Introduction to the Arrhythmias: A Primer

Arrhythmias can be bradycardias or tachycardias. Bradycardias are further divided into sinus bradycardias and heart block. Tachycardias can be supraventricular or ventricular. One should be very careful to describe the arrhythmia before giving a specific diagnosis. Too often one rushes to identify the P waves and QRS, and then leaps to a diagnosis. However, in many cases the diagnosis is not clear and indeed the arrhythmia cannot definitively be known by the surface electrocardiogram. Thus, it is far better to describe the arrhythmia and then given a differential diagnosis. Bradycardias Bradycardia can be caused by sinus bradycardia or heart block. In either, escape rhythms are seen. Junctional escape rhythms are at a heart rate of 40 - 50 beats per minute (bpm); ventricular escape rhythms are at a heart rate of 20 - 30 bpm. Sinus bradycardia is recognized by having a P wave prior to each QRS. However, in the case of a junctional escape rhythm that has a more rapid rate than the sinus bradycardia, one can observe a junctional rhythm with no apparent atrial activity whatsoever. Heart blocks are diagnosed by having more P waves relative to the QRS. First-degree heart block is not truly heart block, but simply a prolongation of the PR interval. Mobitz I or Wenckebach heart block causes progressive lengthening of the PR interval before a P wave not followed by a QRS is observed (i.e., heart block for this beat); the beat following the dropped QRS then has a shortened PR interval. Mobitz II heart block is characterized by no progressive prolongation of the PR interval prior to the blocked beat. Individuals with Mobitz II heart block typically also have a right or left bundle branch block, consistent with His-Purkinje system disease. Complete heart block is diagnosed by the presence of an escape rhythm (20 - 50 bpm), more P waves than QRS complexes, and no relationship between the P waves and QRS complex. Tachycardias Tachycardia nomenclature can be either by mechanism or by descriptive methods. When grouping tachycardias by mechanism, they can be categorized as supraventricular tachycardias (SVT) or ventricular tachycardias (VTs). The descriptive method of nomenclature is to divide tachycardias into a narrow complex (NCT) versus a wide complex (WCT). If the tachycardia QRS is narrow, it must be passing through the AV and His-Purkinje system, and thus by definition is an SVT. If the tachycardia QRS is wide, there are three general possibilities: 1) it is ventricular in origin, such as ventricular tachycardia; 2) it is an SVT conducting down a bypass track; or 3) it is an SVT conducting via a left or right bundle block. Along with the description of wide or narrow, the other features that are very useful in descriptive methodology are rate, onset and regularity. All of these simple descriptive terms should be summarized before looking for atrial activity. Finally, in a descriptive methodology, one will look for the relationship of the P to the QRS and the response to adenosine or other AV nodal blocking agents. Mechanistic nomenclature should only be used after the descriptive method is applied. Adenosine may further clarify the diagnosis, but one must ensure that this short-acting agent reaches the heart before it loses its efficacy (usually 5 - 10 seconds). There are eight SVTs in total, including sinus tachycardia, atrial fibrillation (AF), atrial flutter (AFL), AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT), atrial tachycardia (AT), multifocal atrial tachycardia (MAT), and a very rare junctional tachycardia. Supraventricular Arrhythmias (SVTs) Sinus tachycardia is an appropriate response of the heart to an external stimulus such as fear, anger, exercise, dehydration or anemia. The maximum heart rate is 220 minus their age; however, there is a wide standard deviation. The onset is gradual and the tachycardia is regular (i.e., the tachycardia does not vary in cycle length or beat-to-beat heart rate). P waves are prior to each QRS and are of similar morphology to sinus rhythm. Treatment with adenosine may transiently slow a sinus tachycardia, but will not terminate it. AF is the most common pathologic SVT. The heart rates are between 100 - 250 bpm. The onset can be acute in those with paroxysmal AF, but in those with chronic AF the tachycardia will be gradual. This rhythm is characterized by irregular irregularity. There is no apparent P wave, although occasionally you will see coalescence of fibrillatory waves and the supposed appearance of a P wave. By using adenosine, slowing of the ventricular response may be seen. AFL is a reentrant rhythm around the