Respiratory
Pulmonary physiology, one-lung ventilation, asthma, COPD, sleep apnea, ventilator management. ← All topics
Q1. Hypoxic pulmonary vasoconstriction
Hypoxic pulmonary vasoconstriction is most attenuated by:
A. Halothane more than sevoflurane, isoflurane, or nitrous oxide in dose-dependent fashion
B. Volatile anesthetics modestly and direct pulmonary vasodilators like nitroglycerin, nitroprusside, and milrinone significantly
C. Propofol and other intravenous anesthetics including barbiturates and benzodiazepines in clinical doses
D. Ketamine and other NMDA antagonists along with opioids in typical anesthetic concentrations
E. Dexmedetomidine and other alpha-2 agonists including clonidine when used for sedation or anesthesia
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Answer: B. Hypoxic pulmonary vasoconstriction (HPV) redirects blood flow from poorly ventilated to well-ventilated alveoli, optimizing ventilation-perfusion matching. Modern volatile anesthetics modestly inhibit HPV in a dose-dependent manner, with halothane causing greater inhibition than sevoflurane or isoflurane. Direct pulmonary vasodilators including nitroglycerin, nitroprusside, milrinone, inhaled nitric oxide, and inhaled epoprostenol significantly inhibit HPV, which can worsen V/Q mismatch during one-lung ventilation. Intravenous anesthetics such as propofol, ketamine, dexmedetomidine, barbiturates, benzodiazepines, and opioids have minimal to no effect on HPV at clinical doses.
Q2. One-lung ventilation strategy
Optimal one-lung ventilation settings include:
A. Tidal volume 10 mL/kg predicted body weight with no PEEP to dependent lung
B. Tidal volume 4–6 mL/kg predicted body weight with PEEP 5–10 to dependent lung and CPAP 2–5 to non-dependent lung if hypoxic
C. Tidal volume 12 mL/kg predicted body weight with no PEEP to dependent lung
D. CPAP 20 cm H2O to dependent lung with no ventilation to non-dependent lung
E. Apneic oxygenation only to both lungs with no positive pressure ventilation
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Answer: B. Lung-protective one-lung ventilation uses low tidal volumes of 4–6 mL/kg predicted body weight with PEEP 5–10 cm H2O applied to the ventilated (dependent) lung. If hypoxemia develops, CPAP 2–5 cm H2O can be added to the non-ventilated (non-dependent) lung to recruit alveoli and improve oxygenation without significantly impairing surgical exposure. Higher tidal volumes during one-lung ventilation increase the risk of acute respiratory distress syndrome in cardiothoracic surgery patients, as demonstrated in the PROVHILO trial. CPAP levels of 20 cm H2O would be excessive and impair venous return. Apneic oxygenation alone does not provide ventilation and would lead to hypercarbia and respiratory acidosis.
Q3. Lung volumes — FRC
Functional residual capacity equals:
A. Total lung capacity minus vital capacity
B. Expiratory reserve volume plus residual volume
C. Tidal volume plus inspiratory reserve volume
D. Residual volume minus expiratory reserve volume
E. Inspiratory capacity plus expiratory reserve volume
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Answer: B. Functional residual capacity (FRC) equals expiratory reserve volume plus residual volume, approximately 2300 mL in adults. FRC decreases about 10% with supine positioning, 10% with general anesthesia, and 20% when both are combined. In pregnancy, FRC decreases by 20%. Decreased FRC leads to faster desaturation during apnea. In elderly patients, obese patients, supine positioning, and smokers, closing capacity exceeds FRC, resulting in small airway closure during normal tidal breathing and subsequent atelectasis. Note that TLC minus VC also mathematically equals FRC, but the standard definition uses ERV plus RV.
