Teaching cardiac arrhythmias: A focus on pathophysiology and pharmacology

American Journal of Pharmaceutical Education, Summer 2001 by Sprague, Jon E

PROLOGUE The following manuscript reviews a method of teaching the pathophysiology and pharmacology of cardiac arrhythmias. This manuscript is supplemented with a complimentary web site (http://www.onu.edu/user/fs/jsprague/AJPE.html). Those interested in obtaining further information can use this site for lecture notes, animations of cellular mechanisms, practice case reports, electrocardiograms (ECG) strips, and Powerpoint, lecture presentations. The author hopes that other find this information useful in developing strategies for teaching this subject area.

INTRODUCTION

The teaching of the pathophysiology and pharmacological treatment of cardiac arrhythmias can be a challenging task. The integrated modular system (for description see reference 1) utilized at Ohio Northern University (ONU) allows for the pathophysiology and pharmacology to be followed by the medicinal chemistry and therapeutic principles involved in the management of cardiac arrhythmias. Background material necessary for the comprehension of cardiac arrhythmias is provided in the Biomedical Science Modules. Before entering the Cardiovascular Module, where cardiac arrhythmias are covered in detail, students have been instructed in ion-channel function in muscle contraction, action potential physiology and the basics of ECG. The following text is a summary of a fourhour lecture sequence presented in the Cardiovascular Module on the pathophysiology and pharmacological treatment of cardiac arrhythmias. These lectures are supplemented by a web site that contains primary literature references in a downloadable format, animations of cellular mechanisms and practice case reports, ECG strips, and Powerpoint(R), lecture presentations. This manuscript is written in a fashion to complement a web site created specifically for the readers of the American Journal of Pharmaceutical Education that contains all the above and can be accessed at (http://www.onu.edu/user/ fs/jsprague/AJPE.html). General references utilized in developing these lectures included references 2-4.

MECHANISMS UNDERLYING CARDIAC ARRHYTHMIAS

Most cardiac arrhythmias result from disorders of impulse formation, impulse conduction or a combination of both. Disturbances in impulse formation or automaticity can involve no pathological change in the pacemaker site generating sinus bradycardia ( 100 bpm) due to rapid firing of the SA node. The development of an ectopic focus can also lead to impulse formation abnormalities. An ectopic focus is an impulse originating outside the SA node and can develop as a result of electrolyte disturbances, ischemia, excessive myocardial fiber stretch, drugs, or toxins(5).

Disorders in impulse conduction involve heart blocks. which result in slowed or blocked conduction through the myocardium. The pathological process of reentry is also au impulse conduction abnormality. Figure 1 demonstrates the process of reentry. This figure is animated allowing student tc visually comprehend how impulse conduction circles through the reentry pathway; the animation also draws a corresponding action potential for correlation to heart rate (see web link). In order for a reentry pathway to develop, there must be a unidirectional block within the conduction pathway. This unidirectional block can be the result of ischemia (e.g. following E myocardial infarction). A unidirectional block alone is not suf ficient to generate the arrhythmia. At least one of the following characteristics must be present for the arrhythmia to develop; long reentry pathway, short refractory period, or slowed conduction velocity. All three of these conditions will allow the surrounding myocardial tissue to be out of its refractory period so when the circulating impulse reaches the myocardium a premature contraction is generated. Each of these events is explained in detail. Hand drawings of the reentry pathway illustrating all three pathological events are given to the class. Genetic abnormalities in voltage-gated ion channel function have also been linked to arrhythmia generation(6). For example, the inherited potassium channel disorder that results in the long-QT syndrome(6). These examples are discussed in the previous Biomedical Sciences Module.

TYPES OF CARDIAC ARRHYTHMIAS (5)

After review of a normal ECG and the definitions of some general terminology (Appendix A), the students are introduced to the types of cardiac arrhythmia. The expectation is that they will be able to identify the arrhythmia type on lead II and learn the standard Advanced Cardiac Life Support (ACLS) treatment guidelines for this form of arrhythmia (7,12). ACLS guidelines are also utilized in assisting the students in arrhythmia identification and can be accessed by the students on the courses webpage. After the following types of arrhythmias are discussed, the students are given a handout of twenty different forms of arrhythmias to identify. A sample of the handout strips is in Appendix B and a sample handout can be downloaded from the web link.