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Mechanisms Underlying Supraventricular Tachyarrhythmias
Reentry occurs when the refractory periods and conduction speeds of two separate pathways differ. The initial impulse (marked by blue star) is often a premature complex. It encounters the anterograde limb in a state that can be depolarized, while it encounters the other limb in its refractory period.
Cells with pacemaker ability spontaneously depolarize. The speed of spontaneous depolarization is represented by the slope of phase 4 of the action potential. The steeper the slope, the faster the heart rate. The initial stimulus for these rhythms may be elevated adrenergic tone or toxicity from digitalis.
Afterdepolarizations are triggered by the depolarization in the previous action potential. They can occur during phase 2 or 3 (early after-depolarizations) or during phase 4 of the action potential (late after-depolarizations).
FIGURE 10.1 Schematic of reentry mechanism (A); increased automaticity (B); and triggered mechanism (C).
TABLE 10.1 Comparison of Reentry Mechanisms
Increased adrenergic tone, digitalis toxicity
Narrow Complex Tachycardias Classified
There are a number of ways to classify supraventricular tachyarrhythmias. A common way to separate them is by the underlying mechanisms: reentry, increased automaticity, and triggered activity. “Supraventricular” includes all territory above the bifurcation of the bundle of His (Fig. 10.2A, B
FIGURE 10.2 Schematic of different types of supraventricular rhythms resulting in narrow complex tachycardias. A. Reentry can occur within the sinus node or atrium but most often involves the AV node. B. Foci capable of taking over a rhythm by increased automaticity are located within the atria and the AN and NH segments (shaded in) of the AV node. Several foci may be simultaneously in control.
Atrial fibrillation (AF) is a common arrhythmia characterized by an irregularly irregular ventricular rhythm and extremely rapid atrial waves, called fibrillatory waves. AF is associated with significant morbidity and mortality related to thromboembolic complications.
AF involves different mechanisms. Independent foci with increased automaticity or triggered activity may simultaneously fire to initiate AF. Reentry in multiple circuits may perpetuate the rhythm. Foci within the pulmonary veins are often the origin of AF. They trigger premature depolarizations that propagate across the left atrium which can then activate several macroreentry circuits in the atria. A critical mass in the atria is required for these reentrant circuits to self-perpetuate. Pulmonary vein isolation is an effective method for treating paroxysmal AF.
In AF, the AV node is bombarded with atrial impulses. The ventricular rate depends on the balance of parasympathetic and sympathetic tone at the AV node.
Fibrillatory waves (f waves) represent independent reentrant waves within the atria. The rate of these waves is ≥350 bpm, and they appear as undulations in the baseline. They may be coarse or fine. When very coarse, they may be mistaken for P waves, and when very fine, they may be imperceptible (diagnosis of AF is then based on the irregularity of the R-R intervals). Fibrillatory waves in V1 may appear uniform like flutter waves, but nonuniform undulations of the baseline present in other leads will help to differentiate AF from atrial flutter.
FIGURE 10.3 Schematic of micro- and macroreentrant circuits in atrial fibrillation.
Notable Ventricular Responses
Rapid Ventricular Response
When the QRS complexes are closer together, they may appear regular at first glance and the rhythm may be mistaken for reentrant supraventricular tachycardia (SVT).
Regularized Ventricular Response
Regular R-R intervals in a patient with AF represent complete AV dissociation. Digitalis toxicity is a notable cause. Regular rhythms may also occur if the patient is in an accelerated junctional rhythm or if the patient is paced.
TABLE 10.2 Classification of Atrial Fibrillation
Terminates spontaneously within 7 days
Afib initiated when vagal tone is higher; occurs in subset of patients with paroxysmal AF
Afib initiated in setting of increased sympathetic activity; occurs in a subset of patients with paroxysmal AF
Continuous for more than 7 days
Persistent for more than 1 year
Long-standing AF refractory to cardioversion
AF in patients younger than 60 who do not have structural heart disease or hypertension
Atrial flutter is a macroreentrant rhythm most commonly confined to the right atrium. The reentrant rhythm is usually initiated by a premature atrial beat. The atrial rate is regular and typically occurs at 250 to 350 bpm. In patients treated with antiarrhythmic medications, such as amiodarone, sotalol, or quinidine, the atrial rate can be less than 250 bpm. The ventricular rate depends on AV nodal conduction and is regular unless the rhythm is atrial flutter with variable conduction.