Q4. Asthma bronchospasm intraoperative
A patient with asthma develops bronchospasm during anesthesia. The most appropriate sequence of initial management is:
A. Increase volatile anesthetic depth (sevoflurane), 100% FiO₂, hand-ventilate to assess compliance, then β2 agonist down ETT
B. Administer intravenous lidocaine bolus, maintain current ventilation settings, continue baseline FiO₂, then reassess breath sounds
C. Administer morphine for analgesia, deepen sedation with propofol infusion, maintain current ventilation, then reassess patient
D. Administer intravenous ketorolac or ibuprofen, increase minute ventilation, maintain baseline FiO₂, then assess for improvement
E. Administer vasopressin bolus for hemodynamic support, increase minute ventilation, maintain baseline FiO₂, then reassess compliance
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Answer: A. The appropriate initial management of intraoperative bronchospasm in an asthmatic patient includes hand-ventilating to assess compliance, administering 100% FiO₂, deepening anesthesia with a volatile agent that has bronchodilator properties (sevoflurane or halothane), and administering a β2 agonist such as albuterol via the endotracheal tube. If these measures are insufficient, additional therapies include intravenous epinephrine 10–20 mcg boluses, intravenous ketamine, magnesium sulfate 1–2 grams, and high-dose corticosteroids. Medications to avoid include morphine and atracurium (both cause histamine release), NSAIDs (may trigger bronchospasm in patients with aspirin-exacerbated respiratory disease), and desflurane (airway irritant). Among volatile anesthetics, halothane and sevoflurane are bronchodilators, while nitrous oxide is unique as the only volatile agent that does not depress respiration. Vasopressin has no role in bronchospasm management.
Q5. Closing capacity
Closing capacity exceeds FRC in all of the following EXCEPT:
A. Elderly patients in the upright position
B. Chronic smokers in the upright position
C. Third trimester pregnancy in upright position
D. Obese patients in the upright position
E. Young healthy adults in upright position
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Answer: E. Closing capacity exceeds FRC in elderly patients, obese patients, smokers, supine positioning, and pregnant patients (especially third trimester). In young healthy adults in the upright position, FRC remains greater than closing capacity, so small airways remain patent throughout normal tidal breathing. When closing capacity exceeds FRC, small airways close during normal tidal ventilation, leading to ventilation-perfusion mismatch and atelectasis. This pathophysiology can be reversed with PEEP and recruitment maneuvers to increase FRC above closing capacity.
Q6. Pulmonary function testing — restrictive
A patient with FEV1/FVC of 0.85 and reduced TLC has:
A. Obstructive lung disease with air trapping and hyperinflation
B. Restrictive lung disease with parenchymal or chest wall pathology
C. Asthma with reversible bronchospasm and normal lung volumes
D. COPD with emphysema and chronic airflow limitation
E. Normal lungs with age-appropriate pulmonary function
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Answer: B. This patient has restrictive lung disease. Restrictive patterns show normal or elevated FEV1/FVC ratio (>0.7) with reduced TLC, FVC, and FEV1. The FEV1/FVC of 0.85 is normal to elevated, and the reduced TLC confirms restriction. Restrictive disease includes interstitial lung disease, pulmonary fibrosis, and chest wall disorders. In contrast, obstructive lung disease shows FEV1/FVC <0.7 with relatively preserved FVC and often increased TLC due to air trapping. DLCO is reduced in interstitial disease and emphysema but normal in chronic bronchitis.
Q7. Smoking cessation timing
The benefit of preoperative smoking cessation on cardiovascular outcomes appears at:
A. 12 hours (decreased carboxyhemoglobin and improved oxygen delivery)
B. 1 week (decreased nicotine levels and improved ciliary function)
C. 4 weeks (small reduction in pulmonary complications begins)
D. 8 weeks (significant reduction in pulmonary complications occurs)
E. 1 year (maximal reduction in cardiovascular risk is achieved)
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Answer: D. The cardiovascular benefits of preoperative smoking cessation appear at different time points. At 12–24 hours, carbon monoxide and nicotine levels drop, improving oxygen delivery. At 2–4 weeks, a small reduction in pulmonary complications begins. At 8 or more weeks, a significant reduction in pulmonary complications occurs, which represents the timeframe when meaningful cardiovascular outcome benefits are demonstrated. There is no evidence that brief preoperative cessation worsens outcomes, so clinicians should counsel patients to quit smoking at any timeline before surgery.
Q8. OSA STOPBANG score
A STOPBANG score ≥5 corresponds to:
A. Low risk of obstructive sleep apnea
B. Intermediate risk of obstructive sleep apnea
C. High risk of moderate-to-severe obstructive sleep apnea
D. Insufficient data to stratify obstructive sleep apnea
E. Normal risk equivalent to healthy patient population
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Answer: C. The STOPBANG score is an acronym for eight clinical parameters: Snoring, Tired, Observed apnea, Pressure (hypertension), BMI greater than 35, Age greater than 50, Neck circumference greater than 40 cm, and Gender male. Each parameter scores 1 point. A score of 5 or higher indicates high risk of moderate-to-severe obstructive sleep apnea. These patients should be managed with heightened perioperative vigilance including continuous postoperative pulse oximetry monitoring, minimization of opioid analgesics, multimodal pain control strategies, consideration of regional anesthesia techniques when appropriate, and positioning with lateral decubitus or head-of-bed elevation to reduce upper airway obstruction.
