Haemodynamics & Electrophysiology of the Heart
B.Pharm Pharmacology II, BP503T — Unit I
Introduction to haemodynamics and electrophysiology of heart. → jump to section
This page covers syllabus item (a) only. The other five items in this unit — Unit I(b): Drugs used in congestive heart failure. Unit I(c): Anti-hypertensive drugs. Unit I(d): Anti-anginal drugs. Unit I(e): Anti-arrhythmic drugs. Unit I(f): Anti-hyperlipidemic drugs. — are published as separate pages.
Haemodynamics & Electrophysiology of the Heart
Haemodynamics and the electrical system that drives every heartbeat — the foundation for every cardiovascular drug class that follows.
Haemodynamics basics
Haemodynamics is the study of the forces and mechanics of blood flow through the heart and vessels. The heart is a pressure-and-volume pump: how much blood it ejects, and against how much resistance, together set blood pressure and cardiac performance.
- Cardiac output (CO)
- The volume of blood pumped by the heart per minute. CO = stroke volume (SV) × heart rate (HR).
- Stroke volume (SV)
- The volume ejected per beat, set by preload, afterload and contractility.
- Preload
- The degree of stretch on the ventricle just before contraction, set mainly by venous return (Frank–Starling relationship: within limits, more stretch → a stronger contraction).
- Afterload
- The resistance the ventricle must pump against to eject blood — chiefly the systemic vascular resistance (SVR) and arterial pressure.
- Contractility
- The force of contraction at a given preload/afterload, controlled by sympathetic tone and calcium handling in the myocyte.
- Mean arterial pressure (MAP)
- MAP ≈ CO × SVR. Blood pressure is therefore a product of how much blood the heart pumps and how much the vessels resist that flow.
Electrophysiology of the heart
Two types of myocardial fibre can be distinguished electrophysiologically: fast-response fibres (atrial and ventricular muscle, the His–Purkinje system) and slow-response fibres (the SA and AV nodes, the heart’s natural pacemakers).
- Phase 0 (fast fibres)
- Rapid depolarisation, driven by a fast influx of Na⁺ through voltage-gated sodium channels.
- Phase 1–2
- Brief partial repolarisation, then a plateau maintained by a balance of inward Ca²⁺ current and outward K⁺ current — this plateau is what makes cardiac muscle contract as one long beat rather than tetanising like skeletal muscle.
- Phase 3
- Repolarisation, driven by outward K⁺ current as the calcium channels close.
- Phase 4 (nodal fibres)
- A slow, spontaneous “funny current” (Na⁺ influx) drives the membrane potential gradually up to threshold — this is what gives the SA node its automatic, pacemaking rhythm.
- Refractory period
- The period after an action potential during which the fibre cannot (absolute) or can only partly (relative) be re-excited — this protects the heart from re-entrant, self-sustaining arrhythmias.
Most cardiovascular drug classes act by changing one of these ionic currents or one of these haemodynamic variables: calcium-channel blockers slow the slow inward current; beta-blockers reduce sympathetic drive to contractility and heart rate; diuretics and vasodilators change preload and afterload; anti-arrhythmics act directly on the ion channels that generate each phase.
The conduction system and the ECG
The electrical impulse normally starts in the SA node (the natural pacemaker, right atrium), spreads across both atria, is delayed briefly at the AV node (allowing the atria to finish contracting before the ventricles start), then travels down the bundle of His, the left and right bundle branches, and the Purkinje fibres to activate the ventricles from the inside out.
- PR interval
- SA node to ventricular activation — mostly the AV-node delay. Prolonged by drugs or disease that slow AV conduction (e.g. beta-blockers, verapamil, diltiazem, digoxin).
- QT interval
- Total duration of ventricular depolarisation and repolarisation. Many anti-arrhythmics and some other drugs can prolong it and predispose to the dangerous arrhythmia torsades de pointes.