Cloud Anesthesia

Respiratory

Pulmonary physiology, one-lung ventilation, asthma, COPD, sleep apnea, ventilator management. ← Back to Q-Bank


Q1. Hypoxic pulmonary vasoconstriction

Hypoxic pulmonary vasoconstriction is most attenuated by:

A. Halothane > sevoflurane > isoflurane > nitrous oxide
B. Volatile anesthetics (modestly) and direct pulmonary vasodilators (nitroglycerin, nitroprusside, milrinone) significantly
C. Propofol
D. Ketamine
E. Dexmedetomidine

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Answer: B. HPV redirects blood from poorly ventilated to well-ventilated alveoli. Modern volatiles modestly inhibit HPV; IV anesthetics have minimal effect. Direct pulmonary vasodilators (nitro, NPP, milrinone, inhaled NO/epoprostenol) significantly inhibit HPV → worsened V/Q mismatch during one-lung ventilation.

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Q2. One-lung ventilation strategy

Optimal one-lung ventilation settings include:

A. Tidal volume 10 mL/kg, no PEEP
B. Tidal volume 4–6 mL/kg, PEEP 5–10 to dependent lung, CPAP 2–5 to non-dependent lung if hypoxic
C. Tidal volume 12 mL/kg, no PEEP
D. CPAP 20 to dependent lung
E. Apneic oxygenation only

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Answer: B. Lung-protective OLV: low TV (4–6 mL/kg PBW), PEEP 5–10 to ventilated lung. If hypoxic, add CPAP 2–5 to non-ventilated lung. Higher TV during OLV → ARDS risk in cardiothoracic surgery (PROVHILO).

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Q3. Lung volumes — FRC

Functional residual capacity equals:

A. TLC – VC
B. ERV + RV
C. TV + IRV
D. RV alone
E. IC + ERV

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Answer: B. FRC = expiratory reserve volume + residual volume. ~2300 mL in adult. FRC decreases ~10% with supine, ~10% with GA, ~20% with both. In pregnancy ↓20%. Decreased FRC → faster desaturation during apnea. Closing capacity exceeds FRC in elderly, obese, supine, smokers → small airway closure during normal tidal breathing → atelectasis.

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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. Lidocaine IV bolus
C. Morphine for analgesia
D. NSAIDs
E. Vasopressin

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Answer: A. Bronchospasm: hand-ventilate, 100% FiO₂, deepen anesthetic with sevoflurane (bronchodilator), albuterol via ETT, consider IV epi 10–20 mcg, IV ketamine, magnesium 1–2 g, high-dose steroids. Avoid: morphine (histamine), atracurium (histamine), NSAIDs (potential AERD), desflurane (irritant). Halothane and sevoflurane are bronchodilators; nitrous oxide is the only volatile that doesn't depress respiration.

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Q5. Closing capacity

Closing capacity exceeds FRC in all of the following EXCEPT:

A. Elderly
B. Smokers
C. Pregnancy (third trimester)
D. Obesity
E. Young healthy adult upright

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Answer: E. CC > FRC in elderly, obese, smokers, supine, pregnant — small airways close during tidal breathing → V/Q mismatch and atelectasis. Reverse with PEEP and recruitment maneuvers.

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Q6. Pulmonary function testing — restrictive

A patient with FEV1/FVC of 0.85 and reduced TLC has:

A. Obstructive lung disease
B. Restrictive lung disease (interstitial lung disease, fibrosis, chest wall disease)
C. Asthma
D. COPD
E. Normal lungs

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Answer: B. Restrictive: normal/elevated FEV1/FVC (>0.7), reduced TLC, FVC, FEV1. Obstructive: FEV1/FVC <0.7 with relatively preserved FVC. DLCO reduced in interstitial disease and emphysema, normal in chronic bronchitis.