Q9. Polysomnography AHI severity
Severity of obstructive sleep apnea:
A. AHI 5–15 events/hour is mild, 15–30 is moderate, and >30 is severe
B. AHI 1–5 events/hour is mild, 5–15 is moderate, and >15 is severe
C. AHI 10–20 events/hour is mild, 20–40 is moderate, and >40 is severe
D. AHI 0–10 events/hour is mild, 10–25 is moderate, and >25 is severe
E. AHI 2–10 events/hour is mild, 10–20 is moderate, and >20 is severe
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Answer: A. The apnea-hypopnea index (AHI) measures the number of apnea and hypopnea events per hour of sleep. The standard classification for obstructive sleep apnea severity is: mild OSA is AHI 5–15 events/hour, moderate OSA is AHI 15–30 events/hour, and severe OSA is AHI >30 events/hour. An AHI ≥5 events/hour is diagnostic for OSA. Apnea is defined as ≥10 seconds of complete or near-complete cessation of airflow. Hypopnea is defined as ≥30% reduction in airflow associated with ≥4% oxygen desaturation or an arousal. Treatment options include CPAP (gold standard for obstructive sleep apnea), BiPAP or adaptive servo-ventilation for central sleep apnea, weight loss, oral appliances, and surgical interventions such as uvulopalatopharyngoplasty or maxillomandibular advancement.
Q10. Anesthesia for COPD
Periop considerations for severe COPD include:
A. Aggressive narcotic use to suppress respiratory drive, high tidal volumes to overcome airway resistance, and routine postoperative intubation
B. Avoidance of nitrous oxide due to bullae expansion risk, low tidal volume ventilation with permissive hypercapnia, and regional anesthesia when feasible
C. Routine endotracheal intubation for all procedures, high PEEP to prevent atelectasis, and maximum FiO₂ to ensure adequate oxygenation
D. High PEEP throughout the case to maintain alveolar recruitment, short expiratory times to increase minute ventilation, and avoidance of bronchodilators
E. Strict limitation of FiO₂ to 0.21 regardless of oxygen saturation, aggressive fluid resuscitation, and mandatory general anesthesia for all cases
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Answer: B. In severe COPD, nitrous oxide should be avoided because it can expand bullae and increase pneumothorax risk. Ventilation strategy should include low tidal volumes with permissive hypercapnia and long expiratory times to prevent auto-PEEP. Low PEEP is preferred over high PEEP. Regional or epidural anesthesia is preferred when possible to avoid respiratory depression from general anesthesia and narcotics. Desiccated CO₂ absorbents should be avoided due to compound A formation risk. Bronchodilators should be continued. FiO₂ should be titrated to maintain SpO₂ around 92% rather than being rigidly restricted to room air or maximized, as hyperoxia can worsen outcomes in COPD patients by suppressing hypoxic drive in severe cases.
Q11. Pneumonectomy criteria
A patient cannot undergo pneumonectomy if predicted postoperative FEV1 is:
A. <80% predicted or DLCO <80% or VO2 max <25 mL/kg/min
B. <60% predicted or DLCO <60% or VO2 max <20 mL/kg/min
C. <40% predicted or DLCO <40% or VO2 max <15 mL/kg/min
D. <30% predicted or DLCO <30% or VO2 max <12 mL/kg/min
E. <20% predicted or DLCO <20% or VO2 max <10 mL/kg/min
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Answer: C. Preoperative pulmonary assessment for pneumonectomy occurs in phases. Phase 1 screening includes: PaO₂ <50 mmHg or PaCO₂ >45 mmHg on room air, FVC <50% predicted, FEV1 <2 L, MVV <50% predicted, or DLCO <50% predicted. If any Phase 1 criteria are met, Phase 2 testing with split lung function studies is performed. Predicted postoperative FEV1 <40% predicted, DLCO <40% predicted, or VO2 max <15 mL/kg/min indicate high risk for postoperative respiratory failure and are contraindications to pneumonectomy. These thresholds represent the critical values below which surgical risk becomes prohibitive.
