Heart failure is a clinical syndrome, comprising signs and symptoms that result from impaired efficiency of the heart as a pump (NICE CHF, 2010). It may exist as a chronic state, where patients are symptomatic but functionally stable, or it may present acutely; either as a decompensation of known disease, or with no previous medical history of heart failure.

Impairment of pump function can be broken down in broad terms into either systolic or diastolic dysfunction. Heart failure can be mainly left or right sided, with left sided heart failure often leading to elevated pulmonary resistance and right sided overload, showing signs of right sided heart failure. We will predominantly be discussing left-sided dysfunction, but the principles remain the same. This type of heart failure is initiated by a haemodynamic abnormality, resulting in ventricular remodelling – this in turn leads to further haemodynamic changes, reflecting a progressive disease (Johnson, 2014). Acute decompensation will often occur as a result of increased stress on an already dysfunctional system.

Systolic dysfunction is central in heart failure with reduced ejection fraction (HFrEF) and occurs as a result of decreased myocardial performance as a pump. At this end of the clinical spectrum, the ventricle is unable to expel sufficient volume leading to inadequate cardiac output and increased preload, which may be a result of a dilated and inefficient ventricle. Cardiomyopathy, valvular dysfunction, and ischaemic heart disease are the most common causes leading to HFrEF. Over time, structural changes occur and the ventricle becomes dilated, with eccentric remodelling of the heart (Komamura, 2013; Tania & Frantz, 2016). Mitral regurgitation is a frequent additional mechanical problem, often forgotten or neglected. It is dynamic and worsens with volume overload and increased filling pressure.

Diastolic dysfunction is a hallmark of heart failure with preserved ejection fraction (HFpEF) that develops in a heart with an entirely normal, or only slightly reduced ejection fraction. Diastole is composed of a relaxation phase after the aortic valve closes, followed by ventricular filling until contraction begins, signalling the start of the systolic phase. Myocardial relaxation is an active process, governed by the active uptake of calcium ions into intracellular stores – thus, any disease process that interferes with this may impede relaxation, such as ischaemia or hypertrophy. Myocardial fibrosis and hypertrophy will both increase ventricular stiffness, also hindering ventricular relaxation and filling. As the left ventricle is insufficiently filled, stroke volume is reduced, and adequate cardiac output cannot be maintained. Atrial pressures become raised, resulting in an increased ventricular end-diastolic pressure. This will in turn result in back-pressure via the pulmonary veins, culminating in pulmonary congestion and oedema (Komamura et al., 2013; Tania & Franz, 2016).