Untitled

Which cellular mechanism of arrhythmia involves an area of tissue that conducts impulses more slowly, creating a circuit?

During phase 0 of a myocyte action potential, which ion channel is primarily responsible for the major current flow?

A drug prolongs the repolarization phase in ventricular myocytes. How might this change affect the ECG?

An antiarrhythmic drug selectively blocks $I_{kr}$ channels. What is the most likely effect of this drug on the cardiac action potential?

Which of the following is NOT a fundamental requirement for the establishment of a re-entry arrhythmia?

A patient is prescribed a drug that inhibits HCN channels. What effect would this medication likely have on the heart's electrical activity?

A patient's ECG shows a repeating loop of electrical activity. Which mechanism is most likely responsible, given requirements such as multiple pathways, unidirectional block, and a prolonged conduction time?

A drug is found to have greater effects on arrhythmogenic cells compared to healthy cells. Which of the following properties would best explain this selectivity?

Which of the following statements best describes the role of the sympathetic and parasympathetic nervous systems on nodal firing?

A cardiologist is evaluating a patient with a suspected re-entry arrhythmia. Which diagnostic criterion is MOST critical for confirming this type of arrhythmia?

A patient taking an antiarrhythmic drug develops torsades de pointes. Which ion channel is most likely being excessively blocked by the drug?

A physician is deciding on a treatment strategy for a patient experiencing a re-entry arrhythmia. Which of the following pharmacological approaches would MOST directly target the mechanism underlying the arrhythmia?

A patient is diagnosed with Wolff-Parkinson-White (WPW) syndrome. What makes WPW a type of re-entry arrhythmia?

A patient with supraventricular tachycardia is being treated with a Class 4 antiarrhythmic drug. What is the primary mechanism by which this drug class helps to control the patient's heart rate?

A patient is prescribed esmolol for the management of an arrhythmia. Considering its pharmacokinetic properties, what is the most likely route of administration and a key reason for this?

A cardiologist is choosing between different beta-blockers to treat a patient with both hypertension and a history of asthma. Which property of acebutolol might be a concern in this patient, compared to other beta-blockers?

If a drug prolongs the P-R interval, what effect is it having on the heart?

How do Class 2 antiarrhythmics reduce heart rate?

Which of the following drug properties are associated with Class 4 antiarrhythmics?

A patient with a known hypersensitivity to catecholamines is experiencing arrhythmia. Which class of antiarrhythmic drugs would be most beneficial in managing this patient's condition?

A patient is diagnosed with atrial tachycardia. How do Class 4 antiarrhythmics protect ventricular rate from atrial tachycardia?

A patient with a history of myocardial infarction (MI) is experiencing frequent premature ventricular contractions (PVCs). Which Class 3 antiarrhythmic would be MOST appropriate for long-term suppression of these arrhythmias?

A patient with atrial fibrillation is being considered for pharmacological cardioversion. Which Class 3 antiarrhythmic is specifically indicated for rapid conversion of atrial fibrillation or flutter to normal sinus rhythm?

A patient with a history of paroxysmal atrial fibrillation is being treated with amiodarone. Which potential adverse effect is MOST important to monitor for during long-term amiodarone therapy?

Which of the listed medications carries the HIGHEST risk of Torsades de Pointes (TdP) among Class 3 antiarrhythmics and is therefore the most restricted in its use?

A cardiologist is choosing between amiodarone and dronedarone for a patient with atrial fibrillation. What is the MOST significant advantage of dronedarone over amiodarone?

A patient is prescribed sotalol for the maintenance of normal sinus rhythm following cardioversion of atrial fibrillation. What additional pharmacological effect should the physician be aware of when using this drug?

A patient with congenital Long QT syndrome (LQTS) needs treatment for a bacterial infection. Which class of antibiotic should be AVOIDED due to the risk of precipitating Torsades de Pointes (TdP)?

A patient develops acquired Long QT syndrome (LQTS) while being treated for depression. Which class of antidepressant is MOST likely contributing to the prolongation of the QT interval and increased risk of Torsades de Pointes (TdP)?

Why were many promising drug candidates abandoned early in development?

What is the primary ionic current responsible for the upstroke (phase 0) of the action potential in ventricular myocytes?

Which of the following distinguishes pacemaker cells from ventricular myocytes?

Which ionic current is primarily responsible for the upstroke (phase 0) in pacemaker cells?

