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Cardiovascular physiology for anaesthesia

Blood pressure is the product of cardiac output and vascular resistance, and cardiac output is set by heart rate, preload, afterload and contractility; almost every anaesthetic drug changes one of them, so whoever understands these equations understands why the patient's pressure fell and what to give.

Why it matters in the exam

The exam asks about the Frank–Starling law, calculating systemic vascular resistance, coronary perfusion pressure and why tachycardia is dangerous for an ischaemic heart, the determinants of myocardial oxygen consumption, pressure–volume loops, and reflexes such as the baroreceptor reflex, the Bezold–Jarisch reflex and the Cushing reflex. Questions also cover the effect of anaesthetic drugs on each component.

Cardiac output equals heart rate times stroke volume. By the Frank–Starling law, when the ventricle fills more (higher preload) the fibres stretch and the beat is stronger, up to the point where a diseased heart no longer responds. Afterload is the tension the ventricle must generate to open the valve and eject blood, and by the Laplace law wall tension rises with pressure and ventricular radius and falls with wall thickness. Systemic vascular resistance is calculated as 80 times the difference between mean arterial pressure and central venous pressure, divided by cardiac output. Venous return depends on the difference between mean systemic filling pressure and right atrial pressure, so venodilation under anaesthesia lowers return and output.

The left ventricle receives most of its coronary blood in diastole. Coronary perfusion pressure equals aortic diastolic pressure minus left ventricular end-diastolic pressure; so a low diastolic pressure or a high filling pressure harms supply, and tachycardia shortens diastole and also raises demand. The main determinants of myocardial oxygen consumption are heart rate (the most important), wall tension and contractility. Oxygen delivery to the body is cardiac output times arterial oxygen content times 10. Propofol and volatile agents lower resistance and contractility and blunt the baroreceptor reflex, ketamine stimulates the sympathetic system, and desflurane raised quickly causes tachycardia. The Bezold–Jarisch reflex produces slowing of the heart and a fall in pressure when the ventricle empties and contracts vigorously, for example in a high spinal or the sitting position.

Key points

Summary table

ConceptMain pointExam point
Cardiac outputHeart rate times stroke volume; stroke volume depends on preload, afterload and contractilityFrank–Starling: more filling, a stronger beat
Systemic resistance80 times (mean pressure minus central venous pressure) divided by outputPropofol and volatiles lower it
Coronary perfusionAortic diastolic pressure minus ventricular end-diastolic pressureThe left ventricle is perfused mainly in diastole
Myocardial oxygen consumptionHeart rate, wall tension, contractilityHeart rate is the most important factor
Pressure–volume loopValve stenosis: pressure load; regurgitation: volume loadThe width of the loop is the stroke volume
ReflexesBaroreceptors in the carotid sinus and aortic arch; Bezold–Jarisch; CushingVolatiles blunt the baroreceptor reflex

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Sources

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Reviewed by the Examqo AI Professor · 2026-11-02. The text may contain errors; when in doubt, check the source.