Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR: a comparison with mechanical ventilation

Objective: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. Design: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. Interventions: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. Results: During the first minute of chest compression, mean (± S.D.) minute ventilation was 11.2 ± 5.91 l/min in the mechanically ventilated group and 4.5 ± 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 ± 1.4 1/min and 1.7 ± 1.6 1/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 ± 0.13 compared with 7.30 ± 0.07 units) and Pco₂ was higher (62 ± 19 compared with 35 ± 9 mmHg). Mixed venous Pco₂ was also higher (76 ± 15 compared with 61 ± 8 mmHg). Conclusion: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.