What is the role of the 'funny' current ($i_f$) in pacemaker cells?

How does norepinephrine (NE) influence ion channel signaling in pacemaker cells?

What is the effect of acetylcholine (ACh) on pacemaker cell function?

Which of the following ionic currents is responsible for the repolarization phase (phase 3) in ventricular myocytes?

What is the role of the transient outward potassium current ($iK_{to}$) in myocyte action potentials?

During which phase of the myocyte action potential is the L-type calcium current ($iCa(L)$) most active and what is its primary function?

What is the state of voltage-gated Na+ channels during the absolute refractory period?

Which of the following best describes the relative refractory period (RRP) in cardiac myocytes?

During which phase of the myocyte action potential are voltage-gated K+ channels primarily open?

What is the primary mechanism by which voltage-gated Na+ channels transition from the open to the inactivated state?

What directly triggers the opening of voltage-gated calcium channels in Phase 2 of the myocyte action potential?

Which of the following is a clinical application of Propranolol related to its non-selective beta-adrenergic antagonism, particularly in the context of catecholamine involvement?

Verapamil and Diltiazem, as antiarrhythmics, primarily target which specific mechanism to exert their therapeutic effect?

According to the Vaughan-Williams-Singh classification, which class of antiarrhythmic drugs prolongs the effective refractory period by blocking potassium channels?

How do Class 1A antiarrhythmics like Quinidine affect the cardiac action potential, and what distinguishes this effect from Class 1B and Class 1C?

Lidocaine is a Class 1B antiarrhythmic that is administered intravenously. What is the primary indication for using Lidocaine?

How does Flecainide (Class 1C antiarrhythmic) exert its therapeutic effect on cardiac tissue?

Which of the following describes a key mechanism by which Class 3 antiarrhythmics prolong the action potential duration and increase the effective refractory period (ERP)?

Procainamide is a Class 1A antiarrhythmic. What is a significant adverse effect associated with long-term use of Procainamide?

Quinidine is a Class 1A antiarrhythmic drug. What is a major safety concern associated with its use?

Which Class 1B antiarrhythmic drug, similar in efficacy to lidocaine, is orally available, making it suitable for outpatient management of certain ventricular arrhythmias?

Given its mechanism of action, which antiarrhythmic drug is LEAST likely to be effective in treating atrial fibrillation with a rapid ventricular response?

How does Propafenone, classified as a Class 1C antiarrhythmic, differ from other drugs within its class in terms of pharmacological action?

A patient develops polymorphic ventricular tachycardia characterized by a 'twisting of the points' morphology on the ECG. Which class of antiarrhythmic drugs is most likely implicated in causing this arrhythmia?

What ionic current block characteristic of Class 3 antiarrhythmics increases the risk for early afterdepolarizations (EADs) leading to Torsade de Pointes?

Disopyramide has anti-muscarinic activity. How would this impact heart rate?

Arrhythmia Mechanisms

Action Potential Phases

Action Potential Modulation

AP & ECG Relationship

Antiarrhythmic Selectivity

Antiarrhythmic MOA

Nodal Firing Influence

Key Cardiac Ion Channels

Re-entry arrhythmia

Ischemic Damage (in arrhythmias)

Atrial fibrillation

Monomorphic ventricular tachycardia

Re-Entry Requirements

hERG Channels

In vitro Proarrhythmia Assay

iPSCs-derived cardiomyocytes

Pacemaker Cells

Ventricular Myocytes

iCa

iK

if

iK(ACh)

iNa

iKto

iCa(L)

Phase 0

Refractory Period

Phase 2

Class 1 Antiarrhythmics

Class 2 Antiarrhythmics

Class 3 Antiarrhythmics

Class 4 Antiarrhythmics

Class 2 Antiarrhythmic Action

Class 2 Use Case

Class 4 Antiarrhythmic Action

Esmolol

Amiodarone

Dronedarone

Ibutilide

Sotalol

Dofetilide

Clinical Use of Amiodarone

Clinical Use of Dronedarone

Clinical Use of Sotalol

Propranolol

Propranolol: Clinical Uses

Verapamil/Diltiazem: Mechanism

Verapamil/Diltiazem: Clinical Uses

Class 1A Drugs

Class 1B Drugs

Class 1C Drugs

Class 3 Antiarrhythmics: Mechanism