Critical Care
ARDS, sepsis, hepatorenal syndrome, burn resuscitation, AKI, abdominal compartment syndrome, mechanical ventilation. ← All topics
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 with plateau pressure target below 40 cm H₂O
B. Tidal volume 6 mL/kg PBW with plateau pressure ≤30 cm H₂O and SpO₂ 88–95%
C. Tidal volume 4 mL/kg PBW with PaO₂ target maintained above 100 mmHg
D. APRV mode with P-high 35 cm H₂O and FiO₂ 1.0 until oxygenation improves
E. Permissive hypoxemia strategy with FiO₂ reduced to 0.4 and current PEEP
Show answer
Answer: B. The ARDSnet low tidal volume strategy is the most evidence-based approach for ARDS ventilation. Key parameters include tidal volume of 6 mL/kg predicted body weight, plateau pressure ≤30 cm H₂O, and permissive hypoxemia with SpO₂ goal of 88–95% (corresponding to PaO₂ 55–80 mmHg). Prolonged exposure to FiO₂ >0.6 should be avoided due to oxygen toxicity. Additional evidence-based adjuncts include prone positioning, which improves survival in severe ARDS (PROSEVA trial), and inhaled nitric oxide, which can reduce ventilation-perfusion mismatch. Higher tidal volumes (10 mL/kg) and plateau pressures (>30 cm H₂O) increase ventilator-induced lung injury. Excessively low tidal volumes (4 mL/kg) may worsen hypercapnia without additional benefit. APRV with sustained high FiO₂ 1.0 risks oxygen toxicity. Reducing FiO₂ to 0.4 in a patient with PaO₂ 55 on FiO₂ 0.8 would worsen life-threatening hypoxemia.
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 plus dopamine to increase renal perfusion and urine output
B. Midodrine plus octreotide plus albumin to reverse splanchnic vasodilation
C. Norepinephrine plus albumin infusion for systemic vasoconstriction and volume
D. Terlipressin alone as selective splanchnic vasoconstrictor without albumin
E. Hemodialysis to manage acute kidney injury and rising creatinine
Show answer
Answer: B. This patient has hepatorenal syndrome type 1 based on cirrhosis, rising creatinine (>0.3 mg/dL in 48 hours or doubling to >2.5), oliguria, low FENa (<1%), and failure to respond to albumin challenge. For non-critically ill patients outside the ICU, the most appropriate initial therapy is midodrine (oral alpha-agonist) plus octreotide (splanchnic vasoconstrictor) plus albumin. This combination reverses the splanchnic vasodilation and relative hypovolemia that characterize HRS. In the United States, this regimen has been standard where terlipressin was historically unavailable, though terlipressin received FDA approval in 2022. Critically ill patients in the ICU should receive norepinephrine plus albumin, with or without vasopressin. Terlipressin requires concomitant albumin, not monotherapy. Diuretics worsen HRS by further depleting effective arterial blood volume. Hemodialysis does not address the underlying pathophysiology and is reserved for refractory cases or as a bridge to liver transplantation, which remains the definitive treatment.
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 of lactated Ringer's solution over the next 6 hours
B. 8,400 mL of lactated Ringer's solution over the next 6 hours
C. 14,000 mL of lactated Ringer's solution over the next 6 hours
D. 2,800 mL of lactated Ringer's solution over the next 6 hours
E. 11,200 mL of dextrose 5% in normal saline over the next 6 hours
Show answer
Answer: A. The Parkland formula calculates burn resuscitation as 4 mL/kg/%TBSA over 24 hours. For this patient: 4 × 70 kg × 40% = 11,200 mL total. Half of this volume (5,600 mL) should be given in the first 8 hours from the time of injury. Since 2 hours have already elapsed, the remaining 5,600 mL should be administered over the next 6 hours. Lactated Ringer's is the preferred crystalloid for initial burn resuscitation. Glucose-containing solutions should be avoided in initial resuscitation. Albumin is typically avoided in the first 8–12 hours. Total fluid should be capped at 250–300 mL/kg in the first 24 hours to minimize the risk of abdominal compartment syndrome and ARDS.
