Elevated PaCO2 levels increase pulmonary artery pressure.

Permissive hypercapnia is commonly used in mechanically ventilated patients to avoid lung injury but its effect on pulmonary artery pressure (PAP) is still unclear, particularly in combination with tidal volume (Vt). Therefore, an in vivo study was performed on adult rabbits ventilated with low (9 ml/Kg, LVt group) or high (15 ml/Kg, HVt group) tidal volume (Vt) and alterations in PAP were estimated. Both groups of animals initially were ventilated with FiO2 0.3 (Normocapnia-1) followed by inhalation of enriched CO2 gas mixture (FiCO2 0.10) to develop hypercapnia (Hypercapnia-1). After 30 min of hypercapnia, animals were re-ventilated with FiO2 0.3 to develop normocapnia (Normocapnia-2) again and then with FiCO2 0.10 to develop hypercapnia (Hypercapnia-2). Systolic, diastolic and mean PAP were assessed with a catheter in the pulmonary artery. In HP-1 and HP-2, PaCO2 increased (p < 0.0001) in both LVt and HVt animals compared to baseline values. pH decreased to ≈7.2 in HP-1 and ≈7.1 in HP -2. In normocapnia, the rise in Vt from 9 to 15 ml/Kg induced an increase in static compliance (Cstat), plateau airway pressure (Pplat) and PAP. Hypercapnia increased PAP in either LVt or HVt animals without significant effect on Cstat or Pplat. A two-way ANOVA revealed that there was not a statistically significant interaction between the effects of hypercapnia and tidal volume on mPAP (p = 0.76). In conclusion, increased Vt per se induced an increase in Cstat, Pplat and PAP in normocapnia. Hypercapnia increased PAP in rabbits ventilated with low or high Vt but this effect was not long-lasting.