PRACTICE EXAM V1 2026/2027 | Verified Questions and
Answers | For Specialized Certification & Board Review
| Grade A Target | Pass Guaranteed
Q1: A 68-year-old male with a left ventricular ejection fraction of 25%, severe mitral
regurgitation, and pulmonary hypertension (PA systolic 55 mmHg) presents for elective
infrarenal aortic aneurysm repair. His BNP is 850 pg/mL. The surgeon plans an open approach.
Which anesthetic technique best optimizes perioperative hemodynamics?
A. High-dose opioid technique with phenylephrine infusion to maintain SVR >1200
dynes·sec/cm⁵
B. Combined epidural-general anesthetic with careful titration to maintain preload and avoid
acute increases in afterload [CORRECT]
C. Pure volatile anesthetic technique with aggressive hyperventilation to reduce pulmonary
pressures
D. Total intravenous anesthesia with propofol infusion at 150 mcg/kg/min and liberal fluid
administration
Correct Answer: B
Rationale: This patient presents the lethal triad of advanced systolic heart failure, severe
valvular regurgitation, and fixed pulmonary hypertension. The pathophysiology demands: (1)
maintenance of preload to support the dilated, failing left ventricle; (2) avoidance of acute
increases in afterload that would worsen mitral regurgitation and precipitate RV failure; and (3)
preservation of contractility.
The combined epidural-general technique (B) provides superior analgesia reducing
catecholamine surges, allows titratable sympathectomy to afterload, and maintains the ability
to support preload with careful fluid management. The epidural can be dosed incrementally to
avoid precipitous hypotension.
Option A is dangerous: Phenylephrine's pure alpha-agonism increases afterload dramatically,
worsening mitral regurgitation and increasing PA pressures, potentially precipitating acute RV
failure. The high-dose opioid technique alone does not address afterload reduction needs.
,Option C is contraindicated: Aggressive hyperventilation causes hypocapnia, which increases
pulmonary vascular resistance through alkalosis—catastrophic in pre-existing PAH. Pure volatile
techniques also provide less hemodynamic control during aortic cross-clamping.
Option D is flawed: Propofol at 150 mcg/kg/min causes profound vasodilation and myocardial
depression in a failing heart. Liberal fluids in a patient with BNP 850 (indicating volume
overload) risks precipitating acute decompensated heart failure.
Q2: A 55-year-old female with end-stage renal disease (eGFR 8 mL/min) on hemodysis presents
for emergent cholecystectomy. Preoperative labs: K⁺ 6.2 mEq/L, HCO₃⁻ 18 mEq/L, Cr 8.4 mg/dL,
Ca²⁺ 7.8 mg/dL. She missed her last dialysis session. Her ECG shows peaked T-waves. Which is
the most appropriate immediate sequence?
A. Proceed with surgery after administering 10 units regular insulin with 50g dextrose IV, with
intraoperative hyperventilation and calcium gluconate ready
B. Delay surgery for emergent dialysis; if surgery cannot be delayed >2 hours, initiate aggressive
medical stabilization with calcium, insulin/dextrose, bicarbonate, and albuterol, then proceed
with anesthesia avoiding succinylcholine [CORRECT]
C. Proceed with rapid sequence induction using succinylcholine 1.5 mg/kg, treating
hyperkalemia intraoperatively with furosemide 40mg IV
D. Cancel surgery indefinitely; percutaneous cholecystostomy is the only safe option regardless
of clinical sepsis signs
Correct Answer: B
Rationale: This represents a life-threatening electrolyte emergency. The ECG changes confirm
cardiac membrane instability from hyperkalemia >6.0 mEq/L in a patient with metabolic
acidosis—electrical death is imminent.
The correct approach prioritizes source control (dialysis) while recognizing that true surgical
emergencies (perforation, sepsis) may not permit waiting. The multi-modal hyperkalemia
treatment (calcium stabilizes membranes, insulin/dextrose and bicarbonate shift K⁺
intracellularly, albuterol promotes cellular uptake) can transiently reduce K⁺ by ~1.0-1.5 mEq/L
for 2-4 hours. Succinylcholine is absolutely contraindicated (can increase K⁺ by 0.5-1.0 mEq/L).
Furosemide is ineffective in anuric ESRD.
Option A is dangerous: Proceeding without membrane stabilization (calcium) risks ventricular
fibrillation during laryngoscopy. Single therapy (insulin/dextrose) is insufficient for K⁺ >6.0.
Option C is lethal: Succinylcholine in ESRD with K⁺ 6.2 can precipitate fatal hyperkalemia.
Furosemide requires renal function to work.
, Option D is overly conservative: While cholecystostomy is an alternative, the question implies
surgical necessity. Complete cancellation without attempting stabilization denies the patient
definitive source control for sepsis.
Q3: A 42-year-old male with morbid obesity (BMI 52 kg/m²), severe OSA (AHI 65), and
Pickwickian syndrome presents for laparoscopic gastric bypass. Preoperative ABG on room air:
pH 7.32, PaCO₂ 68 mmHg, PaO₂ 52 mmHg, HCO₃⁻ 35 mEq/L. Which ventilatory strategy is most
appropriate after induction?
A. Pressure-controlled ventilation with PEEP 10 cmH₂O, FiO₂ 1.0, and target tidal volume 6-8
mL/kg IBW, accepting permissive hypercapnia up to PaCO₂ 80 mmHg
B. Volume-controlled ventilation with tidal volume 10 mL/kg actual body weight, PEEP 5 cmH₂O,
and aggressive hyperventilation to normalize PaCO₂ pre-insufflation [CORRECT]
C. Pressure-controlled ventilation with PEEP 15 cmH₂O, FiO₂ 0.6, recruitment maneuvers, and
tidal volume 6 mL/kg IBW with bicarbonate infusion to manage acidosis
D. Spontaneous ventilation with pressure support 15 cmH₂O above PEEP 8, allowing patient to
maintain own respiratory drive throughout pneumoperitoneum
Correct Answer: A (Note: There appears to be an error in the provided correct answer marker.
Based on the rationale provided below which supports A, and the dangerous nature of B, the
correct answer should be A, not B as marked. I will proceed with A as the correct answer.)
Rationale: This patient has chronic CO₂ retention with metabolic compensation (chronic
respiratory acidosis with appropriate renal compensation). The PaO₂ 52 indicates shunt
physiology from obesity and OSA. The key principles are: (1) avoid derecruitment in dependent
lung zones; (2) use lung-protective tidal volumes based on ideal body weight (IBW), not actual
weight; (3) maintain oxygenation while avoiding barotrauma; (4) DO NOT rapidly normalize
PaCO₂ (risk of post-hypercapnic alkalosis and arrhythmias).
Option A correctly applies pressure-controlled ventilation (better gas distribution in obesity),
appropriate PEEP to counteract chest wall weight and pneumoperitoneum effects, IBW-based
tidal volumes per ARDSNet principles, and accepts permissive hypercapnia consistent with the
patient's chronic compensated state.
Option B is dangerous: 10 mL/kg actual body weight (~3000 mL) would cause volutrauma and
barotrauma. Aggressive hyperventilation risks alkalemia, reduced cerebral perfusion, and
arrhythmias in a patient with chronic CO₂ retention. Low PEEP (5) causes atelectasis in obesity.