Critical Events
Malignant hyperthermia, local anesthetic systemic toxicity, anaphylaxis, venous air embolism, severe hyperkalemia, can't-intubate / can't-ventilate. ← All topics
Q1. Earliest sign of malignant hyperthermia
During emergence from a sevoflurane anesthetic in a 22-year-old, the EtCO₂ rises from 38 to 62 mmHg over 10 minutes despite increased minute ventilation. Masseter rigidity is noted. The most reliable earliest clinical sign of malignant hyperthermia is:
A. Core temperature elevation above 38.5°C with ongoing rise
B. Hyperkalemia detected on arterial blood gas analysis
C. Unexplained rise in end-tidal CO₂ despite increased ventilation
D. Sinus tachycardia with heart rate exceeding baseline significantly
E. Masseter muscle rigidity following succinylcholine or volatile exposure
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Answer: C. Unexplained rising end-tidal CO₂ (or spontaneous tachypnea and breathing over the ventilator in a spontaneously ventilating patient) is the most reliable earliest sign of malignant hyperthermia. This reflects the hypermetabolic state with increased CO₂ production. Sinus tachycardia occurs early but is nonspecific and can have many other causes. Masseter rigidity can occur but is also less specific and may be seen in isolation without progression to full MH crisis. Temperature elevation and hyperkalemia are late findings that occur after the hypermetabolic process is well established. Treatment consists of dantrolene 2.5 mg/kg IV every 5 to 10 minutes up to 10 mg/kg, then 1 mg/kg every 4 to 6 hours for 24 to 48 hours, along with discontinuation of triggering agents, hyperventilation, active cooling, and treatment of hyperkalemia and acidosis.
Q2. Local anesthetic systemic toxicity management
A patient receives 0.5% bupivacaine for an interscalene block and develops seizures followed by ventricular dysrhythmia and cardiac arrest. After securing the airway, the most appropriate next step is:
A. Amiodarone 300 mg IV bolus, then 150 mg IV every 10 minutes as needed
B. Lidocaine 1.5 mg/kg IV bolus, then 0.5 mg/kg boluses every 5 minutes
C. 20% lipid emulsion 1.5 mL/kg bolus, then 0.25 mL/kg/min continuous infusion
D. Vasopressin 40 units IV bolus, then repeat 40 units every 3 minutes
E. Calcium chloride 1 g IV bolus, then 1 g IV every 10 minutes
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Answer: C. This is local anesthetic systemic toxicity (LAST) from bupivacaine. The LAST protocol calls for 20% lipid emulsion therapy: give 1.5 mL/kg bolus (approximately 100 mL in an adult) over 2 to 3 minutes, followed by 0.25 mL/kg/min continuous infusion. If the patient remains unstable, repeat the bolus and double the infusion rate to 0.5 mL/kg/min. The maximum recommended cumulative dose is 12 mL/kg. During LAST resuscitation, avoid vasopressin, calcium channel blockers, beta-blockers, and local anesthetics including lidocaine, as these can worsen cardiotoxicity or interfere with lipid rescue. If epinephrine is needed, use reduced doses of 1 mcg/kg or less to avoid impaired myocardial metabolism in the presence of lipophilic local anesthetics.
Q3. Venous air embolism detection sensitivity
During posterior fossa surgery in the sitting position, end-tidal CO₂ abruptly drops from 36 to 22 mmHg with concurrent hypotension. The single most sensitive monitor for the suspected complication is:
A. Precordial Doppler ultrasound positioned over the right atrium
B. End-tidal carbon dioxide monitoring via capnography
C. Transesophageal echocardiography with continuous imaging
D. Esophageal stethoscope listening for mill-wheel murmur
E. Pulmonary artery pressure monitoring via Swan-Ganz catheter
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Answer: C. Venous air embolism detection sensitivity ranks from most to least sensitive as follows: transesophageal echocardiography (TEE) > precordial Doppler > pulmonary artery pressure (PAP) > end-tidal CO₂ (EtCO₂) > right atrial pressure (RAP) > electrocardiogram (EKG) > esophageal stethoscope. TEE can detect air volumes as small as 0.02 mL/kg, making it the most sensitive monitor available. The precordial Doppler can detect approximately 0.05 mL/kg. Management of venous air embolism includes stopping further air entrainment by compressing the jugular veins and flooding the surgical field with saline, administering 100% FiO₂, placing the patient in Durant's position (left lateral decubitus with head down), and attempting aspiration through a central venous catheter if one is accessible.
