CAT 3

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proved sense of quality of life are other factors weighing favorably toward a catheter- based ablative approach to atrial flutter management.

PRACTICE POINT

A strong consideration of catheter-ablation strategy should be considered in patients with atrial flutter and rapid ventricular rate as medical management of rapid ventricular rate is frequently suboptimal.

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA EPIDEMIOLOGY

Atrioventricular nodal reentrant tachycardia (AVnRT) is the most common form of paroxysmal SVT, responsible for almost two-thirds of episodes; it is estimated that 10% of the general population has AVnRT. The palpitations characteristically start abruptly and may last for just a few minutes to as long as a few hours. They terminate as abruptly as they start. Additional symptoms include chest discomfort, dyspnea, lightheadedness, neck pulsations, and associated anxiety. These symptoms are often misdiagnosed as panic attacks if the arrhythmia is not caught while on a monitor. Signs of the arrhythmia include regular tachycardia with a heart rate between 120 and 200 bpm. Vagal maneuvers such as carotid sinus massage or the Valsalva maneuver can break the reentry circuit. This arrhythmia is usually not associated with structural heart disease and carries very little risk of death.

The mechanism of this tachyarrhythmia is a reentry circuit composed of the atrium, AV node or perinodal tissue, and the ventricle. The perinodal tissue or AV node exhibits a dual conduction physiology that reveals a slow pathway with an inherently short refractory period and a fast pathway with a relatively long refractory period.

There are three variants of AVnRT that depend on the routes of conduction. Approximately 90% of AVnRT is called typical AVnRT based on its antegrade conduction via the slow pathway and retrograde conduction via the fast pathway. With this typical conduction the surface ECG has the characteristic P-waves either buried within the QRS complex or just after the QRS. As expected with fast retrograde conduction, the RP interval is shorter than the PR interval. Recognizing the relative length of the RP and PR intervals can further differentiate between the other SVTs. The ECG for the typical AVnRT often demonstrates a pseudo-R’-wave in V1 and pseudo-S’-waves in inferior limb leads. The less common variants include fast/slow and slow/slow, which will demonstrate clear P-waves, inverted in the inferior limb leads with an RP interval longer than the PR interval.

MANAGEMENT

Initial hospital management

Management of AVnRT can follow a straightforward treatment sequence (Figure 132-6). Vagal maneuvers such as the carotid sinus massage and Valsalva maneuver can break

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the reentry circuit 25% of the time. If the tachycardia is refractory to these maneuvers, adenosine will convert the rhythm to sinus in approximately 90% of patients. Due to its very short half-life of less than 10 seconds, it is crucial that adenosine be given as a rapid bolus and immediately followed by 5 to 10 mL of saline. Adenosine is typically dosed in 6 mg increments, but patients usually respond to a 12-mg dose. The expected symptoms with the infusion are dyspnea, facial flushing, and chest discomfort that last under a minute. When using adenosine, the patient’s rhythm should be monitored by telemetry via a continuously running 12-lead ECG to observe the response that occurs within 30 seconds.

Figure 132-6 Treatment sequence for atrioventricular nodal reentrant tachycardia (AVnRT).

PRACTICE POINT

AVnRT can be converted to sinus rhythm with vagal maneuvers in 25% of cases and with adenosine in 90% of cases. Adenosine must be given as a rapid IV bolus and immediately followed by 5-10 mL of saline. The expected symptoms with the infusion are dyspnea, facial flushing, and chest discomfort that last under a minute. When using adenosine, the patient’s rhythm should be monitored continuously with rhythm strip or 12-lead ECG to monitor the response, which occurs within 30 seconds. Recent randomized data demonstrated in 2015 that a “modified Valsalva maneuver” converted 40% of patients with SVT compared to just 17% of those who underwent the standard Valsalva maneuver. The steps to this modified maneuver is as follows: a. semirecumbent position—head of bed at 45° angle b. have patient blow into a 10-cc syringe for ~15 seconds with enough pressure to just

move the plunger c. then, immediately lay patient in the supine position and raise the legs up to ~45°

