ASA 114 Advanced Anesthesiology Practice ACTUAL
PRACTICE EXAM V1 2026/2027 | Verified Questions and
Answers | For Specialized Certification & Board Review
| Grade A Target | Pass Guaranteed
Section 1: Complex Comorbidity Management (Questions 1-20)
Question 1
A 68-year-old male (BMI 42 kg/m², weight 128 kg) presents for elective laparoscopic Roux-en-Y
gastric bypass. He has severe obstructive sleep apnea (AHI 68, on CPAP 16 cm H₂O), pulmonary
hypertension (estimated PASP 58 mmHg on echo), and NYHA Class II heart failure with
preserved ejection fraction (EF 62%). Preoperative arterial blood gas on room air shows pH 7.38,
PaCO₂ 52 mmHg, PaO₂ 64 mmHg, HCO₃ 30 mEq/L. Which anesthetic induction strategy best
balances airway safety with hemodynamic stability in this patient?
A) Rapid sequence induction with succinylcholine and etomidate, followed by immediate nasal
intubation without mask ventilation [CORRECT] B) Standard induction with propofol 2.5 mg/kg
and rocuronium 0.6 mg/kg, gentle mask ventilation with two-person technique, then oral
intubation C) Awake fiberoptic intubation under topical anesthesia with minimal sedation to
avoid any hemodynamic perturbation D) Inhalational induction with sevoflurane while
maintaining spontaneous ventilation, followed by intubation after deep anesthesia
Correct Answer: A
Rationale: This patient presents the lethal triad of morbid obesity, severe OSA, and pulmonary
hypertension—each independently increasing perioperative risk, synergistically creating
extreme vulnerability to hypoxemia and cardiovascular collapse. The arterial blood gas reveals
chronic hypercapnic respiratory failure (PaCO₂ 52 with compensated metabolic alkalosis) and
significant hypoxemia, indicating severe ventilation-perfusion mismatch and limited pulmonary
reserve.
Option A is correct because: Rapid sequence induction (RSI) with etomidate (0.2-0.3 mg/kg)
provides hemodynamic stability in a patient with fixed pulmonary vascular resistance who
,cannot tolerate hypotension or catecholamine surge. Etomidate preserves sympathetic tone
and does not cause histamine release—critical in pulmonary hypertension where systemic
hypotension precipitates right ventricular ischemia and failure. Succinylcholine (1.5 mg/kg ideal
body weight) provides optimal intubating conditions in 45-60 seconds, minimizing the apneic
period during which this patient will desaturate precipitously due to reduced functional residual
capacity (FRC), increased oxygen consumption, and decreased cardiac reserve. Immediate nasal
intubation (preferred route in bariatric surgery) without mask ventilation prevents gastric
insufflation and aspiration risk while avoiding the hemodynamic consequences of positive
pressure ventilation on venous return and right heart function.
Option B is dangerous: Propofol causes dose-dependent vasodilation and myocardial
depression; at 2.5 mg/kg total body weight (320 mg), this represents massive overdose for this
patient (should be ideal body weight or lean body weight dosing). Mask ventilation in severe
OSA with pulmonary hypertension risks gastric insufflation, aspiration, and hemodynamic
compromise from increased intrathoracic pressure reducing venous return and right ventricular
filling.
Option C is suboptimal: While awake fiberoptic intubation is often taught for difficult airways,
this patient's pulmonary hypertension and obesity create a narrow therapeutic window for
sedation. Topical anesthesia alone often provides inadequate conditions, and any sedation risks
respiratory depression and hypercapnic crisis. Additionally, the supine position for fiberoptic
intubation further compromises FRC and oxygenation in obesity.
Option D is contraindicated: Inhalational induction in adults with severe OSA and pulmonary
hypertension is unpredictable, slow, and risks complete airway obstruction during the
excitement phase. Sevoflurane causes dose-dependent myocardial depression and vasodilation,
potentially precipitating cardiovascular collapse before airway control is achieved.
Question 2
A 72-year-old female with severe aortic stenosis (valve area 0.7 cm², mean gradient 48 mmHg,
peak velocity 5.2 m/s), CAD with 70% LAD stenosis, and chronic kidney disease (eGFR 28
mL/min/1.73m²) presents for urgent hemicolectomy for obstructing colon cancer. Her
preoperative hemoglobin is 9.8 g/dL. Intraoperatively, upon peritoneal insufflation for
laparoscopic approach, her arterial pressure drops from 118/72 to 68/42 mmHg with ST-
segment depression in leads II, III, aVF. What is the most appropriate immediate intervention?
