Mechanical ventilation in acute pulmonary embolism: a randomized, 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 (PVR) 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 randomized, 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 (PEEP) (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 (mPAP). mPAP was reduced by a reduction in PEEP (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 PVR showed similar patterns (P < 0.05 for all).

In a porcine model of acute PE reduction of PEEP, permissive hypocapnia through hyperventilation, alkalosis, and increased fraction of inspired oxygen can reduce mPAP.