All these patients were treated with TH, targeting a body temperature between 32 and 34°C for 24 h, according to a standardized institutional protocol, including the use of a cold fluid bolus (20 to 30 mL/kg saline or a balanced crystalloid solution over 30 minutes) and of a water-circulating blanket device (Medi-Therm II, Gaymar, Orchard Park, NY, USA). Midazolam (continuous infusion 0.03 to 0.1 mg/kg/h) and morphine (0.1 to 0.3 mg/kg/h) were administered during the hypothermic phase, while neuromuscular blocking agents (NMBAs, cisatracurium as a bolus of 0.15 mg/kg) were given in the induction phase and, if needed, as a continuous infusion thereafter (1 to 3 mcg/kg/min). Re-warming was performed passively at a maximum rate of 0.5°C/h; sedation, analgesia and NMBAs were discontinued when the body temperature exceeded 37°C.
Patients were kept in a 30° semi-recumbent position; ventilation was set to maintain arterial partial pressure of carbon dioxide (PaCO2) at 35–45 mmHg and peripheral capillary oxygen saturation (SpO2) >94%. Invasive hemodynamic monitoring (PiCCO, Pulsion, Munich, Germany) was placed whenever needed and transesophageal echocardiography was performed within the first 8 to 12 h after ICU admission in all patients. Mean arterial pressure (MAP) was maintained at >65 to 70 mmHg using fluids, dobutamine and/or norepinephrine, whenever needed. Higher levels of MAP were targeted in patients with a history of hypertension and in patients with low (<60%) cerebral oximetry values (Foresight, CasMed, Branford, CT, USA). Intra-aortic balloon counterpulsation (IABP) or extracorporeal membrane oxygenation (ECMO) was initiated in cases of severe cardiogenic shock. A local insulin protocol was applied to keep blood glucose levels between 110 and 150 mg/dL in all patients.
After re-warming the patient and stopping sedative agents, repeated neurologic examination and standard or continuous electroencephalogram (EEG) were performed. Withdrawal of life-support was an interdisciplinary decision based on bilateral absence of the N20 response to somatosensory evoked potentials (SSEPs), persisting deep coma, or presence of status myoclonus or refractory status epilepticus.
Patients were kept in a 30° semi-recumbent position; ventilation was set to maintain arterial partial pressure of carbon dioxide (PaCO2) at 35–45 mmHg and peripheral capillary oxygen saturation (SpO2) >94%. Invasive hemodynamic monitoring (PiCCO, Pulsion, Munich, Germany) was placed whenever needed and transesophageal echocardiography was performed within the first 8 to 12 h after ICU admission in all patients. Mean arterial pressure (MAP) was maintained at >65 to 70 mmHg using fluids, dobutamine and/or norepinephrine, whenever needed. Higher levels of MAP were targeted in patients with a history of hypertension and in patients with low (<60%) cerebral oximetry values (Foresight, CasMed, Branford, CT, USA). Intra-aortic balloon counterpulsation (IABP) or extracorporeal membrane oxygenation (ECMO) was initiated in cases of severe cardiogenic shock. A local insulin protocol was applied to keep blood glucose levels between 110 and 150 mg/dL in all patients.
After re-warming the patient and stopping sedative agents, repeated neurologic examination and standard or continuous electroencephalogram (EEG) were performed. Withdrawal of life-support was an interdisciplinary decision based on bilateral absence of the N20 response to somatosensory evoked potentials (SSEPs), persisting deep coma, or presence of status myoclonus or refractory status epilepticus.
Free full text: Click here
