Antiarrhythmic classification and mechanisms US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Antiarrhythmic classification and mechanisms. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Antiarrhythmic classification and mechanisms US Medical PG Question 1: A molecular biologist is studying the roles of different types of ion channels regulating cardiac excitation. He identifies a voltage-gated calcium channel in the sinoatrial node, which is also present throughout the myocardium. The channel is activated at ~ -40 mV of membrane potential, undergoes voltage-dependent inactivation, and is highly sensitive to nifedipine. Which of the following phases of the action potential in the sinoatrial node is primarily mediated by ion currents through the channel that the molecular biologist is studying?
- A. Phase 2
- B. Phase 3
- C. Phase 1
- D. Phase 4
- E. Phase 0 (Correct Answer)
Antiarrhythmic classification and mechanisms Explanation: ***Phase 0***
- The description of the channel (**activated at -40 mV**, **voltage-dependent inactivation**, sensitive to **nifedipine**) points to an **L-type calcium channel**.
- In the **sinoatrial node**, **L-type calcium channels** are primarily responsible for the **Phase 0 depolarization** (upstroke) of the action potential.
*Phase 2*
- In **myocardial cells**, **Phase 2** (plateau phase) is primarily mediated by **L-type calcium channels**, but the question refers to the **sinoatrial node action potential**.
- **Sinoatrial node cells** typically lack a distinct **Phase 2** plateau, distinguishing them from ventricular myocytes.
*Phase 3*
- **Phase 3** (repolarization) in the **sinoatrial node** is primarily mediated by the **efflux of potassium ions** through various **potassium channels**.
- The described channel, being a **calcium channel**, would contribute to depolarization rather than repolarization.
*Phase 1*
- **Phase 1** (initial repolarization) is characteristic of **ventricular myocytes** and is mediated by a transient outward **potassium current (Ito)**.
- The **sinoatrial node** action potential typically lacks a distinct **Phase 1**, as it does not have this rapid initial repolarization.
*Phase 4*
- **Phase 4** (spontaneous depolarization) in the **sinoatrial node** is primarily driven by the "funny" current (**If**, carried by **HCN channels**) and a gradually increasing **calcium current** (mainly through **T-type calcium channels**), leading to the threshold for **Phase 0**.
- While L-type channels contribute to reaching the threshold, their primary role is the rapid depolarization of **Phase 0**.
Antiarrhythmic classification and mechanisms US Medical PG Question 2: A 54-year-old man comes to the emergency department because of episodic palpitations for the past 12 hours. He has no chest pain. He has coronary artery disease and type 2 diabetes mellitus. His current medications include aspirin, insulin, and atorvastatin. His pulse is 155/min and blood pressure is 116/77 mm Hg. Physical examination shows no abnormalities. An ECG shows monomorphic ventricular tachycardia. An amiodarone bolus and infusion is given, and the ventricular tachycardia converts to normal sinus rhythm. He is discharged home with oral amiodarone. Which of the following is the most likely adverse effect associated with long-term use of this medication?
- A. Angle-closure glaucoma
- B. Hepatic adenoma
- C. Shortened QT interval on ECG
- D. Progressive multifocal leukoencephalopathy
- E. Chronic interstitial pneumonitis (Correct Answer)
Antiarrhythmic classification and mechanisms Explanation: ***Chronic interstitial pneumonitis***
- **Amiodarone** is known to cause several dose-dependent adverse effects, including **pulmonary toxicity** in the form of **interstitial pneumonitis** or fibrosis.
- This adverse effect can manifest as progressive dyspnea, cough, and infiltrates on chest imaging, requiring careful monitoring during long-term use.
*Angle-closure glaucoma*
- While some medications can cause **angle-closure glaucoma**, it is **not a classic or common adverse effect of amiodarone**.
- **Topiramate** and **sulfonamides** are more commonly associated with acute angle-closure glaucoma.
*Hepatic adenoma*
- **Hepatic adenomas** are typically associated with **oral contraceptive use** and sometimes **anabolic steroid use**, not amiodarone.
- Amiodarone can cause **hepatic toxicity** (elevated transaminases, hepatitis), but not specifically hepatic adenoma.
*Shortened QT interval on ECG*
- **Amiodarone** is a Class III antiarrhythmic drug that **prolongs the QT interval** by blocking potassium channels, which is its mechanism of action for suppressing arrhythmias.
- Therefore, a shortened QT interval is the **opposite of what would be expected with amiodarone use**.
*Progressive multifocal leukoencephalopathy*
- **Progressive multifocal leukoencephalopathy (PML)** is a rare, severe opportunistic infection of the brain caused by the **JC virus**, typically seen in immunocompromised individuals.
- It is **not an adverse effect of amiodarone**; drugs like natalizumab or rituximab, which affect the immune system, are associated with PML.
Antiarrhythmic classification and mechanisms US Medical PG Question 3: An investigator is comparing the risk of adverse effects among various antiarrhythmic medications. One of the drugs being studied primarily acts by blocking the outward flow of K+ during myocyte repolarization. Further investigation shows that the use of this drug is associated with a lower rate of ventricular tachycardia, ventricular fibrillation, and torsades de pointes when compared to similar drugs. Which of the following drugs is most likely being studied?
- A. Verapamil
- B. Procainamide
- C. Esmolol
- D. Amiodarone (Correct Answer)
- E. Sotalol
Antiarrhythmic classification and mechanisms Explanation: ***Amiodarone***
- Amiodarone is a **Class III antiarrhythmic drug** that primarily blocks **potassium channels**, thereby prolonging repolarization and the effective refractory period in cardiac myocytes.
- While it has properties of all four Vaughn-Williams classes, its dominant action as a potassium channel blocker makes it highly effective in preventing and treating various arrhythmias, including **ventricular tachycardia (VT)** and **ventricular fibrillation (VF)**, and it has a relatively lower risk of **torsades de pointes (TdP)** compared to other Class III drugs due to its broader ion channel effects.
*Verapamil*
- Verapamil is a **Class IV antiarrhythmic drug (non-dihydropyridine calcium channel blocker)** that primarily blocks **L-type calcium channels**, slowing conduction through the AV node.
- It is mainly used for **supraventricular tachycardias** and rate control in atrial fibrillation, not typically for ventricular arrhythmias like VT/VF.
*Procainamide*
- Procainamide is a **Class IA antiarrhythmic drug** that blocks **sodium channels** and also prolongs repolarization by blocking some potassium channels, but its primary effect is on sodium channels.
- Class IA drugs are known to **increase the QT interval** and carry a significant risk of **torsades de pointes**, making them less favorable for preventing VT/VF with adverse effect concerns.
*Esmolol*
- Esmolol is a **Class II antiarrhythmic drug (beta-blocker)** that primarily acts by **blocking beta-adrenergic receptors**, thereby reducing heart rate, contractility, and AV nodal conduction.
- While useful in some arrhythmias, its main mechanism is not potassium channel blockade, and it is not typically preferred for the direct prevention of VT/VF in situations with concerns about TdP.
*Sotalol*
- Sotalol is a **Class III antiarrhythmic drug** that primarily acts as a **potassium channel blocker**, prolonging the action potential duration and effective refractory period, and also has **beta-blocking properties**.
- While it blocks potassium channels, sotalol carries a **higher risk of torsades de pointes** compared to amiodarone, especially at higher doses and in patients with underlying heart conditions.
Antiarrhythmic classification and mechanisms US Medical PG Question 4: A 63-year-old man with a history of hypertension and atrial fibrillation is brought into the emergency room and found to have a ventricular tachyarrhythmia. Ibutilide is discontinued and the patient is switched to another drug that also prolongs the QT interval but is associated with a decreased risk of torsades de pointes. Which drug was most likely administered in this patient?
- A. Esmolol
- B. Digoxin
- C. Sotalol
- D. Amiodarone (Correct Answer)
- E. Quinidine
Antiarrhythmic classification and mechanisms Explanation: ***Amiodarone***
- **Amiodarone** prolongs the **QT interval** but has a lower risk of **torsades de pointes** compared to other **Class III antiarrhythmics** due to its mixed ion channel blocking properties and consistent action potential prolongation.
- It's a broad-spectrum **antiarrhythmic drug** effective for both **atrial** and **ventricular arrhythmias**, making it a good choice for someone with a history of **atrial fibrillation** presenting with **ventricular tachyarrhythmia**.
*Esmolol*
- **Esmolol** is a **beta-blocker** that does not prolong the **QT interval**; it is used to slow heart rate and can be used for rhythm control but not by **QT prolongation**.
- Its primary action is on **beta-1 receptors**, reducing **myocardial contractility** and **heart rate**, primarily used for acute control of **tachyarrhythmias** or **hypertensive emergencies**.
*Digoxin*
- **Digoxin** is a **cardiac glycoside** that does not prolong the **QT interval**; it primarily works by inhibiting the **Na+/K+-ATPase pump** and increasing **vagal tone**.
- It is used to control **ventricular rate** in **atrial fibrillation** and to manage **heart failure**, but it is not an **antiarrhythmic** in the sense of directly terminating **ventricular tachyarrhythmias** by affecting **QT prolongation**.
*Sotalol*
- **Sotalol** is a **beta-blocker** with **Class III antiarrhythmic properties** that prolongs the **QT interval** and has a significant **dose-related risk of torsades de pointes**, particularly at higher doses.
- While it's effective for both **ventricular** and **supraventricular arrhythmias**, its risk of **TdP** is a major concern, making **amiodarone** a safer alternative when **TdP risk** is to be minimized.
*Quinidine*
- **Quinidine** is a **Class IA antiarrhythmic** that significantly prolongs the **QT interval** and is known for a high risk of causing **torsades de pointes**.
- It primarily blocks **fast sodium channels** and also **potassium channels**, contributing to its **proarrhythmic effects** and making it a less favored option when **TdP risk** needs to be decreased.
Antiarrhythmic classification and mechanisms US Medical PG Question 5: Match the following antiarrhythmic drugs with their mechanism of action:
| Mechanism of action | Drug |
| :-- | :-- |
| 1. Na+ channel blocker | A. Quinidine |
| 2. K+ channel blocker | B. Digoxin |
| 3. Na+K+ ATPase inhibitor | C. Esmolol |
| 4. Beta-blocker | D. Ibutilide |
- A. 1-D, 2-B, 3-A, 4-C
- B. 1-A, 2-D, 3-B, 4-C (Correct Answer)
- C. 1-A, 2-C, 3-D, 4-B
- D. 1-D, 2-C, 3-A, 4-B
Antiarrhythmic classification and mechanisms Explanation: ***1-A, 2-D, 3-B, 4-C***
- **Quinidine** is a Class IA antiarrhythmic drug that primarily blocks **sodium channels**, prolonging the action potential duration and refractoriness.
- **Ibutilide** is a Class III antiarrhythmic drug that blocks **potassium channels**, leading to delayed repolarization and increased effective refractory period.
- **Digoxin** inhibits the **Na+/K+ ATPase pump**, increasing intracellular calcium and affecting AV nodal conduction.
- **Esmolol** is a **beta-blocker** (Class II antiarrhythmic) that reduces heart rate and contractility by blocking β1-adrenergic receptors.
*1-A, 2-C, 3-D, 4-B*
- This option incorrectly matches **Esmolol** (a beta-blocker) with **K+ channel blocker** and **Ibutilide** (K+ channel blocker) with **Na+K+ ATPase inhibitor**.
- It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**.
*1-D, 2-C, 3-A, 4-B*
- This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**.
- It also incorrectly matches **Digoxin** (Na+K+ ATPase inhibitor) with **beta-blocker**.
*1-D, 2-B, 3-A, 4-C*
- This option incorrectly matches **Ibutilide** (K+ channel blocker) with **Na+ channel blocker** and **Digoxin** (Na+K+ ATPase inhibitor) with **K+ channel blocker**.
- It also incorrectly matches **Quinidine** (Na+ channel blocker) with **Na+K+ ATPase inhibitor**.
Antiarrhythmic classification and mechanisms US Medical PG Question 6: An investigator is studying a drug that acts on the thyroid hormone pathway. Levels of serum free T3 and T4 in healthy participants are measured before and after administration of the drug. After administration, there is a decrease in the average serum free T3 level, while the average serum free T4 level is increased compared to initial serum studies. Inhibition of which of the following is the most likely mechanism of action of this drug?
- A. Thyroid-stimulating hormone
- B. Follicular iodotyrosine deiodinase
- C. Follicular thyroid peroxidase
- D. Peripheral 5'-deiodinase (Correct Answer)
- E. Follicular thyroid proteases
Antiarrhythmic classification and mechanisms Explanation: ***Peripheral 5'-deiodinase***
- Inhibition of **peripheral 5'-deiodinase** would decrease the conversion of **T4 to T3** in the periphery, resulting in lower **free T3** and higher **free T4** levels.
- This enzyme is crucial for activating T4 into the more potent T3, and its blockade explains the observed changes in hormone levels.
*Thyroid-stimulating hormone*
- Inhibition of **TSH** would lead to a decrease in the production and release of both **T3 and T4** from the thyroid gland.
- This contradicts the observed increase in **free T4** levels.
*Follicular iodotyrosine deiodinase*
- This enzyme is involved in recycling iodine from **monoiodotyrosine (MIT)** and **diiodotyrosine (DIT)** within the thyroid follicular cells, which is important for efficient thyroid hormone synthesis.
- Its inhibition would primarily affect iodine availability and synthesis, not directly lead to increased T4 and decreased T3 in the periphery.
*Follicular thyroid peroxidase*
- **Thyroid peroxidase (TPO)** is critical for the **iodination of tyrosine residues** on thyroglobulin and the **coupling of MIT and DIT** to form T3 and T4.
- Inhibition of TPO would decrease the synthesis of both **T3 and T4**, contrary to the observed increase in **free T4**.
*Follicular thyroid proteases*
- **Thyroid proteases** cleave thyroglobulin to release mature **T3 and T4** into the bloodstream.
- Inhibition of these proteases would lead to a decrease in the release of both **T3 and T4**, which does not align with the observed increase in **free T4**.
Antiarrhythmic classification and mechanisms US Medical PG Question 7: A 72-year-old man with congestive heart failure is brought to the emergency department because of chest pain, shortness of breath, dizziness, and palpitations for 30 minutes. An ECG shows a wide complex tachycardia with a P-wave rate of 105/min, an R-wave rate of 130/min, and no apparent relation between the two. Intravenous pharmacotherapy is initiated with a drug that prolongs the QRS and QT intervals. The patient was most likely treated with which of the following drugs?
- A. Carvedilol
- B. Verapamil
- C. Flecainide
- D. Quinidine (Correct Answer)
- E. Sotalol
Antiarrhythmic classification and mechanisms Explanation: **Quinidine**
- Quinidine is a **Class IA antiarrhythmic** that blocks fast sodium channels, prolonging both the **QRS complex** (due to slowed conduction) and the **QT interval** (due to prolonged repolarization).
- The ECG findings of **wide-complex tachycardia** and **AV dissociation** (P-wave rate different from R-wave rate without apparent relation) are consistent with ventricular tachycardia, which Class IA drugs can treat.
*Carvedilol*
- Carvedilol is a **beta-blocker** (Class II antiarrhythmic) that primarily slows heart rate and AV nodal conduction, generally **shortening the QT interval** or having no effect, and would not widen the QRS complex.
- Beta-blockers are typically contraindicated in **decompensated heart failure** and **wide-complex tachycardia** due to their negative inotropic effects and risk of worsening decompensation.
*Verapamil*
- Verapamil is a **non-dihydropyridine calcium channel blocker** (Class IV antiarrhythmic) that mainly slows AV nodal conduction. It would not cause QRS widening and can shorten the QT interval.
- Verapamil is generally contraindicated in **wide-complex tachycardias** of unknown origin as it can precipitate cardiovascular collapse if the arrhythmia is ventricular.
*Flecainide*
- Flecainide is a **Class IC antiarrhythmic** that primarily blocks fast sodium channels, causing significant **QRS widening** but has **minimal effect on the QT interval**, which is contrary to the case description.
- Class IC agents are also generally avoided in patients with **structural heart disease** like congestive heart failure due to increased mortality risk.
*Sotalol*
- Sotalol is a **Class III antiarrhythmic** (beta-blocker with potassium channel blockade) that primarily prolongs the **QT interval** by blocking potassium channels. While it prolongs the QT, it does **not significantly widen the QRS complex**.
- Its beta-blocking effects could exacerbate **decompensated heart failure** in this patient, similar to carvedilol.
Antiarrhythmic classification and mechanisms US Medical PG Question 8: A 51-year-old woman with a history of paroxysmal atrial fibrillation comes to the physician for a follow-up visit. She feels well and wants to discuss pausing her only current medication, flecainide. Her pulse is 75/min and regular, blood pressure is 125/75 mm Hg. Physical examination shows no abnormalities. An ECG shows a PR interval of 180 ms, QRS time of 120 ms, and corrected QT interval of 440 ms. Which of the following ECG changes is most likely to be seen on cardiac stress testing in this patient?
- A. Decreased maximal heart rate
- B. Prolonged QRS complex (Correct Answer)
- C. Shortened PR interval
- D. False-positive ST-segment depression
- E. Prolonged QTc interval
Antiarrhythmic classification and mechanisms Explanation: ***Prolonged QRS complex***
- **Flecainide** is a class Ic antiarrhythmic that **blocks fast sodium channels** in myocardial cells, slowing conduction in the atria, ventricles, and His-Purkinje system.
- Its effects are **use-dependent**, meaning the drug binds more effectively to channels that are frequently activated (i.e., at higher heart rates), leading to a **further widening of the QRS complex** during exercise.
*Decreased maximal heart rate*
- While some class II antiarrhythmics (beta-blockers) can decrease maximal heart rate, **flecainide** primarily affects cardiac conduction and does not significantly impact heart rate response to stress.
- The ECG does not suggest sinus node dysfunction that would limit heart rate increase with activity.
*Shortened PR interval*
- Flecainide typically **prolongs the PR interval** by slowing conduction through the atrioventricular (AV) node.
- Exercise would likely exacerbate this effect rather than shorten the PR interval.
*False-positive ST-segment depression*
- While wide QRS complexes (as may occur with flecainide-induced conduction slowing) can cause abnormal ST-segment morphology, the **most prominent and characteristic effect** of flecainide during stress testing is **progressive QRS widening** due to use-dependent sodium channel blockade.
- False-positive ST changes are a nonspecific finding and not the hallmark ECG change expected with flecainide during exercise.
*Prolonged QTc interval*
- Flecainide is generally known to **not significantly prolong the QT interval**; in some cases, it may even shorten it due to its effect on action potential duration.
- Other antiarrhythmics like Class III agents (e.g., amiodarone, sotalol) are more commonly associated with QTc prolongation.
Antiarrhythmic classification and mechanisms US Medical PG Question 9: A previously healthy 52-year-old woman comes to the physician because of a 3-month history of chest pain on exertion. She takes no medications. Cardiopulmonary examination shows no abnormalities. Cardiac stress ECG shows inducible ST-segment depressions in the precordial leads that coincide with the patient's report of chest pain and resolve upon cessation of exercise. Pharmacotherapy with verapamil is initiated. This drug is most likely to have which of the following sets of effects?
$$$ End-diastolic volume (EDV) %%% Blood pressure (BP) %%% Contractility %%% Heart rate (HR) $$$
- A. No change no change no change no change
- B. ↓ ↓ no change ↑
- C. ↓ ↓ ↓ ↑
- D. ↓ ↓ ↓ no change
- E. ↑ ↓ ↓ ↓ (Correct Answer)
Antiarrhythmic classification and mechanisms Explanation: ***↑ ↓ ↓ ↓***
- **Verapamil**, a **non-dihydropyridine calcium channel blocker**, reduces **cardiac contractility**, leading to decreased **heart rate** and **blood pressure**, while increasing **end-diastolic volume**.