Typically, adenosine will convert the AVnRT to a sinus rhythm, but other possible rhythms include ventricular ectopy, transient sinus pause, transient bradyarrhythmias, atrial fibrillation or atrial flutter uncommonly, and, very rarely, polymorphic ventricular tachycardia. The risk of torsades de pointes is increased in patients with a baseline prolonged QTc. Factors that could decrease the efficacy of intravenous adenosine push include the use of methylxanthine products such as theophylline and caffeine, which block the A1 receptors. The use of dipyridamole (persantine, aggrenox) can augment the efficacy of adenosine by slowing its clearance. Due to the potential for exacerbating bronchospams, asthma is a relative contraindication for adenosine use. The transplanted

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heart is hypersensitive to adenosine, therefore a reduced dose or abandoning this approach altogether is appropriate in such patients.

Other options beside adenosine for the acute management of AVnRT include verapamil, β-blockers, and direct cardioversion. Verapamil, a nondihydropyridine calcium channel blocker, will block both fast and slow pathways. Dosing for acute management is 5 mg IV every 10 minutes and has been reportedly 90% effective. The downside to verapamil is the potential for hypotension that could be severe and long lasting. Another option includes digoxin, although this approach is not optimal due to its delayed effect. Direct cardioversion with 10 to 50 J is a final option if the previous interventions prove ineffective.

Outpatient longitudinal therapeutics

If the patient has frequent episodes that negatively impact quality of life, the use of invasive catheter ablation may be considered. The consensus approach by the ACC/AHA guidelines recommends ablation of the slow pathway due to its high efficacy (97%) and low risk of high-grade AV block (1%). The patient does need to consider the possibility of pacemaker placement if high-degree block develops as a complication. Long-term medical management is another option and includes medications such as verapamil, propanolol or class I antiarrhythmic agents such as flecanide and propafenone. The medications can be used on a daily basis to reduce the frequency of occurrences and the length of episodes. Additionally, the “pill-in-the-pocket” method obviates the daily use and could be used just during the episode. Cardiology consultation is indicated when using class I antiarrhythmics due to the risk of malignant ventricular arrhythmias.

ATRIOVENTRICULAR REENTRY TACHYCARDIA EVALUATION

The next most common form of a paroxysmal SVT is atrioventricular reentry tachycardia (AVRT), which is characterized by an accessory conduction pathway between the atrium and ventricle that serves as a conduit for macro reentry. This pathway is a muscular bundle with variable properties of conduction, sometimes with bidirectional properties and in others just unidirectional capabilities. A commonly cited example of AVRT is Wolf- Parkinson-White syndrome, a narrow-complex tachyarrhythmia that manifests symptomatically with palpitations, chest discomfort, dyspnea, presyncope or syncope, and, very rarely, sudden cardiac death.

A baseline ECG when in sinus rhythm may (“revealed”) or may not (“concealed”) demonstrate the delta wave (Figure 132-7). The accessory pathway depolarizes the ventricular myocardium before the normal conduction system and is thus considered “pre- excitation.” On the ECG, this will appear as the short PR interval. Due to the relatively inefficient conduction from myocardial to myocardial cell (in contrast to the efficient His- Purkinje system), the initial portion of the QRS is slurred (delta wave) and gives the QRS a widened appearance (Figure 132-7). This accessory pathway, known as the bundle of Kent in WPW syndrome, provides the electrical wave front a conduit to move from the ventricle to the atrium, completing the macro reentry circuit.

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Figure 132-7 Atrioventricular reentry tachycardia (AVRT). Wolf-Parkinson-White (WPW) syndrome with characteristic short PR interval and delta wave best seen in I, aVL, V3, and V4.

