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

Abstract

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. 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. Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. During the first minute of chest compression, mean (+/- S.D.) minute ventilation was 11.2 +/- 5.9 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 l/min and 1.7 +/- 1.6 l/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). 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.