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Heart failure guidelines
Heart failure interprets the clinical syndrome that develops when the heart cannot maintain sufficient output or can do so only at the expense of elevated ventricular filling pressure. These heart failure guidelines are taken from Davidson’s principle of medicine, 23rd edition.
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 coeval at rest. In clinical practice, heart failure may be diagnosed when a patient with significant heart disease develops the signs or symptoms of low cardiac output, pulmonary congestion or systemic venous congestion at rest or on exercise. Let’s learn about heart failure guidelines.
Types of heart failure
Three types of heart failure are recognized in heart failure guidelines:
Left heart failure guidelines
This is characterised by a reduction in left ventricular output and an increase in left atrial and pulmonary venous pressure. If 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 the right ventricular function.
Right heart failure guidelines
This is characterised 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 terms cor pulmonale’ is used to describe right heart failure that is secondary to chronic lung disease.
Biventricular heart failure guidelines
In biventricular failure, both sides of the heart are affected. This may occur because the disease process, such as dilated cardiomyopathy or ischaemic heart disease, affects both ventricles or because the disease of the left heart leads to chronic levitation of the left atrial pressure, pulmonary hypertension and right heart failure guidelines.
Heart failure guidelines fundamentally begin with the epidemiology of heart failure. Heart failure predominantly affects the elderly; the prevalence rises from 1% in those aged 50-59 years to over 10% in those aged 80—89 years. In the UK, most patients admitted to hospital with heart failure are more than 70 years old; they typically remain hospitalised for a week or more and may be left with chronic disability.
Although the frame of mind depends, to some extent, on the underlying cause of the problem, untreated heart failure guidelines generally carry 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. An accurate diagnosis is important because treatment of the underlying cause may reverse heart failure or prevent its progression.
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. The causes of heart failure are discussed below.
Ventricular performance is related to the degree of myocardial stretching. An accrual in preload (end-diastolic volume, end-diastolic pressure, filling pressure or atrial pressure) will, therefore, enhance function; however, overstretching causes marked deterioration. In heart failure, the curve incites to the right and becomes salve. An increase in myocardial contractility or a reduction in afterload will shift the curve upwards and to the left (green arrow). Pathogenesis of heart failure is segmental allotment of heart failure guidelines.
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 the 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.
A vicious circle may then be fortified because any supplementary fall in cardiac output causes further revival of the SNS and RAAS and an additional increase in peripheral vascular resistance. Activation of the RAAS causes vasoconstriction and sodium and water retention.
This is primarily propitiated by angiotensin II, a potent narrowing of arterioles, in both the kidney and the systemic circulation. Arousal 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. Na and H₂o detainment is further aggrandized by the release of aldosterone, endothelin-1 (a potent vasoconstrictor peptide with marked chattels 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 aerial left and right atrial pressures, and is coagmented by Na and water retention, caused by the deterioration 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 ruination in ventricular function and retrograding heart 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 beriberi, severe anaemia or thyrotoxicosis.
Heart failure can also be caused by valvular disease in which there is impaired filling of the ventricles due to mitral or tricuspid stenosis; where there is an obstruction to ventricular outflow, as occurs in aortic and tricuspid stenosis and hypertrophic cardiomyopathy; or as the result of ventricular overload secondary to valvular regurgitation. So valvular disease is also included in the heart failure guidelines.
Heart failure may develop suddenly, as in Myocardial infarction, or gradually, as in valvular heart disease. When there is a gradual impairment of cardiac function, several compensatory changes take place. The appellation compensated heart failure guidelines are frequently used to describe the condition of those with impaired cardiac function, in whom adaptive changes have prevented the development of overt heart failure. However, a minor event, such as intercurrent infection or development of atrial fibrillation, may precipitate acute heart failure in these circumstances. Similarly, acute heart failure sometimes supervenes as the result of a decompensating episode, on a background of chronic heart failure; this is called acute-on-chronic heart failure.