INPATIENT MANAGEMENT

Management of this macro reentry arrhythmia is identical to the management for nodal reentry tachycardia with vagal maneuvers as a first option and intravenous adenosine push if unsuccessful. As discussed previously, adenosine administration usually converts the rhythm to sinus; however, less frequently atrial fibrillation or atrial flutter can develop. In very rare situations, the electrical impulse could conduct antegrade via the accessory pathway, leading to a very rapid ventricular rate, ventricular instability, and polymorphic ventricular tachycardia. This very rare complication of adenosine in AVRT requires having a crash-cart available during adenosine administration.

In some types of AVRT, the accessory pathway may not be recognizable on the ECG (considered concealed). When the accessory pathway conducts unidirectionally only from the ventricle to the atrium, the characteristic delta wave, short PR interval, and widened QRS are absent. The management remains the same as in the revealed WPW syndrome with very little concern for polymorphic ventricular tachycardia, as the accessory pathway will only conduct unidirectionally in a retrograde fashion from the ventricle to the atrium.

Beyond the acute management of AVRT, the frequency and severity of the palpitations will guide long-term treatments. Infrequent episodes that are short in duration and hemodynamically tolerable require only rest and time to resolve. A pill-in-the-pocket regimen could be considered with class Ia, Ic, or III antiarrhythmics or AV nodal-blocking agents as an option in this scenario in the absence of pre-excitation. However, if the episodes are frequent and prolonged, daily use of these medications can be considered. These antiarrhythmics will prolong the refractory period for both the accessory pathway and the AV node, effectively preventing the arrhythmia or breaking the circuit during the episodes. Radiofrequency ablation of the accessory pathway provides another option

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(with a very high success rate and low complication rate) for permanent rhythm control that obviates the need for chronic medication in AVRT.

PRACTICE POINT

Wolf-Parkinson-White with atrial fibrillation: Atrial fibrillation (AF) in a very young patient should lower clinicians’ threshold to consider WPW syndrome. AF occurs in up to one-third of patients with WPW and is the root cause for sudden death in these patients. The patient with a “revealed” WPW and atrial fibrillation will demonstrate a wide QRS complex on ECG due to the delta wave (often misinterpreted as atrial fibrillation with bundle branch block, BBB). WPW with AF should not be rate controlled with AV node-blocking agents, as atrial impulses would be forced to the incrementally conducting accessory pathway. The ventricular response would become 1:1, leading to unstable ventricular tachycardia (see Figures 132-8 and 132-9).

Figure 132-8 Atrial fibrillation with brief run of aberrant conduction and noticeably wider conduction in the latter half of the ECG strip.

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Figure 132-9 Unstable ventricular tachycardia after patient was given IV adenosine. This AV nodal-blocking agent effectively shunted the atrial electrical impulses to the accessory pathway, which is characterized by nondecremental conduction.

Treatment: IV procainamide or IV amiodarone or electrical cardioversion.

The presence of a delta wave on a resting ECG does not require a cardiology consultation. However, a delta wave with a history of palpitations, syncope, or presyncope, or with a history of atrial fibrillation does require cardiology consultation. The electrophysiologist can perform invasive procedures to stratify some patients with the WPW syndrome for risk of sudden cardiac death, especially when the refractory period for the accessory pathway is short (RR interval of < 250 ms).

MULTIFOCAL ATRIAL TACHYCARDIA

EVALUATION

Multifocal atrial tachycardia (MAT) is recognized on the surface ECG by the presence of tachycardia, at least three distinct P-waves, and at least three distinct PR intervals (Figure 132-10). Correct identification of this arrhythmia helps avoid improperly treating it as another arrhythmia.

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Figure 132-10 Multifocal atrial tachycardia (MAT). Three or more distinct P-wave morphologies with an irregular rhythm. (Reproduced, with permission, from Knoop KJ, Stack LB, Storrow AB, et al. Atlas of Emergency Medicine, 3rd ed. New York, NY: McGraw- Hill; 2009, Fig. 23-29A. Photo contributor: James V. Ritchie, MD.)

