Drug Interactions and Contraindications in Anesthesia Flashcards

A patient taking propranolol for hypertension gets several cartridges of 2% lidocaine with 1:100,000 epinephrine before sedation. Shortly afterward, the monitor shows a sharp rise in blood pressure and the heart rate falls to 48 bpm. What best explains this response?

Answer: Propranolol blocks the beta-2 vasodilation epinephrine normally causes, so alpha-1 vasoconstriction acts unopposed and a baroreceptor reflex slows the heart

Nonselective beta-blockers such as propranolol block beta-2 receptors, so epinephrine can no longer dilate skeletal muscle blood vessels. Its alpha-1 vasoconstriction then acts unopposed and blood pressure rises sharply. The baroreceptors respond by increasing vagal tone, which causes reflex bradycardia. Cardioselective (beta-1) blockers such as metoprolol carry much less of this risk. Patients on nonselective beta-blockers should get the smallest effective dose of vasoconstrictor, with vital signs checked between injections.

A patient scheduled for IV midazolam sedation started a 10-day course of clarithromycin 3 days ago. What interaction should the anesthesia team expect?

Answer: Sedation will be deeper and last longer because clarithromycin inhibits CYP3A4, the main pathway that metabolizes midazolam

Midazolam is metabolized mainly by hepatic CYP3A4. Macrolide antibiotics such as clarithromycin and erythromycin, azole antifungals such as ketoconazole and itraconazole, some HIV protease inhibitors, and grapefruit juice all strongly inhibit CYP3A4. They can raise midazolam levels several-fold, which leads to deeper, longer sedation and a risk of respiratory depression. The dose should be reduced and titrated carefully, with longer monitoring. Rifampin and carbamazepine do the opposite: they induce CYP3A4 and shorten midazolam's effect.

A patient with glaucoma uses echothiophate iodide eye drops. If succinylcholine were given during an airway emergency, which complication would be most likely?

Answer: Prolonged neuromuscular blockade and apnea, because echothiophate inhibits plasma pseudocholinesterase

Echothiophate is a long-acting organophosphate cholinesterase inhibitor. Once absorbed into the bloodstream, it can lower plasma pseudocholinesterase (butyrylcholinesterase) activity for weeks after the drops are stopped. Succinylcholine is normally broken down by pseudocholinesterase within minutes. Without that enzyme, paralysis and apnea can last much longer and may require extended ventilatory support. This is an acquired pseudocholinesterase deficiency, so the medication history matters.

A patient is oversedated after IV midazolam. The patient takes clonazepam daily for a seizure disorder. Why should flumazenil be used with extreme caution, or avoided, in this patient?

Answer: Flumazenil can trigger abrupt benzodiazepine withdrawal and lower the seizure threshold, which may cause seizures

Flumazenil competitively blocks the benzodiazepine binding site on the GABA-A receptor. In a patient who depends on a benzodiazepine for seizure control or takes one long-term, sudden reversal can cause acute withdrawal and seizures. It is also dangerous after mixed overdoses that include tricyclic antidepressants or other proconvulsant drugs. In these patients, the safer course is supportive airway management and ventilation, or very cautious small titrated doses.

A patient taking amitriptyline (a tricyclic antidepressant) needs local anesthesia before a procedure. Which vasoconstrictor approach is most appropriate?

Answer: Avoid levonordefrin and limit epinephrine to small doses with careful aspiration and monitoring

Tricyclic antidepressants block norepinephrine reuptake, which strengthens the pressor effect of sympathomimetic vasoconstrictors. The interaction is most pronounced with levonordefrin and norepinephrine, which can cause severe hypertension and dysrhythmias, so those should be avoided. Epinephrine can still be used at a reduced dose, often cited as about 0.04 mg (roughly two cartridges of 1:100,000), with aspiration to prevent intravascular injection and monitoring of vital signs.

Before a sedation appointment, a patient says they used cocaine about 4 hours ago. Which statement about local anesthetic with a vasoconstrictor is correct?

Answer: Vasoconstrictor-containing local anesthetics should be avoided. The procedure should be postponed, generally at least 24 hours after last use, because of the risk of hypertensive crisis, dysrhythmias, and myocardial infarction

Cocaine blocks reuptake of norepinephrine and other catecholamines and makes the heart more sensitive to them. Adding exogenous epinephrine or levonordefrin can cause severe hypertension, tachydysrhythmias, coronary vasospasm, myocardial infarction, or sudden death. The usual recommendation is to postpone elective treatment and avoid vasoconstrictors until at least 24 hours after last use. Sedation in an acutely intoxicated patient is also contraindicated.