Ventricular Arrhythmias

Chapter 16 Ventricular Arrhythmias


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The three preceding chapters have focused primarily on supraventricular arrhythmias, especially those related to rapidly occurring electrical disturbances arising in the area of the sinus node, the atria, or the atrioventricular (AV) node (junction). Assuming normal ventricular conduction, these all produce narrow (normal duration) complex tachycardias (NCTs).


This chapter considers another essential ECG topic: ventricular arrhythmias—the major, but not the only, cause of wide complex tachycardias (WCTs).


Ectopic (nonsinus) depolarizations frequently arise in the ventricles themselves, or the fascicular system, producing premature ventricular beats (or complexes), ventricular tachycardia (VT), discussed later, and in the most electrophysiologically unstable settings, sometimes ventricular fibrillation (VF) leading to immediate cardiac arrest (also see Chapter 19).



Ventricular Premature Beats


Ventricular premature beats (VPBs) are premature depolarizations arising in the ventricles, analogous to atrial premature beats (APBs) and junctional premature beats (JPBs), which are supraventricular in origin. Recall that with APBs and JPBs, the QRS complex is usually of normal (“narrow”) width because the stimulus spreads synchronously through the bundle branches to the ventricles (unless a bundle branch block or some other cause of aberrancy is present).


With VPBs, however, the premature depolarizations typically arise in either the right or left ventricle. Therefore, the ventricles are not stimulated simultaneously, and the stimulus spreads through the ventricles in an aberrant direction and asynchronous way. Thus, the QRS complexes are wide with VPBs, just as they are with the bundle branch block patterns. Examples of VPBs are shown in Figures 16-1 to 16-8.











VPBs most often precede a sinus P wave. (Occasionally they appear just after a sinus P wave but before the normal QRS complex.) Sometimes, VPBs are followed by retrograde (nonsinus) P waves (negative in lead II) that arise because of reverse stimulation (from bottom to top) of the atria by each VPB. This sequence, called “VA” (ventricular-atrial) conduction, is identical to what may occur with ventricular pacing (see Chapter 21).



Features


Clinicians comment on a number of features of VPBs that may have clinical relevance.



Frequency


The frequency of VPBs refers to the number that is seen per minute or other unit of time. The VPB frequency may range from one or an occasional isolated premature depolarization to many.


VPBs may occur in various combinations. Two in a row (see Fig. 16-4) are referred to as a pair or couplet. Three or more in a row are, by definition, VT (see Fig. 16-5). Sometimes, as shown in Figure 16-6A, isolated VPBs occur so frequently that each normal beat is followed by a VPB. This produces a distinctive repetitive grouping of one normal beat and one VPB, which is called ventricular bigeminy (see Figs. 16-6 and 16-7). The sequence of two normal beats with a VPB is ventricular trigeminy. Three normal beats followed by a VPB constitutes ventricular quadrigeminy.



Morphology and Origin


As you might expect, the appearance of the VPBs will be different depending on the site(s) in the ventricles from which these premature beats originate.



The further away from the middle of the heart VPB origin is, the wider is the QRS. VPBs coming from the top (base) of the heart have “inferior” QRS axis—pointing down and therefore positive in leads II, III, and aVF. They are often called “outflow tract” VPBs because their origin is located close to the pulmonary and aortic valves. Usually they have LBBB-like shape. Outflow tract VPBs (right ventricular outflow tract [RVOT] and left ventricular outflow tract [LVOT]) are the most common variety of “benign” VPBs occurring in a normal heart. VPBs originating closer to the apex and from inferior wall activate the heart from the bottom up and are said to have “superior” axis, with QRS negative in leads II, III, and aVF. VPBs originating in the area of postinfarct myocardial scar often have a qR configuration. Sometimes this allows diagnosing infarct even when no Q waves are seen during sinus rhythm (see Fig. 16-7).


The same principles apply to localization of VT (a run of consecutive VPBs). Localization of the site of ventricular ectopy may be helpful in clinical management, as described later.


The sequence of ventricular repolarization after VPBs is such that ST-T waves are directed in the opposite direction to the main QRS deflection (QRS-T “discordance”), often with prominent ST segment elevations/depressions as expected (see Fig. 16-2). Clinicians need to recognize that these secondary ST-T changes are not due to ischemia and are similar to the QRS-T discordance findings in wide complex beats due to bundle branch block and ventricular pacing. In fact, concordance between QRS and ST-T directions during VPBs may be a sign of myocardial injury.



Jun 11, 2016 | Posted by in CARDIOLOGY | Comments Off on Ventricular Arrhythmias
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