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Cardiovascular Pharmacology Concepts

Richard E. Klabunde, PhD

Clinical Disorders:

Therapeutic Classes:

Mechanism Classes:


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Click here for information on Cardiovascular Physiology Concepts, 2nd edition, a textbook published by Lippincott Williams & Wilkins (2011)

 

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Click here for information on Normal and Abnormal Blood Pressure, a textbook published by Richard E. Klabunde (2013)

 



The Pharmacologic Treatment of Cardiac Arrhythmias cont

Types of Arrhythmias

Arrhythmias can be divided into three 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 call flutter, and can be either atrial or ventricular in origin. Fibrillation occurs (either atrial or ventricular) when the frequency is so high and irregular that the rate cannot be determined.

Premature Beats

Sometimes a cell within the atria or ventricles that is not normally a pacemaker cell (called an ectopic foci) spontaneously fires off an action potential. When this occurs, it can cause what is called a premature beat. If this occurs in the atria the impulse will generally 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

Sometimes a cell within the atria or ventricles that is not normally a pacemaker cell (called an ectopic foci) spontaneously fires off an action potential. When this occurs, it can cause what is called a premature beat. If this occurs in the atria the impulse will generally 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.

Delays in the conduction of electrical impulses within the heart produce abnormal electrical activation of the heart that are 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, only some of the impulses may be able to travel into 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) become completely blocked, the atrial 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 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 do not normally alter the ventricular rhythm, although they will alter ventricular activation and ventricular mechanical function. Special types of partial conduction blocks, sometimes in conjunction with abnormal conduction pathways (e.g., Wolff-Parkinson-White syndrome), can lead to reentry pathways that produce tachycardia.

Specific Arrhythmias - definitions:

Types of AV Nodal Block

First-degree AV nodal block - the conduction velocity is slowed so that the P-R interval is increased to greater than 0.2 seconds.  Can be caused by enhanced vagal tone, digitalis, beta-blockers, calcium channel blockers, or ischemic damage.

Second-degree AV nodal block - the conduction velocity is slowed to the point where some impulses from the atria cannot pass through the AV node.  This can result in P waves that are not followed by QRS complexes.  With a Mobitz type I block, the P-R interval gradually increases until a QRS is dropped. Therefore, the atrial rate will be greater than the ventricular rate.  When there is a Mobitz type II block, the P-R interval is usually normal (<0.2 msec), but there may be 2 or 3 P waves before one is followed by a QRS (as shown in the figure). In this type of block, the ventricular rhythm is less than the sinus rhythm.

Third-degree AV nodal block - conduction through the AV node is completely blocked so that no impulses are able to be transmitted from the atria to the ventricles.  QRS complexes will still occur (escape rhythm), but they will originate from within the AV node, bundle of His, or other ventricular regions.  Therefore, QRS complexes will not be preceded by P waves.  Furthermore, there will be complete asynchrony between the P wave and QRS complexes.  Atrial rhythm may be completely normal, but ventricular rhythm will be greatly reduced depending upon the location of the site generating the ventricular impulse.  Ventricular rate typically range from 30 to 40 beats/min.

Click here to see a table summarizing the types of drugs that may be used to treat the above arrhythmias.

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Causes of Arrhythmias

Revised 03/08/2015

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.