Inpatient management

Multifocal atrial tachycardia usually results from another primary problem that leads to right heart strain or dysfunction (eg, severe COPD with exacerbation or pulmonary embolism). By treating the underlying condition, the arrhythmia usually resolves. However, if the tachycardia needs to be slowed based on clinical effects of the rate, β-blockers represent the first-line treatment. A short-acting β-blocker, IV esmolol, may be considered if concern for bronchospasm or hypotension exists. Some trials support administration of IV magnesium to slow or convert the arrhythmia; however, this has not been well studied. Finally verapamil is another therapeutic option, but may be limited by hypotension. Electrical cardioversion is not effective and thus not recommended. Exacerbating factors for MAT may include commonly used medications for COPD such as β-agonists and theophylline.

JUNCTIONAL TACHYCARDIA

EVALUATION

Junctional tachycardia originates from the AV node or the bundle of His. The paroxysmal form is considered a rare occurrence in the adult population, but the nonparoxysmal form occurs most notoriously in the setting of digoxin toxicity. Particularly with digoxin toxicity, a Wenckebach conduction block in conjunction with junctional tachycardia can manifest. Other settings in which this arrhythmia may manifest include hypokalemia, postcardiac surgery, chronic lung disease, myocardial ischemia, myocarditis, and rarely, underlying

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sinus node dysfunction. Presentation of the arrhythmia under these circumstances allows the clinician to differentiate it from AVnRT, AVRT, and atrial tachycardia (AT).

Inpatient management

By addressing the underlying condition, the rhythm will correct. In the setting of digoxin toxicity, withholding the medication is the treatment of choice. Digoxin binding agents should be considered for judicious use in the setting of ventricular arrhythmias or high- grade AV block.

ATRIAL TACHYCARDIA EVALUATION

An uncommon arrhythmia that falls under the category of SVT is atrial tachycardia. The incidence of this arrhythmia in young persons is less than 1%, however this arrhythmia is comprised of approximately 5% to 15% of patients undergoing electrophysiology studies. The arrhythmia can be seen on 24-hour Holter monitoring, but the asymptomatic patient should not be treated. If symptomatic, the patient may have typical symptoms accompanied with the SVT, including palpitations, lightheadedness, dyspnea, and perhaps syncope or presyncope.

The surface ECG can usually help differentiate AT from the more common rhythm sinus tachycardia by the following three features. Compare the EKG’s in Figures 132-11 and 132-12 which were obtained in the same patient. The former captures an episode of AT with a different P-wave axis and different PR interval. The second EKG, the patient is in a sinus rhythm with a normalized P-wave axis. Review of EKG’s while not in an arrhythmia can be helpful in identifying the SVT. The P-wave axis is usually different from the sinus P- wave, which is upright in leads I and II. The onset and termination of atrial tachycardia is usually very rapid, occurring over a few beats, in contrast to the 30 seconds or minutes it takes sinus tachycardia to develop or terminate. Finally, the PR interval can be variable, which is also known as unhooking.

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Figure 132-11 Atrial tachycardia. Discernible P-waves best seen in III and aVF. Notice the RP interval is greater than the PR interval. The tachycardia started abruptly and spontaneously and abruptly terminated after 20 minutes.

Figure 132-12 Normal sinus rhythm of the patient after spontaneous resolution of atrial tachycardia. Notice the distinctly different P-wave morphology between the two ECGs.

PRACTICE POINT

Atrial tachycardia features:

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P-wave axis is usually different from the sinus P-wave Onset and termination are very rapid Occurring over a few beats (contrast to the 30 seconds or minutes it takes sinus tachycardia to develop or terminate) PR interval variable Potential for developing tachycardia-induced cardiomyopathy (>70% of untreated patients) if the incessant variety Reversible with correction of the tachycardia

Difficulty differentiating this rhythm from a sinus tachycardia occurs when the focus of the arrhythmia is close to the superior portion of the cristas terminalis thereby mirroring the normal P-wave axis (positive in I, II). The importance of rhythm recognition lies in the potential for developing a tachycardia-induced cardiomyopathy if left untreated. Some studies have demonstrated that with an incessant form of atrial tachycardia, over 70% patients demonstrate decreased left ventricular function. Fortunately, this complication is reversible with correction of the tachycardia. Studies have demonstrated that patients with early-onset atrial tachycardia (before the age of 25) frequently spontaneously develop a normal sinus rhythm (Figure 132-12). AT could also be difficult to distinguish from AVRT and AVnRT, but clues such as variable RP intervals make AT more likely. If in doubt, the electrophysiologist should be consulted.

