Heart failure

Heart failure

Heart failure describes the clinical syndrome that develops when the heart cannot maintain an adequate cardiac output, or can do so only at the expense of an elevated filling pressure. In mild to moderate forms of heart failure, cardiac output is adequate at rest and only becomes inadequate when the metabolic demand increases during exercise or some other form of stress.
Worldwide, the incidence of heart failure is variable but increases with advancing age. For example, in Scotland the prevalence of heart failure is high at 7.1 in 1000, increasing with age to 90.1 in 1000 among people over 85 years. In the UK, overall incidence is about 2 in 1000.
prognosis of heart failure has improved over the past 10 years, but the mortality rate is still high with approximately 50% of patients dead at 5 years. Heart failure accounts for 5% of admissions to hospital medical wards. The cost of managing heart failure in the UK exceeds 1 billion per year.
Coronary artery disease is the commonest cause of heart failure in western countries.
Almost all forms of heart disease can lead to heart failure. An accurate aetiological diagnosis (Box 14.17) is important because in some situations a specific remedy may be available .




Mechanisms of heart failureIn coronary artery disease, akinetic or dyskinetic segments contract poorly and may impede the function of normal segments by distorting their contraction and relaxation patterns

⃰ Progressive ventricular dilatation

MI (segmental dysfunction)

⃰ Myocarditis/cardiomyopathy (global dysfunction)

Reduced
Ventricular contractlity


Initially, concentric ventricular hypertrophy allows the ventricle to maintain a normal output by generating a high systolic pressure. Later,
secondary changes in the myocardium and increasing obstruction lead to failure with ventricular dilatation and rapid clinical deteriorationHypertension, aortic stenosis (left heart failure)
Pulmonary hypertension, pulmonary valve stenosis
(right heart failure)Ventricular outflow
obstruction
(pressure
Overload)Small vigorous ventricle, dilated hypertrophied atrium.
Atrial fibrillation is common cause more detoration because ventricular filling depends heavily on atrial contractionMitral stenosis, tricuspid stenosis
Ventricular inflow
obstructionDilatation and hypertrophy allow the ventricle to generate a high stroke volume and help to maintain a normal cardiac output.
However, secondary changes in the myocardium lead to impaired contractility and worsen heart failure
Ventricular septal defect
Right ventricular volume overload (e.g. atrial septal defect)
Increased metabolic demand (high output)Ventricular volume
overload⃰ Tachycardia does not allow for adequate filling of the heart result in reduce cardiac output

■Incessant tachycardia causes myocardial fatigue

■Bradycardia limits cardiac output even if stroke volume is normal
■Atrial fibrillation⃰


■Tachycardia cardiomyopathy

■Complete heart block

Arrhythmia

■Marked fluid retention and peripheral oedema, ascites, pleural effusion and rise JVP

■Bi-atrial enlargement (restrictive filling pattern and high atrial pressures).
■Good systolic function but poor diastolic filling

■Hypotension, elevated jugular veins, pulsus paradoxus, poor urine output

■Constrictive pericarditis

■Restrictive cardiomyopathy

■Left ventricular hypertrophy and fibrosis

■ cardiac tamponade

Diastolic
dysfunction


Pathophysiology
Cardiac output is a function of ⃰ the preload (the volume and pressure of blood in the ventricle at the end of diastole), ⃰ the afterload (the volume and pressure of blood in the ventricle during systole) and ⃰ myocardial contractility;
this is the basis of Starlings Law .
In patients without valvular disease, the primary abnormality is impairment of ventricular function leading to a fall in cardiac output. This activates counter-regulatory neurohumoral mechanisms that in normal physiological circumstances would support cardiac function, but in the
setting of impaired ventricular function can lead to a deleterious increase in both afterload and preload .
A vicious circle may be established because any additional fall in cardiac output will cause further neurohumoral activation and increasing peripheral vascular resistance.
Stimulation of the reninangiotensinaldosterone system leads to vasoconstriction, salt and water retention, and sympathetic nervous system activation. This is mediated by angiotensin II, a potent constrictor of arterioles in both the kidney and the systemic circulation.
Activation of the sympathetic nervous system may initially maintain cardiac output through an increase in myocardial contractility, heart rate and peripheral vasoconstriction. However, prolonged sympathetic
stimulation leads to cardiac myocyte apoptosis, hypertrophy and focal myocardial necrosis Salt and water retention is promoted by the release of aldosterone, endothelin-1 (a potent vasoconstrictor peptide with
marked effects on the renal vasculature) and, in severe heart failure, antidiuretic hormone (ADH).
Natriuretic peptides are released from the atria in response to atrial
stretch, and act as physiological antagonists to the fluid conserving
effect of aldosterone.
After MI, cardiac contractility is impaired and neurohumoral activation causes hypertrophy of non-infarcted segments, with thinning, dilatation and expansion of the infarcted segment (remodelling).
This leads to further deterioration in ventricular function and worsening heart failure.
The onset of pulmonary and peripheral oedema is due to high atrial pressures compounded by salt and water retention caused by impaired renal perfusion and secondary hyperaldosteronism.

