Heart failure

Congestive heart failure (CHF), congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood through the body. It is not to be confused with "cessation of heartbeat", which is known as asystole, or with cardiac arrest, which is the cessation of normal cardiac function with subsequent hemodynamic collapse leading to death. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure".

Congestive heart failure is often undiagnosed due to a lack of a universally agreed definition and difficulties in diagnosis, particularly when the condition is considered "mild". Even with the best therapy, heart failure is associated with an annual mortality of 10%.^[1] It is the leading cause of hospitalization in people older than 65.^[2]

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Signs and symptoms

Symptoms

Symptoms are dependent on two factors. The first is based on the side of the heart, right or left, that is involved. The second factor is based on the type of failure, either diastolic or systolic. Symptoms and presentation may be indistinguishable making diagnosis impossible based on symptoms.

Given that the left side of the heart pumps blood from the lungs to the organs, failure to do so leads to congestion of the lung veins and symptoms that reflect this, as well as reduced supply of blood to the tissues. The predominant respiratory symptom is shortness of breath on exertion (dyspnea, dyspnée d'effort) - or in severe cases at rest - and easy fatigueability. Orthopnea is increasing breathlessness on reclining, measured in the number of pillows required to lie comfortably. Paroxysmal nocturnal dyspnea is a nighttime attack of severe breathlessness, usually several hours after going to sleep. Poor circulation to the body leads to dizziness, confusion and diaphoresis and cool extremities at rest.

The right side of the heart pumps blood returned from the tissues to the lungs to exchange CO₂ for O₂. Hence, failure of the right side leads to congestion of peripheral tissues. This may lead to peripheral edema or anasarca and nocturia (frequent nighttime urination when the fluid from the legs is returned to the bloodstream). In more severe cases, ascites (fluid accumulation in the abdominal cavity) and hepatomegaly (painful enlargement of the liver) may develop.

Heart failure may decompensate easily; this may occur as the result of any intercurrent illness (such as pneumonia), but specifically myocardial infarction (a heart attack), anaemia, hyperthyroidism or arrhythmias. These place additional strain on the heart muscle, which may cause symptoms to rapidly worsen. Excessive fluid or salt intake (including intravenous fluids for unrelated indications), and medication that causes fluid retention (such as NSAIDs and thiazolidinediones), may also precipitate decompensation.

Signs

In examining a patient with possible heart failure, a health professional would look for particular signs. General signs indicating heart failure are a laterally displaced apex beat (as the heart is enlarged) and a gallop rhythm (additional heart sounds) in case of decompensation. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

Predominant left-sided clinical signs are pulmonary edema (abnormal lung sounds due to fluid accumulation), evidence for pleural effusions (fluid collection in the pleural cavity), and cyanosis (due to poor absorption of oxygen by fluid-filled lungs).

Right-sided signs are peripheral edema, ascites and hepatomegaly, an increased jugular venous pressure and hepatojugular reflux and parasternal heave.

Diagnosis

Imaging

Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy.

Chest X-rays are frequently used to aid in the diagnosis of CHF. In the compensated patient, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema.

Electrophysiology

An electrocardiogram (ECG/EKG) is used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block).

Blood tests

Blood tests routinely performed include electrolytes (sodium, potassium), measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. A specific test for heart failure is B-type natriuretic peptide (BNP), which is found to be elevated in heart failure. BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

Angiography

Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery.

Monitoring

Various measures are often used to assess the progress of patients being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts).

Diagnostic criteria

No system of diagnostic criteria has been agreed as the gold standard for heart failure. Commonly used systems are the "Framingham criteria"^[3] (derived from the Framingham Heart Study), the "Boston criteria",^[4] the "Duke criteria",^[5] and (in the setting of acute myocardial infarction) the "Killip class".^[6]

Functional classification is generally done by the New York Heart Association Functional Classification.^[7] This score documents severity of symptoms, and can be used to assess response to treatment. While its use is widespead, the NYHA score is not very reproducible and doesn't reliably predict the walking distance or exercise tolerance on formal testing.^[8] The classes (I-IV) are:

• Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities.
• Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion.
• Class III: marked limitation of any activity; the patient is comfortable only at rest.
• Class IV: any physical activity brings on discomfort and symptoms occur at rest.

