Heart failure occurs when the heart is unable to pump blood at a rate that meets the metabolicrequirements of the peripheral tissue.Compensatory Mechanisms: are triggered during reduced myocardial contractility or increasedhaemodynamic burden.
Activation of neurohormonal systems:noradrenaline, renin-angiotensin system, ANP.
Frank-starling mechanism: Cardiac failure causes
EDP resulting in increased stretch of cardiacmuscle
fibres contract more forcibly, hence
Myocardial structural changes (hypertrophy).This is an adaptation to chronic
since myocytes can’t proliferate, concentric or
eccentric hypertrophy occurs.
Adaptive mechanisms eventually aren’t sufficient with
sustained worsening of heart
pathologic changes (eg.myocyte apoptosis, cytoskeletal changes, altered ECMsynthesis) cause structural and functional disturbances.Classification: resulting failure can be classified by a variety of mechanisms:
Forward failure: diminished cardiac output, reduced tissue perfusion.vs Backward (congestive) failure: back pressure, venous congestion and oedema.
Systolic failure: inability to contract normally and expel blood.vs Diastolic failure: inability to fill ventricles.
High output failure: heart is pumping normally, however tissue demands have greatly increased.vs Low output failure: heart cannot keep pace with basic peripheral demands.
Acute heart failure: quick onset, usually systolic heart failure and hypotension but no oedema.vs Chronic heart failure: long term, often normal BP but with oedema.
Compensated heart failure: if compensatory mechanism produce sufficient COvs Decompensated heart failure: compensatory mechanisms, especially hypertrophy, increaseO
requirements, eventually leading to insufficient CO and increasing risk of ischaemic injury.