Abstract
Dexmedetomidine is widely used for procedural sedation due to its unique combination of sedation, analgesia and anxiolysis with minimal respiratory depression. Transient hypertension has been reported during the use of dexmedetomidine which is usually benign and is taken over by the hypotensive response on continuing the infusion. We report a case of hypertensive crisis following dexmedetomidine infusion used for procedural sedation, necessitating discontinuation of the infusion and treatment of hypertension. The dilemmas involved in treating hypertension caused by dexmedetomidine are discussed.
Key words : Dexmedetomidine, Hypertension, Sedation.
Introduction
Dexmedetomidine, a highly selective centrally acting α2 adrenoceptor agonist …show more content…
He had abrasions over the face, chest and right arm. CT facial bones revealed fracture in the body and condyle of the mandible. CT brain showed no evidence of parenchymal injury and X-ray cervical spine was normal. But for a total leucocyte count of 13,500 /cu.mm, other blood investigations, chest X- ray and ECG were within normal limits. General anesthesia with awake fiberoptic guided nasotracheal intubation was planned, as he had restricted mouth opening.
Dexmedetomidine was chosen for procedural sedation during awake fiberoptic intubation. After premedication with 0.2 mg Glycopyrrolate, a loading dose of one mcg/kg dexmedetomidine was started as an infusion to be given over 20 minutes. The patient’s blood pressure progressively increased from an initial value of 128/86 mmHg to 200/110 mmHg, and the patient started complaining of severe headache. Heart rate decreased from an initial value of 90 beats/ minute to 76 beats/ minute. Dexmedetomidine was discontinued at the 12th minute of infusion. Labetolol was given in boluses of five mgs up to 20 mgs. Blood pressure came down to 130/82 mmHg with a heart rate of 60 beats/ minute and the patient’s headache …show more content…
[4] Dexmedetomidine, a highly selective α2 adrenoceptor agonist was introduced into clinical practice in 1999 as a short term sedative and since then, it has been a valuable tool for providing procedural sedation in the anesthetic armamentarium. It is also widely used for its anesthetic and opioid sparing property, along with minimal respiratory depression, neuroprotection, cardioprotection and renoprotection. [1] Its property as an adjuvant in regional anesthesia is also being explored. Common side effects reported with the use of dexmedetomidine are hypotension and bradycardia. [2] Transient hypertension is also reported during the initial phase of infusion, and subsides on continuing the infusion. This hypertensive response is attributed to the stimulation of peripheral α2b adrenoceptors located in the blood vessels, which on stimulation cause vasoconstriction and increased blood pressure. Nonetheless, this initial response is taken over by stimulation of the central α2a adrenoceptors on continuing the infusion. [3] These central α2a adrenoceptors which are presynaptic prevent the release of norepinephrine, thereby causing hypotension and bradycardia. It is the stimulation of these α2a adrenoceptors which is responsible for the primary actions of
Dexmedetomidine is widely used for procedural sedation due to its unique combination of sedation, analgesia and anxiolysis with minimal respiratory depression. Transient hypertension has been reported during the use of dexmedetomidine which is usually benign and is taken over by the hypotensive response on continuing the infusion. We report a case of hypertensive crisis following dexmedetomidine infusion used for procedural sedation, necessitating discontinuation of the infusion and treatment of hypertension. The dilemmas involved in treating hypertension caused by dexmedetomidine are discussed.
Key words : Dexmedetomidine, Hypertension, Sedation.
Introduction
Dexmedetomidine, a highly selective centrally acting α2 adrenoceptor agonist …show more content…
He had abrasions over the face, chest and right arm. CT facial bones revealed fracture in the body and condyle of the mandible. CT brain showed no evidence of parenchymal injury and X-ray cervical spine was normal. But for a total leucocyte count of 13,500 /cu.mm, other blood investigations, chest X- ray and ECG were within normal limits. General anesthesia with awake fiberoptic guided nasotracheal intubation was planned, as he had restricted mouth opening.
Dexmedetomidine was chosen for procedural sedation during awake fiberoptic intubation. After premedication with 0.2 mg Glycopyrrolate, a loading dose of one mcg/kg dexmedetomidine was started as an infusion to be given over 20 minutes. The patient’s blood pressure progressively increased from an initial value of 128/86 mmHg to 200/110 mmHg, and the patient started complaining of severe headache. Heart rate decreased from an initial value of 90 beats/ minute to 76 beats/ minute. Dexmedetomidine was discontinued at the 12th minute of infusion. Labetolol was given in boluses of five mgs up to 20 mgs. Blood pressure came down to 130/82 mmHg with a heart rate of 60 beats/ minute and the patient’s headache …show more content…
[4] Dexmedetomidine, a highly selective α2 adrenoceptor agonist was introduced into clinical practice in 1999 as a short term sedative and since then, it has been a valuable tool for providing procedural sedation in the anesthetic armamentarium. It is also widely used for its anesthetic and opioid sparing property, along with minimal respiratory depression, neuroprotection, cardioprotection and renoprotection. [1] Its property as an adjuvant in regional anesthesia is also being explored. Common side effects reported with the use of dexmedetomidine are hypotension and bradycardia. [2] Transient hypertension is also reported during the initial phase of infusion, and subsides on continuing the infusion. This hypertensive response is attributed to the stimulation of peripheral α2b adrenoceptors located in the blood vessels, which on stimulation cause vasoconstriction and increased blood pressure. Nonetheless, this initial response is taken over by stimulation of the central α2a adrenoceptors on continuing the infusion. [3] These central α2a adrenoceptors which are presynaptic prevent the release of norepinephrine, thereby causing hypotension and bradycardia. It is the stimulation of these α2a adrenoceptors which is responsible for the primary actions of