Heart Model
Cardiovascular Pharmacology Concepts Richard E. Klabunde, PhD

Cardiovascular Physiology Concepts 3e textbook cover Cardiovascular Physiology Concepts, 3rd edition textbook, Published by Wolters Kluwer (2021)

CNormal and Abnormal Blood Pressure, Physiology, Pathophysiology and Treatment book cover Normal and Abnormal Blood Pressure, published by Richard E. Klabunde (2013)

Types of Arrhythmias

Introduction

Normally, the heart rate is controlled by the sinus node, which triggers action potentials that are first conducted throughout the atria, then pass into the AV node where there is a conduction delay, and finally into and throughout the ventricles via a specialized rapidly conducting system (bundle branches and Purkinje fibers). This normal sequence of events occurs over specific time intervals to ensure coordination of the atrial and ventricular activation and to provide maximal cardiac pumping efficiency. Deviations from this normal pattern result in arrhythmias (also termed dysrhythmias). Arrhythmias can be divided into three broad categories: altered rate, premature beats, and altered conduction.

Altered Rate

Normal resting heart rates are between 60 and 100 bpm. A rate lower than 60 bpm is called bradycardia, and a rate greater than 100 bpm is called tachycardia. There are subcategories of altered rate such as sinus tachycardia or bradycardia (rate is determined by SA node), atrial tachycardia or bradycardia (rate governed by atrial pacemaker site), supraventricular tachycardia, and ventricular tachycardia (rhythm originating from within ventricles). Atrial tachycardias having a rate of 250-350 bpm (>200 bpm in ventricles) are called atrial flutter. Atrial or ventricular fibrillation occurs when their frequency is so high and irregular that the rate cannot be determined.

Premature Beats

Occasionally, a cell within the atria or ventricles spontaneously fires off an action potential (ectopic foci). When this occurs, it can cause what is called a premature beat. If this occurs in the atria, the impulse will often be conducted to the ventricles and produce an early depolarization and contraction of the atria and ventricles. If the premature beat originates from a ventricular ectopic foci, this will lead to an early depolarization and contraction in the ventricles without affecting the atrial rhythm.

Altered Conduction

Delays in the conduction of electrical impulses within the heart produce abnormal electrical activation of the heart, termed conduction defects. These most commonly occur at the AV node. Less severe conduction delays at the AV node will only delay the time it takes for the impulse to reach the ventricles (called a first degree AV block). However, if AV nodal conduction is depressed sufficiently, not all impulses will reach the ventricles, leading to a loss of the one-to-one correspondence between the atria and ventricles (called a second degree AV block). If the AV node (or Bundle of His) becomes completely blocked, the atria will depolarize normally, but ventricular depolarization will no longer be triggered by atrial impulses. When this occurs, pacemaker sites within the ventricle will drive ventricular rate, although at a much lower rate (30-40 bpm) than the normal sinus rate (>60 bpm). This is called a third degree AV block. Conduction blocks can also occur in the ventricular bundle branches. These blocks seldom change the ventricular rhythm, although they will alter the sequence of ventricular activation, leading to an increase in the QRS duration and abnormal QRS shape. This will depress ventricular mechanical function. Special types of partial conduction blocks, sometimes with abnormal conduction pathways (e.g., Wolff-Parkinson-White syndrome), can lead to reentry pathways that produce tachycardia.

To learn more about specific arrhythmias, click here.

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Causes of Arrhythmias

Revised 11/29/2023

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