In its 2001 guidelines, the American College of Cardiology/American Heart Association working group introduced four stages of heart failure:^[9]

• Stage A: a high risk HF in the future but no structural heart disorder;
• Stage B: a structural heart disorder but no symptoms at any stage;
• Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment;
• Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

Classification

There are many different ways to categorize heart failure, including:

• the side of the heart involved, (left heart failure versus right heart failure)
• whether the abnormality is due to contraction or relaxation of the heart (systolic dysfunction vs. diastolic dysfunction)
• whether the abnormality is due to low cardiac output or high systemic vascular resistance (low-output heart failure vs. high-output heart failure)
• the degree of functional impairment conferred by the abnormality (as in the NYHA functional classification)

Causes

Causes and contributing factors to congestive heart failure include the following:^[9]

Pathophysiology

Heart failure is caused by any condition which reduces the efficiency of the myocardium, or heart muscle, through damage or overloading. As such, it can be caused by as diverse an array of conditions as myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and amyloidosis (in which protein is deposited in the heart muscle, causing it to stiffen). Over time these increases in workload will produce changes to the heart itself:

• Reduced contractility, or force of contraction, due to overloading of the ventricle. In health, increased filling of the ventricle results in increased contractility (by the Frank-Starling law of the heart) and thus a rise in cardiac output. In heart failure this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.^[10]
• A reduced stroke volume, as a result of a failure of systole, diastole or both. Increased end systolic volume is usually caused by reduced contractility. Decreased end diastolic volume results from impaired ventricular filling – as occurs when the compliance of the ventricle falls (i.e. when the walls stiffen).
• Reduced spare capacity. As the heart works harder to meet normal metabolic demands, the amount cardiac output can increase in times of increased oxygen demand (e.g. exercise) is reduced. This contributes to the exercise intolerance commonly seen in heart failure.
• Increased heart rate, stimulated by increased sympathetic activity in order to maintain cardiac output. Initially, this helps compensate for heart failure by maintaining blood pressure and perfusion, but places further strain on the myocardium and accelerates the disease process in the long term. It may also cause potentially fatal arrhythmias.
• Hypertrophy (an increase in volume) of the myocardium, caused by the terminally differentiated heart muscle fibres increasing in size in an attempt to improve contractility.
• Enlargement of the ventricles, contributing to the enlargement and spherical shape of the failing heart. The increase in ventricular volume also causes a reduction in stroke volume due to mechanical and contractile inefficiency.^[11]

The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest, and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:

• Arterial blood pressure falls. This stimulates baroreceptors in the carotid body and aortic arch to increase sympathetic stimulation of the blood vessels, resulting in vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart.
• Increased sympathetic stimulation also causes the hypothalamus to secrete ADH, causing further vasoconstriction and fluid retention at the kidneys. This increases the blood volume and blood pressure.
• Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – a hormone which catalyses the production of angiotensin. This hormone and its metabolites cause further vasocontriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume.
• Reduced perfusion of skeletal muscle causes atrophy of the muscle fibres. This can result in weakness, increased fatigueability and decreased peak strength - all contributing to exercise intolerance.^[12]

The increased peripheral resistance and greater blood volume place further strain on the heart and accelerate the process of damage and hypertrophy to the myocardium. Vasconstriction and fluid retention produce an increased hydrostatic pressure in the capillaries. This shifts of the balance of forces in favour of interstitial fluid formation as the increased pressure forces additional fluid out of the blood, into the tissue. This results in oedema (fluid build-up) in the tissues. In right-sided heart failure this commonly in the ankles where venous pressure is high due to the effects of gravity. It may also occur in the abdominal cavity, where the fluid build-up is called ascites. In left-sided heart failure oedema can occur in the lungs - this is called cardiogenic pulmonary oedema. This reduces spare capacity for ventilation, causes stiffening of the lungs and reduces the efficiency of gas exchange by increasing the distance between the air and the blood. The consequences of this are shortness of breath, orthopnoea and paroxysmal nocturnal dyspnea.

The symptoms of heart failure are largely determined by which side of the heart fails. The left side pumps blood into the systemic circulation, whilst the right side pumps blood into the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the system, the main symptoms will be produced by changes to the pulmonary circulation. Reduced ventricular filling and cardiac output on the left side of heart will cause an increase in central venous pressure in the pulmonary veins as blood 'backs up'. Thus the main symptoms of left-sided failure will be pulmonary ones - shortness of breath, orthopnea and paroxysmal noctural dyspnea. However, whilst heart failure usually begins on one side of the heart, the increased central venous pressure on the opposite side causes blood to 'back up,' dramatically increasing the workload of the opposite side of the heart. This will ultimately produce heart failure on the other side if not treated.

Treatment

The treatment of CHF focuses on treating the symptoms and signs of CHF and preventing the progression of disease. If there is a reversible cause of the heart failure (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, or hypertension), that should be addressed as well. Reversible cause treatments can include exercise, eating healthy foods, reduction in salty foods, and abstinence from smoking and drinking alcohol.

Non-pharmacological measures

Patients with CHF are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include:^[13]

• Moderate physical activity, when symptoms are mild or moderate; or bed rest when symptoms are severe.
• Weight reduction – through physical activity and dietary modification, as obesity is a risk factor for heart failure and ventricular hypertrophy.
• Monitor weight - Weight gain of more than 2 pounds is associated with admission to the hospital for heart failure^[14]
• Sodium restriction – excessive sodium intake may precipitate or exacerbate heart failure, thus a "no added salt" diet (60–100 mmol total daily intake) is recommended for patients with CHF. More severe restrictions may be required in severe CHF.
• Fluid restriction – patients with CHF have a diminished ability to excrete free water load. They are also at an increased risk of hyponatremia due to the combination of decreased sodium intake and diuretic therapy. Generally water intake should be limited to 1.5 L daily or less in patients with hyponatremia, though fluid restriction may be beneficial regardless in symptomatic reduction.

Pharmacological management

There is a significant evidence–practice gap in the treatment of CHF; particularly the underuse of ACE inhibitors and β-blockers and aldosterone antagonists which have been shown to provide mortality benefit.^[15] Treatment of CHF aims to relieve symptoms, maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g. spironolactone). It should be noted that while intuitive, increasing heart function with some drugs, such as the positive inotrope Milrinone, leads to increased mortality.^[16][17]

Angiotensin-modulating agents

ACE inhibitor (ACE) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.^[18][9][19] ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy (also referred to as AT₁-antagonists or angiotensin receptor blockers), particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy.^[20][21]

Diuretics

Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure:^[13]

• Loop diuretics (e.g. furosemide) – most commonly used class in CHF, usually for moderate CHF.
• Thiazide diuretics (e.g. hydrochlorothiazide) – useful for mild CHF.
• Potassium-sparing diuretics (e.g. amiloride) – used first-line use to correct hypokalaemia.
  • Spironolactone is used as add-on therapy to ACEI plus loop diuretic in severe CHF.
  • Eplerenone is specifically indicated for post-MI reduction of cardiovascular risk.

If a heart failure patient exhibits a resistance to or poor response to diuretic therapy, ultrafiltration or aquapheresis may be needed to achieve adequate control of fluid retention and congestion. The use of such mechanical methods of fluid removal can produce meaningful clinical benefits in patients with diuretic-resistant heart failure and may restore responsiveness to conventional doses of diuretics.⁹

Beta blockers

Until recently, β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure.^[19] As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, and extended-release metoprolol.

Positive inotropes

Digoxin (a mildly positive inotrope and negative chronotrope), once used as first-line therapy, is now reserved for control of ventricular rhythm in patients with atrial fibrillation; or where adequate control is not achieved with an ACEI, a beta blocker and a loop diuretic.^[19] There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions.^[22] It is contraindicated in cardiac tamponade and restrictive cardiomyopathy.

The inotropic agent dobutamine is advised only in the short-term use of acutely decompensated heart failure, and has no other uses.^[19]

Alternative vasodilators

The combination of isosorbide dinitrate/hydralazine is the only vasodilator regimen, other than ACE inhibitors or angiotensin II receptor antagonists, with proven survival benefits. This combination appears to be particularly beneficial in CHF patients with an African American background, who respond less effectively to ACEI therapy.^[23][24]

Devices and surgery

Patients with NYHA class III or IV, left ventricular ejection fraction (LVEF) of 35% or less and a QRS interval of 120 ms or more may benefit from cardiac resynchronization therapy (CRT; pacing both the left and right ventricles), through implantation of an bi-ventricular pacemaker, or surgical remodelling of the heart. These treatment modalities may make the patient symptomatically better, improving quality of life and in some trials have been proven to reduce mortality.

The COMPANION trial demonstrated that CRT improved survival in individuals with NYHA class III or IV heart failure with a widened QRS complex on EKG.^[25] The CARE-HF trial showed that patients receiving CRT and optimal medical therapy benefited from a 36% reduction in all cause mortality, and a reduction in cardiovascular-related hospitalization.^[26]

Patients with NYHA class II, III or IV, and LVEF of 35% (without a QRS requirement) may also benefit from an implantable cardioverter-defibrillator (ICD), a device that is proven to reduce all cause mortality by 23% compared to placebo. This mortality benefit was observed in patients who were already optimally-managed on drug therapy.^[27]

Another current treatment involves the use of left ventricular assist devices (LVADs). LVADs are battery-operated mechanical pump-type devices that are surgically implanted on the upper part of the abdomen. They take blood from the left ventricle and pump it through the aorta. LVADs are becoming more common and are often used by patients who have to wait for heart transplants.

The final option, if other measures have failed, is cardiac transplant surgery (heart transplant) or implantation of an artificial heart. A radical new type of surgery, which is largely untested and is still in its first stages of development, was invented by Brazilian doctor Randas Batista in 1994. It involves removal of a swath of the left ventricle, to make contractions more efficient and prevent backflow of blood into the left atrium through the bicuspid valve.^[28]

Palliative care and hospice

The growing number of patients with Stage D heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines.

Prognosis

Among several clinical prediction rules for prognosing acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.^[29] Easy methods for identifying low risk patients are:

• ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications.
• BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or less breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications.

References

See also

• Cardiogenic shock
• Heart transplant
• Dor procedure
• ACE inhibitor
• Isosorbide dinitrate/hydralazine
• Killip class
• Ventricular remodeling
• Fluid overload