Q4. Sepsis-3 definition
Per Sepsis-3, septic shock requires all EXCEPT:
A. Sepsis with life-threatening organ dysfunction caused by dysregulated host response to infection
B. Vasopressor requirement to maintain mean arterial pressure of at least 65 mmHg
C. Serum lactate greater than 2 mmol/L persisting despite adequate volume resuscitation
D. Positive blood cultures documenting bacteremia or fungemia from a microbial pathogen
E. None of the above—all four criteria listed are required for septic shock
Show answer
Answer: D. Per Sepsis-3 criteria, septic shock is defined as sepsis (life-threatening organ dysfunction caused by dysregulated host response to infection) plus the need for vasopressors to maintain MAP ≥65 mmHg plus serum lactate >2 mmol/L despite adequate fluid resuscitation. Positive blood cultures are NOT required for the diagnosis of septic shock; in fact, only 30–50% of septic shock cases have positive blood cultures. The diagnosis is clinical and based on hemodynamic and metabolic criteria. qSOFA (RR ≥22, SBP ≤100, altered mentation) is used for screening outside the ICU, while SOFA score is used for diagnosis in the ICU setting.
Q5. Septic shock initial resuscitation
Per Surviving Sepsis Campaign 2021, initial fluid resuscitation in septic shock is:
A. 10 mL/kg crystalloid bolus within the first 3 hours of recognition
B. 30 mL/kg crystalloid bolus within the first 3 hours of recognition
C. 50 mL/kg colloid bolus within the first 3 hours of recognition
D. 1000 mL crystalloid bolus within the first 30 minutes of recognition
E. Minimal fluid bolus with immediate vasopressor initiation within 1 hour
Show answer
Answer: B. The Surviving Sepsis Campaign 2021 guidelines recommend 30 mL/kg of crystalloid fluid within the first 3 hours of recognition of septic shock. Balanced crystalloids such as lactated Ringer's or Plasma-Lyte are preferred over normal saline. After the initial bolus, clinicians should reassess fluid responsiveness using dynamic indices including pulse pressure variation, stroke volume variation, or passive leg raise testing. Norepinephrine is the first-line vasopressor. Vasopressin may be added at 0.03 units per minute for refractory hypotension, and epinephrine can be added if cardiac dysfunction is present. The other volumes listed (10 mL/kg, 50 mL/kg, or fixed 1000 mL doses) do not align with current evidence-based recommendations, and avoiding fluids in favor of immediate pressors contradicts the guideline's emphasis on adequate initial fluid resuscitation.
Q6. Steroids in septic shock
When are corticosteroids indicated in septic shock?
A. All patients meeting sepsis-3 criteria regardless of hemodynamic status or vasopressor requirement
B. Refractory shock despite adequate fluid resuscitation and vasopressor doses exceeding 0.25 mcg/kg/min norepinephrine equivalent
C. Only patients with documented positive blood cultures and microbiologic confirmation of bacterial infection
D. Only patients with biochemically confirmed adrenal insufficiency demonstrated by cosyntropin stimulation testing
E. Never indicated as multiple randomized trials have consistently demonstrated increased mortality with corticosteroid therapy
Show answer
Answer: B. Hydrocortisone 200 mg/day IV (50 mg q6h or continuous infusion) is indicated for refractory septic shock despite adequate fluid resuscitation and vasopressor support, typically defined as norepinephrine doses exceeding 0.25 mcg/kg/min. The ADRENAL and APROCCHSS trials showed conflicting mortality results but consistent acceleration of shock reversal and reduced time on vasopressors. Corticosteroids are not indicated for all septic patients, do not require positive cultures or proven adrenal insufficiency, and do not increase mortality when used appropriately in refractory shock.
Q7. Abdominal compartment syndrome
Abdominal compartment syndrome is diagnosed when:
A. Intra-abdominal pressure >5 mmHg with new organ dysfunction
B. Intra-abdominal pressure >20–25 mmHg with new organ dysfunction
C. Intra-abdominal pressure >12–15 mmHg with new organ dysfunction
D. Intra-abdominal pressure >30 mmHg with new organ dysfunction
E. Intra-abdominal pressure >10 mmHg with new organ dysfunction
Show answer
Answer: B. Abdominal compartment syndrome is defined as sustained intra-abdominal pressure greater than 20–25 mmHg with new organ dysfunction. IAP is measured via bladder pressure transduction, zeroed at the midaxillary line, not via nasogastric tube. The syndrome results from multiple pathophysiologic effects including decreased venous return, decreased cardiac output, increased intracranial pressure, decreased pulmonary compliance, and acute kidney injury from reduced abdominal perfusion pressure (MAP minus IAP). Risk factors include massive volume resuscitation, ruptured abdominal aortic aneurysm, severe pancreatitis, and tense ascites. Surgical decompression is typically indicated when IAP exceeds 25 mmHg with organ dysfunction refractory to medical management. Physical exam findings such as abdominal wall edema or radiographic findings like diaphragmatic elevation may suggest elevated IAP but are not diagnostic criteria for abdominal compartment syndrome.
