Anaes · Applied cardiovascular & respiratory physiology
Cardiac electrophysiology & conduction
Also known as Cardiac conduction system · SA node · AV node · His-Purkinje system · Funny current · Cardiac action potential
The heart generates and propagates its own electrical impulse through a specialised conduction pathway, and the orderly sequence of that propagation is what the ECG records. The framework rests on five exam-critical ideas: the sinoatrial node is the physiological pacemaker because its membrane drifts up to threshold on the funny current (a mixed sodium-potassium inflow through HCN channels) and fires spontaneously; the atrioventricular node deliberately delays conduction (the PR interval) so the atria finish ejecting before the ventricles contract, and conducts slowly and decrementally; the His-Purkinje system then depolarises the ventricles rapidly and synchronously (the QRS); conduction between cells is carried by gap junctions, so disease of the gap junction or of the specialised tissue slows or blocks conduction; and arrhythmia arises by one of three mechanisms — enhanced automaticity, re-entry, or triggered activity — each with drugs and anaesthetic triggers that favour it. Built on the cardiac-conduction and gap-junction biology review (Fujiu 2026), the funny-current structure-function review (Saponaro 2026), the HCN4-in-the-AV-node review (Copier 2025), the HCN4-and-arrhythmia mutations review (Fan 2025), the cardiac ion-channel pharmacology review (Orts 2026), the sudden-cardiac-death genetics review (Lovric Bencic 2025), and the magnesium-treatment review (Anderson 2021).
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Red flags
- The AV node conducts slowly and decrementally — it is the structure that protects the ventricles from rapid atrial rates (atrial fibrillation): only every second or third atrial impulse is conducted, a property called concealed conduction. Disease here causes heart block.
- The PR interval (normally 120 to 200 ms) is the atrioventricular nodal delay; a prolonged PR interval is first-degree heart block, and progressive PR prolongation then a dropped beat is the Wenckebach (Mobitz I) pattern.
- A wide QRS (over 120 ms) means ventricular activation is travelling through slow muscle-to-muscle conduction rather than the fast His-Purkinje system — the defining distinction between a supraventricular rhythm with aberrancy and a ventricular rhythm.
- Re-entry is the commonest mechanism of sustained arrhythmia (AVNRT, atrial flutter, ventricular tachycardia) and requires an anatomical or functional circuit, unidirectional block, and a slow limb that allows recovery — the substrate anaesthetists create or worsen with ischaemia, electrolyte disturbance, and catecholamine surge.
- Congenital and acquired channelopathies (long-QT, Brugada, HCN4 pacemaker mutations) cause sudden arrhythmic death in structurally normal hearts — anaesthesia is a recognised trigger, and QT-prolonging drugs are cumulative and dangerous.
Meet the patient
A 28-year-old woman with known long-QT syndrome presents for an emergency appendicectomy. She has been stable on a beta-blocker, but the anaesthetic plan must now screen every proposed drug for QT liability — inherited channelopathies (Brugada, long-QT, catecholaminergic polymorphic VT) and cardiomyopathies are among the most common causes of sudden death in the young. This is cardiac electrophysiology at the bedside: the action potential phases made visible on the ECG, and the drugs that move them. (Illustrative scenario; the cited genetics review enrolled no anaesthesia patients.)[6]
Hold three things and the topic organises itself: the funny current that fires the SA node, the sodium-calcium-potassium sequence of the ventricular action potential, and the three mechanisms of arrhythmia. Every drug, electrolyte and anaesthetic effect attaches to one of those.[1]
References7ShowHide
- [1]Fujiu K. Cardiac Conduction in Physiology and Disease - Gap Junction Biology, Immune Modulation, and Computational Electrophysiology Circ J, 2026.PMID 41535054
- [2]Saponaro A, et al. Structure mirroring function: What's the 'matter' with the funny current? J Physiol, 2026.PMID 40013960
- [3]Copier JS, et al. HCN4 in the atrioventricular node Heart Rhythm, 2025.PMID 39988103
- [4]Fan W, et al. HCN4 and arrhythmias: Insights into base mutations Mutat Res Rev Mutat Res, 2025.PMID 39922561
- [5]Orts DJB, et al. Chemically induced cardiotoxicity: Role of voltage dependent ion channels Curr Top Membr, 2026.PMID 42082304
- [6]Lovrić Benčić M, Levicki R Genetics of Sudden Cardiac Death Diseases, 2025.PMID 41590224
- [7]Anderson S, et al. Magnesium Treatment in Pediatric Patients J Pediatr Health Care, 2021.PMID 34479684