Atrial Fibrillation

The most common cause of an irregularly irregular heartbeat, AF is particularly common in the elderly, as well as in patients with preexisting cardiopulmonary disease. The mechanism is rapid, quasiperiodic, chaotic reentry within the atria. Consequently, the AV node is bombarded with atrial excitation waves at a high irregular rate. Conduction of signals through the AV node is limited by the refractory period of the nodal tissue. The AV node cannot conduct until the cells have recovered from depolarization and are ready to fire again. This determines the rate of the irregular ventricular response to AF.

The clinician can usually diagnose AF at the bedside by feeling the pulse, listening to the heart sounds, and observing a single-lead cardiac monitor. The ECG may show fine or coarse irregular undulations of the baseline and an absence of regular P waves. The QRS complex is usually normal; however, if the ventricular response is rapid, the QRS complex may be transiently widened because of intermittent aberrant conduction through the His-Purkinje system (Fig. 59.3). This finding, termed the Ashman phenomenon, can occur when areas of the His-Purkinje tissue have a longer refractory period than the AV node does. Such bursts of wide QRS complex tachycardia can be confused with nonsustained VT, but on close inspection the rhythm remains irregularly irregular.

Fig. 59.3 Electrocardiogram showing atrial fibrillation with no clear P waves and an irregularly irregular ventricular response.

Note that the QRS complex is widened in a single beat after a relatively short R-R interval. This is the Ashman phenomenon, which occurs because the His-Purkinje system is still partly refractory to excitation.

The most common treatment issue for patients with AF in the emergency setting is control of the ventricular rate. Depending on the function of the patient’s AV node, the ventricular rate may range up to approximately 150 beats/min in adults. Ventricular rates this fast allow insufficient time for diastolic filling of the heart. The rate can be slowed with a variety of agents that act to lengthen the refractory period of the AV nodal tissue, such as calcium channel blockers,³ beta-blockers,⁴ magnesium,⁵ digoxin, and amiodarone. Digoxin is less useful in the emergency setting because it takes a few hours to work, but the other agents must be used carefully because they can decrease blood pressure to varying degrees. The calcium channel blocker diltiazem usually provides excellent rate control with minimal loss of blood pressure. Beta-blockers may cause a greater loss of blood pressure and must be used with caution in patients with CHF or pulmonary disease. There is no indication for the administration of adenosine in patients with AF. The diagnosis should be made on the basis of findings from the history, physical examination, and ECG. Furthermore, adenosine, which only transiently blocks AV nodal conduction, would have no lasting therapeutic benefit.

If a patient with AF has a rapid ventricular response and associated hypotension, emergency cardioversion should be considered. It is unusual for AF alone to cause hypotension, so the possibility of additional causative conditions that can be corrected, such as dehydration, occult hemorrhage, and the metabolic conditions previously mentioned, should also be considered. Nevertheless, cardioversion can be accomplished by electrical, chemical, or combined therapies. For a patient with cardiovascular instability, emergency direct current cardioversion (DCCV) is most effective and safe. The patient should be sedated if clinical circumstances allow and treatment begun at 100 J with a biphasic or monophasic pulse. A short-acting benzodiazepine such as midazolam is often the first choice for sedation because it is safe and effective and has amnestic properties as well. The defibrillator should be set to the synchronized mode to synchronize the pulse, if possible, with the QRS deflection, even though the QRS waves occur irregularly. If the initial shock is unsuccessful, the energy of the pulse can be escalated as needed.

Cardioversion can also be accomplished chemically when circumstances allow. Agents that slow conduction or increase the refractory period of atrial tissue are used to break the reentrant microcircuits within the atria. Vaughn-Williams class III and class I medications that can accomplish this goal include ibutilide, amiodarone, procainamide, propafenone, and flecainide.^6,7 These agents can terminate AF alone and increase the likelihood of cardioversion of AF with subsequent DCCV. However, their use entails some risk. There is an approximately 2% to 5% chance of causing torsades de pointes (TdP) after the infusion of ibutilide, amiodarone, and procainamide because these agents variably increase the duration of the depolarized phase and the associated QT interval in the ventricles, as well as the atria. The newly developed agent vernakalant may be less likely to cause TdP because of its action in blocking the ultrarapid potassium channels located primarily in the atria. Hypokalemia and hypomagnesemia raise the risk for TdP. Pretreatment with magnesium may be protective in some circumstances, even in patients with normal serum electrolyte levels.⁸ Propafenone and flecainide can slow conduction, exacerbate heart failure, and cause ventricular dysrhythmias. Cardioversion also carries a risk for embolic stroke.