Q12. Bleomycin lung toxicity
A patient with prior bleomycin chemotherapy presents for surgery. Anesthetic priority is:
A. High FiO₂ to prevent atelectasis and maintain oxygen delivery to tissues
B. Minimize FiO₂ to lowest tolerated level; pulmonary toxicity is oxygen-dependent
C. Avoid all narcotics to prevent respiratory depression and hypoventilation
D. Avoid all volatile anesthetics to prevent pulmonary vasodilation and shunting
E. Hyperbaric oxygen pretreatment to optimize tissue oxygenation before anesthesia
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Answer: B. Bleomycin causes oxygen-dependent pulmonary fibrosis via free radical generation. The anesthetic priority is to minimize FiO₂ to the lowest tolerated level, typically 30–40%, titrated to SpO₂ 90–95%. Patients should avoid hyperoxia for life due to ongoing risk. The earliest sign of bleomycin toxicity is decreased DLCO. These patients are at risk for ARDS-like injury when exposed to high oxygen concentrations. High FiO₂ is contraindicated despite theoretical benefits for atelectasis prevention. Narcotics and volatile anesthetics are not absolutely contraindicated and can be used with appropriate monitoring. Hyperbaric oxygen would be harmful given the oxygen-dependent nature of bleomycin toxicity.
Q13. Anterior mediastinal mass anesthesia
An adult with an anterior mediastinal mass and >50% tracheal compression on CT is most at risk for:
A. Easy intubation with standard induction and rapid sequence technique
B. Postoperative respiratory failure and complete airway collapse with neuromuscular paralysis
C. Stridor only during the intraoperative period without other complications
D. Pulmonary embolism from compression of major vessels in the chest
E. Hypertensive emergency from catecholamine release during tumor manipulation
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Answer: B. Anterior mediastinal masses (4 T's: thymoma, teratoma, thyroid, terrible lymphoma) with greater than 50% tracheal compression pose high risk for complete airway collapse and respiratory failure, particularly after induction of general anesthesia and administration of neuromuscular blocking agents. Loss of spontaneous ventilation and muscle tone can lead to critical airway obstruction that may be impossible to ventilate or intubate. Management principles include maintaining spontaneous ventilation with inhalation or slow IV induction, avoiding neuromuscular blockade until the airway is definitively secured, positioning the patient to relieve compression (head of bed up, lateral, or prone), and having rigid bronchoscopy and cardiopulmonary bypass immediately available for rescue in severe cases. Patients with orthopnea, upper body edema, or great vessel compression are at particularly high risk.
Q14. Capnography phases
Phase 3 of the normal capnogram represents:
A. Beginning of expiration with anatomic dead space gas
B. Alveolar plateau with CO₂-rich gas from alveoli
C. Inspiration with rapid downstroke to baseline CO₂
D. Mixed dead space and alveolar gas transition
E. End of inspiration before expiratory phase begins
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Answer: B. The capnogram has four distinct phases. Phase 1 represents dead space with no CO₂ detected. Phase 2 represents the mixing of dead space and alveolar gas as the upstroke begins. Phase 3 is the alveolar plateau, representing CO₂-rich gas from the alveoli; this is the longest phase and has a slight upward slope. Phase 4 is inspiration, characterized by a rapid downstroke to baseline as fresh gas without CO₂ is inhaled. The end-tidal CO₂ (EtCO₂) measured at the end of Phase 3 is usually 2–5 mmHg lower than PaCO₂ in normal patients due to alveolar dead space and V/Q mismatch.
Q15. Heliox use
Heliox (70/30 mix) is most useful for:
A. Lower airway disease with distal obstruction such as asthma or COPD exacerbations
B. Upper airway obstruction such as laryngeal edema, croup, or large airway tumors
C. Acute respiratory distress syndrome with diffuse alveolar damage and poor compliance
D. Pneumonia with consolidation and impaired gas exchange from infectious infiltrates
E. Pulmonary embolism with increased dead space ventilation and ventilation-perfusion mismatch
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Answer: B. Helium is less dense than nitrogen, which reduces turbulent flow resistance through large narrowed airways. Heliox provides the most benefit in upper airway obstruction conditions including post-extubation stridor, tracheal stenosis, croup, laryngeal edema, and large airway tumors. It provides limited benefit in distal obstruction such as asthma or COPD because laminar flow dominates in smaller airways, where gas density has less impact on resistance. Although heliox has been tried in status asthmaticus, the theoretical benefit is greatest when turbulent flow through a large, partially obstructed airway is the primary problem. Heliox does not address the underlying pathophysiology of ARDS, pneumonia, or pulmonary embolism.