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Q7. Smoking cessation timing

The benefit of preoperative smoking cessation on cardiovascular outcomes appears at:

A. 12 hours (decreased carboxyhemoglobin)
B. 1 week
C. 4 weeks
D. 8 weeks (significant decrease in pulmonary complications)
E. 1 year

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Answer: D. 12–24 hr: CO and nicotine drop, improved oxygen delivery. 2–4 weeks: small reduction in pulmonary complications. 8+ weeks: significant reduction in pulmonary complications. There is no evidence that brief preoperative cessation worsens outcomes — counsel patients to quit at any timeline.

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Q8. OSA STOPBANG score

A STOPBANG score ≥5 corresponds to:

A. Low OSA risk
B. Intermediate risk
C. High risk of moderate-to-severe OSA
D. Cannot stratify
E. Healthy patient

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Answer: C. STOPBANG: Snoring, Tired, Observed apnea, Pressure (BP), BMI >35, Age >50, Neck >40 cm, Gender male. ≥5 = high risk. Manage as OSA: monitor postop with continuous oximetry, minimize opioids, use multimodal pain control, consider regional, position lateral/HOB up.

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Q9. Polysomnography AHI severity

Severity of obstructive sleep apnea:

A. AHI 5–15 mild, 15–30 moderate, >30 severe
B. AHI 1–5 mild, 5–15 moderate, >15 severe
C. AHI 10–20 mild, 20–40 moderate, >40 severe
D. AHI 0–10 mild, 10–25 moderate, >25 severe
E. No standard classification

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Answer: A. AHI = apnea-hypopnea index per hour of sleep. ≥5 events/hr is diagnostic. Apnea = ≥10 sec cessation; hypopnea = ≥30% reduced airflow + 4% O₂ desaturation. Treatment: CPAP (gold standard for OSA), BiPAP/ASV for central sleep apnea, weight loss, oral appliance, surgery (UPPP, MMA).

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Q10. Anesthesia for COPD

Periop considerations for severe COPD include:

A. Aggressive narcotic use
B. Avoidance of nitrous oxide (bullae expansion), low tidal volume with permissive hypercapnia, avoid desiccated absorbents, consider regional anesthesia
C. Routine intubation regardless of procedure
D. High PEEP throughout case
E. Limit FiO₂ to 0.21

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Answer: B. COPD: avoid nitrous (expands bullae, risk of PTX); use long expiratory time to avoid auto-PEEP; permissive hypercapnia; low PEEP; bronchodilators; epidural or regional preferred when possible to avoid pulmonary depression; titrate FiO₂ to SpO₂ ~92% to avoid hyperoxia.

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Q11. Pneumonectomy criteria

A patient cannot undergo pneumonectomy if predicted postoperative FEV1 is:

A. <80%
B. <60%
C. <40% predicted (or DLCO <40%, or VO2 max <15 mL/kg/min)
D. <30%
E. <20%

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Answer: C. Phase 1: PaO₂ <50 or PaCO₂ >45 on RA, FVC <50%, FEV1 <2L, MVV <50%, DLCO <50% → trigger Phase 2 testing. Phase 2: split lung function testing, predicted postop FEV1/DLCO <40% or VO2 max <15 mL/kg/min = high risk for postop respiratory failure.

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Q12. Bleomycin lung toxicity

A patient with prior bleomycin chemotherapy presents for surgery. Anesthetic priority is:

A. High FiO₂ to prevent atelectasis
B. Minimize FiO₂ to lowest tolerated; pulmonary toxicity is O₂-dependent
C. Avoid all narcotics
D. Avoid all volatile anesthetics
E. Hyperbaric oxygen pretreatment

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Answer: B. Bleomycin causes O₂-dependent pulmonary fibrosis via free radical generation. Earliest sign: ↓DLCO. Use FiO₂ ≤30–40% (titrated to SpO₂ 90–95%); avoid hyperoxia for life. Watch for ARDS-like injury.

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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
B. Postoperative respiratory failure and complete airway collapse with paralysis
C. Stridor only
D. Pulmonary embolism
E. Hypertensive emergency

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Answer: B. Anterior mediastinal mass (4 T's: thymoma, teratoma, thyroid, terrible lymphoma): >50% tracheal compression, orthopnea, upper body edema, great vessel compression → high risk. Maintain spontaneous ventilation (inhalation induction or slow IV), avoid NMB until airway secured, position to relieve compression (HOB up, lateral, prone), have rigid bronch and CPB on standby for severe cases.

