Cardiac electrophysiology is fundamental to anesthetic practice. The cardiac action potential (AP) orchestrates myocardial conduction and contractility through precise ion fluxes across cardiomyocyte membranes. Anesthetic drugs, electrolyte imbalances, and pathological conditions modulate these ion currents, influencing perioperative rhythm and hemodynamics.
For anesthesiologists, a layered learning approach—Molecular (ion channels) → Cellular (action potential phases) → Clinical (ECG, arrhythmias, drug effects)—provides a powerful framework to anticipate perioperative events and optimize patient safety.
What is the Cardiac Action Potential?
The cardiac AP is the electrical driver of cardiac contraction. Generated by sequential opening and closing of ion channels, it consists of five phases (0–4), each correlated with distinct ionic currents and ECG signatures.
Analogy: Think of the cardiac AP like a stadium wave—each ion channel “section” rises in sequence, passing the signal smoothly. If one section misfires, the rhythm breaks, leading to chaos (arrhythmia).
Why Is It Important for Anesthesiologists?
Anesthetic Drugs Affect Ion Channels → Propofol, sevoflurane, and local anesthetics directly modulate Na⁺, Ca²⁺, and K⁺ channels.
Electrolyte Shifts Are Common → Hypokalemia, hyperkalemia, hypocalcemia, and hypomagnesemia alter action potentials intraoperatively.
High-Risk Patients → Prolonged QT, heart failure, and ischemic cardiomyopathy amplify anesthetic risks.
Monitoring Interpretation → Linking AP phases to ECG helps manage arrhythmias and anticipate instability.
References
Butterworth JF, Mackey DC, Wasnick JD. Morgan & Mikhail’s Clinical Anesthesiology. 7th ed. New York: McGraw-Hill; 2022.
Roden DM. Drug-induced prolongation of the QT interval. N Engl J Med. 2004;350(10):1013-22.
Molecular: Fast Na⁺ influx via Nav1.5 channels.
Cellular: Sharp AP upstroke (~–70 mV to +20 mV).
Clinical (ECG): QRS complex.
Clinical Anesthesia Relevance
Local anesthetics (bupivacaine, lidocaine) block Nav1.5 → conduction block.
Volatile anesthetics reduce Na⁺ influx → decreased excitability.
Pearls & Pitfalls
Pearl: Lidocaine selectively suppresses ischemic myocardium → useful in ventricular arrhythmias.
Pitfall: Bupivacaine binds Na⁺ channels tightly → refractory cardiac arrest unless lipid therapy is given.
References
Miller RD, Cohen NH, Eriksson LI, et al. Miller’s Anesthesia. 9th ed. Philadelphia: Elsevier; 2020.
Neal JM, Mulroy MF, Weinberg GL. ASRA checklist for LAST. Reg Anesth Pain Med. 2012;37(1):16-18.
Molecular: Transient outward K⁺ efflux via Ito channels.
Cellular: Brief notch in AP.
Clinical (ECG): Early ST segment.
Clinical Anesthesia Relevance
Hypokalemia prolongs Phase 1 → favors reentry.
Hyperkalemia blunts repolarization →...