Q8. Emergency hemodialysis indications
The indications for urgent hemodialysis (AEIOU mnemonic) include all EXCEPT:
A. Severe metabolic acidosis with pH less than 7.1 that is refractory to medical therapy
B. Symptomatic hyperkalemia or potassium greater than 6.5 that is refractory to therapy
C. Ingestion of toxic alcohols, salicylates, lithium, or other dialyzable toxins
D. Volume overload with pulmonary edema or heart failure refractory to diuretics
E. Mild uremia with blood urea nitrogen of 60 and no symptoms
Show answer
Answer: E. The AEIOU mnemonic for urgent hemodialysis indications includes: Acidosis (severe metabolic acidosis with pH <7.1 refractory to medical therapy), Electrolytes (symptomatic hyperkalemia or K >6.5 refractory to therapy), Ingestion (toxic alcohols, salicylates, lithium, and other dialyzable toxins such as carbamazepine and sodium valproate, remembered by the CLASS mnemonic: Carbamazepine, Lithium, Alcohols, Salicylates, Sodium valproate), Overload (volume overload refractory to diuretics), and Uremia (symptomatic uremia with encephalopathy, pericarditis, or bleeding, or BUN >100 or creatinine >10). Mild uremia with BUN of 60 and no symptoms does not meet criteria for urgent dialysis, as uremic indications require either severe symptoms or markedly elevated values.
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 (serum creatinine 1.5–1.9 times baseline or absolute rise ≥0.3 mg/dL)
B. Stage 2 AKI (serum creatinine 2.0–2.9 times baseline or urine output criteria met)
C. Stage 3 AKI (serum creatinine ≥3.0 times baseline or creatinine ≥4.0 with acute rise)
D. Not AKI (serum creatinine rise does not meet threshold criteria for any stage)
E. Cannot determine without urine output (serum creatinine alone is insufficient for KDIGO staging)
Show answer
Answer: B. This patient has a creatinine rise from 1.0 to 2.3 mg/dL, representing a 2.3-fold increase from baseline, which meets KDIGO Stage 2 AKI criteria. KDIGO Stage 2 is defined as serum creatinine 2.0–2.9 times baseline OR urine output less than 0.5 mL/kg/h for 12 hours or more. Stage 1 requires creatinine 1.5–1.9 times baseline or an absolute rise of at least 0.3 mg/dL within 48 hours. Stage 3 requires creatinine 3.0 times baseline or more, creatinine 4.0 mg/dL or greater with an acute rise of at least 0.5 mg/dL, initiation of renal replacement therapy, urine output less than 0.3 mL/kg/h for 24 hours or more, or anuria for 12 hours or more. While urine output can also define AKI stages, the serum creatinine criterion alone is sufficient for staging in this case.
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. Postrenal obstruction
D. Acute interstitial nephritis
E. Acute glomerulonephritis
Show answer
Answer: A. This patient has prerenal azotemia. The classic laboratory findings for prerenal azotemia include BUN/Cr ratio greater than 20, FENa less than 1%, urine sodium less than 10 mEq/L, and urine osmolality greater than 500 mOsm/kg. All of these findings are present in this case (BUN/Cr 25, FENa 0.4%, urine Na 8 mEq/L, urine osm 600). In contrast, acute tubular necrosis typically shows BUN/Cr ratio less than 15, FENa greater than 2%, urine sodium greater than 20 mEq/L, and urine osmolality less than 350 mOsm/kg. Postrenal obstruction initially may show prerenal patterns but over time mimics intrinsic renal disease with loss of concentrating ability. Acute interstitial nephritis and glomerulonephritis are intrinsic renal causes that typically show FENa greater than 1% and do not demonstrate the avid sodium retention and concentrated urine seen in prerenal states.
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 orally twice daily starting the day before contrast exposure
B. Sodium bicarbonate infusion at 3 mL/kg/hr for one hour before contrast administration
C. Adequate intravenous crystalloid hydration with isotonic normal saline before and after contrast
D. Mannitol-induced osmotic diuresis initiated at least two hours before the contrast procedure
E. Furosemide 40 mg intravenously administered 30 to 60 minutes before contrast exposure
Show answer
Answer: C. Hydration with isotonic crystalloid is the only intervention with consistent evidence for preventing contrast-induced nephropathy in patients with chronic kidney disease. Normal saline is typically used, though care should be taken to avoid hyperchloremic excess in high-volume resuscitation. N-acetylcysteine is inexpensive and benign but has weak and conflicting evidence for benefit. Sodium bicarbonate infusion showed initial promise in small studies, but the large PRESERVE trial in 2018 demonstrated no benefit over saline hydration. Loop diuretics such as furosemide actually increase the risk of contrast-induced nephropathy and should be avoided. Mannitol has not been shown to provide benefit and may worsen outcomes.
