Principles of Anesthesia Flashcards

A 58-year-old patient undergoing hepatic resection receives isoflurane anesthesia. Intraoperatively, the hepatic artery is temporarily clamped. Which mechanism best explains why isoflurane is relatively hepatoprotective in this setting compared to halothane?

Answer: Isoflurane undergoes less cytochrome P450-mediated oxidative metabolism, producing fewer reactive trifluoroacetyl intermediates

Halothane undergoes ~20% oxidative metabolism via CYP2E1, generating trifluoroacetyl chloride that haptenates hepatic proteins and can trigger immune-mediated hepatotoxicity (halothane hepatitis). Isoflurane undergoes only ~0.2% oxidative metabolism, making this pathway clinically negligible. While isoflurane does have some vasodilatory effects, the primary hepatoprotective advantage is metabolic, not hemodynamic. Mitochondrial complex I inhibition and stellate cell activation are not established mechanisms of isoflurane hepatoprotection.

During total intravenous anesthesia (TIVA) with propofol and remifentanil, a patient's BIS monitor reads 62 and MAC-equivalent is 0 (no volatile agent). The patient suddenly shows a 15% increase in systolic blood pressure and heart rate with purposeful movement. Which pharmacokinetic explanation is MOST likely responsible for this breakthrough response?

Answer: Propofol redistributes from the highly perfused brain compartment to peripheral tissue compartments, decreasing effect-site concentration

During prolonged propofol infusions, the drug redistributes from the central (brain/plasma) compartment to peripheral (muscle, fat) compartments. This reduces the effect-site concentration despite a constant infusion rate, as the peripheral compartment acts as a sink. The BIS of 62 may reflect inadequate depth. Remifentanil's context-sensitive half-time remains ~3–5 minutes regardless of infusion duration due to ester hydrolysis — this is its pharmacokinetic advantage. Plasma esterase saturation does not occur at clinical remifentanil doses. While propofol's volume of distribution does expand, the primary issue here is redistribution lowering effect-site concentration, not a change in Vd per se.

A patient with myasthenia gravis (MG) is scheduled for thymectomy. The anesthesiologist plans to avoid neuromuscular blocking agents. If a short-acting NMB is deemed necessary for intubation, which agent and reversal strategy represents the highest-risk approach in this patient?

Answer: Cisatracurium 0.1 mg/kg reversed with neostigmine 0.07 mg/kg and glycopyrrolate

In myasthenia gravis, patients have dramatically reduced functional acetylcholine receptors, making them exquisitely sensitive to non-depolarizing NMBs — cisatracurium at 0.1 mg/kg (a normal intubating dose) can produce profound, prolonged blockade. Neostigmine reversal is particularly problematic because MG patients are already on cholinesterase inhibitors (e.g., pyridostigmine), and administering neostigmine risks cholinergic crisis in addition to unpredictable reversal. Rocuronium reversed with sugammadex is actually preferred in MG because sugammadex provides predictable, complete reversal independent of receptor status. Succinylcholine is controversial (risk of phase II block) but not requiring reversal. Mivacurium relies on plasma cholinesterase and, if normal enzyme levels, offsets quickly without reversal.

During a laparoscopic procedure, a patient receiving sevoflurane anesthesia develops a sudden end-tidal CO₂ of 68 mmHg, a persistent wave-form abnormality on capnography showing an elevated baseline, and a temperature rise to 38.6°C over 20 minutes. Dantrolene is drawn up. Before administering it, which finding would MOST strongly argue AGAINST a diagnosis of malignant hyperthermia (MH)?

Answer: End-tidal CO₂ that decreased transiently when minute ventilation was doubled

In true MH, the massive increase in cellular metabolism and CO₂ production is so profound that doubling minute ventilation produces only a transient or modest reduction in EtCO₂ before CO₂ rises again — the metabolic source overwhelms ventilatory compensation. A CO₂ that normalizes with increased ventilation suggests the hypercarbia has a ventilatory (e.g., laparoscopic insufflation, hypoventilation) rather than metabolic cause. Absence of rigidity does not rule out MH — it is present in only ~75% of cases. Mixed acidosis is consistent with MH. An early CK of 1,200 U/L is mildly elevated and can appear in early MH; peak CK in MH typically occurs 6–12 hours later and is much higher, but early elevation does not exclude MH.

A 72-year-old patient with chronic kidney disease (eGFR 18 mL/min) requires analgesia following abdominal surgery. The pain team is considering an opioid infusion. Which statement about opioid pharmacokinetics in severe renal failure is MOST accurate?

Answer: Morphine's metabolite morphine-6-glucuronide accumulates and can cause prolonged opioid effect and respiratory depression

Morphine is converted hepatically to morphine-3-glucuronide (M3G, neuroexcitatory, no analgesia) and morphine-6-glucuronide (M6G), both of which are renally excreted. M6G is a potent mu-opioid agonist with a longer duration than morphine itself; it accumulates markedly in renal failure, causing prolonged analgesia and dangerous respiratory depression. Fentanyl does not have a pharmacologically active glucuronide metabolite — it is oxidized to norfentanyl (inactive), making it relatively safer in renal failure. Hydromorphone is actually problematic in renal failure because its metabolite hydromorphone-3-glucuronide (neuroexcitatory) accumulates, and it also produces some active opioid metabolites. Remifentanil is hydrolyzed by nonspecific tissue and plasma esterases unaffected by uremia, making it the safest opioid in severe renal failure.

An anesthesiologist is performing an ultrasound-guided interscalene brachial plexus block for shoulder surgery. After injecting 20 mL of 0.5% ropivacaine, the patient develops sudden hypotension, bradycardia, and loss of consciousness, but the SpO₂ remains 100% on supplemental oxygen. Which mechanism BEST explains this specific clinical picture?

Answer: Inadvertent epidural spread via the interscalene route causing bilateral C3–C5 neuraxial blockade and cardiac sympathectomy

The interscalene groove is immediately adjacent to the epidural space at the cervical level. Large volumes (≥20 mL) can track medially and enter the epidural or even intrathecal space, causing high cervical neuraxial blockade. Blockade of cardiac accelerator fibers (T1–T4) produces profound bradycardia and hypotension, while blockade of C3–C5 can compromise diaphragmatic function. However, in this case, SpO₂ is maintained (arguing against primary respiratory failure from phrenic nerve palsy alone). Intravascular injection causing LAST typically presents with neurological prodrome (tinnitus, circumoral numbness, seizures) before cardiovascular collapse, not the sudden hypotension/bradycardia picture described. While Bezold-Jarisch reflex can cause vasovagal syncope, it doesn't explain loss of consciousness at this severity from a block already completed. High cervical epidural/intrathecal spread is the most complete explanation for this cardiovascular picture.