Corrective effect of norepinephrine on hypotension induced by dexmedetomidine in critically ill patients.

Purpose: To evaluate the corrective effect of norepinephrine on hypotension induced by dexmedetomidine through monitoring sedation status, hemodynamics as well as oxygen metabolism.

Methods: 100 patients administered standard-dose dexmedetomidine therapy with RASS between -2 and 0 in the intensive care unit (ICU) were included in the study. According to the application of norepinephrine to correct hypotension after dexmedetomidine therapy, the patients were divided into two groups: group A and group B. Group A (dexmedetomidine + norepinephrine group): those who had a systolic arterial pressure < 90 mmHg, a mean arterial pressure < 70 mmHg, or a decline in systolic arterial pressure > 40 mmHg or more than 30% of its base value after dexmedetomidine therapy and then received additional norepinephrine intravenously in order to maintain the arterial pressure at its base value. Group B (dexmedetomidine group): patients received the equivalent dose of dexmedetomidine to maintain the pressure at normal value without extra vasoconstrictor substance. Sedation (CPOT and RASS) and hemodynamic and oxygen metabolism indexes (heart rate, mean arterial pressure, respiratory rate, arterial oxygen saturation, central venous pressure, venous oxygen saturation, arteriovenous carbon dioxide difference, blood lactate level, blood lactate clearance rate, and average hourly urine output) were evaluated in the two groups at baseline, 6 hour, 12 hour, and 24 hour after the administration of intravenous dexmedetomidine.

Results: 39 cases were enrolled in group A and 61 cases in group B. Patients of both groups received adequate analgesia and sedation, and there was no significant statistical difference in analgesia and sedation at any point (both p > 0.05). Basal hemodynamic indexes and oxygen metabolism indexes also had no significant statistical difference (both p > 0.05). Central venous pressure (CVP) of group A was significantly higher than that of group B at the 6 hour and 12 hour after administration of intravenous dexmedetomidine (p = 0.005), and the heart rate (HR) of group A was markedly higher than that of group B at the 24 hour after dexmedetomidine therapy (p = 0.017), while the other indexes had no significant difference at any point (both p > 0.05).

Conclusion: Dexmedetomidine plays an important role in ICU patients due to its pharmacological ability of sedation and analgesia. In our study, dexmedetomidine was successfully applied to ensure goal-directed sedation therapy (GDST). Norepinephrine can correct hypotension and bradycardia induced by intravenous dexmedetomidine. According to the hemodynamic indexes and oxygen metabolism indexes, the application of dexmedetomidine or the combination of dexmedetomidine with norepinephrine are both safe and appropriate to maintain the sedation status and hemodynamic situation in ICU patients.
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