AF is associated with unsynchronized, quivering motion of the atrial wall. As a result, there is stasis of blood in the atria and a risk for spontaneous clot formation. AF is an important cause of embolic stroke, with the embolism emanating from the left atrium or its appendage. Long-term anticoagulation with warfarin has been found to reduce the likelihood of embolic stroke, particularly in patients with risk factors, including previous stroke, valvular heart disease, hypertension, diabetes, CHF, and age older than 65 years.

In the acute setting, clot may form within 48 hours after the onset of AF. Cardioversion of AF may cause a new clot to embolize into the systemic circulation. If the patient can clearly discern when he or she is in AF, symptoms have begun within the preceding 1 to 2 days, and the patient is not at high risk for stroke, it is generally safe to perform cardioversion without anticoagulation.⁹ However, if there is any uncertainty about the time of onset of the tachydysrhythmia or if it occurred more than 48 hours ago, the patient should not undergo immediate cardioversion. Instead, the cardiology service should be consulted and transesophageal echocardiography performed to search for atrial clot formation, or cardioversion should be deferred until adequate anticoagulation has been established.¹⁰ The only exception would be cardiovascular instability secondary to AF, which requires emergency DCCV. Continuation of anticoagulation should also be considered for 4 weeks after cardioversion because there may be some delay in return of normal atrial contraction.

The disposition of patients with AF depends on a number of factors, including age, comorbid illnesses and social and outpatient medical support, adequacy of control of the ventricular rate, plans for cardioversion, and the state of anticoagulation.¹¹ If the patient requires ongoing adjustment of medications to control a rapid ventricular response, attempted cardioversion is planned, or new anticoagulation is initiated, hospitalization should be considered. The EP should make this decision in concert with the patient and the consulting cardiologist.

Multifocal Atrial Tachycardia

Multifocal AT (MFAT) is a relatively uncommon tachydysrhythmia that primarily affects older patients with chronic lung diseases such as chronic obstructive pulmonary disease, and it appears to be related to the administration of methylxanthine.¹² Its mechanism is uncertain, but MFAT is thought to occur as a result of DADs in atrial tissue triggering ectopic beats. The diagnosis is made on the basis of the following ECG criteria: at least three consecutive P waves with different morphologies, variable P-P and PR intervals, and a heart rate greater than 100 beats/min. Treatment of MFAT is centered on treating the underlying pulmonary disease and possible hypoxia. Antidysrhythmic agents are poorly effective in slowing the atrial rate or the ventricular response or in terminating MFAT. Nevertheless, a carefully administered trial of a calcium channel blocker or amiodarone is reasonable. Generally, beta-blockers should be avoided in patients with any evidence of bronchospasm. Magnesium therapy, particularly in combination with potassium replacement, may slow the rate or terminate the tachydysrhythmia. Patients usually require admission to treat the pulmonary disease.

Sinus Tachycardia

Sinus tachycardia may be due to a wide variety of physiologic, pathologic, or pharmacologic causes. If necessary, treatment is usually directed toward the underlying cause. In some settings, such as CHF or acute myocardial infarction (MI), treatment of sinus tachycardia with beta-blockers may improve cardiac hemodynamics and outcome. Sinus tachycardia is often part of the differential diagnosis of other regular tachydysrhythmias. Identifying characteristics of sinus tachycardia are (1) regularly occurring identical P waves with a leftward inferior axis in the frontal plane and (2) gradual onset and offset of the tachycardiac rate.

Atrial Flutter

Atrial flutter can occur as a result of a variety of cardiopulmonary and metabolic derangements, often in association with atrial dilation. Patients with atrial flutter also tend to experience AF, but atrial flutter is less common overall. The mechanism of atrial flutter is a macroreentrant circuit in the right atrium (see Fig. 59.1, A). The most common variant of atrial flutter is termed typical atrial flutter and involves a counterclockwise wave of roughly circular excitation when viewed from a position facing the front of the patient. The flutter pathway is constrained in the inferior portion of the circular loop by anatomic structures, and it travels between the tricuspid annulus anteriorly and the inferior vena cava and coronary sinus posteriorly. This segment of the pathway, the isthmus, contains the relatively slower-conducting tissue in the reentrant loop. Atypical atrial flutter most commonly travels over the same pathway, but in the opposite direction.