- Its therapeutic effect in **exertional angina** is primarily due to reduced myocardial oxygen demand, achieved by decreasing **heart rate**, **contractility** (both leading to reduced work of heart), and **afterload** (due to vasodilation which decreases blood pressure).
*No change no change no change no change*
- This option is incorrect because verapamil has significant **pharmacological effects** on the cardiovascular system.
- Verapamil is prescribed to treat the patient's symptoms, implying a need for **hemodynamic changes**, not stasis.
*↓ ↓ no change ↑*
- Verapamil typically **decreases heart rate** due to its action on the sinoatrial (SA) node, making an increase unlikely.
- While it decreases **blood pressure** and **contractility**, the absence of an effect on heart rate and an increase in heart rate are inconsistent with verapamil's known pharmacology.
*↓ ↓ ↓ ↑*
- This option incorrectly suggests an **increase in heart rate**, whereas verapamil is known to cause a dose-dependent **decrease in heart rate**.
- The other parameters (decreased EDV, BP, contractility) are also not fully aligned with verapamil's effects; EDV tends to increase due to better filling time and reduced contractility.
*↓ ↓ ↓ no change*
- This option suggests a **decrease in EDV**, which is generally incorrect; verapamil tends to allow for **increased ventricular filling** due to a reduced heart rate and prolonged diastole.
- The absence of a change in heart rate is also incorrect, as verapamil is a known **negative chronotropic agent**.
Antiarrhythmic classification and mechanisms US Medical PG Question 10: A 39-year-old female presents to the clinic with the complaints of dry skin for a few months. She adds that she also has constipation for which she started eating vegetables and fruits but with no improvement. She lives with her husband and children who often complain when she turns the air conditioning to high as she cannot tolerate low temperatures. She has gained 5 kgs (11.2 lb) since her last visit 2 months back although her diet has not changed much. Her past medical history is relevant for cardiac arrhythmias and diabetes. She is on several medications currently. Her temperature is 98.6° F (37° C), respirations are 15/min, pulse is 57/min and blood pressure is 132/98 mm Hg. A physical examination is within normal limits. Thyroid function test results are given below:
Serum
TSH: 13.0 μU/mL
Thyroxine (T4): 3.0 μg/dL
Triiodothyronine (T3): 100 ng/dL
Which of the following medications is most likely to be responsible for her symptoms?
- A. Amiodarone (Correct Answer)
- B. Digoxin
- C. Metformin
- D. Theophylline
- E. Warfarin
Antiarrhythmic classification and mechanisms Explanation: ***Amiodarone***
- Amiodarone is a known cause of both **hypothyroidism** and **hyperthyroidism** due to its iodine content and direct toxic effects on the thyroid gland. The patient's symptoms (dry skin, constipation, **cold intolerance**, **weight gain**, bradycardia) and thyroid function tests (high TSH, low T4, low T3) are highly consistent with drug-induced hypothyroidism.
- The patient's history of **cardiac arrhythmias** makes amiodarone a plausible medication she would be taking, as it is a common antiarrhythmic drug.
*Digoxin*
- Digoxin is primarily used to treat **heart failure** and certain arrhythmias, but it does not typically cause thyroid dysfunction.
- Its common side effects include gastrointestinal upset, visual disturbances, and various arrhythmias, which do not align with the patient's predominant symptoms of hypothyroidism.
*Metformin*
- Metformin is an oral hypoglycemic agent used to treat **Type 2 diabetes**, a condition the patient also has.
- It does not have substantial effects on thyroid hormone synthesis or metabolism and is not associated with hypothyroidism or hyperthyroidism.
*Theophylline*
- Theophylline is a bronchodilator used in the treatment of **asthma** and **COPD**.
- It is not known to cause thyroid dysfunction, and its side effects mainly involve the central nervous system, gastrointestinal tract, and cardiovascular system.
*Warfarin*
- Warfarin is an **anticoagulant** prescribed to prevent blood clots.
- It has no direct known interaction with thyroid hormone synthesis or metabolism and is not associated with thyroid dysfunction.
More Antiarrhythmic classification and mechanisms US Medical PG questions available in the OnCourse app. Practice MCQs, flashcards, and get detailed explanations.