Q12. Rhabdomyolysis treatment
A trauma patient develops CK >50,000 with dark urine. The most appropriate initial therapy is:
A. Hemodialysis to remove myoglobin and correct electrolyte abnormalities including hyperkalemia
B. Aggressive IV crystalloid to maintain UOP 200–300 mL/hr with urine alkalinization using bicarbonate
C. Mannitol diuresis alone to increase tubular flow and prevent myoglobin cast formation
D. Loop diuretics to maintain high urine output and facilitate clearance of myoglobin
E. Calcium replacement to correct hypocalcemia and prevent cardiac arrhythmias from hyperkalemia
Show answer
Answer: B. The cornerstone of rhabdomyolysis treatment is aggressive IV crystalloid resuscitation (lactated Ringer's or normal saline) targeting urine output of 200–300 mL/hr to prevent acute kidney injury from myoglobin precipitation in renal tubules. Urine alkalinization with sodium bicarbonate to achieve urine pH >6.5 may reduce myoglobin precipitation, though evidence is mixed. Mannitol use is controversial and should not be used alone. Loop diuretics are contraindicated as they concentrate myoglobin and acidify urine. Hemodialysis is reserved for refractory cases with severe electrolyte derangements or AKI. Calcium should be avoided unless symptomatic hypocalcemia occurs, as early administration may worsen tissue calcium deposition. Monitor closely for hyperkalemia, hyperphosphatemia, and hypocalcemia.
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 anticoagulation as monotherapy without additional interventions
B. Systemic thrombolysis if no contraindications, or surgical/catheter embolectomy
C. Inferior vena cava filter placement without systemic anticoagulation
D. Pulmonary vasodilators as monotherapy without additional interventions
E. Volume resuscitation with crystalloid as monotherapy without pressors
Show answer
Answer: B. Massive PE with hemodynamic instability requires immediate reperfusion therapy. Systemic thrombolysis is first-line treatment (alteplase 100 mg over 2 hours or 0.6 mg/kg over 15 minutes) if no contraindications exist. Surgical or catheter-based embolectomy is indicated when thrombolysis is contraindicated or has failed. Heparin anticoagulation should always be initiated but is insufficient as monotherapy in massive PE. Submassive PE (RV strain without shock) requires individualized management. IVC filters are reserved for situations where anticoagulation is contraindicated. Pulmonary vasodilators and volume resuscitation alone do not address the underlying thrombus and are inadequate for massive PE with hemodynamic collapse.
Q14. Mechanical ventilation: PEEP physiology
Increasing PEEP from 5 to 15 cm H₂O most commonly results in:
A. Decreased PaCO₂ due to improved alveolar ventilation and reduced dead space
B. Decreased cardiac output due to reduced venous return and decreased preload
C. Increased CO₂ clearance due to recruitment of previously collapsed alveolar units
D. Decreased peak airway pressure due to improved lung compliance and recruitment
E. Increased systemic vascular resistance due to sympathetic activation and baroreceptor response
Show answer
Answer: B. Increasing PEEP from 5 to 15 cm H₂O most commonly decreases cardiac output by reducing venous return and preload. The increased intrathoracic pressure impedes venous return to the right atrium. PEEP can also increase pulmonary vascular resistance and worsen right ventricular function. While PEEP provides important benefits including alveolar recruitment, improved oxygenation, and reduced shunt fraction, its hemodynamic effects on preload are the most consistent consequence. PEEP typically increases rather than decreases PaCO₂ (by increasing dead space), does not reliably improve CO₂ clearance, increases rather than decreases peak airway pressures, and does not directly increase systemic vascular resistance. Optimal PEEP selection balances oxygenation goals, hemodynamic stability, and lung mechanics.
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 to improve minute ventilation and reduce CO₂ retention
B. Decrease tidal volume and respiratory rate to allow more complete exhalation
C. Increase PEEP to match auto-PEEP level and reduce work of breathing
D. Disconnect from ventilator briefly to allow exhalation; then decrease respiratory rate and increase expiratory time
E. Add inhaled albuterol to reduce bronchospasm and improve expiratory flow
Show answer
Answer: D. Auto-PEEP (intrinsic PEEP or breath stacking) occurs when insufficient expiratory time prevents complete exhalation, leading to progressive hyperinflation. In hemodynamically unstable patients, immediate intervention is critical: briefly disconnect from the ventilator to allow trapped air to escape and relieve the hyperinflation causing hemodynamic compromise. After this acute intervention, adjust ventilator settings for long-term management by decreasing respiratory rate and increasing the inspiratory-to-expiratory (I:E) ratio to allow longer expiratory time. Additional measures include reducing tidal volume, administering bronchodilators, and accepting permissive hypercapnia in severe obstruction. Increasing respiratory rate (choice A) would worsen air trapping. Simply decreasing tidal volume and rate (choice B) addresses the problem but omits the critical immediate step of disconnection in an unstable patient. Increasing PEEP to match auto-PEEP (choice C) may help in stable patients to reduce work of breathing but does not address acute hemodynamic instability from hyperinflation. Bronchodilators (choice E) are important adjuncts but insufficient as sole therapy in this acute scenario.