Q4. Anaphylaxis intraoperative
Five minutes after induction with rocuronium, a patient develops urticaria, profound hypotension, bronchospasm, and SpO₂ falls to 78%. The most appropriate epinephrine dose is:
A. 1 mg IV push as initial bolus, repeat every 3–5 minutes as needed
B. 1 mcg/kg IV bolus (50–100 mcg in adults), repeat and titrate as needed
C. 0.3 mg IM into deltoid or thigh, repeat every 5–15 minutes as needed
D. 10 mcg IV bolus initially, then increase dose every 2–3 minutes as needed
E. Defer epinephrine until after 2 liters crystalloid and 100% oxygen are given
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Answer: B. Intraoperative anaphylaxis requires immediate epinephrine at 1 mcg/kg IV (50–100 mcg in adults), titrated to response and repeated as needed. This dose can be escalated up to code-dose epinephrine (10 mcg/kg) if the patient remains unstable. The 1 mg IV push dose is excessive for initial treatment and risks severe hypertension and arrhythmias. The 0.3 mg IM dose is appropriate for non-intraoperative anaphylaxis when IV access is not available, but IV titration is preferred intraoperatively. A 10 mcg initial bolus is too small for severe anaphylaxis. Delaying epinephrine to wait for fluid response is dangerous; epinephrine and fluids should be given concurrently. Concurrent management includes 100% oxygen, aggressive IV fluid resuscitation (25–50 mL/kg crystalloid), stopping the offending agent, and calling for help. Mast cell tryptase drawn at 1–2 hours can confirm the diagnosis. The most common intraoperative triggers are neuromuscular blocking drugs (succinylcholine > rocuronium), latex, antibiotics, chlorhexidine, and blood products.
Q5. Anaphylaxis triggers in anesthesia
The most common cause of perioperative anaphylaxis is:
A. Volatile anesthetic agents such as sevoflurane or desflurane
B. Neuromuscular blocking drugs such as succinylcholine or rocuronium
C. Local anesthetic agents such as lidocaine or bupivacaine
D. Opioid analgesics such as morphine or fentanyl
E. Intravenous hypnotic agents such as propofol or etomidate
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Answer: B. Neuromuscular blocking drugs are the most common cause of perioperative anaphylaxis, with succinylcholine and rocuronium being the most frequently implicated agents. The second most common cause is latex, followed by antibiotics. Cross-reactivity can occur between aminosteroid NMBDs and over-the-counter products containing quaternary ammonium compounds (found in cosmetics and toothpaste), which means patients may have pre-existing antibodies even without prior anesthetic exposure. Volatile anesthetics, local anesthetics, opioids, and propofol are much less commonly associated with true anaphylaxis, though they may cause anaphylactoid reactions or histamine release.
Q6. Hyperkalemic cardiac arrest
A patient with ESRD on hemodialysis arrives in PEA with K⁺ 7.8 on i-STAT. ACLS is in progress. The most appropriate priority among the following is:
A. Sodium bicarbonate 1 mEq/kg IV to shift potassium intracellularly by alkalinizing serum
B. Calcium chloride 1 g IV to stabilize cardiac membrane and antagonize potassium effects
C. Albuterol 10–20 mg nebulized to shift potassium intracellularly via β₂-receptor activation
D. Regular insulin 10 U IV with D50 to shift potassium intracellularly via Na-K-ATPase
E. Emergent hemodialysis to remove total body potassium and definitively correct the hyperkalemia
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Answer: B. In hyperkalemic cardiac arrest, calcium is the first priority because it stabilizes the cardiac membrane within minutes by antagonizing the effects of potassium on myocardial excitability. Critically, calcium does NOT lower serum potassium but buys time by reducing arrhythmia risk. After calcium administration, the next steps are to shift potassium intracellularly using sodium bicarbonate, insulin with glucose, and beta-2 agonists like albuterol. Finally, total body potassium removal is achieved through hemodialysis or kayexalate. The sequence is: membrane stabilization first (calcium), then intracellular shift (bicarbonate, insulin/glucose, albuterol), then definitive removal (dialysis).
