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Dexmedetomidine adverse effect — FFICM MCQ

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ModeratePharmacologyDexmedetomidine adverse effectFFICM

A 69-year-old man is receiving dexmedetomidine to facilitate NIV for hypercapnic respiratory failure. Two hours after the infusion is increased, he becomes hypotensive with HR 38/min. He is calm and rousable, with no chest pain. ECG shows sinus bradycardia and potassium is normal. What is the most likely diagnosis?

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Correct answer: BDexmedetomidine-associated bradycardia and hypotension

The correct answer is B, dexmedetomidine-associated bradycardia and hypotension. This patient developed sinus bradycardia and hypotension two hours after a dose increase of dexmedetomidine, a highly selective alpha-2 adrenoceptor agonist used off-label in the UK to facilitate NIV tolerance because it preserves respiratory drive. Alpha-2 stimulation in the locus coeruleus and brainstem reduces central sympathetic outflow and augments vagal tone, producing dose-dependent bradycardia and hypotension, an effect the SmPC explicitly warns is common and dose related. The temporal relationship (onset shortly after dose escalation), the patient remaining calm and rousable rather than obtunded, a normal potassium, and a benign sinus bradycardia on ECG all point away from a primary cardiac or metabolic cause and towards a predictable pharmacological effect of the drug itself. Why the other options are wrong: C. Malignant ventricular arrhythmia: the ECG shows sinus bradycardia, not a ventricular rhythm, and the patient is haemodynamically stable enough to be calm and rousable, which is inconsistent with a malignant ventricular arrhythmia. E. Opioid-induced chest wall rigidity: this causes acute hypoventilation and increased airway pressures from truncal rigidity after rapid high-dose opioid, not bradycardia and hypotension, and there is no mention of opioid use or ventilatory difficulty here. D. Serotonin syndrome: this presents with clonus, hyperreflexia, tremor, agitation and hyperthermia from excess serotonergic activity, features entirely absent in a calm, rousable patient with isolated bradycardia. A. Acute anticholinergic toxicity: this classically causes tachycardia, mydriasis, dry skin and delirium, the opposite autonomic picture to the bradycardia and hypotension seen here. Key point: dexmedetomidine reliably causes dose-dependent bradycardia and hypotension via central alpha-2 agonism even though it spares respiratory drive, so haemodynamic monitoring is essential during dose titration.

Reference: Dexdor (dexmedetomidine) Summary of Product Characteristics, electronic medicines compendium (emc), Section 4.4 and 4.8, updated 2023, https://www.medicines.org.uk/emc/medicine/25043