Acute left heart failure guidelines
ALHF demonstrate with an expeditious onset of dyspnoea at rest that rapidly ameliorates to acute respiratory distress, orthopnoea and abashment. Often there is a clear precipitating factor, such as an acute MI, which may be apparent from the history. The patient appears agitated, pale and clammy. The peripheries are cool to the touch and the pulse is rapid, but in some cases, there may be inappropriate bradycardia that may contribute to the acute episode of heart failure. The Blood pressure is usually elevated because of SNS activation, but maybe normal or low if the patient is in cardiogenic shock.
The jugular venous pressure (JVP) is usually raised, particularly with associated fluid overload or right heart failure. In acute heart failure, there has been no time for ventricular dilatation and the apex is not displaced. A ‘gallop’ rhythm, with a third heart sound, is heard quite early in the development of acute left-sided heart failure. A new systolic murmur may signify acute mitral regurgitation or ventricular septal rupture. Chest examination may reveal crepitations at the lung bases if there is pulmonary oedema, or crepitations throughout the lungs if this is severe. There may be an expiratory wheeze. Patients with acute-on-chronic heart failure may have additional features of chronic heart failure (see below). Potential precipitants, such as an upper respiratory tract infection or inappropriate cessation of diuretic medication, may be identified on clinical examination or history-taking.
Chronic heart failure guidelines
Patients with CHF generally follow a relapsing and remitting course, with periods of endurance and episodes of decompensation, leading to sharpening symptoms that may necessitate immediate hospitalisation. The clinical picture depends on the nature of the underlying heart disease, the type of heart failure that it has evoked, and the changes in the SNS and RAAS that have developed.
Low cardiac output causes exhaustion, listlessness and a bankrupt effort tolerance; the peripheries are cold and the BP is low. To perpetuate perfusion of vital organs, blood flow is averted away from skeletal muscle and this may contribute to fatigue and debility. Poor renal perfusion leads to oliguria and uraemia.
Pulmonary oedema due to left heart failure presents with dyspnoea and inspiratory crepitations over the lung bases. In contrast, right heart failure produces a raised JVP with hepatic congestion and relying on peripheral oedema. In ambulant patients, oedema affects the ankles, whereas in bed-bound patients it collects around the thighs and sacrum. Ascites or pleural effusion may occur. Heart failure is not the only cause of oedema.
CHF is sometimes lumped with marked weight loss (cardiac cachexia), compiled by an amalgamation of anorexia and impaired absorption due to GIT congestion, bankrupt tissue perfusion due to a low cardiac output, and skeletal muscle atrophy due to listlessness.
Components that may precipitate or aggravate heart failure in pre-existing heart disease
The heart failure guidelines also include the aggravating components which are enlisted below:
- Myocardial ischaemia or infarction
- Intercurrent illness
- Inappropriate reduction of therapy
- Administration of a drug with negative inotropic (ß-blocker) or fluid-retaining properties (non-steroidal anti-inflammatory drugs, glucocorticoids)
- Pulmonary embolism
- Conditions associated with increased metabolic demand (pregnancy, thyrotoxicosis, anaemia)
- Intravenous fluid overload
Complications of heart failure
Several complications may occur in advanced heart failure. The complication of heart failure is described as heart failure guidelines.
Renal 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 accrue of treatment with potassium-losing diuretics or hyperaldosteronism evoked 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 abundant depletion of potassium stores, even when the plasma concentration is in the citation 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 component of severe heart failure and is a bad 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.
- Imperfect liver function is caused by hepatic venous congestion and poor arterial perfusion, which intermittently cause mild jaundice and abnormal liver function tests; reduced synthesis of clotting factors can make anticoagulant control difficult.
- Deep vein thrombosis and pulmonary embolism may occur due to the effects of 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 customary and may be related to electrolyte changes such as hypokalaemia and hypomagnesaemia, the lurking cardiac disease, and the pro-arrhythmic effects of sympathetic activation. Atrial fibrillation occurs in comparatively 20% of patients with heart failure and causes further stoppage of cardiac function. Ventricular ectopic beats and runs of non-sustained ventricular tachycardia are bourgeois findings in patients with heart failure and are affiliated with an inopportune prognosis.
