Background. Survival after cardiac arrest (CA) remains low worldwide, averaging ≤6% for out-of-hospital and 18% for in-hospital arrest. Mild therapeutic hypothermia (MTH) can improve survival and the neurological outcome after CA by reducing oxygen consumption and numerous deleterious biochemical and physical mechanisms that lead to reperfusion cell damage reducing brain injury and improves neurologic recovery. Aim. The aim of this retrospective study was to determine the agreement between MTH, inflammatory and hemodynamic status of patients after CA Methods. During the observation period (10 months), 11 patients were admitted or have developed CA in our ICU. This group (MTH group) was compared with a group of 11 patients were consecutively admitted in ICU before the introduction of MTH protocol (Baseline group). The goal of the MTH was to achieve a temperature of 32°C to 34°C as soon as possible after CA, for 24 hrs. All patients were sedated with continuous intravenous infusion of fentanyl plus midazolam, neuromuscular blockade was maintained with vecuronium, and they all were mechanically ventilated via endotracheal tubes. After 24 hrs the patient was rewarmed passively and cautiously (≤0.25°C/h). Sedation was stopped at a core temperature of 35°C if underlying disease would permitted. Immediately after ICU admission, MTH group patients have received an intravenous bolus of saline 6 mL/kg at 4°C. Central body temperature was continuously monitored via an esophageal probe. To maintain MTH, ice packs were applied in the groins, axillae and along the neck, instillation of cold saline through the nasogastric tube and bladder tube. The baseline group has not been subjected to hypothermia because admitted in ICU before the introduction of MTH protocol. The hemodynamic management of all patients was based on guideline treatment, and to maintain individual cardiac index (CI) between 1.5 and 2.7 L/min/m2. If indicated, intra-aortic balloon pump (IABP) were implanted in the cath lab before the patients were transferred to the ICU. Heart rate (HR), arterial blood pressure (ABP), CVP, PAOP, lactate plasma levels (LAC), SV, intra-thoracic blood volume (ITBV), global end-diastolic volume (GEDV), were continuously recorded in all patents. To evaluate the inflammatory status, C-reactive protein (CRP) and procalcitonin (PCT) concentrations were recorded daily between day 1 and day 6 after induction of hypothermia. PCT was measured with a high sensitive technology assay. Hemodynamic support with inotropic agents or vasopressors was used as indicated to reach a mean arterial blood pressure (MAP) of 80 mmHg. The dose of the different catecholamines (levosimendan, dobutamine and norepinephrine) was adjusted according to the clinical judgment of the physician on duty, considering MAP, HR, echocardiography results, CI, urine production and underlying disease. Results. In the Baseline group (n=11) the mean SvO2 value was 68.2±11.8% with mean CVP of 13.0±4.9 mmHg, LAC of 6.3±4.2 mmol/l and APACHE II score of 21.7±7.3; in-hospital mortality in this group was 32.0%. In the therapeutic hypothermia group (n=11) the mean time of induction of hypothermia was 5±3.12 hrs, the mean duration of hypothermia was 18±5.35 hrs and mean time for passive re-warming was 7±3.28 hrs. During induction of MTH, the hemodynamic support by norepinephrine infusion could be significantly reduced from 10±2.0 γ/min (arrival ICU) to 4±1.0 γ/min (34°C, p<0.001) and 2±1.0 γ/min (33°C, p<0.001). At the same time, the infusion rate of levosimendan or dobutamine was not changed. Despite reduced epinephrine dosage, the MAP remained stable at 71±18 mmHg (arrival ICU), 72±13 mmHg (34°C) and 79±10 mmHg (33°C). The mean HR significantly decreased from 101±7 bpm (arrival ICU) to 82±7 bpm (34°C, p<0.05) and 80±4 bpm (33°C, p<0.05). Moreover, this group showed a CVP of 13.7±4.6 mmHg, mean ScvO2 values of 78.6±10.2%, LAC of 3.3±2.3 mmol/l and APACHE II score of 22.2±5.4; in-hospital mortality in this group was 28.0%. PCT concentrations were highest on the first day after hypothermia and showed a steady decrease until day 7 without differences in patients with and without presumed infection, and CRP concentrations were higher on fourth day in patients with clinical diagnosis of infection. This increase was unspecific and mirrors rather an inflammatory reaction after cardiac arrest. (Table Presented) Conclusions. In-hospital mortality, in our study, was significantly (p<0.001) lower in the MTH group (28%) compared to the Baseline group (37.2%). This study adds to our knowledge as it demonstrates not only the feasibility of MTH but also its benefit on survival.
Poli, M., Trambaiolo, P., Basso, V., Mustilli, M., Luca, M. D., Likic, V., … Ferraiuolo, G. (2012). MILD THERAPEUTIC HYPOTHERMIA: A SIMPLE WAY TO IMPROVE SURVIVAL AND NEUROLOGICAL OUTCOME AFTER CARDIAC ARREST IN ICU. Journal of the American College of Cardiology, 59(13), E733. https://doi.org/10.1016/s0735-1097(12)60734-7