The effects of cardiac output and pulmonary arterial hypertension on volumetric capnography derived-variables during normoxia and hypoxia

The aim of this study was to test the effect of cardiac output (CO) and pulmonary artery hypertension (PHT) on volumetric capnography (VCap) derived-variables. Nine pigs were mechanically ventilated using fixed ventilatory settings. Two steps of PHT were induced by IV infusion of a thromboxane analogue: PHT₂₅ [mean pulmonary arterial pressure (MPAP) of 25 mmHg] and PHT₄₀ (MPAP of 40 mmHg). CO was increased by 50 % from baseline (CO_up) with an infusion of dobutamine ≥5 μg kg⁻¹ min⁻¹ and decreased by 40 % from baseline (CO_down) infusing sodium nitroglycerine ≥30 μg kg⁻¹ min⁻¹ plus esmolol 500 μg kg⁻¹ min⁻¹. Another state of PHT and CO_down was induced by severe hypoxemia (FiO₂ 0.07). Invasive hemodynamic data and VCap were recorded and compared before and after each step using a mixed random effects model. Compared to baseline, the normalized slope of phase III (Sn_III) increased by 32 % in PHT₂₅ and by 22 % in PHT₄₀. Sn_III decreased non-significantly by 4 % with CO_down. A combination of PHT and CO_down associated with severe hypoxemia increased Sn_III by 28 % compared to baseline. The elimination of CO₂ per breath decreased by 7 % in PHT₄₀ and by 12 % in CO_down but increased only slightly with CO_up. Dead space variables did not change significantly along the protocol. At constant ventilation and body metabolism, pulmonary artery hypertension and decreases in CO had the biggest effects on the Sn_III of the volumetric capnogram and on the elimination of CO₂.