Electrocardiography

Arrhythmias


 

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Arrhythmias
Ventricular
Arrhythmias

The identification and interpretation of cardiac arrhythmias can be difficult. This chapter will address the similarities and differences that exist between various arrhythmias. Supraventricular rhythms, junctional rhythms and ventricular rhythms will be discussed. Management of the various arrhythmias is discussed in the Arrhythmia Module.

Mechanisms of Arrhythmias

There are three types of processes that lead to arrhythmias. They include enhanced automaticity, triggered activity and reentry. Enhanced automaticity can be present in any tissue that has automaticity. Automaticity is the characteristic of cardiac tissue to initiate an impulse. When tissue other than the sinus node generates impulses faster than the sinus node, this is considered enhanced automaticity. Triggered activity results from enhanced "after-repolarization" in phase 4, which, if it reaches threshold, results in another action potential. Reentry requires an available circuit, different refractory periods in the two limbs and a slow response somewhere in the circuit to allow the rest of the circuit to repolarize. Most supraventricular and ventricular arrhythmias are reentry.


 

Supraventricular Arrhythmias

Sinus Arrhythmia

There is beat to beat variation in the discharge of the action potential from the sinus node. The most common cause of this variation is respiratory related. Sinus arrhythmia is a variation greater than normal and is defined as a 10% difference between the greatest R to R interval and the shortest R to R interval.

Premature Atrial Contractions (PAC)

The PAC is an early beat from an ectopic atrial focus and is an example of enhanced automaticity. On the ECG, the P wave may be identified in the baseline segment following the T wave, where it is frequently inverted, but is often located within the T wave. It can be identified because of a change in the T wave from the normal T wave configuration, which may be the only way to distinguish a PAC from a PVC. The PAC is often conducted with the QRS complex unchanged from the sinus beats but also may be aberrantly conducted or not conducted at all. Regardless of the conduction, the interval between the pre-PAC beat and the post-PAC beat is less than two times the R to R interval of consecutive sinus beats (i.e. less than compensatory). When the PAC occurs after every sinus beat, it is referred to as atrial bigeminy. One final comment, PACs that do not result in ventricular activation should be referred to as non-conducted rather than blocked. Blocked suggests pathology of the AV node where the non-conducted PAC is physiologic and simply encounters the AV node during the refractory period.

Atrial Fibrillation

A full description of pathophysiology and treatment for atrial fibrillation is in the Arrhythmia module. The chaos associated with fibrillation of the atria is represented on the ECG as a course baseline. Because there is only partial activation of the atria, the baseline shows low amplitude waves. "Course" atrial fibrillation may have segments of baseline that appear as P waves but these deflections are not consistently associated with QRS complexes. The lack of organization of atrial fibrillation leads to the haphazard activation of the ventricle and results in the irregularly irregular pattern seen on the ECG. The irregularity is due to concealed conduction into the AV node when some atrial impulses partially penetrate the node but do not activate the ventricle.

A normal AV node may conduct at a rate of 180 to 200 beats per minute without rate controlling medicine while a diseased AV node may have a slow ventricular response (<60 beats per minute). In the Wolff-Parkinson-White syndrome (WPW), the refractory period of the accessory pathway determines the rate of atrial conduction. If the refractory period is short, the ventricular rate may reach 300 beats per minute and be mistaken for ventricular tachycardia due to the wide complex QRS associated with WPW.

Although an irregularly irregular rhythm is the hallmark of atrial fibrillation, there are times when the ventricular rhythm may be regular. When this occurs, there is usually complete AV block with either a junctional escape or ventricular escape rhythm. It is also possible the patient has had an AV node ablation with the placement of a ventricular pacemaker.

Atrial Flutter

Atrial flutter is caused by the formation of a circuit in the left atrium and is an example of reentry. Management is covered in the Arrhythmia module. Atrial flutter is more organized than atrial fibrillation. There is a classic "saw-toothed" pattern on the ECG with negative P waves in the inferior leads.

