Problem-Based Learning About Problem-Based Learning: Lessons Learned from a Student-Led Initiative to Improve Tutor Group Interaction

Abstract

This article summarizes a student-led effort to improve tutor group interactions among second-year medical students in a hybrid problem-based learning (PBL) curriculum. Dissatisfaction with PBL had led to superficial tutorial discussions that students escaped to study for board certification exams. Following the PBL principle of using intrinsically motivating problems, the student investigators created board-style questions with accompanying facilitation guides for tutors to present as ‘mini-problems’ to stimulate case-related discussion. Tutor groups used and enjoyed the questions, but interaction quality did not improve. Like the hybrid curriculum itself, the intervention embodied conflicting educational philosophies; implementation challenges reflected the tension between them.

Appendices

Appendix

Sample Question & Tutor Facilitation Guide

Long QT/Electrophysiology

Pose this question. Students may document key question information in whatever format they choose.

Question 1

A 67-year-old with a history of recurrent atrial-fibrillation presents for a follow-up appointment regarding his elevated liver function tests related to medication usage. He has been treated for many years with a medication used to control his refractory atrial fibrillation. On examination, the skin of his face displays a blue-gray hue. The effects of his medication on the QT interval would be most similar to which of the following other antiarrhythmic medications?

• A. Flecainide

• B. Procainamide

• C. Lidocaine

• D. Esmolol

Ask students to select and justify their preferred answer and explain what makes the other answers incorrect.

Tutor Notes

Question Subject/Objective

This patient is displaying signs of amiodarone toxicity. Amiodarone is a class-III antiarrhythmic that can be used to control atrial fibrillation. It has a wide side effect profile that includes thyroid dysfunction, neurologic effects, pulmonary fibrosis, hepatotoxicity, and skin effects such as blue-gray discoloration. This patient is displaying two of those effects in his skin discoloration and elevated LFTs indicating hepatotoxicity.

Class III antiarrhythmics exhibit a potassium channel blocking effect, prolonging phase III of the myocyte action potential, which prolongs the action potential duration and the QT interval. While the main mechanism of class I antiarrhythmics is their blockage of sodium channels, prolonging phase 0 of the action potential, they vary in their effect on the action potential and QT duration. Class IA antiarrhythmics have the unique effect of the ability to block potassium channels, increasing the action potential duration, prolonging phase 3 and the QT interval. Examples of these drugs include Quinidine, Procainamide, and Disopyramide. Class IB on the contrary shorten the action potential duration—drugs include Lidocaine and Mexiletine. Class IC drugs generally have limited effect on the action potential duration and QT interval. Class IC drugs include Flecainide and Propafenone. Beta blockers exert their antiarrhythmic effect in decreasing sympathetic tone on the SA and AV node. Decreased SA nodal sympathetic activity would prolong the spontaneous depolarization of nodal automaticity, decreasing heart rate. Decreased AV node sympathetic activity would delay the conductance of atrial impulses to the ventricle, prolonging the PR interval. These would not affect the duration of phase III of the myocyte action potential.

Discussion Objective

• Students should be able to identify the various classes and subclasses of antiarrhythmics.

• Should be able to identify the various sodium channel blockers and what subclass they belong to (IA – quinidine, procainamide, disopyramide; IB – Lidocaine, Mexiletine; Class IC – flecainide, propafenone). They should be able to identify the effect on action potential length, slope of phase 0, and effect on QRS.

Learning Issues Covered

• 1. Know the rationale, mechanism of action, adverse effects, pharmacokinetics and indications/contraindications of drugs to treat cardiac arrhythmias.

• 2. Classification of antiarrhythmic drugs:

• 3. Know the basis of classification of Class 1.

• 4. EKG and action potential changes associated with antiarrhythmic drugs.

Facilitation Tips

Listen to the students’ discussion, using the below material as a guide, to determine whether their understanding is on track or further facilitation is needed.

• 1. Consider having the students draw out the cardiac action potentials and how they are altered by the various class I and class III antiarrhythmics alter.

• 2. What EKG and action potential changes would be associated with class I antiarrhythmics? Does this vary by the type of Na+ channel blockers? How? What is meant by the term “use dependence”?

• 3. Are there certain contraindications for the various classes of sodium channel blockers?

• 4. How do beta-blockers affect the action potential? Heart rate? How?

Answer Explanations

Correct answer – B – procainamide. This patient is on long term amiodarone, which is suggested by blue-gray skin discoloration and elevated LFTs. Amiodarone works by blocking potassium channels of cardiac myocytes, prolonging phase 3 of the myocyte action potential, which increases the QT interval. Procainamide is a class IA antiarrhythmic. Class IA antiarrhythmics not only block sodium channels, slowing phase 0 of the myocyte action potential, but also exert some potassium channel blocking effect. This will prolong phase 3 of the myocyte action potential, prolonging the QT interval, matching the changes in QT seen with class III antiarrhythmics as seen with amiodarone.

A – Flecainide is a class IC antiarrhythmic. IC antiarrhythmics generally have no effect on phase 3 of the myocyte action potential and thus do not prolong the QT interval.

C – Lidocaine is a class IB antiarrhythmic. IB antiarrhythmics generally shorten the action potential duration and the QT duration.

D – Beta blockers exert their antiarrhythmic effect in decreasing sympathetic tone on the SA and AV node. Decreased SA nodal sympathetic activity would prolong the spontaneous depolarization of nodal automaticity, decreasing heart rate. Decreased AV node sympathetic activity would delay the conductance of atrial impulses to the ventricle, prolonging the PR interval. These would not affect the duration of phase III of the myocyte action potential.