Q16. Pulmonary hypertension classification
WHO Group 1 pulmonary hypertension is:
A. Pulmonary arterial hypertension including idiopathic, heritable, drug-induced, and associated forms
B. Pulmonary hypertension secondary to left-sided heart disease including valvular disorders
C. Pulmonary hypertension due to chronic lung disease and chronic alveolar hypoxia
D. Chronic thromboembolic pulmonary hypertension and other pulmonary artery obstructions
E. Pulmonary hypertension with multifactorial or unclear mechanisms including hematologic disorders
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Answer: A. WHO Group 1 is pulmonary arterial hypertension (PAH), which includes idiopathic PAH, heritable PAH, drug-induced PAH, and PAH associated with connective tissue disease, HIV, schistosomiasis, and other conditions. Vasoreactivity testing guides therapy; responders may use calcium channel blockers, while non-responders receive endothelin receptor antagonists, PDE5 inhibitors, prostacyclins, or riociguat. Group 2 is left heart disease. Group 3 is lung disease and hypoxia. Group 4 is chronic thromboembolic pulmonary hypertension (CTEPH), potentially curable with pulmonary endarterectomy. Group 5 encompasses multifactorial or unclear mechanisms.
Q17. Pulmonary hypertension anesthesia
In a patient with severe PAH, induction priorities include:
A. Avoid hypoxia, hypercarbia, acidosis, and increased PVR; maintain preload and contractility; avoid sudden afterload reduction; have pulmonary vasodilators available
B. Aggressive volume loading to maximize preload; use high-dose α-agonists for blood pressure support; maintain high normal PaCO2; avoid all vasodilators
C. High inspired oxygen with liberal PEEP application; aggressive fluid resuscitation; pure α-agonist infusions; avoid pulmonary vasodilators to prevent systemic hypotension
D. Permissive hypercapnia to reduce ventilator trauma; restrictive fluid management; pure β-agonist support; maintain low inspired oxygen to avoid absorption atelectasis
E. Systemic vasodilation to reduce right ventricular work; moderate hyperventilation; generous crystalloid administration; avoid inotropes to reduce myocardial oxygen consumption
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Answer: A. In severe PAH, induction priorities focus on avoiding all pulmonary vasoconstrictors including hypoxia, hypercarbia, acidosis, pain, and sympathetic stimulation, as these increase PVR and worsen RV function. The RV depends on adequate preload but is vulnerable to volume overload. Contractility must be maintained with inotropes if needed. Sudden drops in systemic vascular resistance from induction agents, mediastinal manipulation, or deep neuraxial blockade can be catastrophic and must be avoided. Inhaled pulmonary vasodilators such as nitric oxide and epoprostenol should be immediately available as they selectively vasodilate the pulmonary circulation without systemic effects. Vasopressin is preferred over pure α-agonists for blood pressure support because it preserves SVR without increasing PVR. High PEEP increases PVR and should be minimized. Aggressive volume loading risks RV failure. Systemic vasodilation worsens the situation by reducing coronary perfusion pressure to an already stressed RV.
Q18. Inhaled NO
Inhaled nitric oxide reduces V/Q mismatch by:
A. Bronchodilation in ventilated alveoli without affecting systemic vascular resistance
B. Selective pulmonary vasodilation in ventilated alveoli without systemic hypotension
C. Increasing pulmonary blood flow universally across both ventilated and collapsed alveoli
D. Direct cardiac inotropy with secondary improvement in pulmonary perfusion pressure
E. Bronchoconstriction in poorly ventilated alveoli to redirect airflow to healthier regions
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Answer: B. Inhaled nitric oxide (iNO) delivered to ventilated alveoli causes local pulmonary vasodilation, which improves V/Q matching by preferentially increasing blood flow to well-ventilated lung units. iNO is rapidly inactivated by hemoglobin once it enters the bloodstream, preventing systemic vasodilation and hypotension. This selective effect distinguishes iNO from systemic vasodilators. Toxic concerns include methemoglobinemia and nitrogen dioxide (NO₂) formation. Clinical uses include ARDS, pulmonary hypertension, and neonatal hypoxic respiratory failure such as persistent pulmonary hypertension of the newborn (PPHN) and congenital diaphragmatic hernia (CDH).