A) Administer phenylephrine 100 mcg bolus to restore afterload and coronary perfusion
pressure [CORRECT] B) Increase insufflation pressure to 18 mmHg to improve surgical exposure
, and complete the case rapidly C) Administer ephedrine 10 mg to increase heart rate and
contractility D) Give a 500 mL crystalloid bolus to increase preload
Correct Answer: A
Rationale: This patient exhibits classic hemodynamic catastrophe from pneumoperitoneum in
severe aortic stenosis (AS). The pathophysiology involves: (1) increased intra-abdominal
pressure reducing venous return and preload, (2) increased systemic vascular resistance (SVR)
from CO₂ absorption and mechanical compression, and (3) reduced myocardial compliance from
hypertrophied, pressure-overloaded left ventricle. The result is decreased cardiac output,
hypotension, and subendocardial ischemia from supply-demand mismatch (ST depression in
inferior leads).
Option A is correct: Phenylephrine, a pure alpha-1 agonist, increases SVR and diastolic blood
pressure, thereby improving coronary perfusion pressure (diastolic pressure minus LVEDP). In
severe AS, cardiac output is fixed (stroke volume cannot increase due to fixed obstruction),
making afterload-dependent coronary perfusion critical. Phenylephrine does not increase heart
rate (unlike ephedrine), avoiding the detrimental effects of tachycardia on diastolic filling time
and myocardial oxygen demand in AS. The goal is to maintain sinus rhythm and adequate
afterload to perfuse the hypertrophied, high-oxygen-demand myocardium.
Option B is lethal: Increasing insufflation pressure further compromises venous return, increases
SVR, and exacerbates the pathophysiology causing the current crisis. This would likely
precipitate cardiac arrest from complete cardiovascular collapse.
Option C is contraindicated: Ephedrine causes tachycardia and increased contractility—both
harmful in severe AS. Tachycardia reduces diastolic filling time (critical in AS where diastolic
dysfunction is common due to LVH), increases myocardial oxygen demand, and may precipitate
ischemia or arrhythmia. Inotropy increases oxygen demand without significantly increasing
output across a fixed stenotic valve.
Option D is ineffective and potentially harmful: In severe AS with reduced ventricular
compliance, volume loading increases LVEDP without significantly increasing stroke volume
(Starling curve is flat), potentially causing pulmonary edema without improving cardiac output
or blood pressure. The problem is afterload mismatch and reduced venous return, not absolute
hypovolemia.
Question 3
A 58-year-old male with end-stage liver disease (MELD 24, Child-Pugh C) secondary to alcoholic
cirrhosis presents for orthotopic liver transplantation. Preoperative labs show: platelets
PRACTICE EXAM V1 2026/2027 | Verified Questions and
Answers | For Specialized Certification & Board Review
| Grade A Target | Pass Guaranteed
Section 1: Complex Comorbidity Management (Questions 1-20)
Question 1
A 68-year-old male (BMI 42 kg/m², weight 128 kg) presents for elective laparoscopic Roux-en-Y
gastric bypass. He has severe obstructive sleep apnea (AHI 68, on CPAP 16 cm H₂O), pulmonary
hypertension (estimated PASP 58 mmHg on echo), and NYHA Class II heart failure with
preserved ejection fraction (EF 62%). Preoperative arterial blood gas on room air shows pH 7.38,
PaCO₂ 52 mmHg, PaO₂ 64 mmHg, HCO₃ 30 mEq/L. Which anesthetic induction strategy best
balances airway safety with hemodynamic stability in this patient?
A) Rapid sequence induction with succinylcholine and etomidate, followed by immediate nasal
intubation without mask ventilation [CORRECT] B) Standard induction with propofol 2.5 mg/kg
and rocuronium 0.6 mg/kg, gentle mask ventilation with two-person technique, then oral
intubation C) Awake fiberoptic intubation under topical anesthesia with minimal sedation to
avoid any hemodynamic perturbation D) Inhalational induction with sevoflurane while
maintaining spontaneous ventilation, followed by intubation after deep anesthesia
Correct Answer: A
Rationale: This patient presents the lethal triad of morbid obesity, severe OSA, and pulmonary
hypertension—each independently increasing perioperative risk, synergistically creating
extreme vulnerability to hypoxemia and cardiovascular collapse. The arterial blood gas reveals
chronic hypercapnic respiratory failure (PaCO₂ 52 with compensated metabolic alkalosis) and
significant hypoxemia, indicating severe ventilation-perfusion mismatch and limited pulmonary
reserve.
Option A is correct because: Rapid sequence induction (RSI) with etomidate (0.2-0.3 mg/kg)
provides hemodynamic stability in a patient with fixed pulmonary vascular resistance who
,cannot tolerate hypotension or catecholamine surge. Etomidate preserves sympathetic tone
and does not cause histamine release—critical in pulmonary hypertension where systemic
hypotension precipitates right ventricular ischemia and failure. Succinylcholine (1.5 mg/kg ideal
body weight) provides optimal intubating conditions in 45-60 seconds, minimizing the apneic
period during which this patient will desaturate precipitously due to reduced functional residual
capacity (FRC), increased oxygen consumption, and decreased cardiac reserve. Immediate nasal
intubation (preferred route in bariatric surgery) without mask ventilation prevents gastric
insufflation and aspiration risk while avoiding the hemodynamic consequences of positive
pressure ventilation on venous return and right heart function.
