Cerebral and hemodynamic variables during cough-induced CPR in dogs

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Abstract
To assess the potential of self administered, cough-induced cardiopulmonary resuscitation (CICPR) to sustain cerebral function during sudden onset ventricular fibrillation (VF), the authors studied four groups of six dogs each. Cough was simulated by: spontaneous gasping (group 1); cough elicited by bilateral electrical stimulation of the vagi (group 2); gasping with artificial glottic closure (group 3); and as a control, apnea under paralysis (group 4). Sudden onset of VF during apnea (group 4) resulted in cessation of arterial blood flow in 11 +/- 3 sec (mean +/- SD) and an isoelectric EEG in 26 +/- 5 sec. Spontaneous gasping (group 1) and cough resulting from vagal stimulation (group 2) resulted in minimal systemic and cerebral perfusion pressures and common carotid artery blood flows (CCABF). CCABF became 0 in group 1 at 31 +/- 12 sec, and in group 2 at 33 +/- 16 sec after the onset of VF. EEG silence occurred at 57 +/- 9 sec and 54 +/- 19 sec in groups 1 and 2, respectively. The decay of vital parameters was delayed further when spontaneous gasping via tracheal tube was against artificial glottic closure, which augments airway pressure fluctuations (group 3); pulselessness occurred at 52 +/- 28 sec and EEG silence at 66 +/- 27 sec. Self-induced fluctuations of intrathoracic pressure generated sufficient blood flow to briefly but statistically significantly (p less than 0.001) prolong EEG activity compared to apneic controls. In this dog preparation, gasping with artificial glottic closure sustained cerebral electrical activity for a maximum of 112 sec. CICPR may offer a means of briefly sustaining consciousness after the sudden onset of VF and, thus, constitutes self-administered CPR.

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