Acid–Base And Electrolyte Emergencies - USMLE Step 2

  1. Which of the following is the most appropriate treatment?
    Answer: Fomepizole and hemodialysis The patient has a severe high-anion-gap metabolic acidosis (Anion Gap = 140 - [100 + 7] = 33). The fluorescence of urine under a Wood's lamp is a classic clue for ethylene glycol (antifreeze) ingestion, as fluorescein is often added to these products. Ethylene glycol is metabolized by alcohol dehydrogenase to toxic metabolites (glycolic acid, oxalic acid) that cause acidosis and renal failure. The definitive treatment is to block this metabolism with an alcohol dehydrogenase inhibitor like fomepizole and to remove the parent alcohol and its toxic metabolites via hemodialysis. N-acetylcysteine is for acetaminophen toxicity. Methylene blue is for methemoglobinemia.
  2. In addition to broad-spectrum antibiotics and continued hemodynamic support, which of the following interventions is most critical to reversing his metabolic acidosis?
    Answer: Urgent urologic consultation for source control The patient's severe lactic acidosis is a direct consequence of tissue hypoperfusion caused by septic shock. The three mainstays of sepsis management are early antibiotics, hemodynamic resuscitation (fluids and vasopressors), and source control. In this case of urosepsis, an obstruction (e.g., kidney stone, prostatic hypertrophy) may be causing ongoing infection and bacteremia. Identifying and draining the source of infection is critical to breaking the inflammatory cycle, improving hemodynamics, and ultimately allowing the clearance of lactate and correction of the acidosis. While the other interventions might be considered, none are as fundamental as source control in reversing the underlying pathophysiology.
  3. Which of the following is the most appropriate intervention?
    Answer: Administer intravenous 5% dextrose in water (D5W) This patient has hypernatremia due to a net water deficit, likely from ongoing insensible losses and hypotonic gastrointestinal losses (diarrhea) without adequate free water replacement. The treatment for hypernatremia is to replace the free water deficit. Intravenous 5% dextrose in water (D5W) is effectively free water, as the dextrose is rapidly metabolized, and is the appropriate fluid for correction. 0.9% saline would worsen the hypernatremia. Desmopressin is used for central diabetes insipidus, which is not suggested here. Decreasing protein might help with urea-induced osmotic diuresis, but the primary issue is a water deficit that needs correction.
  4. A 44-year-old woman presents 36 hours after thyroidectomy with tingling and muscle spasms. She has stridor and is anxious. Labs:
    TestResult
    ABGpH 7.46, PaCO2 33 mm Hg, HCO3− 23 mEq/L
    Ionized Ca2+0.78 mmol/L
    K+4.1 mEq/L
    Mg2+1.8 mg/dL
    Time-sensitive context: airway symptoms are worsening, and IV access is available. Which of the following is the most appropriate initial treatment for this electrolyte imbalance?
    Answer: IV calcium gluconate administration This question tests the ability to diagnose and manage acid-base and electrolyte emergencies in critical care settings. Understanding acid-base balance is critical for managing patients with metabolic acidosis and alkalosis, as well as electrolyte imbalances like hyperkalemia or hyponatremia. In this vignette, the patient's symptoms and lab results provide crucial clues for identifying the underlying condition. The correct answer, choice A, is justified by the acute severe hypocalcemia causing laryngospasm and stridor, requiring immediate IV calcium to stabilize neuromuscular function. Choice B is incorrect due to oral calcium being insufficient for rapid correction in emergent airway-compromising symptoms. To improve student understanding, emphasize the importance of correlating clinical symptoms with laboratory findings and encourage the use of diagnostic algorithms to guide management decisions.
  5. Which of the following is the most appropriate immediate management?
    Answer: Administer a 100 mL bolus of 3% hypertonic saline This patient presents with severe, symptomatic hyponatremia (seizure), likely due to the syndrome of inappropriate antidiuretic hormone (SIADH) from her small cell lung cancer. In a patient with severe neurologic symptoms such as seizures or coma, the immediate goal is to rapidly increase the serum sodium to alleviate cerebral edema. This is achieved with an intravenous bolus of 3% hypertonic saline. Fluid restriction, normal saline, and demeclocycline are treatments for chronic or asymptomatic hyponatremia and are not appropriate for this acute emergency.
  6. Which of the following is the most likely diagnosis?
    Answer: Osmotic demyelination syndrome This patient with chronic hyponatremia experienced overly rapid correction of her serum sodium (14 mEq/L in 24 hours). The recommended safe limit for correction is typically 8-10 mEq/L in 24 hours to allow brain cells to adapt to the changing extracellular osmolality. Rapid correction can lead to osmotic demyelination syndrome (formerly central pontine myelinolysis), which presents with delayed neurologic symptoms (dysarthria, dysphagia, quadriparesis, altered mental status) 2-6 days after the osmotic injury. This clinical picture is classic for this iatrogenic complication.
