Mechanical ventilation in acute pulmonary embolism: A randomised, experimental, crossover study

Acute intermediate-high risk pulmonary embolism (PE) causes a pathological increase in pulmonary artery pressure and right ventricle afterload that may progress to right ventricle failure and cardiopulmonary collapse. Patients may require mechanical ventilation, further increasing pulmonary vascular resistance and artery pressure. We aimed to investigate the ability of ventilator settings adjustments to reduce pulmonary artery pressure in a porcine model. Eleven Danish female pigs (Landrace/Yorkshire/Duroc) of ≈60 kg were used to perform a randomised, blinded, cross-over, experimental study. Following induction of acute PE, the animals were subject to four randomized interventions with wash-out periods in between; 1) changes in positive end-expiratory pressure (from 5 to 0, 10 and 15 cmH2O), 2) 50% and 100% increase in minute ventilation (hypocapnia), 3) increase in fraction of inspired oxygen (FiO2, from 21% to 40%), and 4) infusion of sodium bicarbonate to induce alkalosis. The main outcome was mean pulmonary artery pressure. Mean pulmonary artery pressure was reduced by reduction in positive end-expiratory pressure (28 ± 6 vs 26 ± 5 mmHg, p=0.011), hypocapnia (27 ± 6 vs. 23 ± 5 mmHg, p=0.0004), alkalosis (27 ± 4 vs 25 ± 5 mmHg, p=0.003) and increased fraction of inspired oxygen (28 ± 6 vs. 23 ± 5 mmHg, p<0.0001). Changes in pulmonary vascular resistance showed similar patterns (p<0.05 for all). In a porcine model of acute PE reduction of positive end-expiratory pressure, permissive hypocapnia through hyperventilation, alkalosis and increased fraction of inspired oxygen can reduce mean pulmonary artery pressure.