Q19. Lung-protective ventilation in non-ARDS surgery
Lung-protective ventilation in major abdominal surgery (IMPROVE trial) shows benefit at:
A. TV 12 mL/kg PBW, zero PEEP, no recruitment maneuvers
B. TV 6–8 mL/kg PBW, PEEP 6–8, recruitment maneuvers
C. TV 4 mL/kg PBW, zero PEEP, no recruitment maneuvers
D. CPAP 20 cm H₂O throughout surgery, no ventilation
E. APRV mode with P-high 25, P-low 5, no recruitment
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Answer: B. The IMPROVE trial (2013) demonstrated that lung-protective ventilation in non-ARDS major abdominal surgery significantly reduces pulmonary complications. The protocol consisted of tidal volumes of 6–8 mL/kg predicted body weight, PEEP of 6–8 cm H₂O, and recruitment maneuvers performed every 30 minutes. This approach has become the standard of care across abdominal, thoracic, and cardiac surgery. Higher tidal volumes (12 mL/kg) without PEEP represent traditional ventilation associated with increased complications. Very low tidal volumes (4 mL/kg) without PEEP provide inadequate ventilation. CPAP alone does not provide ventilation during surgery. APRV mode was not studied in IMPROVE and is not standard for elective abdominal surgery.
Q20. ARDS prone positioning
The PROSEVA trial showed prone positioning improves survival in severe ARDS at:
A. P/F ratio <100 with prone positioning for 4 hours per day
B. P/F ratio <150 with prone positioning ≥16 hours per day
C. P/F ratio <200 with prone positioning for 8 hours per day
D. P/F ratio <250 with prone positioning for 12 hours per day
E. Any P/F ratio with prone positioning for 1 hour per day
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Answer: B. The PROSEVA trial demonstrated that prone positioning for at least 16 hours per day in patients with severe ARDS, defined as a P/F ratio less than 150, significantly reduced mortality. Prone positioning should be initiated within 36 hours of ARDS onset to maximize benefit. The extended duration of proning (≥16 hours daily) is critical to the mortality benefit observed in the trial. Important risks associated with prone positioning include pressure injuries to the face and anterior chest, as well as accidental dislodgement of endotracheal tubes, central lines, and other critical access devices. The trial excluded less severe ARDS and shorter durations of prone positioning.
Q21. ABG: A-a gradient
The alveolar-arterial gradient on FiO₂ 0.21 is normally:
A. <5 mmHg in all age groups at sea level on room air
B. <15 mmHg in young patients; rises with age (estimate: age/4 + 4)
C. <50 mmHg in all age groups at sea level on room air
D. Equal to PaO₂ minus the respiratory quotient adjustment factor
E. Always >25 mmHg regardless of patient age or clinical status
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Answer: B. The A-a gradient equals PAO₂ minus PaO₂. Using the alveolar gas equation, PAO₂ = FiO₂(Patm – PH₂O) – PaCO₂/RQ = 0.21(760 – 47) – 40/0.8 = approximately 100 mmHg at sea level on room air. The normal A-a gradient is less than 15 mmHg in young patients but rises with age due to increased closing capacity and V/Q mismatch; a useful estimate is (age/4 + 4). On 100% oxygen, the normal A-a gradient can rise to approximately 60 mmHg. An elevated A-a gradient suggests V/Q mismatch, shunt, or diffusion limitation. Normal A-a gradient with hypoxemia indicates hypoventilation or low FiO₂ as the cause.
