Cloud Anesthesia

Critical Care

ARDS, sepsis, hepatorenal syndrome, burn resuscitation, AKI, abdominal compartment syndrome, mechanical ventilation. ← Back to Q-Bank


Q1. ARDS ventilator strategy

A 65-year-old with severe ARDS has PaO₂ 55 on FiO₂ 0.8 with PEEP 14. Which strategy is most evidence-based?

A. Tidal volume 10 mL/kg PBW, plateau <40 cm H₂O
B. Tidal volume 6 mL/kg PBW, plateau ≤30 cm H₂O, SpO₂ goal 88–95%
C. Tidal volume 4 mL/kg PBW, PaO₂ goal >100
D. APRV with P-high 35, FiO₂ 1.0 indefinitely
E. Permissive hypoxemia with FiO₂ 0.4

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Answer: B. ARDSnet: 6 mL/kg PBW, plateau ≤30, SpO₂ 88–95% (PaO₂ 55–80). Avoid sustained FiO₂ >0.6. Inhaled NO reduces V/Q mismatch as adjunct. Prone positioning improves survival in severe ARDS (PROSEVA).

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Q2. Hepatorenal syndrome treatment

A 56-year-old with cirrhosis (MELD 28) develops oliguria, Cr rising 1.0 → 2.4, FENa <1%, no improvement after 48 hr of albumin challenge. Most appropriate initial pharmacologic therapy outside the ICU is:

A. Furosemide + dopamine
B. Midodrine + octreotide + albumin
C. Norepinephrine + albumin only
D. Terlipressin alone
E. Hemodialysis

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Answer: B. HRS type 1 in non-critically ill: midodrine + octreotide + albumin (US, where terlipressin was historically unavailable; terlipressin now FDA-approved 2022). Critically ill: norepi + albumin ± vasopressin. Definitive: liver transplant. Diuretics worsen the syndrome.

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Q3. Burn fluid resuscitation

A 35-year-old, 70 kg patient presents with 40% TBSA full-thickness burns 2 hours ago. Calculate Parkland fluid for the next 6 hours.

A. 5,600 mL LR
B. 8,400 mL LR
C. 14,000 mL LR
D. 2,800 mL LR
E. 11,200 mL D5NS

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Answer: A. Parkland: 4 mL/kg/%TBSA in 24 hr = 4 × 70 × 40 = 11,200 mL. 50% in first 8 hr from injury = 5,600 mL. 2 hr already elapsed → remaining 5,600 mL over next 6 hr. Avoid glucose-containing solutions in initial resuscitation; avoid albumin in first 8–12 hr; cap at 250–300 mL/kg in first 24 hr to avoid abdominal compartment syndrome/ARDS.

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Q4. Sepsis-3 definition

Per Sepsis-3, septic shock requires all EXCEPT:

A. Sepsis (life-threatening organ dysfunction caused by dysregulated host response to infection)
B. Vasopressors needed to maintain MAP ≥65
C. Serum lactate >2 mmol/L despite adequate fluid resuscitation
D. Positive blood cultures
E. None — all are required

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Answer: D. Sepsis-3: septic shock = sepsis + need for pressors to keep MAP ≥65 + lactate >2 after fluid resuscitation. Positive cultures are not required (only ~30–50% positive). qSOFA (RR ≥22, SBP ≤100, altered mentation) for screening; SOFA score for ICU diagnosis.

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Q5. Septic shock initial resuscitation

Per Surviving Sepsis Campaign 2021, initial fluid resuscitation in septic shock is:

A. 10 mL/kg crystalloid bolus
B. 30 mL/kg crystalloid within 3 hours
C. 50 mL/kg colloid
D. 1000 mL LR over 30 min then reassess
E. Avoid fluids, go directly to pressors

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Answer: B. SSC 2021: 30 mL/kg crystalloid (preferably balanced — LR, Plasma-Lyte) within first 3 hr. Reassess fluid responsiveness with dynamic indices (PPV, SVV, passive leg raise). Norepi first-line pressor; vasopressin added at 0.03 U/min for refractory; epinephrine added if cardiac dysfunction.

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Q6. Steroids in septic shock

When are corticosteroids indicated in septic shock?

