Cardiac power output is associated with cardiovascular related mortality in the ICU in post-cardiac arrest patients.

AIM: Although brain injury is the main determinant of poor outcome following cardiac arrest (CA), cardiovascular failure is the leading cause of death within the first days after CA. However, it remains unclear which hemodynamic parameter is most suitable for its early recognition. We investigated the association of cardiac power output (CPO) with early mortality in intensive care unit (ICU) after CA and with mortality related to post-CA cardiovascular failure. METHODS: Retrospective analysis of adult comatose survivors of CA admitted to the ICU of a University Hospital. Exclusion criteria were treatment with extracorporeal cardiopulmonary resuscitation, ECMO or intra-aortic balloon pump. We retrieved CA characteristics; we recorded mean arterial pressure, cardiac output, CPO (as derived parameter) and the vasoactive-inotropic score for the first 72 hours after ROSC, at intervals of 8 hours. ICU death was defined as related to post-CA cardiovascular failure when death occurred as a direct consequence of shock, secondary CA or fatal arrhythmia, or related to neurological injury if this led to withdrawal of life-sustaining therapy or brain death. RESULTS: Among the 217 patients (median age 66 years, 65% male, 61.8% out-of-hospital CA), 142 (65.4%) died in ICU: 99 (69.7%) patients died from neurological injury and 43 (30.3%) from cardiovascular-related causes. Comparing the evolution over time of CPO between survivors and non-survivors, a statistically significant difference was found only at +8 hours after CA (p = 0.0042). In multivariable analysis, CPO at 8-hour was significantly associated with cardiovascular-related mortality (p = 0.007). CONCLUSIONS: In post-CA patients, the 8-hour CPO is an independent factor associated with ICU cardiovascular-related mortality.

Cervical Ganglion Sympathectomy to Treat Cerebral Vasospasm in Subarachnoid Hemorrhage.

Delayed cerebral ischemia (DCI) is still a significant cause of death and disability after aneurysmal subarachnoid hemorrhage. Cerebral vasospasm represents one of the most reported mechanisms associated with DCI. The management of DCI-related vasospasm remains a significant challenge for clinicians; induced hypertension, intraarterial vasodilators, and/or intracranial vessel angioplasty-particularly in refractory or recurrent cases-are the most used therapies. Because an essential role in the pathophysiology of cerebral vasospasm has been attributed to the adrenergic sympathetic nerves, a "sympatholytic" intervention, consisting of a temporary interruption of the sympathetic pathways using local anesthetics, has been advocated to minimize the vascular narrowing and reverse the consequences of cerebral vasospasm on tissue perfusion. In this review, we have analyzed the existing literature on the block of the cervical ganglions, particularly the stellate ganglion, in managing refractory cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. These findings could help clinicians to understand the potential role of such intervention and to develop future interventional trials in this setting.

Predictors of poor outcome after extra-corporeal membrane oxygenation for refractory cardiac arrest (ECPR): A post hoc analysis of a multicenter database.

BACKGROUND: The objective was to assess predictors for unfavorable neurological outcome (UO) in out-of-hospital (OHCA) and in-hospital (IHCA) cardiac arrest patients treated with Extracorporeal cardiopulmonary resuscitation (ECPR). METHODS: A post hoc analysis of retrospective data from five European ECPR centers (January 2012-December 2016) was performed. The primary composite endpoint was 3-month UO defined as survival with a cerebral performance category (CPC) of 3-4 or death (CPC 5). RESULTS: A total of 413 patients treated with ECPR were included (median age was 57 [48-65] years, male gender 78%): 61% of patients (n = 250) suffered OHCA. The median time from collapse to ECMO placement was 63 [45-82] minutes. Overall, 81% patients (n = 333) showed unfavorable UO, which was higher in OHCA patients (90% vs 66%), as compared to IHCA. In OHCA, prolonged time from collapse to ECMO initiation (OR 1.02, p < 0.01) and higher ECMO blood flow (OR 1.99, p = 0.01) were associated with UO while initial shockable rhythm (OR 0.04, p < 0.01), previous heart disease (OR 0.20, p < 0.01) and pre-hospital hypothermia (OR 0.08, p < 0.01) had a protective role. In IHCA, prolonged time from arrest to ECMO implantation (OR 1.02, p = 0.03), high lactate level on admission (OR 1.15, p < 0.01) and higher body weight (OR 1.03, p < 0.01) were independently associated with UO. CONCLUSIONS: IHCA and OHCA patients receiving ECPR have different predictors of UO at presentation, suggesting that selection criteria for ECPR should be decided according to the location of CA. After ECMO initiation, ECMO blood flow management and mean arterial pressure targets might also impact neurological recovery.

How to Manage Withdrawal of Sedation and Analgesia in Mechanically Ventilated COVID-19 Patients?

COVID-19 patients suffering from severe acute respiratory distress syndrome (ARDS) require mechanical ventilation (MV) for respiratory failure. To achieve these ventilatory goals, it has been observed that COVID-19 patients in particular require high regimens and prolonged use of sedatives, analgesics and neuromuscular blocking agents (NMBA). Withdrawal from analgo-sedation may induce a "drug withdrawal syndrome" (DWS), i.e., clinical symptoms of anxiety, tremor, agitation, hallucinations and vomiting, as a result of adrenergic activation and hyperalgesia. We describe the epidemiology, mechanisms leading to this syndrome and our strategies to prevent and treat it.