Heart failure: classification and pathophysiology

Heart failure (HF) is a clinical syndrome and not a stand-alone diagnosis – identification of the aetiology of the underlying cardiac abnormality and the whole body’s response to it is key to providing optimal management of the individual patient. The classic triad of clinical features – breathlessness, fatigue and fluid retention – can be the result of any disorder (genetic or acquired) affecting the structure or function of the heart in a manner that impairs its ability to act as an efficient pump. Despite improved understanding of the pathophysiology, and a wider range of therapeutic options, HF remains a serious condition with considerable morbidity and mortality. It is a global problem, though the relative importance of different aetiologies differs between the developed world – where the syndrome is most commonly a consequence of ischaemic heart disease – and the developing world, where rheumatic fever remains an important cause. HF can present either de novo, as a consequence of acute myocardial insult, or in its chronic form, where decompensation secondary to coincident medical problems often requires acute management. The HF syndrome is characterized by cardiac dysfunction with haemodynamic, renal and neurohormonal changes attempting to maintain circulatory homeostasis. Ultimately, such changes are maladaptive and result in excessive sodium and fluid retention, changes in muscle blood flow, altered breathing pattern, arrhythmia, and an inflammatory state with immune activation. Current evidence-based therapies ameliorate these responses and improve survival and quality of life.