OBJECTIVES: Coincident with "agonal" gasping during cardiac arrest, there are prominent increases in stroke volumes even in the absence of chest compression. In the present study, we tested the hypothesis that gasps also increase carotid blood flow (CBF) during untreated cardiac arrest. MATERIALS AND METHODS: The tracheas of nine domestic male pigs, weighing 39+/-2kg, were intubated and animals were ventilated mechanically. Ventricular fibrillation (VF) was induced electrically and untreated for 5min. Coincident with the onset of VF, mechanical ventilation was discontinued. The right femoral artery and vein were cannulated. Intrathoracic pressure (ITP) was measured with the aid of a balloon tipped catheter advanced into the esophagus for a distance of 35cm. A transonic flowprobe was placed around the right common carotid artery for measurement of CBF. RESULTS: Gasps increased in frequency during the first 4min of untreated VF together with increases in CBF. The CBF produced by gasping averaged 220+/-102mL/min, which represented approximately 59% of a pre-cardiac arrest CBF. Significant increases in CBF were highly correlated with the decreases in ITP during the inspiratory phase of the gaspings (r=0.78) and with the increases in aortic pressure during the expiratory phase of the gaspings (r=0.76). CONCLUSIONS: Spontaneous gasps produce significant increases in CBF during untreated cardiac arrest. The present study therefore confirmed beneficial effects of gasping during cardiac arrest.
OBJECTIVES: Coincident with "agonal" gasping during cardiac arrest, there are prominent increases in stroke volumes even in the absence of chest compression. In the present study, we tested the hypothesis that gasps also increase carotid blood flow (CBF) during untreated cardiac arrest. MATERIALS AND METHODS: The tracheas of nine domestic male pigs, weighing 39+/-2kg, were intubated and animals were ventilated mechanically. Ventricular fibrillation (VF) was induced electrically and untreated for 5min. Coincident with the onset of VF, mechanical ventilation was discontinued. The right femoral artery and vein were cannulated. Intrathoracic pressure (ITP) was measured with the aid of a balloon tipped catheter advanced into the esophagus for a distance of 35cm. A transonic flowprobe was placed around the right common carotid artery for measurement of CBF. RESULTS: Gasps increased in frequency during the first 4min of untreated VF together with increases in CBF. The CBF produced by gasping averaged 220+/-102mL/min, which represented approximately 59% of a pre-cardiac arrest CBF. Significant increases in CBF were highly correlated with the decreases in ITP during the inspiratory phase of the gaspings (r=0.78) and with the increases in aortic pressure during the expiratory phase of the gaspings (r=0.76). CONCLUSIONS: Spontaneous gasps produce significant increases in CBF during untreated cardiac arrest. The present study therefore confirmed beneficial effects of gasping during cardiac arrest.
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