Does the ventricle limit cardiac contraction rate in the anoxic turtle (Trachemys scripta)? II. In vivo and in vitro assessment of the prevalence of cardiac arrhythmia and atrioventricular block

Previous studies have reported evidence of atrio-ventricular (AV) block in the oxygen-limited Trachemys scripta heart. However, if cardiac arrhythmia occurs in live turtles during prolonged anoxia exposure remains unknown. Here, we compare the effects of prolonged anoxic submergence and subsequent reoxygenation on cardiac electrical activity through in vivo electrocardiogram (ECG) recordings of 21 °C- and 5 °C-acclimated turtles to assess the prevalence of cardiac arrhythmia. Additionally, to elucidate the influence of extracellular conditions on the prominence of cardiac arrhythmia, we exposed spontaneously contracting T. scripta right atrium and electrically coupled ventricle strip preparations to extracellular conditions that sequentially and additively approximated the shift from the normoxic to anoxic extracellular condition of warm- and cold-acclimated turtles. Cardiac arrhythmia was prominent in 21 °C anoxic turtles. Arrhythmia was qualitatively evidenced by groupings of contractions in pairs and trios and quantified by an increased coefficient of variation of the RR interval. Similarly, exposure to combined anoxia, acidosis, and hyperkalemia induced arrhythmia in vitro that was not counteracted by hypercalcemia or combined hypercalcemia and heightened adrenergic stimulation. By comparison, cold acclimation primed the turtle heart to be resilient to cardiac arrhythmia. Although cardiac irregularities were present intermittently, no change in the variation of the RR interval occurred in vivo with prolonged anoxia exposure at 5 °C. Moreover, the in vitro studies at 5 °C highlighted the importance of adrenergic stimulation in counteracting AV block. Finally, at both acclimation temperatures, cardiac arrhythmia and irregularities ceased upon reoxygenation, indicating that the T. scripta heart recovers from anoxia-induced disruptions to cardiac excitation.