Inpatient management

In the acute setting, AV node-blocking calcium channel blockers (diltiazem, verapamil) or β-blockers can at times terminate the arrhythmia, or simply slow the ventricular rate via increased blockade at the AV node. Adenosine can also terminate the arrhythmia. The alternatives that are considered efficacious are sotalol and amiodarone; however, the side effects do need to be considered, especially if amiodarone is used for chronic management. The vagal maneuvers usually do not work, but electrical cardioversion may work, especially if the underlying reason for the AT is micro reentry or triggered activity. Long-term management may include the medications discussed previously or electrophysiologic ablation.

SINUS TACHYCARDIAS The sinus tachycardias represent a heterogeneous group of arrhythmias comprised of normal sinus tachycardia, inappropriate sinus tachycardia, postural orthostasis tachycardia syndrome (POTS), and sinus node reentry tachycardia (SNRT). All have the same ECG findings, which include a pulse rate >100 bpm, upright P-waves in limb leads I and II (normal P-wave vector). The clinical presentation varies from the asymptomatic to regular palpitations accompanied by syncope or presycope. Normal sinus tachycardia, as one would expect, is a result of physiologic demand and requires the appropriate workup.

POSTURAL ORTHOSTASIS TACHYCARDIA SYNDROME

Postural orthostasis tachycardia syndrome (POTS) is usually found in a young population between the ages of 18 and 50 with a female predominance of 5:1. The postulated

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mechanisms include partial dysautonomia and the less common central β-hypersensitivity form. POTS also has pronounced sympathetic characteristics such as tremors, anxiety, and palpitations. The evaluation of this condition includes the head-up tilt-table (HUTT) test documenting the patient’s symptoms and tachycardic response greater than 30 bpm over baseline and usually greater than 120 bpm. Other diagnostic studies include 24-hour urine sodium collection, serum norepinephrine measurement (>600 pg/dL), and postganglionic antibody testing. The use of physical maneuvers to increase muscle tone in the lower extremities, compression garments, volume expanders (ie, mineralocorticoids, increased salt diet, increase fluid intake), peripheral vasoconstrictors, and centrally acting β-blockers (ie, pindolol) are the therapeutic options, however they have limited efficacy.

INAPPROPRIATE SINUS TACHYCARDIA

Inappropriate sinus tachycardia (IST) characteristically has daytime tachycardia at rest or with minimal exertion and normalization of the pulse during sleep. The sinus node regulation is dysfunctional with enhanced sensitivity to sympathetic stimulus or decreased regulation by the parasympathetic system. In contrast to sinus node reentry tachycardia (SNRT), the onset and termination of this rhythm is gradual, and atrial overdrive pacing has no influence on the arrhythmia. Treatment of IST requires high doses of β-blockers or calcium channel blockers. Other treatment options include antiarrhythmics or even catheter ablation in the event of medical failure.

SINUS NODE REENTRY TACHYCARDIA

Sinus node reentry tachycardia (SNRT) originates within or very close to the sinus node. It usually starts and ends abruptly. Bedside interventions such as vagal maneuvers or intravenous adenosine or verapamil can terminate this arrhythmia. Following the SVT recognition algorithm (see Figure 132-1), this rhythm is categorized within the arrhythmias with an RP interval greater than the PR interval.

CONSULTATION AND REFERRAL A variety of instances of SVTs meet indications to consult general cardiology or electrophysiology cardiology (Table 132-11).

