Profound reflex bradycardia produced by transient hypoxia or hypercapnia in man.

A quadraplegic patient was able to breathe adequately for the first 3 days after his cervical spinal cord was transected by a bullet. However, for several days thereafter spontaneous ventilation became inadequate, most likely due to edema of the cord, and mechanical ventilation was required. When the ventilator was disconnected for required tracheal aspiration, before there was any tracheal stimulation, profound bradycardia, hypotension and syncope occurred within a few seconds. The bradycardia could be diminished by atropine and its onset delayed by prior ventilation with oxygen. Because of the rapid onset of the hemodynamic changes and their correlation with relatively small changes in PaO2 and PaCO2, it is suggested that this vagally mediated bradycardia represents the primary cardiac reflex response to peripheral chemoreceptor stimulation, which, although extensively studied in experimental animals, has not before been described in man. Just as in animals, it seems likely that the inability to hyperventilate permitted the primary cardiac reflex to occur rather than the usual response of tachycardia to chemoreceptor stimulation which is prepotent with spontaneous ventilation. An understanding of this reflex was important in the clinical mangement of this patient.