tricuspid valve. Because this is a reentrant rhythm, it is quite regular and typically at a heart rate of 150 bpm. AFL may be acute in onset in people who convert from sinus to atrial flutter, or it can be gradual in people who are in chronic AFL. AFL is generally a regular rhythm, but can occasionally be irregular if AV nodal agents are utilized. There is no P wave in atrial flutter, but the flutter waves can often be seen in the inferior leads in V1 in a classic saw-tooth pattern. Similar to AF, adenosine will transiently slow the ventricular response but will not terminate the tachycardia. AVNRT occurs because of a reentry circuit in the AV node. The heart rate is typically between 150 and 250 bpm, and onset is acute. In this regular rhythm, there is no apparent P wave, although occasionally one can see an R primed in V1 consistent with atrial activation. Adenosine will terminate AVNRT. AVRT is the arrhythmia seen with bypass tracks. Onset is acute, and the rates are from 150 to 250 bpm. AVRT is a regular rhythm and the P wave is seen after the QRS, although at the time it will be difficult to find because of the T wave. AVRT can occur with conduction down the AV node and retrograde through the bypass track, in which case, the resulting tachycardia will be a NCT. AVRT may also conduct antegrade via the bypass track and retrograde via the AV node, in which case, the resulting SVT will be a WCT. Patients with Wolff-Parkinson-White (WPW) syndrome are at a higher risk of atrial fibrillation, and therefore, an irregular WCT could be atrial fibrillation with WPW. AVRT is broken by adenosine. AT is less common than AVNRT and AVRT. This rhythm also has a heart rate of 150 - 250 bpm, is acute in onset, and is regular (similar characteristics to AVNRT and AVRT). There is evidence of atrial activation prior to each QRS. Morphology of the P wave is reflective of the location of atrial tachycardia. Adenosine will terminate 60 - 80% of AT cases; the remainder will have transiently slow heart rates or will not experience a change in their heart rate with adenosine administration. MAT is the response of the atrium to poisoning, seen in severe pulmonary disease treated with beta-adrenergic agents and theophylline. Heart rates are between 100 - 150 bpm, and rarely go above 150. The onset is gradual, because in general the sinus tachycardia rate would be quite similar to the MAT rates. It is an irregular rhythm, but not quite as irregular as atrial fibrillation. There are P waves prior to each QRS, and these P waves are of varying morphologies. MAT does not respond to adenosine. Lastly, junctional tachycardia cases are extremely rare, except in infancy. In the adult, heart rates run between 100 and 150 bpm. It is acute in onset and very regular. P waves are not generally observed. In general, junctional tachycardia will not respond to adenosine. Ventricular Arrhythmias Ventricular arrhythmias can be divided into monomorphic ventricular tachycardia and polymorphic ventricular arrhythmias. Polymorphic rhythms can be further subdivided into ventricular fibrillation (VF) and polymorphic ventricular tachycardia (PMVT), although it is usually difficult to separate these tachycardias. Ventricular tachycardia has rates usually in the 180 - 300 bpm range, although in a patient with chronic heart disease or on amiodarone you can occasionally see VT at rates as low as 120. It is acute in onset, regular, and has a wide complex. The P wave can either follow the QRS, if there is 1:1 retrograde conduction, or there can be AV disassociation with a P wave at a slower rate than the VT. There is no response to adenosine. In addition, the response to calcium channel blockers can be fatal because of the vasodilatory effects. VF is characterized by a very irregular ventricular rhythm. The initial phase of VF is quite coarse, and with time it becomes of lower amplitude and finer. Polymorphic VT or torsade is also an irregular rhythm, but there appears to be some repeating pattern of organization. Often, it is very difficult to distinguish between VF and polymorphic VT; in fact, these arrhythmias mechanistically share similarities. Torsade is generally caused by long QT syndromes that are either acquired or congenital, whereas VF is generally caused by ischemic conditions and underlying structural heart disease. Conclusion In summary, the differential diagnosis of arrhythmia should be descriptive, relying on readily apparent features such as rate, regularity, and onset. Once these simple features are described, then the relationship of the atrial activity to the ventricular activity should be sought and a differential diagnosis can be made.