Does hypoxia or hypercarbia independently affect resuscitation from cardiac arrest?

STUDY OBJECTIVE

In a previous cardiopulmonary resuscitation (CPR) study in swine, ventilation was associated with improved rate of return of spontaneous circulation (ROSC) compared with nonventilated animals, which had greater hypoxia and hypercarbic acidosis. We used the same model to determine the independent effect of hypoxia and hypercarbic acidosis on ROSC after cardiac arrest.

DESIGN

Laboratory model of cardiac arrest.

SETTING

University teaching hospital laboratory.

PARTICIPANTS

Domestic swine (23 to 61 kg).

INTERVENTIONS

Twenty-four swine were randomly assigned to three groups receiving ventilation during CPR with 85% O2/15% N2 (control), 95% O2/5% CO2 (hypercarbia), or 10% O2/90% N2 (hypoxia). All animals had ventricular fibrillation for 6 min without CPR, then CPR with one of the ventilation gases for 10 min, then defibrillation. Animals without ROSC received epinephrine, 85% O2, CPR for another 3 min, and defibrillation.

MEASUREMENTS AND RESULTS

During the tenth minute of CPR, the hypercarbic group had more mean (SD) arterial hypercarbia than the control group (PCO2, 47 +/- 6, compared with 34 +/- 6; p < 0.01), and greater mixed venous hypercarbia (PCO2, 72 +/- 14, compared with 59 +/- 8; p < 0.05), while mean arterial and mixed venous PO2 was not significantly different. The hypoxic group had significantly less mean arterial (43 +/- 9 compared with 228 +/- 103 mm Hg) and mixed venous (22 +/- 5 compared with 35 +/- 7 mm Hg) PO2 when compared with the control group (p < 0.01), while mean arterial and mixed venous PCO2 were not significantly different. Thus, the model succeeded in producing isolated hypercarbia without hypoxia in the hypercarbic group and isolated hypoxia without hypercarbia in the hypoxic group. The rate of ROSC was 6/8 (75%) for the control group, 1/8 (13%) for the hypercarbic group, and 1/8 (13%) for the hypoxic group (p < 0.02).

CONCLUSIONS

Both hypoxia and hypercarbia independently had an adverse effect on resuscitation from cardiac arrest. In this model with a prolonged interval of untreated cardiac arrest, adequate ventilation was important for resuscitation.