Q16. DKA fluid management
The initial fluid of choice in DKA is:
A. D5W at 250 mL/hr initially, then titrate based on serum glucose levels
B. 0.9% normal saline 15–20 mL/kg in the first hour, then 0.45% NS with K⁺
C. Lactated Ringer solution at 500 mL/hr initially, then adjust for electrolyte balance
D. Plasma-Lyte at 15–20 mL/kg in the first hour, then maintenance fluids
E. 3% saline at 1–2 mL/kg/hr initially to correct severe hyponatremia
Show answer
Answer: B. The initial fluid of choice in DKA is 0.9% normal saline given as a bolus of 15–20 mL/kg in the first hour to restore intravascular volume. Once the patient is euvolemic and serum sodium is corrected, switch to 0.45% normal saline with potassium supplementation as appropriate (when K⁺ >3.3 mEq/L). Add dextrose to maintenance fluids once glucose drops below 250 mg/dL while continuing insulin infusion at 0.1 U/kg/hr. D5W lacks the necessary sodium and volume expansion needed in DKA. Lactated Ringer and Plasma-Lyte contain potassium and may worsen hyperkalemia that can be present initially in DKA despite total body potassium depletion. Hypertonic saline (3% saline) is not indicated as DKA patients typically have elevated serum sodium when corrected for hyperglycemia. In pediatric patients, avoid overly rapid correction to prevent cerebral edema.
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 with secondary hypercalcemia and hypomagnesemia
B. Hypophosphatemia with concurrent hypomagnesemia and hypokalemia
C. Hypercalcemia with secondary hypermagnesemia and hyperkalemia
D. Hyponatremia with concurrent hypocalcemia and hyperphosphatemia
E. Hypocalcemia with secondary hypokalemia and hypermagnesemia
Show answer
Answer: B. This patient has refeeding syndrome, which occurs when nutrition is reintroduced to malnourished patients. The insulin surge triggered by refeeding drives potassium, phosphate, and magnesium intracellularly, causing severe extracellular depletion of all three electrolytes. The triad of hypophosphatemia, hypomagnesemia, and hypokalemia leads to cardiac arrhythmias, muscle weakness, respiratory failure, and altered mental status. Prevention requires starting TPN slowly in at-risk patients, monitoring electrolytes daily, and aggressively repleting deficiencies. Thiamine should be given before glucose administration to prevent Wernicke encephalopathy in malnourished patients.
Q18. Hypercalcemia treatment
Severe symptomatic hypercalcemia (15 mg/dL) is initially managed with:
A. Calcitonin alone for rapid onset of action
B. IV 0.9% saline with calcitonin and bisphosphonate
C. Loop diuretics with aggressive fluid resuscitation
D. Hemodialysis as the initial first-line therapy
E. Steroids for all causes of hypercalcemia
Show answer
Answer: B. Severe hypercalcemia (>14 mg/dL or symptomatic) requires multimodal initial management. IV 0.9% normal saline provides volume resuscitation and promotes calciuresis. Calcitonin is added for rapid onset of action (within hours) though its effect is brief and subject to tachyphylaxis. Bisphosphonates such as zoledronic acid are administered concurrently for long-term control, with onset in 2–4 days and durable effect. Loop diuretics should be avoided unless the patient is volume overloaded, as they can worsen hypercalcemia. Steroids are reserved for vitamin D-mediated hypercalcemia such as sarcoidosis or lymphoma. Hemodialysis is indicated only when cardiac or renal failure precludes aggressive hydration.
Q19. SIADH lab pattern
Classic SIADH lab findings include:
A. Hyponatremia, low serum osmolality, high urine osmolality, urine sodium greater than 20 mEq/L
B. Hypernatremia, high serum osmolality, low urine osmolality, urine sodium greater than 20 mEq/L
C. Hyponatremia, low serum osmolality, low urine osmolality, urine sodium less than 20 mEq/L
D. Hyponatremia, low serum osmolality, high urine osmolality, urine sodium less than 20 mEq/L
E. Hyperkalemia, low serum osmolality, high urine osmolality, urine potassium greater than 20 mEq/L
Show answer
Answer: A. SIADH presents with euvolemic hyponatremia and a characteristic laboratory pattern: serum osmolality less than 275 mOsm/kg, urine osmolality greater than 100 mOsm/kg (often exceeding 300), urine sodium greater than 20 mEq/L, and low uric acid and BUN. The key is inappropriate antidiuretic hormone secretion causing water retention despite low serum osmolality, with continued renal sodium excretion. Common causes include CNS lesions, pulmonary disease, drugs (SSRIs, opioids, NSAIDs, carbamazepine), and small cell lung cancer producing ectopic ADH. Treatment begins with fluid restriction; vaptans (vasopressin receptor antagonists) are reserved for refractory cases. Choice D represents hypovolemic hyponatremia with appropriate renal sodium retention. Choice C suggests primary polydipsia or reset osmostat.