Typical atrial flutter is at a rate of 300 beats per minute. The AV node will not conduct at the normal flutter rate and there is AV block which is not considered pathological (therefore, second degree AV block should not be coded). Although the conduction of the flutter waves to the ventricle may be variable, it typically occurs at a rate of either 4:1 or 2:1. When the block is 4:1, it is easy to see the flutter waves on the baseline ECG. Block at a 2:1 rate may be more difficult because the non-conducted flutter wave may be buried in the QRS complex. Therefore, whenever a ventricular rate of approximately 150 beats per minute is observed, careful inspection needs to be done to look for hidden flutter waves.

Multiple clinical scenarios may alter the anatomy of atrial flutter. Antiarrhythmic drugs can slow the flutter circuit making the flutter rate less than 150 beats per minute and can increase the degree of block at the AV node lowering the ventricular rate. An enlarged right atrium can also increase the distance the circuit needs to travel also slowing the flutter rate. Disease of the conduction system can increase the block at the AV node decreasing the ventricular rate.

There are times when clinically atrial fibrillation and atrial flutter cannot be distinguished and both may be present on the same ECG. At these times, a diagnosis of atrial fibrillation / flutter is made and attempts to distinguish them are forsaken.

Atrial Tachycardia

This arrhythmia can usually be distinguished from atrial flutter and multifocal atrial tachycardia. The rate is normally lower than atrial flutter with a rate of 225-280 beats per minute but the typical flutter waves are not present. Similar to atrial flutter, the ventricular rate is a fraction of the atrial rate which is physiologic due to the refractory period of the AV node and should not be coded as AV block. The P waves are usually inverted in the inferior leads suggesting a focus of the rhythm is not from the sinus node.

Multifocal Atrial Tachycardia / Wandering Atrial Pacemaker

These are two ECG diagnoses which are closely related and differ only in the rate. Both describe an arrhythmia that has multiple atrial foci participating in the generation of the rhythm. For the diagnosis to be done by ECG, there must be at least three different P wave morphologies and the rhythm must be irregular. If the ventricular rate is over 100 beats per minute, then multifocal atrial tachycardia is diagnosed. If the ventricular rate is under 100 beats per minute, then the diagnosis of wandering atrial pacemaker is made.

Supraventricular Tachycardia

Supraventricular tachycardias are predominantly reciprocating tachycardias which are a form of a reentry circuit. They include arrhythmias with microcircuits including AV nodal reentry tachycardia and macrocircuits involving both antidromic and orthodromic pathways. Supraventricular tachycardia is a waste basket term used to describe any tachycardia originating in the atria or AV node. For the purposes of this module, atrial flutter, atrial fibrillation, atrial tachycardia, sinus tachycardai, multifocal tachycardia and the junctional rhythms have been given separate diagnoses. The remainder of the supraventricular tachycardias are classified here.

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Junctional Arrhythmias

Premature Junctional Contractions (PJC)

Premature junctional contractions are represented on the ECG by a premature beat without an associated P wave. If the QRS morphology is the same as the normal rhythm and there is no P wave, then a PJC can be diagnosed. If the PJC is conducted with aberrancy, there is no way on the surface ECG to differentiate a PJC from a premature ventricular contraction.

Junctional Escape Rhythm

A junctional rhythm originates in the AV junction and the wave of propagation travels both antegrade through the His-Purkinje system and retrograde into the atria. Based upon the location of the pacing focus and the rate of propagation, the P wave may be in front of the QRS complex, buried within the QRS complex or just after the QRS complex. If there is normal conduction in the His-Purkinje system, the QRS complex will be narrow.

A distinction exists between a junctional rhythm and an idiojunctional rhythm. Idiojunctional rhythm refers to an independent rhythm from the atrium. In this situation, an escape junctional beat may temporarily take over the pacing function of the ventricles while AV dissociation is present.

