POST‐EXERCISE HYPERPNEA AND CARDIAC ASYSTOLE

Abstract

We have recently reported that, in resting conditions, spontaneous eupneic respiration is maintained following a cardiac arrest (CA) in humans and in an animal model of ventricular fibrillation. This response deprived from any relevant role in arterial blood gas homeostasis, as circulation is abolished, still results in the production of a low level of rhythmic arterial blood pressure and in a reduction in alveolar PCO2. We are reporting here that, in a sheep model, the ventilatory control system retains during a CA the fundamental property of maintaining breathing, for 70± 41 seconds, in proportion to the level of metabolism preceding the period of asystole. As a result, ventilation persists during CA following muscle contractions but at a much higher level than at rest, despite the lack of pulmonary blood flow and cardiac output. We discuss the view that this response could be the expression of a yet unrecognised rudimentary defence mechanism aimed at limiting the consequences of an acute failure of the cardiac pump in mammals. Moreover, this “protective” response is not predictable from the traditional respiratory control feedback systems thought to be involved during exercise or its recovery.