A. All septic patients
B. Refractory shock despite fluid + adequate vasopressor (NE >0.25 mcg/kg/min)
C. Only with positive cultures
D. Only with adrenal insufficiency
E. Never — increases mortality

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Answer: B. Hydrocortisone 200 mg/day IV (50 mg q6h or continuous infusion) for refractory septic shock. Steroid stress dose accelerates shock reversal (ADRENAL, APROCCHSS trials show conflicting mortality but consistent shock resolution).

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Q7. Abdominal compartment syndrome

Abdominal compartment syndrome is diagnosed when:

A. Intra-abdominal pressure >5 mmHg
B. Intra-abdominal pressure >20–25 mmHg with new organ dysfunction
C. Intra-abdominal pressure measured via NG tube
D. Abdominal wall edema visible on exam
E. Visible diaphragmatic elevation on CXR

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Answer: B. ACS = IAP >20–25 mmHg + new organ dysfunction. Measured via bladder pressure (zeroed at midaxillary line). Effects: ↓ venous return, ↓ CO, ↑ ICP, ↓ pulmonary compliance, AKI from MAP – IAP perfusion drop. Risk: massive volume resuscitation, ruptured AAA, pancreatitis, ascites. Treatment: decompression at IAP >25.

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Q8. Emergency hemodialysis indications

The indications for urgent hemodialysis (AEIOU mnemonic) include all EXCEPT:

A. Severe metabolic acidosis (pH <7.1) refractory to medical therapy
B. Symptomatic hyperkalemia or K >6.5 refractory to therapy
C. Ingestion of toxic alcohols, salicylates, lithium
D. Volume overload refractory to diuretics
E. Mild uremia (BUN 60) with no symptoms

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Answer: E. AEIOU: Acidosis, Electrolyte (K), Ingestion (Carbamazepine, Lithium, Alcohols, Salicylates, Sodium valproate = CLASS), Overload, Uremia (symptomatic — encephalopathy, pericarditis, bleeding; or BUN >100 / Cr >10).

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Q9. RIFLE / KDIGO AKI staging

A patient's serum creatinine rises from 1.0 to 2.3 mg/dL. Per KDIGO, this is:

A. Stage 1 AKI (1.5–1.9× baseline)
B. Stage 2 AKI (2.0–2.9× baseline)
C. Stage 3 AKI (≥3× baseline or Cr ≥4 with acute rise of 0.5)
D. Not AKI
E. Cannot determine without urine output

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Answer: B. KDIGO Stage 2: Cr 2–2.9× baseline OR UO <0.5 mL/kg/h for ≥12 hr. Stage 1: 1.5–1.9× or ≥0.3 mg/dL rise in 48 hr. Stage 3: ≥3× baseline or Cr ≥4 with acute rise ≥0.5, or RRT initiation, or UO <0.3 mL/kg/h for ≥24 hr, or anuria for ≥12 hr.

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Q10. Prerenal vs intrinsic AKI

A patient with oliguria has urine Na 8 mEq/L, FENa 0.4%, BUN/Cr ratio 25, urine osm 600. The most likely diagnosis is:

A. Prerenal azotemia
B. Acute tubular necrosis
C. Post-renal obstruction
D. Acute interstitial nephritis
E. Glomerulonephritis

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Answer: A. Prerenal: BUN/Cr >20, FENa <1%, urine Na <10, urine osm >500. ATN: BUN/Cr <15, FENa >2%, urine Na >20, urine osm <350. Postrenal mimics intrinsic over time.

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Q11. Contrast-induced nephropathy prevention

The most evidence-supported prevention for contrast-induced nephropathy in a patient with CKD is:

A. N-acetylcysteine 1200 mg BID
B. Sodium bicarbonate infusion
C. Adequate IV crystalloid hydration with normal saline
D. Mannitol diuresis
E. Furosemide before procedure

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Answer: C. Hydration with isotonic crystalloid (avoid hyperchloremic excess) is the only intervention with consistent evidence. NAC is inexpensive and benign but has weak evidence. Bicarbonate showed promise but PRESERVE trial (2018) was negative. Loop diuretics increase risk.

