Intubation of critically ill patients: A pilot study of minute-by-minute physiological changes within an Australian tertiary intensive care unit.

BACKGROUND: There are no published minute-by-minute physiological assessment data for endotracheal intubation (ETT) performed in the intensive care unit (ICU). The majority of physiological data is available from Europe and North America where etomidate is the induction agent administered most commonly. AIMS: The aim of this study was to describe the feasibility of obtaining minute-by-minute physiological and medication data surrounding ETT in an Australian tertiary ICU and to assess its associated outcomes. METHODS: We performed a single-centre feasibility observational study. We obtained minute-by-minute data on physiological variables and medications for 15 min before and 30 min after ETT. We assessed feasibility as enrolled to screened patient ratio and completeness of data collection in enrolled patients. Severe hypotension (systolic blood pressure < 65 mmHg) and severe hypoxaemia (pulse oximetry saturation < 80%) were the secondary clinical outcomes. RESULTS: We screened 43 patients and studied 30 patients. The median age was 58.5 (interquartile range: 49-70) years, and 18 (60%) were male. Near-complete (97%) physiological and medication data were obtained in all patients at all times. Overall, 15 (50%) ETTs occurred after hours (17:30-08:00) and 90% were by video laryngoscopy with a 90% first-pass success rate. Prophylactic vasopressors were used in 50% of ETTs. Fentanyl was used in all except one ETT at a median dose of 2.5 mcg/kg. Propofol (63%) or midazolam (50%) were used as adjuncts at low dose. Rocuronium was used in all but one patient. There were no episodes of severe hypotension and only one episode of short-lived severe hypoxaemia. CONCLUSION: Minute-by-minute recording of ETT-associated physiological changes in the ICU was feasible but only fully available in two-thirds of the screened patients. ETT was based on fentanyl induction, low-dose adjunctive sedation, and frequent prophylactic vasopressor therapy and was associated with no severe hypotension and a single short-lived episode of severe hypoxaemia.

A pilot study of the pharmacokinetics of continuous magnesium infusion in critically ill patients.

Objective: The pharmacokinetics and haemodynamic effect of continuous magnesium infusion in non-cardiac intensive care unit (ICU) patients are poorly understood. We aimed to measure serum and urine magnesium levels during bolus and continuous infusion in critically ill adults, compare serum levels with those of a control population, and assess its haemodynamic effect. Design: Pharmacokinetic study Setting: A single tertiary adult ICU. Participants: Mechanically ventilated adults requiring vasopressor support. Intervention: A 10 mmol bolus of magnesium sulfate followed by 1.5-3 mmol/h infusion for 24 hours. Main outcome measures: The primary outcome was the change in total serum magnesium concentration. The main secondary outcome was mean arterial pressure (MAP)- adjusted vasopressor dose. Results: We matched 31 treated patients with 93 controls. Serum total magnesium concentration increased from a median 0.94 mmol/L (interquartile range [IQR], 0.83-1.10 mmol/L) to 1.38 mmol/L (IQR, 1.25-1.69 mmol/L; P < 0.001) and stabilised between a median 1.64 mmol/L (IQR, 1.38-1.88 mmol/L) at 7 hours and 1.77 mmol/L (IQR, 1.53-1.85 mmol/L) at 25 hours. This was significantly greater than in the control group (P < 0.001). The MAP-adjusted vasopressor dose decreased during magnesium infusion (P < 0.001). Conclusion: In critically ill patients, a magnesium sulfate bolus followed by continuous infusion achieved moderately elevated levels of total serum magnesium with a decrease in MAP-adjusted vasopressor dose. Trial registration number: ACTRN12619000925145.

A pilot, feasibility, randomised controlled trial of midodrine as adjunctive vasopressor for low-dose vasopressor-dependent hypotension in intensive care patients: The MAVERIC study.

PURPOSE: To assess the feasibility and physiological efficacy of adjunctive midodrine in patients with vasopressor-dependent hypotension. MATERIALS AND METHODS: This was a pilot, open label, randomised controlled trial. Patients were enrolled from two tertiary intensive care units on low dose intravenous vasopressor therapy for more than 24 h. We randomly assigned patients to receive either adjunctive midodrine (10 mg every 8 h) or usual care. The primary efficacy outcome was time to cessation of intravenous vasopressor therapy. Secondary outcomes included protocol compliance, ICU and hospital length of stay. RESULTS: We screened 381 patients over 22-months and enrolled 62 (32 in midodrine group, 30 in usual care group). Median time to cessation of vasopressor infusion was 16.5 h for midodrine vs 19 h for usual care (p = 0.22). Time in ICU (50 [25.50, 74.00] hours for midodrine v 59 [38.50, 93.25] hours for usual care, p = 0.14) and hospital length of stay (9 days vs. 7.5 days, p = 0.92) were similar. Protocol compliance was 96.9%. One patient ceased midodrine early due to symptomatic bradycardia. CONCLUSIONS: Adjunctive midodrine therapy was feasible with acceptable compliance, duration of therapy, and safety profile. However, at the chosen dose, there was no evidence of physiological or clinical efficacy.