Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO₂.

AIMS: Ventilation at high respiratory rates is considered detrimental during CPR because it may increase intrathoracic pressure limiting venous return and forward blood flow generation. We examined whether ventilation at high, yet clinically plausible, tidal volumes could also be detrimental, and further examined effects on end-tidal pCO(2) (P(ET)CO(2)).

METHODS

Sixteen domestic pigs were randomized to one of four ventilatory patterns representing two levels of respiratory rate (min(-1)) and two levels of tidal volume (ml/kg); i.e., 10/6, 10/18, 33/6, and 33/18 during chest compression after 8 min of untreated VF.

RESULTS

Data (mmHg, mean ± SD) are presented in the order listed above. Ventilation at 33/18 prompted higher airway pressures (p<0.05) and persistent expiratory airway flow (p<0.05) before breath delivery demonstrating air trapping. The right atrial pressure during chest decompression showed a statistically insignificant increase with increasing minute-volume (7 ± 4, 10±3, 12 ± 1, and 13 ± 3; p=0.055); however, neither the coronary perfusion pressure (23 ± 1, 17 ± 6, 18 ± 6, and 21 ± 2; NS) nor the cerebral perfusion pressure (32 ± 3, 23 ± 8, 30 ± 12, and 31 ± 3; NS) was statistically different. Yet, increasing minute-volume reduced the P(ET)CO(2) demonstrating a high dependency on tidal volumes delivered at currently recommended respiratory rates.

CONCLUSIONS

Increasing respiratory rate and tidal volume up to a minute-volume 10-fold higher than currently recommended had no adverse hemodynamic effects during CPR but reduced P(ET)CO(2) suggesting that ventilation at controlled rate and volume could enhance the precision with which P(ET)CO(2) reflects CPR quality, predicts return of circulation, and serve to guide optimization of resuscitation interventions.