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Q12. Rhabdomyolysis treatment

A trauma patient develops CK >50,000 with dark urine. The most appropriate initial therapy is:

A. Hemodialysis
B. Aggressive IV crystalloid to maintain UOP 200–300 mL/hr; consider urine alkalinization
C. Mannitol diuresis alone
D. Loop diuretics
E. Calcium replacement

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Answer: B. Aggressive crystalloid (LR or NS) targeting UOP 200–300 mL/hr. Urine alkalinization with bicarbonate to pH >6.5 may reduce myoglobin precipitation in tubules (evidence mixed). Mannitol controversial. Watch for hyperkalemia, hyperphosphatemia, hypocalcemia.

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Q13. Pulmonary embolism massive

A patient develops sudden hemodynamic collapse and TEE shows large RV and clot in transit. The most appropriate immediate therapy is:

A. Heparin alone
B. Systemic thrombolysis (tPA) if no contraindications, or surgical/catheter embolectomy
C. Inferior vena cava filter
D. Pulmonary vasodilators alone
E. Volume resuscitation

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Answer: B. Massive PE (hemodynamic instability) → thrombolysis (alteplase 100 mg over 2 hr or 0.6 mg/kg over 15 min) or surgical/catheter-based embolectomy. Sub-massive PE (RV strain without shock) → individualized. Heparin always; IVC filter if anticoagulation contraindicated.

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Q14. Mechanical ventilation: PEEP physiology

Increasing PEEP from 5 to 15 cm H₂O most commonly results in:

A. Decreased PaCO₂
B. Decreased cardiac output via reduced preload
C. Increased CO₂ clearance
D. Decreased peak airway pressure
E. Increased systemic vascular resistance

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Answer: B. PEEP reduces venous return → ↓ preload → ↓ CO. Also can increase pulmonary vascular resistance and worsen RV function. Benefits: alveolar recruitment, improved oxygenation, reduced shunt. Optimal PEEP balances oxygenation, hemodynamics, and lung mechanics.

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Q15. Auto-PEEP

A COPD patient on mechanical ventilation has elevated peak and plateau pressures with hemodynamic instability. End-expiratory hold reveals 12 cm H₂O above set PEEP. The most appropriate intervention is:

A. Increase respiratory rate
B. Decrease tidal volume and respiratory rate to allow complete exhalation
C. Increase PEEP to match auto-PEEP
D. Disconnect from ventilator briefly to allow exhalation; then ↓RR / ↑I:E ratio for longer expiration
E. Add inhaled albuterol

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Answer: D. Auto-PEEP (breath stacking) → hyperinflation → hemodynamic collapse. Immediate: disconnect from ventilator to allow exhalation. Long-term: ↓RR, ↑expiratory time, ↓TV, bronchodilators. In severe obstruction may need permissive hypercapnia.

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Q16. DKA fluid management

The initial fluid of choice in DKA is:

A. D5W
B. 0.9% normal saline 15–20 mL/kg in the first hour, then 0.45% NS with K⁺ as appropriate
C. Lactated Ringer
D. Plasma-Lyte
E. 3% saline

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Answer: B. DKA: NS bolus → switch to half-NS once euvolemic and Na corrected. Add dextrose to maintenance once glucose <250 mg/dL while continuing insulin. Insulin infusion 0.1 U/kg/hr after K replete (K >3.3). Watch for cerebral edema in pediatrics — avoid rapid correction.

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Q17. Refeeding syndrome

A previously malnourished patient is started on TPN and develops cardiac arrhythmias, weakness, and altered mental status on day 3. The most likely electrolyte disturbance is:

A. Hyperkalemia
B. Hypophosphatemia, hypomagnesemia, hypokalemia
C. Hypercalcemia
D. Hyponatremia
E. Hypocalcemia alone

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Answer: B. Refeeding syndrome: insulin surge with refeeding drives K⁺, phosphate, Mg²⁺ intracellularly → severe depletion. Start TPN slowly, monitor electrolytes daily, replete aggressively. Thiamine before glucose to prevent Wernicke encephalopathy.

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Q18. Hypercalcemia treatment

Severe symptomatic hypercalcemia (15 mg/dL) is initially managed with:

A. Calcitonin alone
B. IV 0.9% saline + calcitonin + bisphosphonate (zoledronic acid) for long-term
C. Loop diuretics
D. Hemodialysis as first line
E. Steroids

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Answer: B. Severe (>14 or symptomatic): NS volume resuscitation (calciuresis), calcitonin (fast onset, brief), bisphosphonates (onset 2–4 days, durable). Avoid loops unless volume overloaded. Steroids for vitamin D-mediated hypercalcemia (sarcoidosis, lymphoma). Dialysis if cardiac/renal failure precludes hydration.

