Abstract

Out-of-hospital cardiac arrest (OHCA) patients are often circulatory unstable and have high mortality in the first days following resuscitation. An increase in lactate will reflect the severity and duration of hypoperfusion in out-of-hospital cardiac arrest (OHCA). Further, the severity of hypoperfusion could modify the effect on survival and neurological injury of different mean arterial blood pressure (MAP) targets. In this sub-study of the BOX trial, adults successfully resuscitated comatose OHCA patients (n=789) with a presumed cardiac cause were randomized to a MAP 63 mmHg vs. 77 mmHg. Patients were arbitrarily grouped in low-lactate: <25%, medium-lactate: 25%-75%, and high >75 % according to blood lactate levels at hospital arrival as a surrogate of severity of hypoperfusion. Invasive evaluations were performed using an arterial line and pulmonary artery catheter (PAC). Logistic regression analysis evaluated whether lactate levels (as continuous and categorical) modify the effect of MAP targets on 1-year mortality. The three lactate groups were: low-lactate: <2.9 mmol/L, medium-lactate: 2.9-7.9 mmol/L, and high-lactate >7.9 mmol/L. The vasoactive inotropic score was higher with increasing initial lactate level with the largest difference at 6 hours (low-lactate: 7.8 (95%CI: 5.7 - 10.1) vs. high-lactate: 16.4 (95%CI: 13.4 - 19.6). No difference in the cardiac index or systemic vascular resistance was observed between lactate groups. The initial lactate level modified the effect of the two MAP targets (p=0.044), with a tendency to higher mortality for high-lactate patients if the MAP target were 77 mmHg (odds ratio: 1.7 (95%CI: 0.9-3.0, p=0.08). Comatose OHCA patients with high initial lactate levels required more vasoactive drugs on the first two days of ICU admission to meet the blood pressure target and have a poorer prognosis. The results do not support a higher MAP target benefit for patients with an initial high lactate level in the first 48 hours.

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