In typical atrial flutter, the rhythm is conducted counterclockwise up the atrial septal wall and down the free wall of the right atrium. This occurs in 90% of atrial flutter. Flutter waves are usually more obvious in the inferior leads.
Reverse Typical AFlutter
In reverse typical atrial flutter, the atrial conduction proceeds down the septal wall and up the free wall of the atrium (clockwise in the frontal plane). Flutter waves are more obvious in the right precordial leads. This occurs in 10% of atrial flutter.
FIGURE 10.4 A. Typical atrial flutter mechanism and ECG appearance. B. Atypical atrial flutter mechanism and ECG appearance.
The reentrant circuit of atrial flutter can also occur in the left atrium or around surgical scars.
Because atrial conduction follows a single reentrant circuit, the atrial rate in this atrial rhythm is regular. The atrial rate is at least 240 bpm. Flutter waves can be difficult to recognize, especially when there is 2:1 conduction. They can appear as follows:
When they distort the QRS complex.
Within the QRS complex.
Inverted T Waves
When they are between two QRS complexes.
Motion artifact may appear as coarse P waves with some regularity. This can occur in Parkinson disease.
Atrial flutter with 2:1 block and atrial tachycardia with 2:1 block can look similar. The atrial rate of atrial tachycardia (200 +/− 50 bpm) is slower than that of atrial flutter (300 +/− 50 bpm). In atrial tachycardia, the P waves in the inferior limb leads are typically upright with a discernible isoelectric line.
An abrupt cessation of the rhythm to vagal maneuvers or AV nodal agents is diagnostic of SVT. These agents will slow the ventricular response to atrial flutter but not convert flutter into sinus rhythm.
AV Nodal Reentrant Tachycardia (Typical)
AV nodal reentrant tachycardia (AVNRT) is the most common cause of paroxysmal SVT. A reentrant circuit can occur within nodal tissue when there is a difference in conduction velocity and refractory period length between two groups of cells.
The reentrant pathway is triggered by a premature atrial beat that encounters the fast AV nodal pathway in its refractory period. By default, the impulse is conducted down the available slow pathway. If anterograde conduction down the slow pathway is slow enough, it will encounter a fast pathway that is no longer in its refractory period. The impulse then conducts in a retrograde fashion up this fast pathway (Fig. 10.5
FIGURE 10.5 Mechanism of typical AVNRT.
Anterograde Ventricular Activation
The resulting QRS is narrow and normal appearing since activation of ventricular tissue occurs along the normal pathway from the AV node to the bundle of His and down both bundle branches. An abnormal QRS morphology results only if the patient has preexisting bundle branch or fascicular blocks.
The ventricular rate is typically between 150 and 250 bpm.
Retrograde Atrial Activation
Atrial conduction occurs in a retrograde fashion.
The P wave is often obscured by the QRS because ventricular and atrial activation from this reentry circuit occur nearly simultaneously. If P waves are visible, they are located very close to the QRS waveform. The P wave may be close enough to give the appearance of a pseudo-q wave if it occurs before the QRS or a pseudo-s or r wave if it occurs after the QRS complex.
Retrograde P Waves Can
AVNRT most commonly appears as a regular, narrow complex tachycardia with no visible P waves.
FIGURE 10.6 Relationship of P waves to QRS complexes in typical AVNRT.
AV Nodal Reentrant Tachycardia (Atypical AVNRT)
In atypical AVNRT, the impulse conducts retrogradely to the atria through the slow pathway and anterograde down the fast pathway to the ventricles. The reentrant rhythm is initiated by an ectopic ventricular impulse.
The ECG will appear as a regular, narrow complex tachycardia. Retrograde P waves will precede QRS complexes (Fig. 10.7
FIGURE 10.7 Schematic of ECG in atypical AVNRT.
A more common cause of inverted P waves preceding QRS waves is atrial tachycardia.
Orthodromic Atrioventricular Reciprocating Tachycardia
This is a regular, narrow complex tachycardia, with a bypass tract that connects the atrium to the ventricle.
FIGURE 10.10 Schematic of AVRT involving a left-sided bypass tract and initiated by a PAC.
Retrograde P waves typically appear separated from QRS complexes because ventricular and atrial impulses in orthodromic atrioventricular reciprocating tachycardia (AVRT) often occur at distinct times.
QRS complexes are narrow since both ventricles are activated simultaneously through the AV node.
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