Chronic heart failure Flashcards
The major determinants of variation of cardiac output are:
Heart rate
Myocardial contractility
Preload
Afterload
Heart failure
A condition in which the heart fails to maintain a circulation adequate for the body’s needs
Signifies inability of the heart to discharge its contents adequately
Characterised by cardiac dysfunction associated with dyspnoea and/or fatigue
Acute heart failure
Sudden circulatory collapse
e.g. haemorrhagic shock, cardiogenic shock during acute MI
Chronic (congestive) heart failure
A condition in which the heart fails to maintain a circulation adequate for the body despite adequate venous return
High prevalence
Annual incidence of new diagnoses approximately 3-5 per 1000
Median 5 year mortality is ~50% with an annual mortality of 60% for more severe heart failure
Forward HF
Backward HF
Forward HF: predominant problem is reduced output
Backward HF: near normal output but venous congestion
Systolic HF
Diastolic HF
Systolic HF: reduced ventricular contractility
Diastolic HF: reduced ventricular filling
Low-output HF
High output HF
Low output: implies reduced output
High output HF: high output but still insufficient e.g. in severe anaemia or thyrotoxicosis
Compensated HF
Decompensated HF
Compensated HF: stable, adequately controlled symptoms
Decompensated HF: acute overt episode on chronic background (relapsing/ remitting course)
Aetiology of CHF
Usually there is some form of cardiomyopathy
Many causes: inherited- congenital hypertrophic CM, arrhythmogenic RV CM
Acquired- ischaemic cardiomyopathy, pressure overload, valvular disease, infection/ inflammation, chronic volume overload
Acquired Cardiomyopathies
Ischaemic cardiomyopathy- post myocardial infarction (LV with/without RV)
Increased ventricular afterload- systemic hypertension, pulmonary disease or pulmonary hypertension, aortic valve stenosis, pulmonary valve stenosis
Valvular disease- mitral valve stenosis
Infection/ inflammation- viral/ bacterial myocarditis, alcoholic cardiomyopathy, doxorubicin-induced myocarditis etc.
Gradual reduction in cardiac function results in clinical signs/ symptoms
Reduced cardiac contractility Reduced cardiac output Reduced tissue perfusion Reduced venous return and volume expansion Dyspnoea, fatigue and oedema
Oedema in heart failure
A characteristic feature of congestive heart failure: limb extremities especially ankles (pitting oedema), intra-abdominal fluid accumulation (ascites), pulmonary oedema causes crepitations and dyspnoea
Neurohormonal response to decreased cardiac output
Primary response to a fall in CO is a Neurohormonal reflex to maintain perfusion of vital organs
In evolutionary terms, it is an ancient conserved neuroendocrine defence reaction to massive blood loss
Major features are: peripheral vasoconstriction, reduced fluid excretion through sympathetic nervous system activation and renin-angiotensin system activation
Some neurohormones promote proliferative signalling
Angiotensin II and NAd promote myocyte hypertrophy and fibroblast mitosis
Aldosterone promotes cardiac collagen synthesis