St. Thomas Hospital Cardioplegia #2 fails to suppress slow reaction pacemaker cell electrical activity

Background Inadequate right atrial myocardial preservation during cardioplegic arrest may promote postoperative supraventricular arrhythmias (SVA). We determined (1) if oxygenated St. Thomas Hospital Cardioplegia #2 (STH2) alone causes slow reaction pacemaker cell (SR) quiescence; and (2) if hypothermia, higher [K⁺], lower [Ca²⁺], and verapamil in STH2 suppresses SR electrical activity. Materials and methods A glass microelectrode recorded SA node SR membrane action potentials (AP) in rabbits (n = 23, 1.93 ± 0.45 kg) randomized to normothermic STH2 (33°C, n = 6), hypothermia (20°C, n = 4), hypothermic STH2 (22°C, n = 3), lower calcium STH2 (n = 3), higher potassium STH2 (n = 4), and STH2 plus Verapamil (n = 3). Results Normothermic STH2 depressed SR action potential amplitude and action potential duration (APD), but did not completely suppress action potential generation. Hypothermia alone prolonged APD and sinus cycle length and suppressed SR AP. STH2 with hypothermia (to 20°C) completely suppressed propagating AP and STH2 plus 0.04 Ca²⁺ mEq/L inhibited SR AP generation. STH2 plus 30 mEq K⁺ and STH2 plus 2.5 mmol/L verapamil failed to generate SR AP. Conclusion STH2 cannot prevent SA node SR myocardial cells from low-amplitude AP autogeneration above 21°C. STH2 with 30 mEq/L K⁺, STH2 with 0.02mEq/L Ca²⁺, and STH2 plus 2.5 mmol/L verapamil can arrest AP generation in SR and potentially prevent postoperative SVA.