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

Abstract

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 (COup) with an infusion of dobutamine≥5 μg kg(-1) min(-1) and decreased by 40% from baseline (COdown) infusing sodium nitroglycerine≥30 μg kg(-1) min(-1) plus esmolol 500 μg kg(-1) min(-1). Another state of PHT and COdown 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 (SnIII) increased by 32% in PHT25 and by 22% in PHT40. SnIII decreased non-significantly by 4% with COdown. A combination of PHT and COdown associated with severe hypoxemia increased SnIII by 28% compared to baseline. The elimination of CO2 per breath decreased by 7% in PHT40 and by 12% in COdown but increased only slightly with COup. 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 SnIII of the volumetric capnogram and on the elimination of CO2.

Correlation between minute carbon dioxide elimination and pulmonary blood flow in single‐ventricle patients after stage 1 palliation and 2‐ventricle patients with intracardiac shunts: A pilot study

“…Alteration of minute ventilation changes EtCO 2 and VCO 2 in opposite directions, while changes in Qp or metabolism move EtCO 2 and VCO 2 in the same direction. However, in steady‐state conditions, when metabolism and minute ventilation are maintained at a constant, carbon dioxide elimination and, hence VCO 2 , represents an assessment of Q p and by extension CO in patients with normal cardiac physiology and anatomy . Among critically ill patients on mechanical ventilation and sedation, there may be very little variation in metabolic rate and minute ventilation at any given time within each individual patient.…”

The Influence of Acute Pulmonary Hypertension on Cardiac Output Measurements

“…To assess CO with a modified Fick method (FICK), the CO 2 production per minute was calculated from the area under the curve of the capnogram during in-and expiration multiplied with the respiratory rate. 16 The CO 2 production was divided by a respiratory quotient of 0.8 to receive O 2 consumption. This value was divided by the arterio-venous O 2 content difference to receive FICK CO values.…”

Volumetric Capnography in Pediatric Extracorporeal Membrane Oxygenation: A Case Series

“…Under stable minute ventilation and metabolic conditions, VCO 2 becomes a very sensitive indirect indicator of Q p and by extension cardiac output in patients with normal cardiac physiology and anatomy. [8][9][10] Volumetric capnometry correlates well with Q p in patients with stable single ventricle physiology and with Q p and cardiac output in patients with structurally normal hearts. In contrast, poor correlation between cardiac output and VCO 2 is seen in patients with single ventricle physiology and significant intracardiac shunts.…”