Cardiovascular Physiology
The cardiovascular system maintains perfusion to all tissues through coordinated heart function, vascular tone, and blood volume regulation. Cardiac output (CO): 5-6 L/min (HR 60-100 bpm × SV 60-100 mL); determined by...
What matters first
The cardiovascular system maintains perfusion to all tissues through coordinated heart function, vascular tone, and blood volume regulation. Cardiac output (CO): 5-6 L/min (HR 60-100 bpm × SV 60-100 mL); determined by...
Cardiogenic shock with low cardiac output
2 Feb 2026
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Clinical board
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Urgent signals
Safety-critical features pulled from the topic metadata.
- Cardiogenic shock with low cardiac output
- Severe arrhythmias compromising perfusion
- Acute coronary syndrome with ST elevation
- Pulmonary oedema with respiratory failure
Exam focus
Current exam surfaces linked to this topic.
- ANZCA Primary Written
- ANZCA Primary Viva
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Cardiovascular physiology forms the foundation of critical care practice, informing haemodynamic monitoring, vasoactive ... CICM Fellowship Written, CICM Fellow
The cardiovascular system maintains perfusion to all tissues through coordinated heart function, vascular tone, and blood volume regulation. Cardiac output (CO): 5-6 L/min (HR 60-100 bpm × SV 60-100 mL); determined by...
Clinical explanation and evidence
Quick Answer
The cardiovascular system maintains perfusion to all tissues through coordinated heart function, vascular tone, and blood volume regulation. Cardiac output (CO): 5-6 L/min (HR 60-100 bpm × SV 60-100 mL); determined by preload (venous return, Frank-Starling mechanism), contractility (inotropy, catecholamines, calcium), afterload (SVR, arterial impedance), heart rate. Frank-Starling law: Increased ventricular end-diastolic volume (preload) increases stroke volume up to physiological limit; beyond this, further stretch reduces contractility (ventricular failure). Blood pressure: MAP = CO × SVR; normal MAP 70-105 mmHg; systolic pressure determined by stroke volume and arterial compliance, diastolic pressure determined by SVR and arterial elasticity. Autonomic control: Sympathetic (β1 receptors—HR, contractility; α1 receptors—vascular constriction); parasympathetic (vagus—reduces HR, minimal vascular effect); baroreceptor reflex (carotid and aortic arch sensors maintain BP via rapid HR and vascular adjustments). Coronary circulation: Left coronary (LAD, circumflex—supplies LV, anterior septum, lateral wall), right coronary (supplies RV, inferior wall, SA/AV nodes in most); coronary perfusion occurs during diastole (80%), especially important in tachycardia (reduced diastolic time); autoregulation maintains flow across MAP 60-180 mmHg. Electrophysiology: SA node pacemaker (60-100 bpm), AV node delay (0.1 sec), Purkinje conduction; action potential phases (0—fast Na+ influx, 1—transient K+ efflux, 2—Ca2+ influx plateau, 3—K+ efflux repolarization, 4—resting); refractory periods prevent tetany. Anaesthetic implications: Most anaesthetics reduce myocardial contractility and vasodilate (reduce afterload); compensate with fluids, vasopressors; volatile agents preserve autoregulation better than IV agents; ketamine maintains BP via sympathetic stimulation; propofol causes profound vasodilation and myocardial depression. Vascular function: Arteries (pressure reservoir, compliance), arterioles (resistance vessels, regulated by autonomic and local factors), capillaries (exchange), veins (capacitance vessels, 70% blood volume). Indigenous populations: Higher rates of cardiovascular disease (2-3×); careful assessment and management of coronary risk essential. [1-10]