We measured the changes in atrial dynamics, pulse pressure, stroke volume, cAMP efflux, as well as the secretion of atrial natriuretic peptide (ANP).
The slope differences in mean arterial pressure, diastolic arterial pressure, stroke volume index and CI were −4 mmHg/h, p = 0.02, −3 mmHg/h, p = 0.04, −2.2 L/min/m2, p < 0.01 and −0.17 L/min/m2/h, p = 0.02, respectively (Additional file 1: Table SDC2).
The study started when patients were sedated with a constant value of the stroke volume in semi-recumbent position for 10 min and the first set of hemodynamic measurements was recorded, including the heart rate, systemic arterial pressure, diastolic arterial pressure, mean arterial pressure, central venous pressure, stroke volume, PtcO2 and PtcCO2.
Of these measurements, only those that are clinically available or inferable were used in to identify pig-specific computer models of the CVS, including the aortic and pulmonary artery pressure, stroke volume, heart rate, global end diastolic volume, and mitral and tricuspid valve closure times.
No significant differences were found in blood pressure (mean arterial and pulse pressure), stroke volume, or respiratory rate.
No significant decrease in mean arterial pressure, stroke volume or cardiac output occurred during the recruitment (T20/30).
Unsurprisingly, conventional ventilation resulted in reduced blood pressure, stroke volume and cardiac performance, including systemic oxygen delivery.
MAP and mean pulmonary arterial pressure, stroke volume, and systemic and pulmonary vascular resistances were calculated from standard formulae.
All volatile inhalation anaesthetics cause dose-dependent and drug-specific changes in cardiovascular performance: decreased arterial blood pressure, stroke volume, and peripheral vascular resistance.
For calculating these parameters we use preload alterations (most often induced by respiration) and the resulting changes in either right atrial pressure, blood pressure, pulse pressure, stroke volume or cardiac output.