Q7. Can't-intubate / can't-ventilate
In a failed mask ventilation and failed intubation scenario, after a single attempt with a supraglottic airway fails, the next definitive step is:
A. Additional intubation attempts with different laryngoscope blade
B. Emergent cricothyrotomy using scalpel-bougie-tube technique
C. Awake fiberoptic intubation after reversal of induction agents
D. Increase volatile anesthetic concentration and deepen anesthesia
E. Lateral positioning with head-down tilt for ventilation
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Answer: B. Per the ASA Difficult Airway Algorithm, the cannot-intubate/cannot-ventilate scenario with failed supraglottic airway requires immediate transition to emergency invasive airway access. Cricothyrotomy is the gold standard technique, typically performed using the scalpel-bougie-tube method. The key principle is to limit total time in this life-threatening situation; when SpO₂ falls below 80% or after a single failed supraglottic airway attempt, the clinician must transition directly to surgical airway rather than persisting with additional laryngoscopy attempts. Further intubation attempts waste critical time in a desaturating patient. Awake fiberoptic intubation is not feasible once the patient is anesthetized and hypoxemic. Deepening anesthesia worsens the situation. Repositioning does not address the failed ventilation and intubation.
Q8. Laryngospasm management
A 5-year-old develops laryngospasm during inhalation induction. After applying CPAP at 20 cm H₂O with 100% O₂ and a jaw thrust, the next step is:
A. Administer propofol 1 mg/kg IV to deepen anesthesia
B. Administer succinylcholine 4 mg/kg IM immediately
C. Administer atropine 0.02 mg/kg IV as pretreatment
D. Administer lidocaine 1 mg/kg IV to relax
E. Wait and continue CPAP with jaw thrust maneuver
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Answer: A. The laryngospasm management ladder proceeds stepwise: first apply jaw thrust with CPAP at 20 cm H₂O and 100% oxygen, then deepen anesthesia with propofol 1 mg/kg IV if laryngospasm persists. If this fails, proceed to succinylcholine 0.25–2 mg/kg IV or 4–5 mg/kg IM. Atropine 0.01–0.02 mg/kg should be given before succinylcholine in children to prevent bradycardia, but is not the next step after failed CPAP and jaw thrust. Lidocaine has no established role in acute laryngospasm management. Simply waiting after failed initial maneuvers risks hypoxemia and is inappropriate when pharmacologic deepening is indicated.
Q9. Acute hemolytic transfusion reaction
A patient receiving pRBCs develops fever, flank pain, hemoglobinuria, and hypotension within 30 minutes of transfusion start. The most likely mechanism is:
A. Cytokine release from leukocytes accumulated during storage
B. ABO incompatibility causing IgM-mediated intravascular hemolysis
C. Donor anti-leukocyte antibodies reacting with recipient leukocytes
D. IgE-mediated mast cell degranulation with histamine release
E. Bacterial contamination with endotoxin release and septic shock
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Answer: B. Acute hemolytic transfusion reaction results from ABO mismatch leading to IgM-mediated complement activation and intravascular hemolysis. The presentation of fever, flank pain, hemoglobinuria, and hypotension within 30 minutes is classic. Treatment includes immediately stopping the transfusion, supporting hemodynamics, administering generous IV fluids and diuretics to maintain urine output, treating hyperkalemia, and monitoring for DIC. Send the blood product back to the blood bank along with a fresh patient sample for retype and crossmatch and direct Coombs test. Febrile nonhemolytic reactions (choice A) cause fever but not hemoglobinuria or hypotension. TRALI (choice C) presents with respiratory distress. Anaphylaxis (choice D) causes bronchospasm and urticaria without hemoglobinuria. Bacterial contamination (choice E) can cause hypotension but typically lacks the hemoglobinuria seen with intravascular hemolysis.
Q10. TRALI vs TACO
A patient develops respiratory distress and bilateral pulmonary infiltrates within 4 hours of FFP transfusion. CVP is normal, BNP is normal. The diagnosis is:
A. Transfusion-associated circulatory overload (TACO) with cardiogenic pulmonary edema and elevated filling pressures
B. Transfusion-related acute lung injury (TRALI) with non-cardiogenic pulmonary edema and normal filling pressures
C. Anaphylactic reaction with bronchospasm, urticaria, hypotension, and elevated serum tryptase levels
D. Bacterial contamination with fever, hypotension, rigors, and positive blood cultures from transfused product
E. Acute hemolytic reaction with hemoglobinuria, flank pain, fever, and ABO incompatibility on workup
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Answer: B. This patient has TRALI, which is non-cardiogenic pulmonary edema occurring within 6 hours of transfusion. The normal CVP and BNP exclude cardiogenic causes and point away from TACO. TRALI is caused by donor anti-leukocyte antibodies, most often from multiparous female donors, which activate recipient neutrophils leading to capillary leak and pulmonary edema. Treatment includes lung-protective ventilation with low tidal volumes and supportive care. TACO presents with elevated BNP and CVP due to volume overload and responds to diuresis. The other options (anaphylaxis, bacterial contamination, hemolytic reaction) present with different clinical features not seen in this case.