  7. Which of the following is the most appropriate immediate step in management?
    Answer: Administer intravenous calcium gluconate This patient has life-threatening hyperkalemia, evidenced by the serum potassium level and significant ECG changes (widened QRS), which indicate cardiac membrane instability. The most immediate priority is to stabilize the cardiac membrane to prevent progression to ventricular fibrillation or asystole. Intravenous calcium gluconate is the first-line agent for this purpose. It does not lower the serum potassium level but acts within minutes to antagonize the cardiotoxic effects of hyperkalemia.
  8. Which of the following is the most appropriate intravenous fluid for resuscitation?
    Answer: Lactated Ringer's solution This patient has a normal anion gap metabolic acidosis (NAGMA), calculated as 138 - (115 + 15) = 8. This is characteristic of bicarbonate loss from severe diarrhea. When resuscitating a patient with NAGMA, using large volumes of 0.9% saline (which has a high chloride content) can worsen the acidosis (hyperchloremic metabolic acidosis). Lactated Ringer's is a balanced crystalloid solution; the lactate is metabolized to bicarbonate, which helps correct the acidosis, making it the preferred resuscitation fluid in this setting. D5 1/2NS is hypotonic and inappropriate for resuscitation, and 3% saline is for severe symptomatic hyponatremia.
  9. Which of the following best describes his acid-base status?
    Answer: Mixed metabolic acidosis and respiratory acidosis The patient's pH is 7.15, indicating a significant acidemia. The elevated PaCO2 of 60 mm Hg (normal ~40) indicates a primary respiratory acidosis, likely due to his severe COPD exacerbation. The low bicarbonate of 16 mEq/L (normal ~24) indicates a concurrent metabolic acidosis, consistent with DKA. In a simple metabolic acidosis, the expected respiratory compensation (Winter's formula: PaCO2 = 1.5 * HCO3 + 8 ± 2) would be a PaCO2 of approximately 32 mm Hg. Since the actual PaCO2 is much higher, there is a superimposed respiratory acidosis. Therefore, this is a mixed disorder.
  10. Which of the following is the most appropriate next step in managing her severe acidemia?
    Answer: Continue fluid resuscitation and optimize vasopressor therapy The patient has a severe high-anion-gap metabolic acidosis due to lactic acidosis from septic shock. The primary treatment for this condition is to correct the underlying cause, which is poor tissue perfusion. Therefore, continuing aggressive hemodynamic support with fluids and vasopressors to improve organ perfusion is the most critical intervention. Sodium bicarbonate is controversial in lactic acidosis as it can worsen intracellular acidosis and has not been shown to improve outcomes. Increasing minute ventilation would cause a respiratory alkalosis, which is not the primary problem. Renal replacement therapy may be needed later for renal failure but is not the immediate step to address the cause of the acidosis.
  11. After administering calcium gluconate, which of the following is the most important next step in management?
    Answer: Administer aggressive intravenous hydration and rasburicase This patient has tumor lysis syndrome (TLS), a life-threatening emergency characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia, often leading to acute kidney injury. After stabilizing the cardiac membrane with calcium, the cornerstone of management is aggressive intravenous hydration to promote renal excretion of metabolites and administration of a hypouricemic agent. Rasburicase is preferred over allopurinol in established, high-risk TLS because it rapidly breaks down existing uric acid, preventing further renal damage. Sevelamer (phosphate binder) and sodium polystyrene sulfonate are adjunctive but secondary to hydration and uric acid management.
  12. Which of the following is the most appropriate next step?
    Answer: Check and replete magnesium levels This patient has refractory hypokalemia, which is persistent hypokalemia despite adequate potassium replacement. In patients with a history of alcohol use disorder, concurrent hypomagnesemia is extremely common. Magnesium is a cofactor for the renal outer medullary potassium (ROMK) channels, which are responsible for potassium reabsorption. In the setting of hypomagnesemia, these channels are dysfunctional, leading to persistent renal potassium wasting. Therefore, repletion of magnesium is necessary to allow for effective correction of the hypokalemia.
  13. Which of the following is the most appropriate management?
    Answer: Administer intravenous potassium chloride at 10 mEq/hr via a peripheral line The patient has severe, symptomatic hypokalemia (potassium < 2.5 mEq/L) with ECG changes, which is a medical emergency requiring intravenous potassium replacement. Oral replacement is too slow for this acuity. The standard safe rate for IV potassium replacement via a peripheral line is 10 mEq/hr to avoid venous irritation and cardiac toxicity. Rates higher than 10 mEq/hr (up to 20-40 mEq/hr) require a central line and continuous cardiac monitoring, but 10 mEq/hr is the most appropriate initial choice for urgent but controlled repletion. Spironolactone would be for long-term management, not acute replacement.
  14. Which of the following is the most appropriate immediate intervention?
    Answer: Administer intravenous calcium gluconate This patient is exhibiting classic signs and symptoms of acute, symptomatic hypocalcemia (perioral paresthesias, Trousseau's sign), which is a common complication of total thyroidectomy due to iatrogenic hypoparathyroidism. Symptomatic hypocalcemia is a medical emergency that can progress to seizures, laryngospasm, and cardiac arrhythmias. The most appropriate immediate management is intravenous calcium gluconate to rapidly raise serum calcium levels and stabilize the patient. Oral calcium is for mild or chronic hypocalcemia. Awaiting lab results would dangerously delay treatment in a symptomatic patient.
