Key result
Dexmedetomidine and propofol were associated with similar incidences of the primary composite of severe hypotension and severe bradycardia in neurocritical care patients (28% vs. 35%, p=0.35).
Why the study?
Does dexmedetomidine compared to propofol reduce the incidence of severe hypotension and bradycardia in neurocritical care patients?
Cohort (n=190)
Yes
Does dexmedetomidine compared to propofol reduce the incidence of severe hypotension and bradycardia in neurocritical care patients?
Absolute Event Rate: 28% vs 35%
p-value: p=0.35
Dexmedetomidine and propofol are associated with similar rates of severe hypotension and bradycardia when used for sedation in neurocritical care patients.
Supports similar hemodynamic safety in neurocritical care; leaves open need for randomized confirmation before practice change.
Introduction: Dexmedetomidine and propofol are commonly used sedatives in neurocritical care as they allow facilitation of frequent neurologic assessments. Both agents are associated with hemodynamic adverse effects including hypotension and bradycardia which have been shown to increase mortality and poor neurologic outcomes in those with severe brain injuries. Methods: This was a multicenter, retrospective, propensity-matched cohort study conducted in neurocritical care units at two academic medical centers with dedicated neurocritical care teams and board certified neurointensivists. Patients admitted between 7/09 and 9/12 who received at least 4 hours of propofol or dexmedetomidine were evaluated and matched 1:1 based on propensity scoring. Primary composite outcome was a combination of severe hypotension (mean arterial blood pressure <60 mmHg) and severe bradycardia (<50 beats per minute). Patients who received dexmedetomidine did not receive a bolus dose and dose increases were limited to every 30 minutes, with a maximum dose of 1.4 mcg/kg/hr. Results: A total of 342 patients were identified (105 dexmedetomidine and 237 propofol) with 190 patients included for analysis after propensity matching. There was no difference in baseline characteristics and the primary composite outcome between the two groups (28 vs. 35%, p=0.35). When analyzed separately, there were also no differences in the incidences of severe hypotension (24% vs. 31%, p=0.33) or bradycardia (6.3% vs. 6.3%, p=1.00). Common interventions for those that developed hypotension were administration of an intravenous fluid bolus (52%), decreasing sedative dose (40%), and stopping sedative entirely (21%). There were no significant differences between the rates of hypotension requiring intervention between groups. Conclusions: Severe hypotension and bradycardia were common and occur at similar incidences in neurocritical care patients who receive dexmedetomidine or propofol when dosed as described. Providers should weigh the risk of hemodynamic instability before starting either sedative.
No takes yet. Share an insight, caveat, or question.
Erdman et al. (2013) conducted a cohort in Neurocritical care patients (n=190). Dexmedetomidine vs. Propofol was evaluated on combination of severe hypotension (mean arterial blood pressure <60 mmHg) and severe bradycardia (<50 beats per minute) (p=0.35). Dexmedetomidine and propofol were associated with similar incidences of the primary composite of severe hypotension and severe bradycardia in neurocritical care patients (28% vs. 35%, p=0.35).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: