Pharmacology Quiz: Qt Prolongation And Torsades Risk
20 questions · exam conditions
0:00
Qt Prolongation And Torsades RiskQuestion 1 of 20

A physician is reviewing ECGs for two patients. Patient A has a heart rate of 50 bpm and a QT interval of 470 ms. Patient B has a heart rate of 100 bpm and a QT interval of 410 ms. Using Bazett's formula (QTc = QT / √RR), which patient has a more concerning corrected QT interval?

Patient A, because bradycardia itself is a risk factor for Torsades de Pointes.
Patient B, because Bazett's formula over-corrects at high heart rates, revealing a significantly prolonged QTc.
Patient A, because Bazett's formula under-corrects at low heart rates, revealing a significantly prolonged QTc.
Both patients have a similarly concerning QTc of approximately 470 ms after correction.
← Back to quizzes

Pharmacology Quiz

Pharmacology Quiz: Qt Prolongation And Torsades Risk

Practice Qt Prolongation And Torsades Risk in Pharmacology with focused quiz questions that help you check what you know, review explanations, and build confidence with test-style prompts.

What this quiz covers

This quiz focuses on Qt Prolongation And Torsades Risk, giving you a quick way to practice the rules, question types, and explanations that matter most for Pharmacology.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

All questions

Question 1

A physician is reviewing ECGs for two patients. Patient A has a heart rate of 50 bpm and a QT interval of 470 ms. Patient B has a heart rate of 100 bpm and a QT interval of 410 ms. Using Bazett's formula (QTc = QT / √RR), which patient has a more concerning corrected QT interval?

  1. Patient A, because bradycardia itself is a risk factor for Torsades de Pointes.
  2. Patient B, because Bazett's formula over-corrects at high heart rates, revealing a significantly prolonged QTc. (correct answer)
  3. Patient A, because Bazett's formula under-corrects at low heart rates, revealing a significantly prolonged QTc.
  4. Both patients have a similarly concerning QTc of approximately 470 ms after correction.
Explanation: This question requires a two-step analysis: calculation and interpretation. First, calculate the QTc for each patient. The RR interval in seconds is 60/HR. For Patient A (HR=50): RR = 1.2 s. QTc = 470 / √1.2 ≈ 429 ms. For Patient B (HR=100): RR = 0.6 s. QTc = 410 / √0.6 ≈ 529 ms. Patient B has a markedly prolonged QTc (>500 ms), which is highly concerning for TdP risk. This illustrates a key limitation of Bazett's formula: it tends to over-correct for tachycardia, but in doing so, it correctly identifies the high-risk patient in this scenario.

Question 2

During preclinical testing, a new antiarrhythmic drug is found to be a potent blocker of the I_Kr channel. However, it is also discovered to have moderate blocking effects on the late sodium current (I_Na-late) and the L-type calcium current (I_CaL). How would this multi-channel effect likely alter its clinical risk profile compared to a pure I_Kr blocker like dofetilide?

  1. It would have a significantly higher risk of Torsades de Pointes (TdP).
  2. It would lose all antiarrhythmic efficacy due to conflicting channel effects.
  3. It would have a greater effect on the PR interval than the QT interval.
  4. It would have a similar or potentially lower risk of TdP. (correct answer)
Explanation: When evaluating antiarrhythmic drugs that block multiple ion channels, you need to understand how different channel effects interact to influence proarrhythmic risk, particularly for Torsades de Pointes (TdP). The correct answer is D because this multi-channel blocker would likely have similar or lower TdP risk compared to pure I_Kr blockers like dofetilide. Here's why: While I_Kr blockade prolongs repolarization and increases TdP risk, blocking late sodium current (I_Na-late) actually shortens action potential duration and reduces early afterdepolarizations - a key TdP trigger. Additionally, L-type calcium channel blockade reduces calcium overload and further decreases the likelihood of triggered arrhythmias. These opposing effects on repolarization create a more balanced electrophysiological profile. Option A is incorrect because the additional channel blocks would counteract, not amplify, the proarrhythmic effects of I_Kr blockade. The late sodium and calcium channel effects actually provide protective mechanisms against TdP. Option B is wrong because conflicting channel effects don't eliminate antiarrhythmic efficacy - they can actually create more comprehensive rhythm control while reducing adverse effects. Many successful antiarrhythmics work through multiple mechanisms. Option C is incorrect because I_Kr blockade primarily affects ventricular repolarization (QT interval), not atrioventricular conduction (PR interval). The described channel combination wouldn't shift the primary effect from QT to PR interval prolongation. Remember: Multi-channel antiarrhythmics often have improved safety profiles because complementary mechanisms can offset individual channel risks. Pure channel blockers frequently carry higher proarrhythmic risk than balanced multi-channel agents.

Question 3

A 45-year-old man on methadone maintenance therapy presents with palpitations. An ECG shows a QTc of 510 ms. He reports no changes to his methadone dose but mentions he recently started taking a new over-the-counter supplement to 'help with his stomach.'

Which of the following supplements is most likely responsible for the patient's increased QTc interval?

  1. St. John's Wort
  2. Cimetidine (correct answer)
  3. Ginkgo biloba
  4. Echinacea
Explanation: Methadone is metabolized primarily by CYP3A4 and CYP2B6. Cimetidine, an H2-receptor antagonist available over-the-counter for heartburn, is a moderate inhibitor of several CYP enzymes, including CYP3A4. By inhibiting methadone's metabolism, cimetidine can lead to increased plasma concentrations of methadone, potentiating its QT-prolonging effect. St. John's Wort is a CYP3A4 inducer and would likely lower methadone levels. Ginkgo and Echinacea do not have a well-established, clinically significant interaction of this type.

Question 4

Hypokalemia is a well-established risk factor for Torsades de Pointes (TdP), especially in patients taking I_Kr blocking drugs. What is the primary electrophysiological mechanism by which low extracellular potassium potentiates the effects of these drugs?

  1. Low potassium alters the hERG channel conformation, increasing drug binding affinity. (correct answer)
  2. Low potassium causes hyperpolarization, which increases the driving force for calcium entry.
  3. Low potassium upregulates the synthesis of new hERG channels in the sarcolemma.
  4. Low potassium directly inhibits the Na+/K+-ATPase pump, leading to sodium overload.
Explanation: When you encounter questions about Torsades de Pointes and hypokalemia, focus on the molecular mechanisms of how potassium affects ion channel function, particularly the hERG channel that mediates the delayed rectifier potassium current (I_Kr). The correct answer is A because low extracellular potassium fundamentally alters hERG channel structure through conformational changes. The hERG channel's outer vestibule contains high-affinity potassium binding sites that are crucial for normal channel gating. When extracellular potassium is reduced, these binding sites become less occupied, causing the channel to adopt a conformation that has dramatically increased affinity for I_Kr blocking drugs. This means drugs that might cause minimal QT prolongation at normal potassium levels become much more potent blockers during hypokalemia, significantly increasing TdP risk. Option B is incorrect because hypokalemia actually causes depolarization of the resting membrane potential, not hyperpolarization, and this mechanism doesn't explain the specific drug interaction effect. Option C misses the mark entirely—the issue isn't about channel synthesis or upregulation, but about immediate conformational effects on existing channels. Option D describes a secondary effect that doesn't directly explain why I_Kr blocking drugs become more potent during hypokalemia. Study tip: Remember that hypokalemia enhances drug-induced QT prolongation through a "conformational trap"—low potassium changes the hERG channel shape to create a higher-affinity binding site for drugs. This is why maintaining normal potassium levels is critical when prescribing any QT-prolonging medication.

Question 5

A 68-year-old female with a history of paroxysmal atrial fibrillation and major depressive disorder is treated with citalopram 40 mg daily. Her cardiologist plans to initiate antiarrhythmic therapy. Her baseline QTc is 465 ms. The options considered are flecainide and sotalol.

Given the patient's current medication and baseline QTc, which of the following represents the most significant concern regarding the initiation of one of these antiarrhythmics?

  1. Flecainide will cause a significant increase in the QRS duration, which is additive to the QTc prolongation from citalopram.
  2. Sotalol's beta-blocking properties will be antagonized by citalopram, reducing its antiarrhythmic efficacy.
  3. The combination of sotalol and citalopram creates a high risk for Torsades de Pointes due to their additive I_Kr blocking effects. (correct answer)
  4. Flecainide is a potent inhibitor of CYP2D6, which will lead to toxic levels of citalopram and subsequent QT prolongation.
Explanation: Both sotalol (a Class III antiarrhythmic) and citalopram are known to prolong the QT interval, primarily through blockade of the I_Kr potassium channel. Using them concurrently creates an additive pharmacodynamic effect, significantly increasing the risk of excessive QT prolongation and Torsades de Pointes (TdP), especially in a patient with a borderline-high baseline QTc.

Question 6

A 71-year-old female with congestive heart failure (EF 30%) is being treated with furosemide. She is admitted for a ventricular arrhythmia, and the physician is considering initiating dofetilide. Which of the following electrolyte abnormalities would most significantly potentiate the risk of dofetilide-induced Torsades de Pointes?

  1. Hyperkalemia (K+ = 5.8 mEq/L)
  2. Hyponatremia (Na+ = 129 mEq/L)
  3. Hypomagnesemia (Mg2+ = 1.3 mg/dL) (correct answer)
  4. Hypercalcemia (Ca2+ = 11.2 mg/dL)
Explanation: Both hypokalemia and hypomagnesemia are major risk factors for Torsades de Pointes, particularly in the presence of QT-prolonging drugs like dofetilide. Hypomagnesemia impairs the function of multiple ion channels and transport systems critical for repolarization and can predispose to early afterdepolarizations. Hypokalemia directly enhances the blocking effect of drugs on the I_Kr channel. Among the choices, hypomagnesemia is a critical and common risk factor, often co-occurring with hypokalemia in patients on diuretics like furosemide.

Question 7

The QT-prolonging effect of Class III antiarrhythmics like sotalol and dofetilide is most pronounced at slower heart rates. This phenomenon is known as 'reverse use-dependence'. In which clinical scenario would this property be most concerning?

  1. A patient with atrial fibrillation with a rapid ventricular response.
  2. A patient experiencing sinus bradycardia during sleep. (correct answer)
  3. A patient undergoing an exercise stress test.
  4. A patient with paroxysmal supraventricular tachycardia.
Explanation: Reverse use-dependence means that the drug has a greater effect (in this case, more I_Kr channel blockade and more action potential prolongation) at slower heart rates. Bradycardia allows more time for the drug to bind to the channel in its resting/open state. Therefore, the risk of excessive QT prolongation and TdP is highest during periods of low heart rate, such as sleep-associated sinus bradycardia. During tachycardia (atrial fibrillation with RVR, exercise, PSVT), the channel block is less pronounced.

Question 8

A 55-year-old male with schizophrenia is treated with haloperidol. He develops community-acquired pneumonia and is prescribed clarithromycin. Several days later, he experiences a syncopal episode and an ECG reveals Torsades de Pointes. The combination of these two drugs likely precipitated this event through which shared mechanism?

  1. Inhibition of the rapid component of the delayed rectifier potassium current (I_Kr). (correct answer)
  2. Blockade of fast inward sodium channels (I_Na), leading to slowed conduction.
  3. Synergistic inhibition of the CYP3A4 enzyme, leading to haloperidol toxicity.
  4. Activation of L-type calcium channels (I_CaL), causing early afterdepolarizations.
Explanation: The primary mechanism by which most drugs cause QT prolongation and increase the risk for TdP is by blocking the rapid component of the delayed rectifier potassium current (I_Kr), which is crucial for ventricular repolarization. Both haloperidol and clarithromycin are well-known I_Kr blockers. Their concurrent use leads to an additive effect on QT prolongation. While clarithromycin is a CYP3A4 inhibitor and could increase haloperidol levels (a pharmacokinetic interaction), the core pharmacodynamic mechanism causing TdP is I_Kr blockade.

Question 9

A 24-year-old female is diagnosed with Long QT Syndrome Type 2 (LQT2) following a genetic workup after a syncopal episode. This condition is caused by a loss-of-function mutation in the KCNH2 gene. Which of the following medications would be most hazardous for this patient?

  1. Metoprolol
  2. Verapamil
  3. Lidocaine
  4. Erythromycin (correct answer)
Explanation: The KCNH2 gene (also known as hERG) encodes the alpha subunit of the potassium channel responsible for the I_Kr current. Patients with LQT2 have a reduced baseline I_Kr function. Erythromycin is an antibiotic known to block the I_Kr channel. Administering an I_Kr blocker to a patient with a pre-existing genetic defect in this same channel would result in a profound reduction of repolarizing current, creating an extremely high risk for Torsades de Pointes. Metoprolol (a beta-blocker) is actually used to treat LQTS. Verapamil (calcium channel blocker) and lidocaine (sodium channel blocker) do not primarily target the I_Kr channel.

Question 10

A patient on methadone for opioid use disorder develops onychomycosis. Their physician is considering prescribing an oral antifungal.

Which of the following antifungal agents would pose the greatest risk for a serious cardiac arrhythmia in this patient?

  1. Terbinafine
  2. Nystatin
  3. Fluconazole (correct answer)
  4. Griseofulvin
Explanation: This scenario involves a critical drug-drug interaction. Methadone is a known QT-prolonging agent that is primarily metabolized by CYP3A4. Fluconazole is an azole antifungal that is also a known QT-prolonging agent and a potent inhibitor of CYP3A4. Co-administration would lead to a dangerous interaction on two levels: 1) a pharmacokinetic interaction where fluconazole inhibits methadone metabolism, increasing its concentration and QT effect, and 2) a pharmacodynamic interaction where both drugs have additive QT-prolonging effects. Terbinafine, nystatin, and griseofulvin have a much lower risk of this specific interaction.

Question 11

Amiodarone is known to cause more significant QT interval prolongation than many other antiarrhythmics, yet it has a relatively low incidence of Torsades de Pointes (TdP). Which property of amiodarone best accounts for this paradoxical safety profile?

  1. Amiodarone exhibits 'reverse use-dependence,' meaning its QT-prolonging effects are diminished at slower heart rates.
  2. Its primary metabolite, desethylamiodarone, antagonizes the I_Kr blocking effects of the parent drug.
  3. Amiodarone also blocks sodium and calcium channels, which reduces transmural dispersion of repolarization. (correct answer)
  4. The drug's extensive tissue distribution leads to low peak plasma concentrations, preventing critical channel blockade.
Explanation: The relatively low TdP risk with amiodarone, despite significant QT prolongation, is attributed to its complex pharmacology. In addition to blocking I_Kr, amiodarone also blocks inactivated sodium channels and L-type calcium channels. This multi-channel blockade is thought to create a more homogeneous prolongation of the action potential across the ventricular wall (i.e., less transmural dispersion of repolarization), which is a key substrate for TdP. This protective effect counteracts the risk from I_Kr blockade alone.

Question 12

Amiodarone is known to cause more significant QT interval prolongation than many other antiarrhythmics, yet it has a relatively low incidence of Torsades de Pointes (TdP). Which property of amiodarone best accounts for this paradoxical safety profile?

  1. Amiodarone exhibits 'reverse use-dependence,' meaning its QT-prolonging effects are diminished at slower heart rates.
  2. Its primary metabolite, desethylamiodarone, antagonizes the I_Kr blocking effects of the parent drug.
  3. Amiodarone also blocks sodium and calcium channels, which reduces transmural dispersion of repolarization. (correct answer)
  4. The drug's extensive tissue distribution leads to low peak plasma concentrations, preventing critical channel blockade.
Explanation: The relatively low TdP risk with amiodarone, despite significant QT prolongation, is attributed to its complex pharmacology. In addition to blocking I_Kr, amiodarone also blocks inactivated sodium channels and L-type calcium channels. This multi-channel blockade is thought to create a more homogeneous prolongation of the action potential across the ventricular wall (i.e., less transmural dispersion of repolarization), which is a key substrate for TdP. This protective effect counteracts the risk from I_Kr blockade alone.

Question 13

A 71-year-old female with congestive heart failure (EF 30%) is being treated with furosemide. She is admitted for a ventricular arrhythmia, and the physician is considering initiating dofetilide. Which of the following electrolyte abnormalities would most significantly potentiate the risk of dofetilide-induced Torsades de Pointes?

  1. Hyperkalemia (K+ = 5.8 mEq/L)
  2. Hyponatremia (Na+ = 129 mEq/L)
  3. Hypomagnesemia (Mg2+ = 1.3 mg/dL) (correct answer)
  4. Hypercalcemia (Ca2+ = 11.2 mg/dL)
Explanation: Both hypokalemia and hypomagnesemia are major risk factors for Torsades de Pointes, particularly in the presence of QT-prolonging drugs like dofetilide. Hypomagnesemia impairs the function of multiple ion channels and transport systems critical for repolarization and can predispose to early afterdepolarizations. Hypokalemia directly enhances the blocking effect of drugs on the I_Kr channel. Among the choices, hypomagnesemia is a critical and common risk factor, often co-occurring with hypokalemia in patients on diuretics like furosemide.

Question 14

A patient in the intensive care unit develops Torsades de Pointes after receiving an intravenous dose of haloperidol for acute agitation. The patient is hemodynamically unstable.

After stopping the offending agent and initiating defibrillation for instability, which pharmacological intervention is the most appropriate next step in management?

  1. Intravenous amiodarone 150 mg bolus
  2. Intravenous magnesium sulfate 2 g (correct answer)
  3. Intravenous lidocaine 100 mg
  4. Intravenous procainamide infusion
Explanation: The first-line pharmacological treatment for Torsades de Pointes, regardless of the patient's baseline magnesium level, is intravenous magnesium sulfate. Magnesium is thought to stabilize the cardiac membrane and may block the influx of calcium, which helps to terminate the early afterdepolarizations that trigger TdP. Administering other antiarrhythmics like amiodarone or procainamide that also prolong the QT interval would be contraindicated and could worsen the arrhythmia. Lidocaine is generally ineffective for TdP.

Question 15

A 24-year-old female is diagnosed with Long QT Syndrome Type 2 (LQT2) following a genetic workup after a syncopal episode. This condition is caused by a loss-of-function mutation in the KCNH2 gene. Which of the following medications would be most hazardous for this patient?

  1. Metoprolol
  2. Verapamil
  3. Lidocaine
  4. Erythromycin (correct answer)
Explanation: The KCNH2 gene (also known as hERG) encodes the alpha subunit of the potassium channel responsible for the I_Kr current. Patients with LQT2 have a reduced baseline I_Kr function. Erythromycin is an antibiotic known to block the I_Kr channel. Administering an I_Kr blocker to a patient with a pre-existing genetic defect in this same channel would result in a profound reduction of repolarizing current, creating an extremely high risk for Torsades de Pointes. Metoprolol (a beta-blocker) is actually used to treat LQTS. Verapamil (calcium channel blocker) and lidocaine (sodium channel blocker) do not primarily target the I_Kr channel.

Question 16

The QT-prolonging effect of Class III antiarrhythmics like sotalol and dofetilide is most pronounced at slower heart rates. This phenomenon is known as 'reverse use-dependence'. In which clinical scenario would this property be most concerning?

  1. A patient with atrial fibrillation with a rapid ventricular response.
  2. A patient experiencing sinus bradycardia during sleep. (correct answer)
  3. A patient undergoing an exercise stress test.
  4. A patient with paroxysmal supraventricular tachycardia.
Explanation: Reverse use-dependence means that the drug has a greater effect (in this case, more I_Kr channel blockade and more action potential prolongation) at slower heart rates. Bradycardia allows more time for the drug to bind to the channel in its resting/open state. Therefore, the risk of excessive QT prolongation and TdP is highest during periods of low heart rate, such as sleep-associated sinus bradycardia. During tachycardia (atrial fibrillation with RVR, exercise, PSVT), the channel block is less pronounced.

Question 17

During preclinical testing, a new antiarrhythmic drug is found to be a potent blocker of the I_Kr channel. However, it is also discovered to have moderate blocking effects on the late sodium current (I_Na-late) and the L-type calcium current (I_CaL). How would this multi-channel effect likely alter its clinical risk profile compared to a pure I_Kr blocker like dofetilide?

  1. It would have a significantly higher risk of Torsades de Pointes (TdP).
  2. It would lose all antiarrhythmic efficacy due to conflicting channel effects.
  3. It would have a greater effect on the PR interval than the QT interval.
  4. It would have a similar or potentially lower risk of TdP. (correct answer)
Explanation: When evaluating antiarrhythmic drugs that block multiple ion channels, you need to understand how different channel effects interact to influence proarrhythmic risk, particularly for Torsades de Pointes (TdP). The correct answer is D because this multi-channel blocker would likely have similar or lower TdP risk compared to pure I_Kr blockers like dofetilide. Here's why: While I_Kr blockade prolongs repolarization and increases TdP risk, blocking late sodium current (I_Na-late) actually shortens action potential duration and reduces early afterdepolarizations - a key TdP trigger. Additionally, L-type calcium channel blockade reduces calcium overload and further decreases the likelihood of triggered arrhythmias. These opposing effects on repolarization create a more balanced electrophysiological profile. Option A is incorrect because the additional channel blocks would counteract, not amplify, the proarrhythmic effects of I_Kr blockade. The late sodium and calcium channel effects actually provide protective mechanisms against TdP. Option B is wrong because conflicting channel effects don't eliminate antiarrhythmic efficacy - they can actually create more comprehensive rhythm control while reducing adverse effects. Many successful antiarrhythmics work through multiple mechanisms. Option C is incorrect because I_Kr blockade primarily affects ventricular repolarization (QT interval), not atrioventricular conduction (PR interval). The described channel combination wouldn't shift the primary effect from QT to PR interval prolongation. Remember: Multi-channel antiarrhythmics often have improved safety profiles because complementary mechanisms can offset individual channel risks. Pure channel blockers frequently carry higher proarrhythmic risk than balanced multi-channel agents.

Question 18

Hypokalemia is a well-established risk factor for Torsades de Pointes (TdP), especially in patients taking I_Kr blocking drugs. What is the primary electrophysiological mechanism by which low extracellular potassium potentiates the effects of these drugs?

  1. Low potassium alters the hERG channel conformation, increasing drug binding affinity. (correct answer)
  2. Low potassium causes hyperpolarization, which increases the driving force for calcium entry.
  3. Low potassium upregulates the synthesis of new hERG channels in the sarcolemma.
  4. Low potassium directly inhibits the Na+/K+-ATPase pump, leading to sodium overload.
Explanation: When you encounter questions about Torsades de Pointes and hypokalemia, focus on the molecular mechanisms of how potassium affects ion channel function, particularly the hERG channel that mediates the delayed rectifier potassium current (I_Kr). The correct answer is A because low extracellular potassium fundamentally alters hERG channel structure through conformational changes. The hERG channel's outer vestibule contains high-affinity potassium binding sites that are crucial for normal channel gating. When extracellular potassium is reduced, these binding sites become less occupied, causing the channel to adopt a conformation that has dramatically increased affinity for I_Kr blocking drugs. This means drugs that might cause minimal QT prolongation at normal potassium levels become much more potent blockers during hypokalemia, significantly increasing TdP risk. Option B is incorrect because hypokalemia actually causes depolarization of the resting membrane potential, not hyperpolarization, and this mechanism doesn't explain the specific drug interaction effect. Option C misses the mark entirely—the issue isn't about channel synthesis or upregulation, but about immediate conformational effects on existing channels. Option D describes a secondary effect that doesn't directly explain why I_Kr blocking drugs become more potent during hypokalemia. Study tip: Remember that hypokalemia enhances drug-induced QT prolongation through a "conformational trap"—low potassium changes the hERG channel shape to create a higher-affinity binding site for drugs. This is why maintaining normal potassium levels is critical when prescribing any QT-prolonging medication.

Question 19

A 62-year-old woman with depression is treated with citalopram. Her dose was recently increased from 20 mg to 60 mg daily due to an incomplete response. An ECG performed one week later shows a QTc of 525 ms, increased from a baseline of 450 ms.

What is the most appropriate management step for this patient?

  1. Add a beta-blocker such as propranolol to mitigate the risk of arrhythmia.
  2. Immediately reduce the citalopram dose to a maximum of 20 mg daily. (correct answer)
  3. Continue the current dose but monitor serum potassium and magnesium levels weekly.
  4. Switch to another SSRI with similar QT prolongation potential, such as escitalopram.
Explanation: Citalopram causes dose-dependent QT prolongation. The FDA has issued a warning against doses exceeding 40 mg/day (and 20 mg/day in patients >60 years old, with hepatic impairment, or on CYP2C19 inhibitors) due to an increased risk of TdP. A QTc >500 ms is a significant warning sign. The most appropriate action is to immediately reduce the dose to within the recommended range (20 mg for this patient >60) and reassess the ECG. While adding a beta-blocker or monitoring electrolytes is part of risk management, neither addresses the primary issue of drug overdose. Switching to escitalopram is not ideal as it also prolongs QT (max dose 10 mg in this population).

Question 20

A patient presents with a wide-complex tachycardia on the cardiac monitor. Which of the following ECG findings would most specifically suggest Torsades de Pointes (TdP) rather than monomorphic ventricular tachycardia (VT)?

  1. A heart rate greater than 150 beats per minute.
  2. A QRS duration greater than 160 milliseconds.
  3. A cyclical, progressive change in the QRS axis and morphology. (correct answer)
  4. The presence of atrioventricular (AV) dissociation.
Explanation: The pathognomonic feature of Torsades de Pointes ('twisting of the points') is the progressive, cyclical change in the QRS complex's amplitude and axis, appearing as if it is twisting around the isoelectric baseline. While both TdP and monomorphic VT are wide-complex tachycardias and can have rates >150 bpm and AV dissociation, the QRS morphology in monomorphic VT remains uniform. The 'twisting' appearance is specific to TdP.