Q11. Massive hemorrhage venous air
The fatal volume of air that produces an "air lock" in the right ventricle is approximately:
A. 10 mL bolus of air or 1–2 mL/kg of CO₂
B. 100 mL bolus of air or 5–7 mL/kg of CO₂
C. 300–500 mL bolus of air or 10–15 mL/kg of CO₂
D. 1000 mL bolus of air or 20–25 mL/kg of CO₂
E. Any volume above 5 mL regardless of rate
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Answer: C. The fatal volume of air that produces an air lock in the right ventricle is approximately 300–500 mL (or 3–5 mL/kg) when delivered as a bolus. Carbon dioxide is less dangerous and requires 10–15 mL/kg to produce cardiovascular collapse because it is more soluble in blood than air. Common clinical sources of venous air embolism include open neck veins during sitting craniotomy, large open wounds above heart level, central line placement or removal, and laparoscopy with CO₂ insufflation. Smaller volumes of air (0.5 mL/kg) can be detected by precordial Doppler or transesophageal echocardiography but are usually not fatal.
Q12. Pediatric bradycardia
A 4-month-old infant under sevoflurane anesthesia develops HR 75. First action:
A. Administer IV atropine 20 mcg/kg and reassess heart rate
B. Confirm adequate oxygenation and ventilation, then treat hypoxia
C. Begin chest compressions at 100-120 compressions per minute
D. Administer IV epinephrine 1 mcg/kg and reassess heart rate
E. Apply transcutaneous pacing pads and prepare for cardiac pacing
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Answer: B. Pediatric bradycardia is hypoxia until proven otherwise. The first action is to confirm adequate oxygenation and ventilation by checking the airway, ventilation quality, FiO₂, and endotracheal tube position if intubated. Hypoxia is the most common cause of bradycardia in infants and children. If heart rate remains less than 60 bpm despite 30 seconds of effective positive pressure ventilation with supplemental oxygen, then chest compressions should be initiated. Pharmacologic interventions such as atropine and epinephrine come later in the resuscitation algorithm after addressing oxygenation and ventilation.
Q13. Negative pressure pulmonary edema
A 28-year-old wrestler develops pink frothy sputum and bilateral infiltrates immediately after extubation that was preceded by 30 seconds of laryngospasm. The mechanism is:
A. Direct alveolar barotrauma from forceful inspiratory effort against a closed glottis causing membrane rupture
B. Large negative intrathoracic pressure against a closed glottis increasing venous return and decreasing LV afterload
C. Aspiration of gastric contents during laryngospasm causing chemical pneumonitis and bilateral alveolar infiltrates
D. Anaphylaxis to residual neuromuscular blocker causing increased capillary permeability and bilateral pulmonary edema
E. Cardiogenic pulmonary edema from acute LV failure due to catecholamine surge during emergence hypertension
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Answer: B. This is Type I negative pressure pulmonary edema (NPPE), which follows obstructed inspiration against a closed glottis during laryngospasm or tube biting. Forceful inspiratory effort generates large negative intrathoracic pressure (sometimes below -100 cm H₂O), which increases venous return to the right heart and simultaneously decreases left ventricular afterload. The combination leads to increased pulmonary capillary hydrostatic pressure and transudation of fluid into the alveoli. Young, muscular males are at highest risk because they can generate the most negative intrathoracic pressure. Treatment includes supplemental oxygen and PEEP or CPAP; the condition typically resolves within 24 to 48 hours. Type II NPPE occurs after relief of chronic upper airway obstruction.