- Sudden death occurs in up to 50% of patients with heart failure and is most probably due to ventricular fibrillation.
A chest X-ray should be performed in all cases. This may show abnormal distension of the upper lobe pulmonary veins with the patient in the erect position. Vascularity of the lung fields becomes more prominent and the right and left pulmonary arteries dilate. Subsequently, interstitial oedema causes thickened interlobular septa and dilated lymphatics.
These are axiomatic as horizontal lines in the costophrenic angles (septal or ‘Kerley B’ lines). More progressive changes due to alveolar oedema cause a hazy opacification spreading from the hilar regions, and pleural effusions. Echocardiography is very useful and should be considered in all patients with heart failure guidelines in order to:
- determine the aetiology
- observe hitherto unsuspected valvular heart disease, such as occult mitral stenosis, and other conditions that may be amenable to specific remedies
- Distinguish patients who will benefit from long-term drug therapy.
Serum urea, creatinine and electrolytes, haemoglobin and thyroid function may succour to establish the nature and grimness of the underlying heart disease and detect any intricacy. BNP is elevated in heart failure and is a prognostic marker, as well as being useful in differentiating head failure from other causes of breathlessness or peripheral oedema.
Management of acute heart failure
AHF with pulmonary oedema is a medical emergency that should be treated urgently. The patient should originally be kept rested, with steady monitoring of cardiac rhythm, BP and pulse oximetry. IV opiates can be of value in distressed patients but must be used sparingly, as they may cause respiratory depression and exacerbation of hypoxaemia and hypercapnia.
If these measures prove ineffective, inotropic agents such as dobutamine (2.5—10 gg/kg/min) may be required to augment cardiac output, particularly in hypotensive patients. Interpolation of an intra-aortic balloon pump may be beneficial in patients with acute cardiogenic pulmonary oedema and shock. Following management of the acute episode, additional measures must be instituted to control heart failure in the longer term, as discussed below and included in heart failure guidelines.
Management of chronic heart failure
The aims of treatment in chronic heart failure guidelines are to improve cardiac function by increasing contractility, optimising preload or decreasing afterload, and controlling cardiac rate and rhythm. This can be achieved by a combination of drug treatment or non-drug treatments, as discussed below.
Education of patients and their relatives about the causes and treatment of head failure can improve adherence to a management plan. Some patients may need to weigh themselves daily, as a measure of fluid load, and adjust their diuretic therapy accordingly.
A wide variety of drug treatments are now available for the treatment of heart failure guidelines. Drugs that reduce preload are appropriate in patients with high end-diastolic filling pressures and evidence of pulmonary or systemic venous congestion, whereas those that reduce afterload or increase myocardial contractility are more useful in patients with signs and symptoms of low cardiac output.
Diuretics promote urinary sodium and water excretion, leading to a reduction in blood plasma volume, which in turn reduces preload and improves pulmonary and systemic venous congestion. They may also abate afterload and ventricular volume, leading to a fall in ventricular wall pressure and boost cardiac efficiency. Although a fall in preload (ventricular filling pressure) normally reduces cardiac output, patients with heart failure are beyond the apex of the Starling curve, so there may be a substantial and beneficial fall in filling pressure with either no change or an improvement in cardiac output. Nevertheless, the dose of diuretics needs to be titrated carefully so as to avoid excessive volume depletion, which can cause a fall in cardiac output with hypotension, lethargy and renal failure. This is especially likely in patients with a marked diastolic component to their heart failure.
Oedema may persist, despite oral loop diuretic therapy, in some patients with severe chronic heart failure, particularly if there is renal impairment. Under these circumstances, an intravenous infusion of furosemide (5-10 mg/hr) may initiate a diuresis. Combining a loop diuretic with a thiazide diuretic such as bendroflumethiazide (5 mg daily) may also prove effective but care must be taken to avoid an excessive diuresis.