Accelerated Junctional Rhythm

An acclerated junctional rhythm is defined as a junctional rhythm that is over 60 beats per minute. Similar to the idiojuntional rhythm, there is AV dissociation with occasional ventricular capture by the sinus beats. Occasionally there will be atrial fibrillation with an accelerated junctional rhythm that is strongly associated with digoxin toxicity.

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Ventricular Arrhythmias


Premature Ventricular Contractions (PVC)

The PVC is an early beat from an ectopic venticular focus and is an example of enhanced automaticity. The impulse generated from the PVC may partially penetrate the AV node but will infrequently advance into the atrium. Following a PVC, there is a compensatory pause. The compensatory pause represents ongoing sinus node activity despite the PVC. When the PVC occurs, the sinus beat occurring just after the PVC is not conducted through the AV node because of the partial penetration from the PVC and therefore is blocked. Because the PVC did not penetrate the atria, the rhythm of the sinus node is not interrupted and the next sinus impulse comes on time resulting in a normal QRS complex. The result is that the two sinus beats that bookend the PVC are exactly two times the R to R interval of the preceding sinus beats and this is referred to as a compensatory pause on the ECG.

Consecutive PVCs are referred to as couplets and if there are more than two consecutive ventricular beats then the rhythm is referred to as ventricular tachycardia. Multifocal PVCs refers to PVCs of different morphologies from different foci. When making the diagnosis of multifocal PVC's, it is important to look at the same lead for all the PVCs as the same focus will look different in different leads.

Idioventricular Rhythm

An idioventricular rhythm is similar in concept to the idiojunctional rhythm. The focus of the rhythm is from the ventricle and may temporarily take over control of the ventricle. There remains a sinus focus with AV dissociation. Occasionally, a sinus beat may recapture control of the ventricle. This rhythm is frequently seen after reperfusion following a total occlusion of a coronary artery either by thrombolytic therapy or percutaneous intervention.

Ventricular Tachycardia (VT)

Ventricular tachycardia is a reentry circuit that exists in the ventricle. Ventricular tachycardia is categorized as either non-sustained ventricular tachycardia (NSVT) which is three or more consecutive ventricular complexes or sustained ventricular tachycardia (what is usually meant by the term VT) which is consecutive ventricular complexes lasting greater than 30 seconds. The biggest challenge with a wide complex QRS tachycardia is differentiating ventricular tachycardia versus supraventricular tachycardia with aberrant conduction. Many criteria have been documented in the literature to help distinguish between the two arrhythmias. The following are supportive for VT rather than a supraventricular tachycardia with aberrancy.

    1. P waves not associated with the QRS complexes
    2. Fusion beats

    3. Left bundle branch block morphology with right axis deviation

    4. Negative concordance

    5. Positive concordance

    6. LBBB morphology with QRS duration greater than 160 milliseconds

    7. RBBB morphology with QRS duration greater than 140 milliseconds

When referring to concordance, the term is used to identify the major deflection of the QRS complex. Negative concordance refers to all QRS complexes in the precordial leads having the major deflection be negative. Positive concordance has all major QRS deflections being positive. Negative concordance is more specific to VT than positive concordance.

Torsades de Pointes

Torsades de pointes is French for twisting of the points. It is a form of multifocal ventricular tachycardia where the wide QRS complexes vary in height and directionality on the ECG. It is strongly associated with a prolonged QT interval as well as hypomagnesemia.. Because the QT interval is prolonged with slower heart rates, torsades de points is more common in bradycardia than in faster heart rates.

Ventricular Fibrillation

Ventricular fibrillation is a terminal event and only rarely resolves spontaneously. It is due to erratic ventricular activity and course fibrillatory waves on the ECG. It is frequently preceded by ventricular tachycardia and torsades de pointes and a common cause of sudden cardiac death. It may also occur without a preceding ventricular arrhythmia when an R on T extrasystole happens.


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