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Q14. Capnography phases

Phase 3 of the normal capnogram represents:

A. Beginning of expiration with anatomic dead space
B. Alveolar plateau (CO₂-rich gas from alveoli)
C. Inspiration
D. Mixed dead space + alveolar gas
E. End of inspiration

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Answer: B. Phase 1: dead space (no CO₂). Phase 2: mixing of dead space + alveolar. Phase 3: alveolar plateau (CO₂-rich). Phase 4: inspiration (rapid downstroke to baseline). EtCO₂ usually 2–5 mmHg < PaCO₂ in normal patient.

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Q15. Heliox use

Heliox (70/30 mix) is most useful for:

A. Lower airway disease (asthma, COPD distal obstruction)
B. Upper airway obstruction (laryngeal edema, large airway tumors)
C. ARDS
D. Pneumonia
E. Pulmonary embolism

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Answer: B. Helium is less dense than nitrogen → reduces turbulent flow resistance through large narrowed airways. Most benefit in upper airway obstruction (post-extubation stridor, tracheal stenosis, croup). Limited benefit in distal obstruction (laminar flow dominates) — though tried in status asthmaticus.

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Q16. Pulmonary hypertension classification

WHO Group 1 pulmonary hypertension is:

A. Pulmonary arterial hypertension (idiopathic, heritable, drug-induced, connective tissue disease, HIV, schistosomiasis)
B. Due to left heart disease
C. Due to chronic lung disease/hypoxia
D. Chronic thromboembolic pulmonary hypertension
E. Multifactorial/unclear mechanisms

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Answer: A. WHO groups: 1) PAH (vasoreactive testing → CCB; otherwise endothelin antagonists, PDE5 inhibitors, prostacyclins, riociguat); 2) left heart disease; 3) lung disease/hypoxia; 4) CTEPH (pulmonary endarterectomy curative); 5) multifactorial.

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Q17. Pulmonary hypertension anesthesia

In a patient with severe PAH, induction priorities include:

A. Avoid hypoxia, hypercarbia, acidosis, increased PVR; maintain preload and contractility; avoid sudden afterload reduction; have inhaled NO/epoprostenol available
B. Aggressive volume loading
C. High inspired PEEP
D. Pure α-agonists only
E. Vasodilation to reduce work of right heart

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Answer: A. PAH: avoid all pulmonary vasoconstrictors (hypoxia, hypercarbia, acidosis, pain, sympathetic stim). RV depends on preload but vulnerable to overload. Vasopressin preserves SVR without ↑PVR (preferred over α-agonists which also ↑PVR). Inhaled NO and epoprostenol selectively vasodilate the lung. Avoid sudden SVR drops (induction, mediastinal manipulation, deep neuraxial).

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Q18. Inhaled NO

Inhaled nitric oxide reduces V/Q mismatch by:

A. Bronchodilation only
B. Selective pulmonary vasodilation in ventilated alveoli without systemic hypotension
C. Increasing pulmonary blood flow universally
D. Direct cardiac inotropy
E. Bronchoconstriction

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Answer: B. iNO delivered to ventilated alveoli → local pulmonary vasodilation → improved V/Q. Rapidly inactivated by hemoglobin → no systemic effect. Toxic concerns: methemoglobinemia, NO₂ formation. Used in ARDS, PHTN, neonatal hypoxic respiratory failure (PPHN, CDH).

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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, no PEEP
B. TV 6–8 mL/kg PBW, PEEP 6–8, recruitment maneuvers
C. TV 4 mL/kg, no PEEP
D. CPAP 20 throughout
E. APRV mode

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Answer: B. IMPROVE (2013): lung-protective ventilation in non-ARDS major abdominal surgery reduces pulmonary complications. TV 6–8 mL/kg PBW, PEEP 6–8, recruitment maneuvers q30 min. Standard of care across abdominal, thoracic, and cardiac surgery.