Mineralocorticoid receptor antagonists, such as spironolactone and eplerenone, are potassium-sparing diuretics that are of particular benefit in patients with heart failure with severe left ventricular systolic dysfunction. They have been shown to improve long-term clinical outcome in individuals with severe heart failure or heart failure following acute MI but may cause hyperkalaemia, particularly when used with an ACE inhibitor.
Angiotensin-converting enzyme inhibitors
ACE inhibitors play a central role in the management of heart failure since they interrupt the vicious circle of neurohumoral activation that is characteristic of the disease by forbidding the exchange of angiotensin I to angiotensin II. This, in turn, reduces peripheral vasoconstriction, activation of the sympathetic nervous system, and salt and water retention due to aldosterone release, as well as preventing the activation of the renin-angiotensin system caused by diuretic therapy.
In moderate and severe heart failure guidelines, ACE inhibitors can produce a substantial improvement in effort tolerance and in mortality. They can also emend outcome and hinder the onset of overt heart failure in patients with poor residual left ventricular function following MI.
Adverse effects of ACE inhibitors include symptomatic hypotension and impairment of renal function, especially in patients with bilateral renal artery stenosis or those with pre-existing renal disease. An increase in serum potassium concentration may also occur, which can be beneficial in offsetting the hypokalaemia associated with loop diuretic therapy. Short-acting ACE inhibitors can engender marked falls in Blood pressure, explicitly in the elderly or when started in the presence of hypotension, hypovolaemia or hyponatraemia. In anchored patients without low BP(systolic BP over 100 mmHg), ACE inhibitors can usually be safely started in the community. In other patients, however, it is usually advisable to withhold diuretics for 24 hours before starting treatment with a small dose of a long-acting agent, preferably given at night. Renal function and serum potassium must be monitored and should be checked 1—2 weeks after starting therapy.
Angiotensin receptor blockers
ARBs act by arresting the action of angiotensin II on the heart, peripheral vasculature and kidney. In heart failure, they compose beneficial haemodynamic changes that are comparable to the effects of ACE inhibitors but are generally better countenance. They have equipollent effects on mortality and are useful flipside for patients who cannot tolerate ACE inhibitors. Like ACE inhibitors they should be commenced at a low dose and titrated upwards, revolving on response. Disastrously, they share all the more serious adverse effects of ACE inhibitors, counting renal dysfunction and hyperkalaemia. ARBs are normally used as an alternative to ACE inhibitors, but the two can be combined in patients with resistant or recurrent heart failure.
The only drug present in this class is sacubitril, a small-molecule inhibitor of neprilysin, which is censurable for the breakdown of the endogenous diuretics ANP and BNP. Used in combination with the ARB valsartan (sacubitril—valsartan), it has been shown to produce additional symptomatic and mortality benefit over ACE inhibition and is now recommended in the management of resistant heart failure.
These drugs are beneficial in chronic heart failure when ACE inhibitors or ARBS are contraindicated. Vasodilators, such as nitrates, reduce preload, and arterial dilators, for example, hydralazine, reduce afterload. Their use is limited by pharmacological tolerance and hypotension.
Beta-blockade helps to counteract the deleterious effects of enhanced sympathetic stimulation and reduces the risk of arrhythmias and sudden death. When originated in authoritative doses lb-blockers may precipitate acute-on-chronic heart failure, but when given in bantam incremental doses they can increase ejection fraction. Ameliorate symptoms, reduce the frequency of hospitalisation and reduce mortality in patients with chronic heart failure. A typical regimen is bisoprolol, starting at a dose of 1.25 mg daily and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily. Beta-blockers are more effective at reducing mortality than ACE inhibitors, with a relative risk reduction of 33% versus 20%, respectively.
Ivabradine acts on the l, inward current in the SA node. resulting in a reduction of heart rate. It reduces hospital admission and mortality rates in patients with heart failure due to moderate or severe left ventricular systolic impairment. In trials, its effects were most marked in patients with a relatively high heart rate (over 77/min), so ivabradine is best suited to patients who cannot take b-blockers or whose heart rate remains high despite ß-blockade. It is ineffective in patients with atrial fibrillation.