TABLE 132-11 Consultation for Supraventricular Tachyarrhythmias

Rhythm Consult Cardiology

Consider Direct Electrophysiology (EP) Consult

Atrial fibrillation 1. Refractory to multiple medications

2. Need for cardioversion (chemical, electrical, or both)

3. Desire to maintain sinus rhythm

4. Lone atrial fibrillation

1. Presence of sick sinus syndrome (SSS)—potential ablate-pace strategy

2. Refractory to medical management: potential for RFA

3. Presence of pre-excitation (WPW)

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Atrial flutter 1. Refractory to multiple medications

2. Need for cardioversion 3. Desire to maintain sinus

rhythm

Strong consideration for RFA strategy as first-line treatment

Atrioventricular nodal reentry tachycardia

Refractory to vagal maneuvers and IV adenosine

Frequent and debilitating palpitations: potential need for RFA

Atrioventricular tachycardia

All WPW patients 1. History of syncope/presyncope

2. Presence of atrial fibrillation or atrial flutter

Multifocal atrial tachycardia

   

Atrial tachycardia   Incessant: risk of cardiomyopathy

Sinus tachycardia • Sinus reentry • Inappropriate sinus

tachycardia • Postural orthostatic

tachycardia syndrome (POTS)

Inability to define etiology  

Junctional tachycardia Concern for digitalis toxicity  

RFA, radiofrequency ablation; SSS, sick sinus syndrome; WPW, Wolff-Parkinson-White syndome.

CONCLUSION A systematic algorithmic approach to SVTs will aid in differentiating the common from the uncommon (see Figure 132-1). In the setting of hemodynamic instability, other concerns fall to the wayside, and direct cardioversion should be performed without delay (except with sinus tachycardia, where the underlying cause should be identified and treated) (Table 132-12).

TABLE 132-12 Evidence-based Medicine: Key References for Supraventricular Tachyarrhythmias

Reference Methodology Results Bottom Line AFFIRM Wyse DG, et al. N Engl J Med. 2002;347(23):1825- 1833.

Randomized trial (rate control vs rhythm control for atrial fibrillation) • N = 4,060

No difference in overall mortality after 5 years of follow-up 23.8% vs 21.3% P = 0.08

Rhythm control not better than rate control

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• Patients age >65 or risk factors for stroke

AF CHF Roy D, et al. N Engl J Med. 2008;358(25):2667- 2676.

Randomized trial (rate control vs rhythm control for atrial fibrillation in systolic CHF) • N = 1376 • Ejection fraction

≤35%

No difference in time to death from cardiovascular causes (25% vs 27%) after 37 months

Rhythm control not better than rate control in systolic CHF

Validation of Clinical Classification Schemes for predicting stroke. Gage BF, et al. JAMA. 2001;285(22):2854- 2870.

Comparison of CHADS2 to AFI and SPAF risk classification schemes

CHADS2 c statistic of 0.82 compared to 0.68 and 0.74 for AFI and SPAF respectively

CHADS2 performs better at predicting strokes than prior classification schemes

RE-LY: Randomized evaluation of long- term anticoagulation therapy study group. Connolly SJ, et al. New Engl J Med. 2009;361:1139-1151.

Randomized trial in atrial fibrillation warfarin versu dabigatran • N = 18113 patients • Dabigatran 2 doses:

110 mg twice a day, 150 mg twice a day

• primary outcome • stroke or systemic

embolism • follow-up 2 years

Coumadin event rate= 1.69%/year Dabigatran 110 mg = 1.53%/y RR 0.91 P < 0.001 for noninferiority Dabigatran 150 mg = 1.11%/y RR 0.66 P < 0.001 for superiority

Higher-dose dabigatran prevents more strokes, but has equal major bleeding complications as coumadin

CHF, congestive heart failure.

SUGGESTED READINGS Blomström-Lundqvist C, Scheinman M, Aliot E, et al. ACC/AHA/ESC guidelines for the

management of patients with supraventricular arrhythmias: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias). J Am Coll Cardiol. 2003;42:1493

Fuster V, Ryden, L, Cannom M, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of

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Cardiology/American Heart developed in collaboration with the European Heart Rhythm Association and