Principles of Anesthesia Flashcards

A 58-year-old patient undergoing laparoscopic cholecystectomy develops sudden hypotension and desaturation 20 minutes into the procedure. End-tidal CO₂ abruptly drops to 12 mmHg while peak airway pressure rises. Which diagnosis best explains this triad?

Answer: CO₂ gas embolism from venous insufflation

CO₂ venous gas embolism classically produces a sudden drop in EtCO₂ (CO₂ washed out of pulmonary circulation by the gas lock), hypotension from right heart outflow obstruction, and increased airway pressure. Tension pneumothorax would show absent breath sounds unilaterally and rising EtCO₂, not a drop. Anaphylaxis does not explain the sharp EtCO₂ fall. Esophageal intubation would have been apparent from the start.

During sevoflurane anesthesia at low fresh gas flows (<1 L/min), a nephrotoxic compound can accumulate. Which mechanism best explains this toxicity risk?

Answer: Compound A formation via CO₂ absorbent degradation reacting with renal β-lyase

Compound A (fluoromethyl-2,2-difluoro-1-(trifluoromethyl)vinyl ether) is produced when sevoflurane reacts with soda lime or Baralyme at low flows. It undergoes renal β-lyase metabolism into nephrotoxic thiol compounds. While inorganic fluoride was historically implicated (methoxyflurane era), sevoflurane's fluoride levels rarely reach clinically nephrotoxic thresholds. Carbon monoxide from desiccated absorbent is an issue with desflurane/isoflurane, not the primary nephrotoxicity pathway for sevoflurane.

A patient with a known dibucaine number of 20 receives succinylcholine for rapid sequence intubation. What is the most appropriate immediate management after failed spontaneous reversal at 45 minutes?

Answer: Maintain sedation, continue controlled ventilation, and await plasma cholinesterase reconstitution

A dibucaine number of 20 indicates homozygous atypical pseudocholinesterase — the patient cannot hydrolyze succinylcholine, resulting in prolonged (hours) paralysis. The correct management is to maintain sedation and mechanically ventilate until the block spontaneously dissipates. Sugammadex only encapsulates aminosteroid NDMBs (rocuronium/vecuronium) — it has no effect on succinylcholine. Neostigmine inhibits acetylcholinesterase and may worsen a phase II block rather than reliably reverse it. FFP contains pseudocholinesterase but response is inconsistent and takes time; it is not first-line.

Which pharmacokinetic property most accurately explains why context-sensitive half-time increases dramatically for fentanyl but NOT for remifentanil during prolonged infusions?

Answer: Remifentanil is hydrolyzed by nonspecific plasma and tissue esterases independent of organ blood flow

Remifentanil contains a methyl ester linkage that is cleaved by ubiquitous nonspecific esterases in blood and tissues, giving it a context-insensitive offset (half-time ~3–5 min regardless of infusion duration). Fentanyl, despite redistribution early on, accumulates in fat and muscle peripheral compartments during prolonged infusion; when the infusion stops, drug continues to transfer back to plasma, markedly extending clinical effect. While remifentanil does have a smaller Vdss, this alone does not fully account for its unique kinetics — the ester metabolism is the defining mechanism.

Intraoperatively, a patient develops masseter muscle rigidity after succinylcholine administration. Core temperature is 37.2°C and the patient is hemodynamically stable. Which action is MOST appropriate at this time?

Answer: Discontinue all triggering agents, monitor creatine kinase, lactate, and temperature closely, and have dantrolene immediately available

Isolated masseter muscle rigidity (MMR) after succinylcholine is considered a forme fruste or harbinger of malignant hyperthermia (MH) susceptibility in a significant proportion of cases — estimates range from 15–50%. The current evidence-based approach is to discontinue volatile agents and succinylcholine, convert to TIVA if the case must continue, monitor continuously for MH signs (rising EtCO₂, temperature, acidosis, myoglobinuria), and have dantrolene immediately at bedside. Prophylactic dantrolene without MH signs is not mandatory but must be available. Simply observing (B) underestimates risk; proceeding with TIVA without vigilance (D) ignores the ongoing MH risk window.

A patient on chronic buprenorphine therapy for opioid use disorder requires general anesthesia for an emergent bowel resection. Which intraoperative analgesic strategy is BEST supported by current pharmacological understanding?

Answer: Continue buprenorphine perioperatively and supplement with multimodal analgesia plus higher-dose full µ-agonists, accepting partial ceiling effect

Buprenorphine is a partial µ-agonist with very high receptor affinity and slow dissociation, making displacement by full agonists difficult. Current guidelines (ASAM, SOAP) recommend continuing buprenorphine perioperatively — abrupt discontinuation risks undertreated pain and relapse. Full µ-agonists (e.g., hydromorphone, fentanyl) can still provide analgesia at higher doses by occupying unbound or cycling receptors. Multimodal analgesia (NSAIDs, ketamine, regional) reduces the opioid requirement. Methadone transition is impractical in an emergent setting and carries its own QTc risks. Ketamine alone is insufficient for major abdominal surgery.