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. Urine sodium concentration — CSW is low, SIADH is elevated
C. Urine osmolality — CSW is low, SIADH is elevated
D. Serum osmolality — CSW is normal, SIADH is decreased
E. Blood urea nitrogen — CSW is elevated, SIADH is low
Show answer
Answer: A. Volume status is the key differentiator between cerebral salt wasting and SIADH. In CSW, patients are hypovolemic with increased urine output, elevated hematocrit, and clinical signs of dehydration. Urine sodium is typically elevated (>40 mEq/L) due to renal salt wasting. In SIADH, patients are euvolemic with decreased urine output and variable urine sodium. Both conditions can have elevated urine sodium, low serum osmolality, and elevated urine osmolality, making these less reliable differentiators. BUN may be elevated in CSW due to hypovolemia and low-normal in SIADH due to euvolemia, but this is less specific than volume status. Treatment differs significantly: CSW requires salt and volume replacement, while SIADH requires fluid restriction.
Q21. Hyponatremia correction rate
Maximum safe correction rate of chronic hyponatremia is approximately:
A. 1 mEq/L per hour for the first 24 hours
B. 4–6 mEq/L in 24 hours, maximum 8 mEq/L in 24 hours
C. 10 mEq/L in 12 hours, maximum 15 mEq/L in 24 hours
D. 12–15 mEq/L in 24 hours with careful monitoring
E. Correct to 135 mEq/L within the first 24 hours
Show answer
Answer: B. For chronic hyponatremia (present for more than 48 hours), the maximum safe correction rate is 4–6 mEq/L in 24 hours, with an absolute maximum of approximately 8 mEq/L in 24 hours. This conservative approach prevents osmotic demyelination syndrome (ODS), formerly known as central pontine myelinolysis. Higher correction rates may be acceptable initially for acute severe symptomatic hyponatremia presenting with seizures or other neurologic emergencies. Major risk factors for developing ODS include chronic alcoholism, malnutrition, potassium depletion, and liver disease. Overly rapid correction, even by a few mEq/L beyond recommended limits, significantly increases the risk of this devastating complication.
Q22. ICU sedation choice
For sedation of a mechanically ventilated patient, evidence supports:
A. Continuous benzodiazepine infusion with daily sedation holidays and delirium screening
B. Minimal sedation with daily awakening trials, preferring propofol or dexmedetomidine over benzodiazepines
C. Deep sedation throughout intubation with continuous propofol infusion and delirium monitoring
D. Ketamine infusion as first-line sedation with daily interruption and early mobility protocols
E. Etomidate continuous infusion with intermittent boluses and daily breathing trial assessments
Show answer
Answer: B. Evidence-based ICU sedation follows the ABCDEF bundle principles: Awakening trials, Breathing trials, Choice of sedation, Delirium screening, Early mobility, and Family engagement. Minimal sedation strategies with daily awakening trials improve outcomes. Benzodiazepines increase delirium incidence and prolong ICU length of stay. Dexmedetomidine reduces delirium and mortality compared to lorazepam, as demonstrated in the SEDCOM and MENDS trials. Propofol is acceptable for short-term sedation. Deep sedation is associated with worse outcomes. Ketamine is not first-line for routine ICU sedation. Etomidate is not appropriate for continuous infusion due to adrenal suppression.