Option B is dangerous: Propofol causes dose-dependent vasodilation and myocardial
depression; at 2.5 mg/kg total body weight (320 mg), this represents massive overdose for this
patient (should be ideal body weight or lean body weight dosing). Mask ventilation in severe
OSA with pulmonary hypertension risks gastric insufflation, aspiration, and hemodynamic
compromise from increased intrathoracic pressure reducing venous return and right ventricular
filling.
Option C is suboptimal: While awake fiberoptic intubation is often taught for difficult airways,
this patient's pulmonary hypertension and obesity create a narrow therapeutic window for
sedation. Topical anesthesia alone often provides inadequate conditions, and any sedation risks
respiratory depression and hypercapnic crisis. Additionally, the supine position for fiberoptic
intubation further compromises FRC and oxygenation in obesity.
Option D is contraindicated: Inhalational induction in adults with severe OSA and pulmonary
hypertension is unpredictable, slow, and risks complete airway obstruction during the
excitement phase. Sevoflurane causes dose-dependent myocardial depression and vasodilation,
potentially precipitating cardiovascular collapse before airway control is achieved.
Question 2
A 72-year-old female with severe aortic stenosis (valve area 0.7 cm², mean gradient 48 mmHg,
peak velocity 5.2 m/s), CAD with 70% LAD stenosis, and chronic kidney disease (eGFR 28
mL/min/1.73m²) presents for urgent hemicolectomy for obstructing colon cancer. Her
preoperative hemoglobin is 9.8 g/dL. Intraoperatively, upon peritoneal insufflation for
laparoscopic approach, her arterial pressure drops from 118/72 to 68/42 mmHg with ST-
segment depression in leads II, III, aVF. What is the most appropriate immediate intervention?
A) Administer phenylephrine 100 mcg bolus to restore afterload and coronary perfusion
pressure [CORRECT] B) Increase insufflation pressure to 18 mmHg to improve surgical exposure
, and complete the case rapidly C) Administer ephedrine 10 mg to increase heart rate and
contractility D) Give a 500 mL crystalloid bolus to increase preload
Correct Answer: A
Rationale: This patient exhibits classic hemodynamic catastrophe from pneumoperitoneum in
severe aortic stenosis (AS). The pathophysiology involves: (1) increased intra-abdominal
pressure reducing venous return and preload, (2) increased systemic vascular resistance (SVR)
from CO₂ absorption and mechanical compression, and (3) reduced myocardial compliance from
hypertrophied, pressure-overloaded left ventricle. The result is decreased cardiac output,
hypotension, and subendocardial ischemia from supply-demand mismatch (ST depression in
inferior leads).
Option A is correct: Phenylephrine, a pure alpha-1 agonist, increases SVR and diastolic blood
pressure, thereby improving coronary perfusion pressure (diastolic pressure minus LVEDP). In
severe AS, cardiac output is fixed (stroke volume cannot increase due to fixed obstruction),
making afterload-dependent coronary perfusion critical. Phenylephrine does not increase heart
rate (unlike ephedrine), avoiding the detrimental effects of tachycardia on diastolic filling time
and myocardial oxygen demand in AS. The goal is to maintain sinus rhythm and adequate
afterload to perfuse the hypertrophied, high-oxygen-demand myocardium.
Option B is lethal: Increasing insufflation pressure further compromises venous return, increases
SVR, and exacerbates the pathophysiology causing the current crisis. This would likely
precipitate cardiac arrest from complete cardiovascular collapse.
Option C is contraindicated: Ephedrine causes tachycardia and increased contractility—both
harmful in severe AS. Tachycardia reduces diastolic filling time (critical in AS where diastolic
dysfunction is common due to LVH), increases myocardial oxygen demand, and may precipitate
ischemia or arrhythmia. Inotropy increases oxygen demand without significantly increasing
output across a fixed stenotic valve.
Option D is ineffective and potentially harmful: In severe AS with reduced ventricular
compliance, volume loading increases LVEDP without significantly increasing stroke volume
(Starling curve is flat), potentially causing pulmonary edema without improving cardiac output
or blood pressure. The problem is afterload mismatch and reduced venous return, not absolute
hypovolemia.
Question 3
A 58-year-old male with end-stage liver disease (MELD 24, Child-Pugh C) secondary to alcoholic
cirrhosis presents for orthotopic liver transplantation. Preoperative labs show: platelets