Q14. Tension pneumothorax
In a mechanically ventilated patient, sudden hypotension, tracheal deviation, decreased breath sounds, and rising peak airway pressures suggest tension pneumothorax. The most appropriate immediate intervention is:
A. CT scan of the chest to confirm pneumothorax before any intervention
B. Needle thoracostomy at the 2nd intercostal space, midclavicular line
C. Bronchoscopy to evaluate for endobronchial obstruction or mucus plugging
D. Increased PEEP to improve oxygenation and recruit collapsed alveoli
E. Albuterol nebulizer to treat suspected bronchospasm causing high pressures
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Answer: B. Tension pneumothorax is a clinical diagnosis that requires immediate needle decompression without waiting for imaging confirmation. The classic approach is needle thoracostomy at the 2nd intercostal space, midclavicular line, though the 4th-5th intercostal space at the anterior axillary line is an alternative site with potentially higher success rates due to chest wall thickness. This should be followed by definitive chest tube placement. While chest X-ray can confirm the diagnosis, treatment must not be delayed in a hemodynamically unstable patient with classic clinical findings. CT scan would cause dangerous delay. Bronchoscopy does not address pneumothorax. Increasing PEEP would worsen a tension pneumothorax by increasing intrathoracic pressure. Albuterol treats bronchospasm, not pneumothorax.
Q15. Serotonin syndrome perioperative
A patient on fluoxetine, tramadol, and ondansetron develops hyperthermia, clonus, agitation, and rigidity post-anesthesia. The most likely diagnosis is:
A. Malignant hyperthermia from volatile anesthetic exposure causing muscle rigidity and hyperthermia
B. Neuroleptic malignant syndrome from antipsychotic medication causing rigidity and hyperthermia
C. Serotonin syndrome from combined serotonergic agents causing clonus and hyperthermia
D. Thyroid storm from uncontrolled hyperthyroidism causing agitation and hyperthermia
E. Anticholinergic toxicity from muscarinic blockade causing agitation and hyperthermia
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Answer: C. Serotonin syndrome presents with the classic triad of mental status changes (agitation, confusion), autonomic hyperactivity (hyperthermia, diaphoresis, tachycardia), and neuromuscular abnormalities (clonus, hyperreflexia, mydriasis). Clonus is typically more prominent in lower extremities than upper. This patient has three serotonergic agents: fluoxetine (SSRI), tramadol (weak serotonin reuptake inhibitor and releaser), and ondansetron (5-HT₃ antagonist with serotonergic effects). Other culprit drugs include meperidine, methadone, MAOIs, methylene blue, and linezolid. Treatment involves stopping all serotonergic agents, supportive care with benzodiazepines for agitation, cyproheptadine (a 5-HT₂ antagonist) as a specific antidote, and dantrolene for severe hyperthermia refractory to other measures. Malignant hyperthermia would require volatile anesthetic or succinylcholine exposure. Neuroleptic malignant syndrome requires antipsychotic use and typically has lead-pipe rigidity rather than clonus.
Q16. Methylene blue + SSRI
A patient on sertraline is given methylene blue for vasoplegic shock. Why is this combination concerning?
A. Methylene blue inhibits cytochrome P450 metabolism of sertraline leading to toxic accumulation
B. Methylene blue is a potent reversible MAOI leading to risk of serotonin syndrome
C. SSRIs prevent catecholamine release and block the vasopressor response to methylene blue
D. Methylene blue inhibits guanylate cyclase causing paradoxical worsening of vasoplegia with SSRIs
E. Both agents oxidize hemoglobin iron causing additive risk of severe methemoglobinemia
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Answer: B. Methylene blue is a reversible monoamine oxidase inhibitor (MAOI) at doses greater than 5 mg/kg, which creates a significant risk of serotonin syndrome when combined with serotonergic agents like SSRIs. Serotonin syndrome is a potentially life-threatening condition resulting from excessive serotonergic activity. If methylene blue is needed solely for ureteral identification during surgery, indigo carmine can be used as a safer alternative in patients on serotonergic medications. However, methylene blue remains an important therapeutic option for treating vasoplegic shock and methemoglobinemia when the benefits outweigh the risks, though careful monitoring is essential in patients taking SSRIs or other serotonergic agents.
