Spontaneous gasping generates cardiac output during cardiac arrest

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Abstract

Objectives

To measure stroke volumes coincident with spontaneous gasping during untreated ventricular fibrillation and to evaluate the effects of gasping.

Design

Prospective study in laboratory animals.

Setting

University-affiliated research institute.

Subjects

Male Yorkshire-X domestic pigs.

Interventions

Pigs were anesthetized (ketamine, 20 mg/kg intramuscularly and sodium pentobarbital, 30 mg/kg intravenously), intubated, and mechanically ventilated. Ventricular fibrillation was electrically induced and untreated for 7 mins. The right femoral artery and vein were cannulated. A 5.5/7.5-MHz biplanar transesophageal echocardiography transducer was advanced into the esophagus.

Measurements and Main Results

Stroke volumes were measured as the product of the transaortic blood flow velocity and transesophageal echocardiographic measurements of valve area. In addition, left ventricular volumes were echocardiographically estimated at peak inspiration and at peak expiration of each gasp by transesophageal methods. The stroke volume produced by gasping averaged 23 ± 6 mL, which represented approximately 60% of a precardiac arrest stroke volume (38 ± 8 mL, p < .001). Increases in end-tidal carbon dioxide tension coincident with each gasp were consistent with comparable increases in pulmonary blood flow and therefore stroke volumes. Both were associated with increases in aortic pressure from 20 ± 3 to 33 ± 8 mm Hg (p < .001) and coronary perfusion pressure from 4 ± 3 to 13 ± 7 mm Hg (p < .001).

Conclusions

Our studies confirm that preterminal gasping during ventricular fibrillation increases both ventilation and forward blood flow.

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