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Q19. SIADH lab pattern

Classic SIADH lab findings include:

A. Hyponatremia, low serum osmolality, high urine osmolality, urine Na >20
B. Hypernatremia, high serum osmolality, low urine osmolality
C. Hyponatremia with low urine osmolality
D. Hyponatremia with hypovolemia and low urine Na
E. Hyperkalemia and high urine osmolality

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Answer: A. SIADH: euvolemic hyponatremia, serum osm <275, urine osm >100 (often >300), urine Na >20, low uric acid and BUN. Causes: CNS lesions, pulmonary disease, drugs (SSRIs, opioids, NSAIDs, carbamazepine), small cell lung cancer (ectopic). Treatment: fluid restriction first; vaptans for refractory.

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Q20. CSW vs SIADH

A neurosurgical patient develops hyponatremia. Differentiating cerebral salt wasting from SIADH:

A. Volume status — CSW is hypovolemic, SIADH is euvolemic
B. Sodium level alone
C. Urine osmolality
D. Serum osmolality
E. BUN

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Answer: A. Volume status is the key differentiator. CSW: ↑UOP, hypovolemia, ↑urine Na (>40), elevated hematocrit, dry. SIADH: euvolemic, ↓UOP, urine Na variable. Treatment differs: CSW needs salt + volume; SIADH needs fluid restriction.

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Q21. Hyponatremia correction rate

Maximum safe correction rate of chronic hyponatremia is approximately:

A. 1 mEq/L/hour
B. 4–6 mEq/L in first 24 hours, with maximum ~8 mEq/L in 24 hr
C. 10 mEq/L in 12 hours
D. 15 mEq/L in 24 hours
E. Correct to 135 within 24 hours

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Answer: B. Chronic (>48 hr) hyponatremia: max 4–6 mEq/L in 24 hr to prevent osmotic demyelination syndrome. Higher rates acceptable for acute severe symptomatic hyponatremia (seizures) initially. Risk factors for ODS: alcoholism, malnutrition, K depletion, liver disease.

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Q22. ICU sedation choice

For sedation of a mechanically ventilated patient, evidence supports:

A. Continuous benzodiazepine infusion
B. Minimal sedation with daily awakening trials, prefer propofol or dexmedetomidine over benzos
C. Deep sedation throughout intubation
D. Ketamine infusion as first-line
E. Etomidate continuous infusion

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Answer: B. ABCDEF bundle (Awakening, Breathing trials, Choice of sedation, Delirium screening, Early mobility, Family). Benzos increase delirium and length of stay. Dexmedetomidine reduces delirium and mortality compared to lorazepam (SEDCOM, MENDS trials). Propofol acceptable short-term.

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Q23. Prone positioning ARDS

In severe ARDS (P/F <150), prone positioning improves outcomes by:

A. Decreasing intrathoracic pressure
B. Improving V/Q matching, reducing atelectasis in dorsal lung, more uniform stress distribution
C. Reducing oxygen consumption
D. Cardiopulmonary stretch reflex activation
E. Direct effect on cytokine clearance

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Answer: B. PROSEVA trial: 16 hours prone in severe ARDS reduces mortality. Recruits dorsal lung, redistributes ventilation more uniformly, reduces ventral hyperinflation. Risk: pressure injuries, line/tube dislodgement, transient hemodynamic changes.

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Q24. Stress ulcer prophylaxis

Stress ulcer prophylaxis with PPI is most indicated in:

A. All ICU patients
B. Mechanical ventilation >48 hr, coagulopathy, GI bleeding history, sepsis, head injury, burns
C. Only patients with documented active bleeding
D. Trauma patients only
E. Patients on systemic steroids regardless of other factors

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Answer: B. SUP indicated for high-risk: ventilation >48 hr, coagulopathy (plt <50k or INR >1.5), prior GI bleed, sepsis with shock, severe TBI/SCI, burns >35%, hepatic failure. Discontinue when risk resolves. PPIs may increase risk of C. diff and PNA.

