Drug Interactions and Contraindications in Anesthesia Flashcards

A patient taking propranolol for essential tremor gets two cartridges of 2% lidocaine with 1:100,000 epinephrine. A few minutes later the monitor shows BP 196/110 mmHg and HR 48 bpm. What is the most likely mechanism?

Answer: Epinephrine stimulates alpha-1 receptors without beta-2 vasodilation to oppose it, and the sudden pressure rise triggers a reflex vagal bradycardia

Propranolol is a nonselective beta-blocker, so it blocks both beta-1 and beta-2 receptors. Normally epinephrine's beta-2 effect dilates skeletal muscle blood vessels and offsets its alpha-1 vasoconstriction. With beta-2 blocked, alpha-1 vasoconstriction is unopposed, so blood pressure rises sharply. The baroreceptor reflex then slows the heart through the vagus nerve. Propranolol can reduce hepatic blood flow and raise lidocaine levels, but lidocaine toxicity shows up as CNS signs and cardiovascular depression, not a hypertensive crisis. Cardioselective (beta-1) blockers carry much less of this risk.

A patient takes phenelzine (an MAO inhibitor) for treatment-resistant depression. Which agent in the dental sedation setting is truly contraindicated because of a potentially fatal interaction?

Answer: Meperidine

Meperidine combined with an MAOI can cause serotonin syndrome: hyperthermia, agitation, rigidity, autonomic instability and possibly death. It is an absolute contraindication. Many students pick epinephrine, but epinephrine is broken down mainly by COMT, not MAO, so dental doses are generally considered safe with MAOIs. Midazolam and nitrous oxide have no clinically significant MAOI interaction.

A sedation patient was started on clarithromycin three days ago for a respiratory infection. The usual IV midazolam titration is planned. What is the most clinically relevant concern?

Answer: Clarithromycin inhibits CYP3A4, so midazolam sedation may be deeper and longer, with more risk of respiratory depression

Midazolam is metabolized almost entirely by CYP3A4. Macrolides such as clarithromycin and erythromycin are strong CYP3A4 inhibitors, as are azole antifungals (ketoconazole, itraconazole), HIV protease inhibitors and grapefruit juice. They can raise midazolam levels several-fold, especially oral midazolam. The result is deeper, longer sedation and a higher risk of respiratory depression. Titrate in smaller increments, extend monitoring, or choose an alternative. Azithromycin causes much less CYP3A4 inhibition.

A patient taking dapsone for dermatitis herpetiformis needs extensive mandibular work. Which local anesthetic choice is the most problematic for this patient?

Answer: 4% prilocaine plain at maximum dose

Dapsone causes methemoglobinemia on its own. Prilocaine's metabolite, o-toluidine, oxidizes hemoglobin to methemoglobin, so the two effects add up and can cause cyanosis and tissue hypoxia that pulse oximetry does not reliably detect. High prilocaine doses are especially dangerous. The same caution applies to topical benzocaine and, to a lesser extent, articaine. Lidocaine, bupivacaine and mepivacaine are not significant methemoglobin inducers at clinical doses. The antidote is IV methylene blue, which is itself contraindicated in G6PD deficiency.

A patient on long-term clonazepam for a seizure disorder becomes oversedated after IV midazolam but is breathing adequately with supplemental oxygen. Why is giving flumazenil especially hazardous here?

Answer: Abruptly reversing all benzodiazepine effect can trigger acute withdrawal and seizures in a benzodiazepine-dependent patient with a seizure disorder

Flumazenil is a competitive GABA-A benzodiazepine-site antagonist that reverses all benzodiazepines, including clonazepam. In a patient who is physically dependent and whose seizures are controlled by a benzodiazepine, flumazenil can cause sudden withdrawal and seizures that are hard to treat, since the usual first-line seizure drugs are now blocked. Flumazenil is also relatively contraindicated after tricyclic antidepressant overdose. When ventilation is adequate, supportive care (airway, oxygen, monitoring) is preferred over reversal.

A patient takes amitriptyline (a tricyclic antidepressant) for chronic neuropathic pain. Which vasoconstrictor approach is most appropriate?

Answer: Avoid levonordefrin, and use epinephrine in limited amounts with aspiration and slow injection

Tricyclic antidepressants block neuronal reuptake of norepinephrine, which strengthens the pressor response to injected adrenergic vasoconstrictors. The effect is most dramatic with levonordefrin and norepinephrine, which are mainly alpha agonists. Studies show a markedly exaggerated hypertensive response with levonordefrin, so it should be avoided. Epinephrine is not contraindicated but should be limited (commonly about 0.05 mg, roughly 3 cartridges of 1:100,000 per visit), with careful aspiration and slow injection. Option A sounds reasonable but is the trap: levonordefrin's strong alpha activity makes it the worst choice.