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

Abstract

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 pCO₂ (P_ETCO₂).

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_ETCO₂ 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_ETCO₂ suggesting that ventilation at controlled rate and volume could enhance the precision with which P_ETCO₂ reflects CPR quality, predicts return of circulation, and serve to guide optimization of resuscitation interventions.

Introduction

Positive pressure ventilation at high respiratory rates is considered hemodynamically detrimental during CPR consequent to increases in intrathoracic pressure limiting venous return and the corresponding blood flow that can be generated by chest compression. The 2010 Guidelines for CPR recommend delivery of 8–10 breaths/min unsynchronized to compressions after securing an artificial airway.1, 2 However, professional rescuers may deliver breaths at higher rates.3, 4 Contrasting with the available data on respiratory rate, there is virtually no data on the effects of tidal volume. Current guidelines recommend delivery of 6–7 ml/kg, yet the effects of varying tidal volume have not been examined. We postulated that increases in tidal volumes could exert comparable detrimental effects, with the combination of high respiratory rates and high tidal volumes being particularly detrimental.

Varying ventilation during CPR could also affect end-tidal PCO₂ (P_ETCO₂) and its ability to assess blood flow generation. P_ETCO₂ reflects the combined effects of CO₂ generation, CO₂ transport, and alveolar ventilation, which, in turn, depends on dead space and minute-volume. If dead space and minute-volume are constant, P_ETCO₂ becomes an excellent surrogate of systemic and regional blood flow during CPR.5, 6, 7 However, the clinical variability in respiratory rate and the likely variability in tidal volume8, 9 are expected to reduce the accuracy with which P_ETCO₂ reflects blood flow during CPR.

We used a swine model of ventricular fibrillation (VF) to determine whether increases in respiratory rate, tidal volume, or a combination thereof could be hemodynamically detrimental during CPR while simultaneously examining the effects on P_ETCO₂.