Q23. Prone positioning ARDS
In severe ARDS (P/F <150), prone positioning improves outcomes by:
A. Decreasing intrathoracic pressure and reducing right ventricular afterload through improved thoracic compliance
B. Improving V/Q matching, reducing dorsal atelectasis, and redistributing ventilator-induced stress more uniformly
C. Reducing total body oxygen consumption and decreasing metabolic demand through improved chest wall mechanics
D. Activating cardiopulmonary stretch reflexes and modulating autonomic tone through altered mechanoreceptor signaling
E. Enhancing cytokine clearance through direct effects on lymphatic drainage and pulmonary inflammatory mediator removal
Show answer
Answer: B. The PROSEVA trial demonstrated that prone positioning for 16 hours per day in severe ARDS (P/F ratio <150) significantly reduces mortality. The mechanism involves recruiting collapsed dorsal lung regions, redistributing ventilation more uniformly across all lung zones, and reducing ventral hyperinflation and ventilator-induced lung injury. By placing previously dependent (dorsal) regions in a non-dependent position, atelectasis is reduced and ventilation-perfusion matching improves. The more homogeneous distribution of transpulmonary pressure reduces regional stress and strain, protecting against ventilator-induced lung injury. Risks of prone positioning include pressure injuries (face, chest, knees), accidental line or endotracheal tube dislodgement, and transient hemodynamic changes during position changes. Prone positioning does not primarily work through changes in intrathoracic pressure, oxygen consumption, stretch reflexes, or direct cytokine effects.
Q24. Stress ulcer prophylaxis
Stress ulcer prophylaxis with PPI is most indicated in:
A. All patients admitted to the intensive care unit regardless of individual risk factors
B. Mechanical ventilation exceeding 48 hours, coagulopathy, prior gastrointestinal bleeding, sepsis, traumatic brain injury, or burns
C. Only patients with endoscopically documented active gastrointestinal bleeding at time of admission
D. Trauma patients admitted through the emergency department regardless of injury severity or location
E. Patients receiving systemic corticosteroids at any dose regardless of other clinical risk factors
Show answer
Answer: B. Stress ulcer prophylaxis with PPIs is indicated for high-risk ICU patients, including those with mechanical ventilation exceeding 48 hours, coagulopathy (platelets less than 50,000 or INR greater than 1.5), history of prior gastrointestinal bleeding, sepsis with shock, severe traumatic brain injury or spinal cord injury, burns exceeding 35% body surface area, or hepatic failure. Prophylaxis should be discontinued when the risk factors resolve. Important considerations include that PPIs may increase the risk of Clostridioides difficile infection and pneumonia. Universal prophylaxis for all ICU patients is not recommended due to these risks and lack of benefit in low-risk patients.
Q25. Lactate clearance
A patient in septic shock has initial lactate 6, then 4.5 at hour 6. Lactate clearance is:
A. 25%, calculated as the change in lactate divided by the initial lactate times 100
B. 50%, calculated as the change in lactate divided by the final lactate times 100
C. 60%, calculated as the final lactate divided by the initial lactate times 100
D. 80%, calculated as the change in lactate divided by the average lactate times 100
E. Cannot calculate without knowing the patient's weight and volume of distribution for lactate
Show answer
Answer: A. Lactate clearance is calculated as (initial lactate – current lactate) / initial lactate × 100%. In this case: (6 – 4.5) / 6 × 100% = 1.5 / 6 × 100% = 25%. This formula measures the percentage reduction in lactate from baseline. Target lactate clearance of ≥10% per 6 hours correlates with improved mortality in septic shock. The ANDROMEDA-SHOCK trial (2019) demonstrated that a peripheral perfusion-guided resuscitation strategy was non-inferior to lactate-guided resuscitation. Common errors include dividing by the final lactate value instead of the initial value, or confusing clearance with the percentage of lactate remaining.
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 + K) − (Cl + HCO₃) ≈ 12–16 mEq/L
C. (Na + Albumin) − (Cl + Lactate) ≈ 38–40 mEq/L
D. (Na + K + Cl) − (HCO₃ + Albumin) ≈ 8–12 mEq/L
E. (Na + Ca) − (Cl + Phosphate) ≈ 35–38 mEq/L
Show answer
Answer: A. Per Stewart's approach, the strong ion difference (SID) equals the sum of strong cations minus the sum of strong anions, which is (Na + K + Ca + Mg) − (Cl + Lactate), and normally approximates 40–42 mEq/L. A decreased SID causes acidosis, as seen with NaCl administration (which dilutes the SID) or renal chloride retention. An increased SID causes alkalosis. This framework is particularly useful for understanding hyperchloremic metabolic acidosis that occurs after large-volume normal saline resuscitation, where excess chloride reduces the SID and produces acidosis independent of changes in bicarbonate or pCO₂.
