Excerpt
Our study simply establishes an association between hypotension and mortality following pediatric cardiac arrest. Like all observational studies, this association neither proves causality nor does it guarantee that treatment will improve outcomes. In our analysis, we controlled for multiple potential confounders, including first documented rhythm and number of epinephrine doses. Although we agree with Dr. Spentzas (1) that duration of cardiopulmonary resuscitation (CPR) was greater than 26 minutes for 25% patients with postarrest hypotension and greater than 19 minutes for 25% of patients without postarrest hypotension, we did not adjust for duration of CPR because it was collinear with the number of doses epinephrine administered. We note that adjustment for multiple potential confounders did not change the results. Recent data from Get With the Guidelines-Resuscitation showed a survival rate of 17.8% for patients who received 16–35 minutes of CPR and 15.9% for more than 35 minutes of CPR (4). Based on these data, 25% of patients in both the hypotension and no hypotension groups would have similar risk for mortality.
Of the 383 patients evaluated in our study, 56% had early postarrest hypotension. Adult data from the Project Impact database showed a hypotension prevalence of 47%, with a strongly associated mortality of 65% (5). Most interestingly, of the 3,030 adult patients with hypotension, 9% received vasopressor support, had no further hypotension over a 24-hour period, and had a significantly higher survival to discharge rate than those with persistent hypotension.
Unfortunately, we did not have access to data regarding volumes of fluids administered for the treatment of postarrest hypotension, nor did any of these patients have continuous and invasive monitoring with intracranial pressure monitors or pulmonary artery catheters. As Dr. Spentzas (1) notes, this study is only the first step in defining the association between postarrest hypotension and outcomes. We believe that future prospective trials should evaluate the association of duration and severity of hypotension and myocardial dysfunction on outcomes while using cerebral end-organ measurements of hypoxia, ischemia, and cellular metabolic crisis. Future interventional trials should assess treatment bundles including IV fluids, vasopressor support, and cardiac and cerebral monitoring targets as any one single treatment approach is unlikely to be effective (6).
We agree that there are markers of injury severity that predict outcome postarrest, such as patient factors, arrest factors, and postarrest neuromonitoring biomarkers. Although prognosis is important to the care we provide, we must be careful not to overinterpret associations as determinants of death. We did not focus our analysis on the prediction of postarrest outcomes. During the early hours following resuscitation from cardiac arrest, prediction of mortality is fraught with uncertainty and clinicians are often unable to reliably predict outcome (7). Therefore, we would encourage clinicians to use our data to heighten their awareness of the association of early postresuscitation hypotension with poor outcome. It is only with these observational data that we can go further to ask and answer the next questions with the hopes of improving resuscitation outcomes.