Reduced oxygen consumption (VO2), either due to insufficient oxygen delivery (DO2), microcirculatory hypoperfusion and/or mitochondrial dysfunction, has an impact on the adverse short- and long-term survival of patients after cardiac surgery. However, it is still unclear whether VO2 remains an efficient predictive marker in a population in which cardiac output (CO) and consequently DO2 is determined by a left ventricular assist device (LVAD). We enrolled 93 consecutive patients who received an LVAD with a pulmonary artery catheter in place to monitor CO and venous oxygen saturation. VO2 and DO2 of in-hospital survivors and non-survivors were calculated over the first 4 days. Furthermore, we plotted receiver-operating curves (ROC) and performed a cox-regression analysis. VO2 predicted in-hospital, 1- and 6-year survival with the highest area under the curve of 0.77 (95%CI: 0.6-0.9; p = 0.0004). A cut-off value of 210 mL/min VO2 stratified patients regarding mortality with a sensitivity of 70% and a specificity of 81%. Reduced VO2 was an independent predictor for in-hospital, 1- and 6-year mortality with a hazard ratio of 5.1 (p = 0.006), 3.2 (p = 0.003) and 1.9 (p = 0.0021). In non-survivors, VO2 was significantly lower within the first 3 days (p = 0.010, p < 0.001, p < 0.001 and p = 0.015); DO2 was reduced on days 2 and 3 (p = 0.007 and p = 0.003). In LVAD patients, impaired VO2 impacts short- and long-term outcomes. Perioperative and intensive care medicine must, therefore, shift their focus from solely guaranteeing sufficient oxygen supply to restoring microcirculatory perfusion and mitochondrial functioning.
Keywords: cardiac surgery; intensive care medicine; left ventricular assist device; metabolic and hemodynamic parameters; mitochondrial dysfunction; oxygen consumption; oxygen delivery.