Abstract
The aim of this study was to assess the risk of unfavorable outcomes according to the timing of hypotension episodes in cardiac arrest patients. This prospectively conducted multicenter observational study included 1373 out-of-hospital cardiac arrest patients treated with 33 °C targeted temperature management (TTM). Unfavorable neurological outcome and the incidence of complications were analyzed according to the timing of hypotension. Compared with hypotension before TTM initiation (adjusted hazard ratio (aHR) 1.51), hypotension within 6 h after TTM initiation was associated with an increased risk of unfavorable neurologic outcome (aHR 1.693), and after 24 h of TTM, was connected with decreased risk (aHR 1.277). The risk of unfavorable neurological outcome was gradually reduced over time after TTM initiation. Hypotension, persisting both before and during TTM, demonstrated a greater risk (aHR 2) than transient hypotension (aHR 1.265). Hypotension was correlated with various complications. Differences in lactate levels were persistent, regardless of the initial fluid therapy (p < 0.001). Hypotension showed a strong correlation with unfavorable neurological outcome, especially in the early phase after TTM initiation, and complications. It is essential to manage hypotension that occurs at the beginning of TTM initiation to recover cerebral function in cardiac arrest patients.
Highlights
Low stroke volume and systolic and diastolic dysfunction after cardiac arrest can often result from myocardial stunning [1], a reversible myocardial dysfunction that is observed within the first 24 h after cardiac arrest
The patients were further divided according to hypotension episodes before temperature management (TTM) initiation as follows: 1074 and 299 patients in the early phase within 12 h after TTM initiation, respectively, and 793 and 580 patients in the late phase after 24 h of TTM, respectively (Figure 1)
Patients with hypotension found before TTM initiation were shown to be older in age and to have a longer relative anoxic time, more frequent occurrences of an asystole pattern, and less frequent occurrences of ventricular fibrillation in initial electrocardiography, lower four-scale scores, slightly higher target temperatures, and longer TTM durations than those with no hypotension found before TTM initiation (Table 1)
Summary
Low stroke volume and systolic and diastolic dysfunction after cardiac arrest can often result from myocardial stunning [1], a reversible myocardial dysfunction that is observed within the first 24 h after cardiac arrest. This condition usually takes two to three days to recover, but mortality due to persisting hypotension in non-recovering patients tends to be high [1,2]. Myocardial dysfunction and vasodilatation due to myocardial stunning, hypovolemia, sepsis, etc., can cause hypotension in post-cardiac arrest patients For management of these causes, several treatments have been used. Infusion of relatively large volumes of fluid is endurable in patients with cardiac arrest [8]
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