Q22. Apneic oxygenation
Apneic oxygenation can extend safe apnea time by:
A. Cooling the body to reduce oxygen consumption and slow metabolic demand during the apneic period
B. Delivering oxygen to alveoli via mass flow during apnea, prolonging safe apnea to 5–10 minutes in select patients
C. Sympathetic stimulation increasing oxygen extraction efficiency and improving tissue oxygen delivery during apnea
D. Increased cardiac output enhancing oxygen delivery to tissues and compensating for lack of ventilation
E. Decreased metabolic rate reducing oxygen consumption requirements and extending time to desaturation during apnea
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Answer: B. Apneic oxygenation (via transtracheal oxygen, NODESAT, THRIVE, or high-flow nasal oxygen) maintains SpO₂ during prolonged apnea by delivering oxygen to the alveoli via passive mass flow while CO₂ continues to diffuse out. This technique can prolong safe apnea time to 5–10 minutes in select patients. It is particularly useful in difficult airway management, awake fiberoptic intubation, and jet ventilation cases. During apnea, CO₂ rises approximately 3 mmHg per minute. The other options do not describe the mechanism by which apneic oxygenation works, though some (like cooling or decreased metabolic rate) could theoretically extend apnea time through different mechanisms unrelated to apneic oxygenation techniques.
Q23. Post-pneumonectomy considerations
The major risk in the first 72 hr after pneumonectomy is:
A. Deep venous thrombosis from immobility and hypercoagulable state
B. Post-pneumonectomy pulmonary edema and cardiac herniation through pericardial defect
C. Surgical site infection from contamination and impaired wound healing
D. Atrial fibrillation from atrial stretch and autonomic nervous system disruption
E. Postoperative nausea and vomiting from anesthetic agents and opioid use
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Answer: B. Post-pneumonectomy pulmonary edema is the major risk in the first 72 hours after pneumonectomy and carries high mortality. It is related to fluid overload, lymphatic disruption, and endothelial damage. Management includes restrictive fluid administration (less than 2 mL/kg/hr) and avoiding blood transfusion unless absolutely needed. Cardiac herniation through a pericardial defect is another catastrophic early complication; repositioning the patient may help. While atrial fibrillation is also common after pneumonectomy and should be treated with rate control, it is not the major risk in the immediate postoperative period. DVT, surgical site infection, and PONV are general postoperative concerns but not the primary risks specific to pneumonectomy in the first 72 hours.
Q24. Tracheal extubation criteria
Standard extubation criteria include:
A. SpO₂ >98% on 100% FiO₂, heart rate <100 bpm, systolic blood pressure >90 mmHg, patient awake and following commands
B. Adequate gas exchange (PaO₂/FiO₂ >150), spontaneous ventilation with adequate tidal volume, hemodynamic stability, sufficient mental status to protect airway, TOF >0.9
C. Resolution of underlying pneumonia, negative chest radiograph, normal white blood cell count, afebrile for 48 hours, able to ambulate independently
D. Negative CT chest for infiltrates, bronchoscopy showing clear airways, sputum culture negative, procalcitonin <0.5 ng/mL, CRP normalized
E. Negative blood cultures for 72 hours, resolution of sepsis, lactate <2 mmol/L, vasopressors discontinued, urine output >0.5 mL/kg/hr
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Answer: B. Comprehensive extubation criteria include respiratory parameters (PaO₂/FiO₂ ratio >150, RSBI <105, NIF <−20 cmH₂O, adequate tidal volume and respiratory rate), hemodynamic stability, adequate mental status for airway protection (including gag and swallow reflexes), and reversal of neuromuscular blockade (TOF >0.9). Cuff leak test should be performed in at-risk patients, with a leak volume <110 mL predicting increased risk of post-extubation stridor. Extubation does not require resolution of all underlying disease, complete radiographic clearance, or negative cultures—only that the patient can maintain adequate ventilation and oxygenation independently while protecting their airway.
Q25. Diffusing capacity (DLCO) interpretation
Reduced DLCO is seen in all EXCEPT:
A. Pulmonary embolism due to reduced vascular bed
B. Emphysema due to alveolar surface area loss
C. Pulmonary fibrosis due to thickened alveolar membrane
D. Asthma due to preserved alveolar-capillary interface
E. Anemia due to reduced hemoglobin concentration
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Answer: D. DLCO measures carbon monoxide transfer across the alveolar-capillary membrane and is reduced in parenchymal disease (emphysema, interstitial pulmonary fibrosis, sarcoidosis), vascular disease (pulmonary embolism, pulmonary hypertension), and anemia. Asthma typically has normal or elevated DLCO because the alveolar-capillary interface remains intact despite airway obstruction. DLCO is elevated in polycythemia, alveolar hemorrhage, left-to-right shunts, and during exercise.