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Pharmacology · patient case question

Why does propranolol increase the risk of lidocaine toxicity?

Patient case: A long medication list before an extraction

Patient: Male, 58 years old

Chief Complaint: Presents for extraction of a non-restorable maxillary premolar.

Background: Hypertension and migraine. Longstanding depression.

Medications: Propranolol 80 mg twice daily · imipramine 75 mg nightly · sumatriptan as required · acetaminophen as required

Vital Signs: BP 138/86 mmHg · HR 58 bpm · RR 16

Findings: Tooth #5 is non-restorable. Following an infiltration in the maxillary buccal vestibule he is temporarily unable to raise the upper lip on that side, which alarms him.

  1. It inhibits plasma cholinesterase, slowing hydrolysis of the anaesthetic
  2. It displaces lidocaine from plasma protein binding sites
  3. It reduces hepatic clearance of lidocaine, both by lowering cardiac output and by competing for the same hepatic enzymes
  4. It increases the rate of absorption of lidocaine from the injection site
Show answer and explanation

Correct answer: C. It reduces hepatic clearance of lidocaine, both by lowering cardiac output and by competing for the same hepatic enzymes

  • A. Plasma (pseudo)cholinesterase hydrolyses the ESTER anaesthetics — procaine, benzocaine, tetracaine. Lidocaine is an AMIDE and is metabolised in the liver, which is the entire reason this hepatic interaction exists.
  • B. Protein binding displacement is not the mechanism. Lidocaine is roughly 65% protein bound and beta blockers do not displace it to any clinically meaningful degree.
  • C. CORRECT, and by TWO distinct mechanisms, which is what the question is testing. First, a non-selective beta blocker reduces CARDIAC OUTPUT and therefore hepatic blood flow; lidocaine is a high-extraction drug whose clearance is flow-limited, so less liver perfusion directly means slower elimination. Second, propranolol and the amide local anaesthetics COMPETE for the same hepatic microsomal enzyme pathways. Both effects raise and prolong the plasma lidocaine concentration — which is why the DURATION OF ACTION of lidocaine is increased in the presence of propranolol, and why the maximum dose should be reduced, injection made slowly, and aspiration performed carefully.
  • D. The rate of absorption from the site is governed by the vasoconstrictor concentration and by the vascularity of the tissue, not by a systemic beta blocker.

Note: There is a SECOND and separate propranolol interaction that must not be confused with this one. Epinephrine given to a patient on a NON-SELECTIVE beta blocker produces UNOPPOSED ALPHA-1 stimulation, since the vasodilatory beta-2 response is blocked — the result is a hypertensive response with reflex bradycardia. Limit the epinephrine dose, aspirate, and monitor blood pressure. Cardioselective agents such as metoprolol and atenolol carry considerably less of this risk. Note this patient's resting pulse of 58.

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