  15. Which of the following is the most appropriate management for her acid-base disturbance?
    Answer: Initiate anticoagulation and provide supplemental oxygen The patient has an acute respiratory alkalosis (high pH, low PaCO2) secondary to hypoxemia and anxiety from her pulmonary embolism. The primary management of any respiratory acid-base disorder is to treat the underlying cause. In this case, the cause is the pulmonary embolism. Therefore, initiating anticoagulation and providing supplemental oxygen to correct the hypoxemia and treat the PE is the most appropriate step. Sedating the patient or having her rebreathe CO2 does not address the life-threatening underlying pathology and could be harmful.
  16. Which of the following is the most appropriate next step?
    Answer: Increase the respiratory rate on the ventilator The patient has an acute respiratory acidosis (low pH, high PaCO2), likely due to a decrease in his spontaneous respiratory drive from increased sedation, leading to decreased minute ventilation. In a patient on volume-control ventilation, the most direct way to increase minute ventilation (and thus CO2 removal) is to increase the respiratory rate. Increasing the tidal volume above 6 mL/kg is generally avoided in ARDS (lung-protective strategy). Increasing PEEP primarily affects oxygenation, not ventilation. Sodium bicarbonate does not address the underlying problem of inadequate ventilation.
  17. A 58-year-old woman with hypertension and CKD stage 3 takes lisinopril and spironolactone. She presents with progressive muscle weakness and palpitations for 2 hours. BP 148/86, HR 54. ECG shows peaked T waves and QRS widening. Labs:
    TestResult
    ABGpH 7.36, PaCO2 40 mm Hg, HCO3− 22 mEq/L
    Na+138 mEq/L
    K+7.2 mEq/L
    Cl−104 mEq/L
    BUN/Cr44/2.6 mg/dL
    Glucose118 mg/dL
    Time-sensitive context: telemetry shows intermittent runs of ventricular ectopy. Differential includes medication effect vs hemolysis vs acidosis. Management steps being considered: - Stabilize myocardium - Shift potassium intracellularly - Remove potassium from body - Stop offending agents Which of the following is the most appropriate initial treatment for this electrolyte imbalance?
    Answer: IV calcium gluconate administration This question tests the ability to diagnose and manage acid-base and electrolyte emergencies in critical care settings. Understanding acid-base balance is critical for managing patients with metabolic acidosis and alkalosis, as well as electrolyte imbalances like hyperkalemia or hyponatremia. In this vignette, the patient's symptoms and lab results provide crucial clues for identifying the underlying condition. The correct answer, choice B, is justified by the ECG changes of peaked T waves and QRS widening in hyperkalemia, requiring immediate myocardial stabilization with calcium gluconate. Choice A is incorrect due to albuterol being a temporizing measure for shifting potassium but not the initial step when ECG changes indicate urgent membrane protection. To improve student understanding, emphasize the importance of correlating clinical symptoms with laboratory findings and encourage the use of diagnostic algorithms to guide management decisions.
  18. Laboratory studies are most likely to show a severe deficiency of which of the following electrolytes?
    Answer: Phosphate This patient is experiencing refeeding syndrome, a life-threatening condition that occurs when nutrition is reintroduced in severely malnourished individuals. The sudden influx of carbohydrates stimulates insulin release, which drives phosphate, potassium, and magnesium into cells for glycolysis and ATP production. The resulting acute and profound hypophosphatemia is the hallmark of the syndrome and can cause widespread organ dysfunction, including respiratory muscle weakness leading to respiratory failure, cardiac failure, and rhabdomyolysis.
  19. Which of the following is the most likely cause of his hyponatremia?
    Answer: Administration of hypotonic fluids This patient's hyponatremia is most likely iatrogenic. Postoperative patients often have elevated levels of ADH due to surgical stress and pain. The administration of large volumes of hypotonic fluid (0.45% saline) in the setting of high ADH levels leads to free water retention and subsequent dilutional hyponatremia. While SIADH also involves high ADH, the primary iatrogenic driver here is the administration of hypotonic fluids. Cerebral salt wasting is less common and characterized by volume depletion. Adrenal insufficiency would typically present with hyperkalemia.
  20. What is the most likely cause of the initial laboratory finding?
    Answer: Pseudohyperkalemia Pseudohyperkalemia is an artificially elevated potassium level due to the in vitro release of potassium from cells during or after phlebotomy. It is a common finding in patients with extreme thrombocytosis or leukocytosis. During clotting in the collection tube, the large number of platelets release intracellular potassium, falsely elevating the measured serum level. The discrepancy between the high lab value and the normal ECG, along with the normal result from a whole blood (heparinized) sample, confirms this diagnosis. It is a lab artifact, not a true representation of the patient's in vivo potassium level.

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