Q27. TPN complications
Long-term TPN complications include:
A. Hyperglycemia, hepatic dysfunction, biliary stasis with gallstones, copper deficiency, and catheter-related infections
B. Hypernatremia, renal tubular acidosis, nephrolithiasis with calcium stones, and recurrent urinary tract infections
C. Hyperthyroidism, pancreatic insufficiency, intestinal bacterial overgrowth, and vitamin B12 deficiency with neuropathy
D. Hypertension, left ventricular hypertrophy, accelerated atherosclerosis, and chronic thromboembolic disease from catheters
E. Metabolic acidosis, osteoporosis with pathologic fractures, selenium deficiency, and central line thrombosis
Show answer
Answer: A. Long-term TPN complications include catheter-related infections, hyperglycemia, hypoglycemia from abrupt cessation, electrolyte disturbances (hypophosphatemia, hypomagnesemia, hypokalemia), trace element deficiencies including copper deficiency causing anemia and zinc deficiency causing impaired wound healing, hepatic dysfunction with elevated AST/ALT that can be treated with vitamin K, and gallstones from biliary stasis due to lack of enteral stimulation. The other options list complications not typically associated with long-term TPN use. Diabetes insipidus, hypothyroidism, primary hypertension, and restrictive lung disease are not direct consequences of parenteral nutrition.
Q28. Hypercapnia and CBF
For each 1 mmHg rise in PaCO₂, cerebral blood flow increases by approximately:
A. 0.1 mL/100g/min per mmHg change in PaCO₂
B. 1–2 mL/100g/min per mmHg change in PaCO₂
C. 5 mL/100g/min per mmHg change in PaCO₂
D. 10 mL/100g/min per mmHg change in PaCO₂
E. No change occurs with any PaCO₂ variation
Show answer
Answer: B. Cerebral blood flow increases by 1–2 mL/100g/min for each 1 mmHg rise in PaCO₂. Normal baseline CBF is approximately 50 mL/100g/min. This CO₂ reactivity forms the basis for using hyperventilation to transiently reduce intracranial pressure, though the effect dissipates over 6–8 hours due to CSF bicarbonate buffering. Extreme hyperventilation should be avoided because cerebral blood flow can fall to ischemic levels below 20 mL/100g/min, risking cerebral ischemia.
Q29. Anion gap interpretation
A patient has Na 140, Cl 100, HCO₃ 14. Anion gap is:
A. 12, which is within the normal reference range for anion gap
B. 24, which represents a moderately elevated anion gap metabolic acidosis
C. 26, which represents a significantly elevated anion gap metabolic acidosis
D. 30, which represents a severely elevated anion gap metabolic acidosis
E. Cannot be calculated accurately without the serum potassium concentration
Show answer
Answer: C. The anion gap is calculated as AG = Na − (Cl + HCO₃) = 140 − 114 = 26. The normal anion gap range is 8–12 mEq/L, so this patient has a significantly elevated anion gap indicating a high anion gap metabolic acidosis. Common causes are remembered by the mnemonic MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol/paraldehyde, isoniazid/iron, lactic acidosis, ethylene glycol, and salicylates. When interpreting the anion gap, it is important to correct for hypoalbuminemia, as each 1 g/dL decrease in albumin lowers the calculated anion gap by approximately 2.5 mEq/L. Potassium is not required for the standard anion gap calculation, though some formulas include it.
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. 60 mmHg
Show answer
Answer: B. Winter's formula predicts the expected PaCO₂ for appropriate respiratory compensation in metabolic acidosis: expected PaCO₂ = 1.5 × HCO₃ + 8 ± 2. For HCO₃ of 15, this calculates to 1.5(15) + 8 = 30.5 ± 2, giving a range of 28.5–32.5 mmHg. The answer choice 24–32 mmHg encompasses this expected range. If the actual PaCO₂ is higher than predicted, a concurrent respiratory acidosis is present. If the actual PaCO₂ is lower than predicted, a concurrent respiratory alkalosis is present. This formula helps distinguish appropriate compensation from mixed acid-base disorders.
Q31. SAH vasospasm prophylaxis
In aneurysmal subarachnoid hemorrhage, vasospasm prevention is achieved with:
A. Hydralazine 10 mg IV q6h for 21 days to reduce arterial tone
B. Nimodipine 60 mg PO q4h for 21 days to improve neurologic outcome
C. Magnesium sulfate infusion titrated to serum level 2-4 mEq/L
D. Atorvastatin 80 mg PO daily for 14 days to reduce inflammation
E. Labetalol 200 mg PO q12h for 14 days to control blood pressure
Show answer
Answer: B. Nimodipine 60 mg PO every 4 hours for 21 days is the only proven vasospasm prophylaxis in aneurysmal subarachnoid hemorrhage. It improves neurologic outcomes despite no demonstrable reduction in angiographic vasospasm. Vasospasm typically peaks between days 3 and 14 after the initial hemorrhage. Triple-H therapy (hypertension, hemodilution, hypervolemia) was historically used, but current management focuses on euvolemia combined with induced hypertension. Transcranial Doppler ultrasonography is used for monitoring vasospasm. Magnesium, statins, and other agents have been studied but have not shown consistent benefit in large randomized trials.