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Q20. ARDS prone positioning

The PROSEVA trial showed prone positioning improves survival in severe ARDS at:

A. P/F <100 prone 4 hr/day
B. P/F <150 with prone ≥16 hr/day
C. P/F <200 prone 8 hr/day
D. Any severity prone 1 hr/day
E. Not beneficial

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Answer: B. Severe ARDS (P/F <150) with prone ≥16 hr/day → reduced mortality. Begin within 36 hr of ARDS onset. Risk: pressure injuries, line/tube dislodgement.

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Q21. ABG: A-a gradient

The alveolar-arterial gradient on FiO₂ 0.21 is normally:

A. <5 mmHg
B. <15 mmHg in young patients; rises with age (estimate: age/4 + 4)
C. <50 mmHg
D. Equal to PaO₂
E. Always >25 mmHg

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Answer: B. A-a gradient = PAO₂ – PaO₂. PAO₂ = FiO₂(Patm – PH₂O) – PaCO₂/RQ = 0.21(760 – 47) – 40/0.8 = ~100 at sea level RA. Normal A-a <15 in young, rises with age (closing capacity), and to ~60 on 100% O₂. Elevated A-a → V/Q mismatch, shunt, or diffusion limitation. Normal A-a with hypoxemia → hypoventilation or low FiO₂.

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Q22. Apneic oxygenation

Apneic oxygenation can extend safe apnea time by:

A. Cooling the body
B. High-flow nasal oxygen continues to deliver O₂ to alveoli via mass flow during apnea; can prolong safe apnea to 5–10 min in select patients
C. Sympathetic stimulation
D. Increased cardiac output
E. Decreased metabolic rate

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Answer: B. Apneic oxygenation (transtracheal O₂, NODESAT, THRIVE) maintains SpO₂ during prolonged apnea via passive O₂ flow + apneic CO₂ rise. Particularly useful in difficult airway, awake fiberoptic, jet ventilation cases. CO₂ rises ~3 mmHg/min during apnea.

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Q23. Post-pneumonectomy considerations

The major risk in the first 72 hr after pneumonectomy is:

A. DVT
B. Post-pneumonectomy pulmonary edema (Slinger), and cardiac herniation
C. Surgical site infection
D. Atrial fibrillation
E. PONV

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Answer: B. Post-pneumonectomy pulmonary edema: high mortality, related to fluid overload + lymphatic disruption + endothelial damage. Restrictive fluid (<2 mL/kg/hr), avoid blood unless needed. Cardiac herniation through pericardial defect: catastrophic, repositioning may help. AFib also common — treat with rate control.

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Q24. Tracheal extubation criteria

Standard extubation criteria include:

A. SpO₂ >98% on 100% FiO₂
B. Adequate gas exchange (PaO₂/FiO₂ >150), spontaneous ventilation with adequate TV, hemodynamic stability, sufficient mental status to protect airway, TOF >0.9, cuff leak test for at-risk patients
C. Resolution of all underlying disease
D. CT chest negative
E. Negative blood cultures

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Answer: B. Comprehensive extubation criteria: respiratory (P/F ratio, RSBI <105, NIF <−20, adequate TV/RR), hemodynamic stability, mental status, airway protection (gag, swallow), reversal of NMB. Cuff leak test (<110 mL leak) predicts post-extubation stridor.

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Q25. Diffusing capacity (DLCO) interpretation

Reduced DLCO is seen in all EXCEPT:

A. Pulmonary embolism
B. Emphysema
C. Pulmonary fibrosis
D. Asthma (typically)
E. Anemia

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Answer: D. DLCO measures CO transfer; reduced in: parenchymal disease (emphysema, IPF, sarcoid), vascular disease (PE, PHTN), anemia. Asthma typically has normal or elevated DLCO. DLCO elevated in: polycythemia, alveolar hemorrhage, left-to-right shunts, exercise.

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