compensate to an extent for the sodium-conserving effect of aldosterone, but this mechanism is overwhelmed in heart failure.
Pulmonary and peripheral oedema occurs because of high left and right atrial pressures, and is compounded by sodium and water retention, caused by impairment of renal perfusion and by secondary hyperaldosteronism.
If the underlying cause is a myocardial infarction, cardiac contractility is impaired and SNS and RAAS activation causes hypertrophy of non-infarcted segments, with thinning, dilatation and expansion of the infarcted segment. This leads to further deterioration in ventricular function and worsening heart failure.
Other classification of HF ;
High out put HF
Left , right, congestive HF
Acute versus chronic HF
Systolic versus diastolic HF
Forward versus backward HF
High-output failure
Sometimes cardiac failure can occur in patients without heart disease due to a large arteriovenous shunt, or where there is an excessively high cardiac output due to beri-beri, severe anaemia or thyrotoxicosis.Factors and causes that can precipitate or exacerbate or aggravate HF
Complications
Several complications may occur in advanced heart failureRenal failure is caused by poor renal perfusion due to low cardiac output and may be exacerbated by diuretic therapy, ACE inhibitors and angiotensin receptor blockers (ARBs).
Hypokalaemia may be the result of treatment with potassium-losing diuretics or hyperaldosteronism caused by activation of the renin–angiotensin system and impaired aldosterone metabolism due to hepatic congestion. Most of the body’s potassium is intracellular and there may be substantial depletion of potassium stores, even when the plasma concentration is in the reference range.
Hyperkalaemia may be due to the effects of drugs that promote renal resorption of potassium, in particular the combination of ACE inhibitors, ARBs and mineralocorticoid receptor antagonists. These effects are amplified if there is renal dysfunction due to low cardiac output or atherosclerotic renal vascular disease.
Hyponatraemia is a feature of severe heart failure and is a poor prognostic sign. It may be caused by diuretic therapy, inappropriate water retention due to high vasopressin secretion, or failure of the cell membrane ion pump.
Impaired liver function is caused by hepatic venous congestion and poor arterial perfusion, which frequently cause mild jaundice and abnormal liver function tests; reduced synthesis of clotting factors can make anticoagulant control difficult.
Thromboembolism. Deep vein thrombosis and pulmonary embolism may occur due to the effects of a low cardiac output and enforced immobility. Systemic emboli occur in patients with atrial fibrillation or flutter, or with intracardiac thrombus complicating conditions such as mitral stenosis, MI or left ventricular aneurysm.
Atrial and ventricular arrhythmias are very common and may be related to electrolyte changes such as hypokalaemia and hypomagnesaemia, the underlying cardiac disease, and the pro-arrhythmic effects of sympathetic activation. Atrial fibrillation occurs in approximately 20% of patients with heart failure and causes further impairment of cardiac function. Ventricular ectopic beats and runs of non-sustained ventricular tachycardia are common findings in patients with heart failure and are associated with an adverse prognosis.
Sudden death occurs in up to 50% of patients with heart failure and is most probably due to ventricular fibrillation.