Oxygen Consumption Predicts Long-Term Outcome of Patients with Left Ventricular Assist Devices

Abstract

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.

Figure 1

CO, CI, VO₂, DO₂, O₂ER and SvO₂ levels of in-hospital survivors and non-survivors after LVAD implantation. In non-survivors CO, CI and DO₂ were significantly lower compared to survivors on days 2 and 3 (A–C). VO₂ was significantly lower in non-survivors compared to survivors during the first 3 days after surgery (D). Non-survivors had significantly lower O₂ER values on postoperative days 0 and 1 compared to survivors (E). SvO₂ was significantly higher in non-survivors compared to survivors on day 1 (F). There was no difference in Hb and CVP between survivors and non-survivors (G,H). In contrast, there were significantly higher MAP levels in survivors compared to non-survivors from day 1 until day 3 (I). TPR did not differ between survivors and non-survivors (J). CO, continuous cardiac output; CVP, central venous pressure; DO₂, oxygen delivery; O₂ER, oxygen extraction ratio; SvO₂, mixed venous oxygen saturation; VO₂, oxygen consumption; * p < 0.05.

Figure 2

VO₂ levels during the first 4 days after surgery of 1- and 5-years non-survivors, patients on pump and patients undergoing transplantation. ns, not significant; VO₂, oxygen consumption; * p < 0.05, ** p < 0.01, *** p < 0.001.

Figure 3

The association of VO₂, CO and DO₂ and short- and long-term outcomes. Elevated VO₂ predicted in-hospital, 1-year and 6-year survival and successful transplantation within 5 years (A–D). Increased CO and DO₂ levels predicted 1-year survival (E,F). Increased VAD flow and O₂ER did not predict 1-year survival (G,H). AUC, area under the curve, CO, cardiac output; VAD ventricular assist device; VO₂, oxygen consumption.