Digoxin can be used to accommodate rate control in patients with heart failure and atrial fibrillation. In patients with severe heart failure (NYHA class lll-IV), digoxin reduces the likelihood of hospitalisation for heart failure, although it has no effect on long-term survival.
This is a dynamic anti-arrhythmic drug that has a little negative inotropic effect and may be beneficial in patients with poor left ventricular function. It is effective only in the treatment of symptomatic arrhythmias and should not be used as a preventative agent in asymptomatic patients. Amiodarone is used for prevention of symptomatic atrial arrhythmias and of ventricular arrhythmias when other pharmacological options have been exhausted.
Implantable cardiac defibrillators
These devices are indicated in patients with symptomatic ventricular arrhythmias and heart failure since they improve prognosis and survival.
In patients with marked intraventricular conduction delay, prolonged depolarization may lead to uncoordinated left ventricular contraction. When this is associated with severe symptomatic heart failure, cardiac resynchronization devices may be helpful. Here, both the Left ventricular and Right ventricular are paced synchronously to generate a more coordinated left ventricular contraction and amend cardiac output. This is associated with improved symptoms and survival.
Coronary artery bypass surgery or percutaneous coronary intervention may amend function in areas of the myocardium that are ‘hibernating’ because of deficient blood supply and can be used to treat carefully prefered patients with heart failure and coronary artery disease. If necessary, ‘hibernating’ myocardium can be identified by stress echocardiography and specialised nuclear or magnetic resonance imaging.
Cardiac transplantation is an established and successful treatment for patients with intractable heart failure. Coronary artery disease and dilated cardiomyopathy are the most common indications. The appliance of transplantation is limited by the efficacy of the modern drug and device therapies, as well as the possibility of donor’s hearts, so it is generally reserved for young patients with severe symptoms despite optimal therapy.
Conventional heart transplantation is contraindicated in patients with pulmonary vascular disease due to long-standing left heart failure, complex congenital heart disease such as Eisenmenger’s syndrome, or primary pulmonary hypertension because the RV of the donor’s heart may abort in the face of high pulmonary vascular resistance. However, heart-lung transplantation can be successful in patients with Eisenmenger’s syndrome, and lung transplantation has been used for primary pulmonary hypertension.
Despite, cardiac transplantation usually percolate a dramatic improvement in the recipient’s quality of life, serious entanglement may occur:
- Rejection. In spite of routine therapy with cyclosporin A, azathioprine and glucocorticoids, episodes of rejection are common and may present with heart failure, arrhythmias or subtle ECG changes. The cardiac biopsy is often used to confirm the diagnosis before starting treatment with high-dose glucocorticoids.
- Accelerated atherosclerosis. Isochronal heart failure is often due to advancing atherosclerosis in the coronary arteries of the donor’s heart. This is not confined to patients who underwent transplantation for coronary artery disease and is probably a manifestation of chronic rejection. Anginal pain is rare because the heart has been denervated.
- Opportunistic infection with organisms such as cytomegalovirus or Aspergillus remains a major cause of death in transplant recipients.
Ventricular assist devices
Because of the limited supply of donor organs, ventricular assist devices (VAD) may be employed as a bridge to cardiac transplantation and as short-term restoration therapy following a potentially reversible insult such as viral myocarditis. In some patients, VADs may be used as a long-term therapy if no other options exist.
These devices assist cardiac output by using a roller, centrifugal or pulsatile pump that, in some cases, is implantable and portable. They abjure blood through cannulae inserted in the atria or ventricular apex and draw it into the pulmonary artery or aorta. They are designed not only to unload the ventricles but also to provide support to the pulmonary and systemic circulations. Their more pandemic application is limited by high complication rates (haemorrhage, systemic embolism, infection, neurological and renal sequelae), supposing some improvements in survival and quality of life have been manifested in patients with severe heart failure.