Types of heart failure (Clinical syndromes of heart failure)

Left, right and biventricular heart failure
The left side of the heart comprises the functional unit of the LA and LV, together with the mitral and aortic valves; the right heart comprises the RA, RV, and tricuspid and pulmonary valves.
Left-sided heart failure. There is a reduction in the left ventricular output and an increase in the left atrial or pulmonary venous pressure. An acute increase in left atrial pressure causes pulmonary congestion
or pulmonary oedema; a more gradual increase in left atrial pressure, as occurs with mitral stenosis, leads to reflex pulmonary vasoconstriction, which protects the patient from pulmonary oedema at the cost of increasing pulmonary hypertension.
Right-sided heart failure. There is a reduction in right ventricular output for any given right atrial pressure. Causes of isolated right heart failure include chronic lung disease (cor pulmonale), multiple pulmonary emboli and pulmonary valvular stenosis.
Biventricular heart failure. Failure of the left and right heart may develop because the disease process, such as dilated cardiomyopathy or ischaemic 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.


Diastolic and systolic dysfunction
Heart failure may develop as a result of impaired myocardial contraction (systolic dysfunction) but can also be due to poor ventricular filling and high filling pressures caused by abnormal ventricular relaxation (diastolic
dysfunction). The latter is caused by a stiff non-compliant ventricle and is commonly found in patients with left ventricular hypertrophy. Systolic and diastolic dysfunction often coexist, particularly in patients with coronary artery disease.
High-output failure
Conditions such as large arteriovenous shunt, beri-beri, severe anaemia or thyrotoxicosis can occasionally cause heart failure due to an excessively high cardiac output.
Acute and chronic heart failure
Heart failure may develop suddenly, as in MI, or gradually, as in progressive valvular heart disease. When there is gradual impairment of cardiac function, a variety of compensatory changes may take place.
The term compensated heart failure is sometimes used to describe those with impaired cardiac function in whom adaptive changes have prevented the development of overt heart failure. A minor event, such as an intercurrent infection or development of atrial fibrillation, may precipitate overt or acute heart failure (Box 18.13). Acute left heart failure occurs either de novo or as an acute decompensated episode on a background of chronic heart failure, so-called acute-on-chronic heart failure.

Clinical assessment

Acute left heart failure
Acute de novo left ventricular failure presents with a sudden onset of dyspnoea at rest that rapidly progresses to acute respiratory distress, orthopnoea and prostration
The patient appears agitated, pale and clammy. The peripheries are cool to the touch and the pulse is rapid. Inappropriate bradycardia or excessive tachycardia should be identified promptly, as this may be the precipitant for the acute episode of heart failure. The BP is usually high because of sympathetic nervous system activation, but may be normal or low if the patient is in cardiogenic shock.
The jugular venous pressure (JVP) is usually elevated, particularly with associated fluid overload or right heart failure. In acute de novo heart failure, there has been no time for ventricular dilatation and the apex is not displaced.
Auscultation occasionally identifies the murmur of a catastrophic valvular or septal rupture, or reveals a triple gallop rhythm. Crepitations are heard at the lung bases, consistent with pulmonary oedema.
Acute-on-chronic heart failure will have additional features of long-standing heart failure (see below).
Potential precipitants, such as an upper respiratory tract infection or inappropriate cessation of diuretic medication, should be identified. Chronic heart failure
Patients with chronic heart failure commonly follow a relapsing and remitting course. The clinical picture depends on the nature of the underlying heart disease, the type of heart failure that it has evoked, and the neurohumoral changes that have developed .
A low cardiac output causes fatigue, listlessness and a poor effort tolerance; the peripheries are cold and the BP is low. To maintain perfusion of vital organs, blood flow is diverted away from skeletal muscle and this may contribute to fatigue and weakness. Poor renal perfusion leads to oliguria and uraemia.
Pulmonary oedema due to left heart failure presents as described above and with inspiratory crepitations over the lung bases. In contrast, right heart failure produces a high JVP with hepatic congestion and dependent peripheral oedema. In ambulant patients, the oedema affects the ankles, whereas in bed-bound patients it collects around the thighs and sacrum. Ascites or pleural effusion occurs in some cases.
Chronic heart failure is sometimes associated with marked weight loss (cardiac cachexia) caused by acombination of anorexia and impaired absorption due to gastrointestinal congestion, poor tissue perfusion due to a low cardiac output, and skeletal muscle atrophy due to immobility. Complications
In advanced heart failure, the following may occur:
Renal failure is caused by poor renal perfusion due to a low cardiac output and may be exacerbated by diuretic therapy, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers.
Hypokalaemia may be the result of treatment with potassium-losing diuretics or hyperaldosteronism caused by activation of the reninangiotensin system and impaired aldosterone metabolism due to hepatic congestion. Most of the bodys potassium is intracellular and there may be substantial depletion of potassium stores, even when the plasma potassium concentration is in the normal range.
Hyperkalaemia may be due to the effects of drug treatment, particularly the combination of ACE inhibitors and spironolactone (which both promote potassium retention), and renal dysfunction.
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 ADH 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, whereas systemic emboli may be related to arrhythmias, atrial flutter or fibrillation, or 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 (e.g. hypokalaemia, hypomagnesaemia), the underlying structural heart disease, and the pro-arrhythmic effects of increased circulating catecholamines or drugs. Sudden death occurs in up to 50% of patientswith heart failure and is often due to a ventricular
arrhythmia. Frequent 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.