To observe the effect of different airway pressure on ventilation, organ perfusion and return of spontaneous circulation (ROSC) of cardiac arrest (CA) pigs during cardiopulmonary resuscitation (CPR), and to explore the possible beneficial mechanism of positive airway pressure during CPR. Twenty healthy landrace pigs of clean grade were divided into low airway pressure group (LP group, n = 10) and high airway pressure group (HP group, n = 10) with random number table. The model of ventricular fibrillation (VF) was reproduced by electrical stimulation, and mechanical chest compressions and mechanical ventilation (volume-controlled mode, tidal volume 7 mL/kg, frequency 10 times/min) were performed after 8 minutes of untreated VF. Positive end expiratory pressure (PEEP) in LP group and HP group was set to 0 cmH2O and 6 cmH2O (1 cmH2O = 0.098 kPa) respectively. Up to three times of 100 J biphasic defibrillation was delivered after 10 minutes of CPR. The ROSC of animals were observed, and the respiratory parameters, arterial and venous blood gas and hemodynamic parameters were recorded at baseline, 5 minutes and 10 minutes of CPR. The number of animals with ROSC in the HP group was significantly more than that in the LP group (8 vs. 3, P < 0.05). Intrathoracic pressure during chest compression relaxation was negative in the HP group, and its absolute value was significantly lower than that in LP group at the same time [intrathoracic negative pressure peak (cmH2O): -4.7±2.2 vs. -10.8±3.5 at 5 minutes, -3.9±2.8 vs. -6.5±3.4 at 10 minutes], however, there was significantly difference only at 5 minutes of CPR (P < 0.01). Intrathoracic pressure variation during CPR period in the HP group were significantly higher than those in the LP group (cmH2O: 22.5±7.9 vs. 14.2±4.4 at 5 minutes, 23.1±6.4 vs. 12.9±5.1 at 10 minutes, both P < 0.01). Compared to the LP group, arterial partial pressure of oxygen [PaO2 (mmHg, 1 mmHg = 0.133 kPa): 81.5±10.7 vs. 68.0±12.1], venous oxygen saturation (SvO2: 0.493±0.109 vs. 0.394±0.061) at 5 minutes of CPR, and PaO2 (mmHg: 77.5±13.4 vs. 63.3±10.5), arterial pH (7.28±0.09 vs 7.23±0.11), SvO2 (0.458±0.096 vs. 0.352±0.078), aortic blood pressure [AoP (mmHg): 39.7±9.5 vs. 34.0±6.9], coronary perfusion pressure [CPP (mmHg): 25.2±9.6 vs. 19.0±7.6], and carotid artery flow (mL/min: 44±16 vs. 37±14) at 10 minutes of CPR in the HP group were significantly higher (all P < 0.05). Arterial partial pressure of carbon dioxide (PaCO2) in the HP group was significantly lower than that in the LP group at 10 minutes of CPR (mmHg: 60.1±9.7 vs. 67.8±8.6, P < 0.05). Compared to low airway pressure, a certain degree of positive airway pressure can still maintain the negative intrathoracic pressure during relaxation of chest compressions of CPR, while increase the degree of intrathoracic pressure variation. Positive airway pressure can improve oxygenation and hemodynamics during CPR, and is helpful to ROSC.
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