Q17. Neuroleptic malignant syndrome
NMS classically presents with:
A. Hyperthermia, lead-pipe rigidity, autonomic instability, altered mental status, and elevated creatine kinase
B. Hyperthermia, clonus, hyperreflexia, mydriasis, diaphoresis, and gastrointestinal hyperactivity
C. Sudden flaccid paralysis, areflexia, sensory loss, autonomic dysfunction, and urinary retention
D. Polyuria, polydipsia, hyperglycemia, dehydration, altered mental status, and electrolyte abnormalities
E. Bradycardia, hyperthermia, dry flushed skin, urinary retention, mydriasis, and altered mental status
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Answer: A. Neuroleptic malignant syndrome (NMS) classically presents with hyperthermia, lead-pipe (not cogwheel) rigidity, autonomic instability, altered mental status, and elevated creatine kinase in a patient taking dopamine antagonists such as haloperidol, metoclopramide, or prochlorperazine. NMS results from D2 receptor antagonism and has a slower onset than serotonin syndrome. Treatment includes stopping the offending drug, supportive care, bromocriptine (a D2 agonist), and dantrolene for muscle rigidity. Choice B describes serotonin syndrome. Choice C describes acute spinal cord injury or Guillain-Barré syndrome. Choice D describes diabetic ketoacidosis or hyperosmolar hyperglycemic state. Choice E mixes anticholinergic toxidrome features with bradycardia, which is inconsistent.
Q18. Carcinoid crisis
During induction for tumor debulking in a patient with metastatic carcinoid, severe hypotension, bronchospasm, and flushing develop. The most appropriate immediate management is:
A. Epinephrine 1 mg IV bolus to treat refractory hypotension and bronchospasm
B. Octreotide 100 mcg IV bolus to inhibit mediator release from tumor
C. Phenylephrine infusion to restore systemic vascular resistance and blood pressure
D. Diphenhydramine and steroids to block histamine receptors and reduce inflammation
E. β-blocker administration to control tachycardia and reduce myocardial oxygen demand
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Answer: B. Carcinoid crisis results from massive tumor release of vasoactive mediators including serotonin, histamine, and kallikrein. The key pathophysiologic feature is that β-agonists such as epinephrine and ephedrine can paradoxically worsen hypotension by stimulating kallikrein release, which generates bradykinin and causes profound vasodilation. Octreotide is the first-line treatment because it directly inhibits mediator release from carcinoid tumor cells. Standard practice includes preoperative prophylaxis with octreotide 100 mcg subcutaneously three times daily for several days before surgery, plus a 100 mcg infusion intraoperatively. Pure α-agonists like phenylephrine may be used for blood pressure support but do not address the underlying mediator release. Antihistamines and steroids are insufficient for acute crisis management.
Q19. Hyperkalemia ECG progression
The earliest ECG sign of hyperkalemia is:
A. Sine wave pattern with loss of all discrete waveforms
B. Peaked T waves with narrow base and increased amplitude
C. Wide QRS complexes with increased duration beyond 120 ms
D. Loss of P waves with absent atrial depolarization
E. PR prolongation with first-degree atrioventricular block pattern
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Answer: B. The earliest ECG sign of hyperkalemia is peaked T waves with narrow base and increased amplitude. Hyperkalemia ECG changes follow a predictable progression as potassium levels rise: peaked T waves appear first, followed by PR prolongation and short QT interval, then P wave flattening, then QRS widening, then sine wave pattern, and finally asystole or ventricular fibrillation. Treatment is guided by severity: for peaked T waves or potassium greater than 6.5 mEq/L, shift potassium intracellularly; for additional ECG changes or potassium greater than 7 mEq/L, stabilize the membrane with calcium, shift potassium intracellularly, and remove potassium from the body.
Q20. Aspiration risk factors
Risk factors for clinically significant aspiration pneumonitis (Mendelson syndrome) include:
A. Gastric volume >0.4 mL/kg, pH <2.5, presence of particulates
B. Gastric volume >0.2 mL/kg, pH <3.5, presence of bile
C. Gastric volume >0.1 mL/kg, pH <4.0, regardless of particulates
D. Gastric volume >0.3 mL/kg, pH <5.0, presence of blood
E. Gastric volume >0.5 mL/kg, pH <1.5, solid food only
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Answer: A. Mendelson syndrome (clinically significant aspiration pneumonitis) occurs when three criteria are met: aspirate volume greater than 0.4 mL/kg, pH less than 2.5, and presence of particulate matter. The combination of adequate volume, high acidity, and particulates creates the chemical pneumonitis that defines this syndrome. Modern fasting guidelines to reduce aspiration risk recommend clear liquids 2 hours, breast milk 4 hours, formula or light meal 6 hours, and fatty meal 8 hours before elective surgery. The other options present incorrect threshold values for volume, pH, or particulate requirements that do not meet established Mendelson criteria.