Heart failure is a clinical syndrome that results from an inability of the heart to maintain adequate cardiac output.
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:
There are a number of key terms to be aware of to better understand heart failure.
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.
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.
The pathogenesis of heart failure is complex and follows from mechanisms that result in a failure of cardiac output.
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.
In patients with suspected heart failure, the first step is taking a detailed history and performing a clinical examination. The next step is measuring a BNP, which is used to risk stratify patients and determine the urgency of referral. At this point, an ECG should be performed in all patients. Consideration should be made regarding further blood tests, chest radiograph, urinalysis and lung function testing (if alternative diagnosis is suspected). However, it is reasonable to await the BNP result.
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. It has an exclude negative predictive value, which means a negative test should warrant investigation into others causes of the patients symptoms.
The BNP, along with a detailed history and examination and other relevant investigations, may be used to decide who to refer for further assessment:
A transthoracic echocardiography (TTE) is the main investigation for the confirmation of heart failure. It should be completed in patients with an elevated BNP. A TTE may still be warranted, regardless of BNP, if clinical examination reveals a murmur or the ECG is abnormal for example.
The main determinant of an TTE is to look at the ejection fraction of the heart. This helps to differentiate suspected heart failure into three groups:
NOTE: additional echo criteria are used to help diagnose HFpEF or 'diastolic heart failure'. These are broadly based on ventricular thickness, chamber size and other features
Investigations are essential to determine the aetiology, complications associated with heart failure and modifiable risk factors.
Management follows NICE guidance and is based upon the type of heart failure, although there are some general management principles.
ACE inhibitors and beta blockers are the mainstay of management.
NOTE: these second-line agents should be prescribed following specialist assessment by a clinician that manages heart failure.
Insufficient evidence exists for the role of ACE-inhibitors, ARBs, and beta-blockers in heart failure with preserved LVEF.
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