Heart failure is a clinical syndrome that results from an inability of the heart to maintain adequate circulation.
It is a progressive disorder associated with high morbidity and mortality. Prognosis is generally poor; approximately 50% die within five years.
A wide range of classifications reflects the complexity of the condition.
The New York Heart Association (NYHA) classifies the symptoms of heart failure as follows:
Cardiac remodelling refers to changes in cardiac size, shape and function in response to cardiac injury or increased load (e.g. exercise).
Pathological remodelling may occur after conditions such as myocardial infarction or cardiomyopathy.
The aetiology of heart failure is complex.
Though systemic disease may cause heart failure it will typically do so through one of the pathologies listed below (often cardiomyopathy). The exception are the high-output heart failures which are discussed separately.
These are the most common causes of heart failure.
Cardiomyopathy is a common cause of heart failure. Dilated cardiomyopathies are often idiopathic.
Valvular disease may lead to either acute or chronic heart failure.
Arrhythmias (abnormalities of normal conduction) may cause acute heart failure through decompensation.
Typically heart failure is caused by a reduced cardiac output. In some cases, however, the cardiac output may be raised but the systemic vascular resistance very low. Causes include:
Stroke volume: the amount of blood pumped out of the heart from each contraction.
Cardiac output: the amount of blood pumped out of the heart in one minute, equivalent to HR x SV.
Preload: stretching of cardiomyocytes at the end of diastole.
Afterload: pressure or load against which the ventricles must contract.
Inotropy: refers to myocardial contractility (i.e. the force of muscular contractions).
The relationship between ventricular stretching and contractility. Essentially stretching of cardiac muscle (within physiological limits) will increase the force of contraction.
Discovered in the mid-19th century by Otto Frank and Ernest Starling. The ability of the heart to respond to increased venous return by increasing the stroke volume is essential to normal cardiac function. Failure to do so would result in input-output mismatch and pooling of blood in either the systemic or pulmonary circulation.
The titles of the axis may vary slightly. Here we display stroke volume (SV) and left ventricular end-diastolic volume (LVEDV) - essentially the preload.
In a normal heart, increased venous pressures lead to increased venous return and raised end diastolic volume (EDV). This increased EDV means an increase in the preload (see definition above), as there is increased stretch on the cardiomyocytes. This increased stretching - an increase in the length of the sarcomere - leads to a more forceful contraction. In turn, this increase in contractility leads to an increase in the stroke volume.
Interestingly, the heart does not sit on a single curve, rather it is affected by afterload and the inotropic state.
In effect, venous return governs where on the curve the heart sits while the pre-existing afterload and inotropic environment control which curve it sits on.
In summary, the primary determinants of stroke volume are:
The relationship between increasing preload and increasing stroke volume does not continue unfettered. At a point, increases in preload lead to a depression of contractility and stroke volume - this concept is crucial in understanding heart failure.
As a heart fails the amount of blood left after each contraction increases i.e. the ejection fraction decreases. This increased end-systolic volume (ESV) means the myocardium experiences greater stretch. In a normal heart this would lead to an increase in myocardial contractility by the Frank-Starling principle.
However, in a failing heart, this causes a reduction in stroke volume (and thus cardiac output).
The body may compensate for this in a number of ways:
To maintain cardiac output, the heart undergoes hypertrophy of the stressed myocardium. This accompanied by other compensatory mechanisms discussed above may mean that patients are asymptomatic at rest. However, physical activity may lead to decompensation and the development of symptoms.
CHF typically manifests with dyspnoea and fatigue (which may limit exercise tolerance) and symptoms associated with fluid retention.
NICE recommends echocardiography and specialist assessment in patients with suspected heart failure. BNP is used to stratify risk in those without previous history of myocardial infarction.
Indications for urgent specialist assessment within 2 weeks:
B-type natriuretic peptide (BNP) is a protein released by cardiomyocytes in response to excessive stretching. It is used to assess the likelihood of heart failure. Conditions other than heart failure which may raise BNP levels include diabetes, sepsis, old age, hypoxaemia (PE and COPD), kidney disease, and liver cirrhosis.
Management follows NICE guidance and is based upon the type of heart failure, although there are some general management principles.
Angiotensin receptor blockers (ARBs) such as losartan may be used in those individuals who have intolerable side effects with ACE inhibitors.
Insufficient evidence exists for the role of ACE-inhibitors, ARBs, and beta-blockers in heart failure with preserved LVEF.
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