JOURNAL ARTICLE

The effectiveness of intramuscular dexmedetomidine on hemodynamic responses during tracheal intubation and anesthesia induction of hypertensive patients: a randomized, double-blind, placebo-controlled study

Kudret Dogru, Tugba Arik, Karamehmet Yildiz, Cihangir Bicer, Halit Madenoglu, Adem Boyaci
Current Therapeutic Research, Clinical and Experimental 2007, 68 (5): 292-302
24692761

BACKGROUND: Hypertensive patients are at risk for increased hemodynamic response to tracheal intubation. Sympatholytic drugs administered during the preinduction period may prevent adverse events.

OBJECTIVE: We assessed the effectiveness of a single preinduction IM bolus dose of dexmedetomidine (DMED) 2.5 μg/kg in attenuating hemodynamic responses to tracheal intubation and rapid-sequence anesthesia induction in hypertensive patients treated with angiotensin-converting enzyme inhibitors.

METHODS: Adult patients (American Society of Anesthesiologists classification II and III) with essential hypertension, scheduled for elective abdominal or gynecologic surgery, were enrolled in this randomized, double-blind, placebo-controlled study. Patients were assigned to i of 2 groups: the DMED group received IM DMED 2.5 μg/kg and the placebo group received IM saline 0.9% 45 to 60 minutes before induction of anesthesia. General anesthesia was induced with thiopental, fentanyl, and vecuronium and maintained with a sevoflurane-nitrous oxide-oxygen mixture. Hemodynamic values were recorded before (baseline) and after anesthesia induction, before endotracheal intubation, and 1, 3, and 5 minutes after intubation. The patients were monitored for hypotension (systolic arterial pressure [SAP] decreased ≥25% from baseline or to <90 mm Hg) or bradycardia (heart rate [HR] decreased ≥25% from baseline or to <50 beats/min).

RESULTS: Nine hundred sixty patients were assessed for enrollment during a 6-month period. Sixty patients (49 women, 11 men; mean [SD] age, 59.16 [8.39] years) were eligible for the study. There were no significant differences in baseline hemodynamic values between the groups. SAP and diastolic arterial pressure (DAP) before anesthesia induction, 1 and 3 minutes after intubation, and DAP 1 minute after intubation were significantly lower in the DMED group than in the placebo group (all, P < 0.05). There were no significant between-group differences in SAP or DAP 5 minutes after intubation. HR before anesthesia induction, before intubation, and 1, 3, and 5 minutes after intubation were lower in the DMED group than in the control group (all, P < 0.05). In the DMED group, SAP after intubation, DAP before intubation, 3 and 5 minutes after intubation, HR before induction, before intubation, and 3 and 5 minutes after intubation were significantly decreased compared with baseline values (all, P < 0.05). In the control group, SAP at all times, DAP before intubation, 1, 3, and 5 minutes after intubation, HR before intubation, and 3 and 5 minutes after intubation were significantly decreased compared with baseline values (all, P < 0.05). Hypotension and bradycardia were observed together in 3 patients, and hypotension alone was observed in 1 patient 3 minutes after intubation in the DMED group; hypotension was observed in 1 patient at 3 minutes after intubation in the control group.

CONCLUSION: The results of this study suggest that IM DMED 2.5 μg/kg administered 45 to 60 minutes before anesthesia induction attenuated, but did not completely prevent, hemodynamic responses to tracheal intubation in these patients with essential hypertension.

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