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Q25. Lactate clearance

A patient in septic shock has initial lactate 6, then 4.5 at hour 6. Lactate clearance is:

A. 25%
B. 50%
C. 60%
D. 80%
E. Cannot calculate

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Answer: A. Clearance = (initial – current) / initial × 100% = (6 – 4.5)/6 = 25%. Target clearance ≥10% per 6 hr correlates with improved mortality. Lactate-guided resuscitation (ANDROMEDA-SHOCK 2019) showed peripheral perfusion-guided strategy non-inferior.

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Q26. Strong ion difference

Per Stewart's approach to acid-base, the strong ion difference (SID) is approximately:

A. (Na + K + Ca + Mg) − (Cl + Lactate) ≈ 40–42 mEq/L
B. Na − Cl
C. Anion gap minus albumin
D. Hbg / pH
E. Bicarb / pCO₂

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Answer: A. SID = strong cations − strong anions ≈ 40–42 mEq/L normally. ↓SID = acidosis (NaCl administration dilutes SID; renal Cl retention). ↑SID = alkalosis. Useful in hyperchloremic acidosis from large-volume NS resuscitation.

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Q27. TPN complications

Long-term TPN complications include:

A. Hyperglycemia, hepatic dysfunction with elevated AST/ALT, biliary stasis with gallstones, copper deficiency anemia, catheter infections
B. Diabetes insipidus
C. Hypothyroidism
D. Hypertension
E. Restrictive lung disease

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Answer: A. TPN complications: catheter infections, hyperglycemia, hypoglycemia from abrupt cessation, hypophosphatemia/hypomagnesemia/hypokalemia, copper deficiency (anemia), zinc deficiency (impaired wound healing), liver dysfunction (treat with vit K), gallstones (biliary stasis without enteral stimulation).

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Q28. Hypercapnia and CBF

For each 1 mmHg rise in PaCO₂, cerebral blood flow increases by approximately:

A. 0.1 mL/100g/min
B. 1–2 mL/100g/min
C. 5 mL/100g/min
D. 10 mL/100g/min
E. No change

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Answer: B. ΔCBF = 1–2 mL/100g/min per mmHg ΔPaCO₂. Normal CBF ~50 mL/100g/min. Hyperventilation can transiently reduce ICP but effect dissipates over 6–8 hr due to bicarb buffering. Avoid extreme hyperventilation (CBF can fall to ischemic levels <20).

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Q29. Anion gap interpretation

A patient has Na 140, Cl 100, HCO₃ 14. Anion gap is:

A. 12
B. 24
C. 26
D. 30
E. Cannot calculate without K

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Answer: C. AG = Na − (Cl + HCO₃) = 140 − 114 = 26. Normal 8–12. Elevated AG metabolic acidosis (MUDPILES: methanol, uremia, DKA, propylene glycol/paraldehyde, INH/iron, lactic acidosis, ethylene glycol, salicylates). Correct for hypoalbuminemia: ↓1 g/dL albumin → ↓2.5 mEq AG.

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Q30. Winter's formula

For a metabolic acidosis with HCO₃ 15, expected PaCO₂ for appropriate respiratory compensation is approximately:

A. 18 mmHg
B. 24–32 mmHg
C. 40 mmHg
D. 50 mmHg
E. Cannot predict

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Answer: B. Winter's formula: expected PaCO₂ = 1.5 × HCO₃ + 8 ± 2 = 1.5(15) + 8 = 30.5 ± 2 (28.5–32.5). If actual PaCO₂ is higher → concurrent respiratory acidosis; if lower → concurrent respiratory alkalosis.

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Q31. SAH vasospasm prophylaxis

In aneurysmal subarachnoid hemorrhage, vasospasm prevention is achieved with:

A. Hydralazine
B. Nimodipine 60 mg PO q4h × 21 days
C. Magnesium infusion
D. Statins
E. Beta-blockers

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Answer: B. Nimodipine PO is the only proven vasospasm prophylaxis (improves neurologic outcome despite no demonstrable reduction in angiographic spasm). Vasospasm peaks days 3–14. Triple-H therapy (hypertension, hemodilution, hypervolemia) historically used; current focus on euvolemia + induced hypertension. Transcranial Doppler for monitoring.

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