Right heart dysfunction remains a frequent cause of morbidity and mortality after cardiac surgery. Respiratory acidosis, particularly when accompanied by hypoxemia, plays a significant role in right heart failure, primarily by increasing right ventricular afterload through pulmonary vasoconstriction and elevated pulmonary arterial pressures. This phenomenon leads to increased right ventricular workload, causing dilation, decreased contractility, and ultimately right heart failure. The study aims to evaluate the effect of respiratory acidosis on right ventricular function after cardiac surgery.
Previously included and complete study NCT05886413 or NCT06826794
Absence of one or more of the following hemodynamic measurements: systolic or diastolic pulmonary artery pressure, central venous pressure, cardiac output
Absence of arterial blood gas on arrival to the intensive care unit
Adult patients who underwent cardiac surgery mechanically ventilated in controlled mode, and had an arterial blood gas within the first hour following admission.
Cohort
Retrospective
Not applicable- observational study
Other interventionNo intervention
Right ventricular function per central hemodynamic assessment
Calculation of different predictor: Cardiac index, PAPi (pulmonary artery pulse pressure over central venous pressure) , RVSWI ((mean pulmonary artery pressure- central venous pressure) X stroke volume index X 0.0136) and RV-CPO
Intensive care unit length of stay
Intensive care unit admission through Intensive care unit discharge
Mechanical ventilation duration
Time spent with invasive mechanical ventilation between intensive care unit admission and hospital discharge
Vasopressor duration
Duration of vasopressor or inotrope administration
Acute renal failure
Rate of acute renal failure during coronary unit length of stay. Renal failure will be defined according to the usual criteria, i.e., an increase of \>27 umol/L creatinine in 48 hours or 1.5x over the baseline
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