The rate of atrial flutter waves ranges from 250 to 350 beats/min. The diagnosis is made from the ECG tracing, which demonstrates typical sawtooth-shaped flutter waves at the appropriate rate, generally most prominent in the inferior limb leads (II, III, and aVF) and lead V₁. The flutter waves tend to be identical and to recur regularly, and there is no isoelectric or flat ECG segment between the waves (Figs. 59.4 and 59.5). As in AF, the refractory period of the AV node usually controls the ventricular response to atrial flutter. The most common response is 2 : 1 AV conduction; however, higher, lower, or variable ratios of conduction are also possible. The ratio of conduction depends on the atrial flutter rate, the health of the AV node, and any modifying physiologic, metabolic, or pharmacologic factors. Because atrial flutter is most commonly manifested as flutter waves at 300 beats/min, 2 : 1 AV conduction, and a ventricular response rate of 150 beats/min, atrial flutter should be the first diagnosis considered in all patients with a regular tachycardia at 150 beats/min. It is important to remember, however, that pharmacologic agents can slow the rate of atrial flutter and decrease or increase AV nodal conduction, thereby altering the usual characteristics.

Fig. 59.4 Electrocardiogram showing atrial flutter with 2 : 1 conduction and a regular ventricular rate of 150 beats/min.

Fig. 59.5 Electrocardiogram showing atrial flutter at approximately 260 beats/min with regularly irregular 3 : 2 conduction (3 flutter waves per 2 QRS complexes).

Note the variable flutter-to–QRS conduction interval (Wenckebach pattern) and alternating QRS complex morphology. These findings suggest that the heart rate is on the cusp of the refractory period of both the atrioventricular node and the His-Purkinje system.

Management of atrial flutter is similar to that for AF but can be a bit more difficult. Agents that lengthen the refractory period of the AV node tend to gradually decrease the ventricular response rate to AF. In the setting of atrial flutter, the decrease in the ventricular response rate with the same agents may be stepwise and incremental and thus more difficult to control. Furthermore, concomitant slowing of the atrial flutter waves may paradoxically allow greater efficiency of AV nodal conduction. For example, slowing flutter from 280 to 180 beats/min could lead to augmentation of the ventricular response from 2 : 1 conduction at 140 beats/min to 1 : 1 conduction at 180 beats/min.

Control of the ventricular rate in patients with atrial flutter can usually be achieved with a calcium channel antagonist such as diltiazem, a beta-blocker, or digoxin. Both electrical cardioversion and chemical cardioversion have a high success rate. Synchronized DCCV should start at 50 J, and the shock should be repeated with higher energy if the first is ineffective. Chemical cardioversion can be achieved with a variety of agents, including class III antidysrhythmics such as ibutilide and amiodarone, class I agents such as procainamide, and the beta-blocker esmolol. Rate control should generally be achieved before attempted chemical cardioversion. These agents can slow the atrial flutter rate with adverse enhancement of the conduction ratio as previously described, or in the case of procainamide or quinidine, the agent’s vagolytic properties may independently enhance AV nodal conduction.

Cardioversion of atrial flutter is associated with thromboembolism, although the association is probably weaker than that with cardioversion of AF.¹⁰ For this reason, cardioversion of atrial flutter should probably not be undertaken in the ED unless the indication is an emergency because of cardiovascular instability, the combined duration of atrial flutter and AF is less than 48 hours, the patient has been adequately anticoagulated before arrival in the ED, or the patient is newly anticoagulated without evidence of atrial thrombi on transesophageal echocardiography. The decision to hospitalize patients with atrial flutter involves weighing issues similar to those described for AF.

Atrial Tachycardia

Regular AT is a relatively uncommon tachydysrhythmia. It may be due to cardiopulmonary disease with dilated atria and a reentrant mechanism; toxicity from digoxin, methylxanthines, or adrenergic agents with increased automaticity; or other causes. AT is distinguished from atrial flutter by separate identifiable P waves with an intervening isoelectric baseline and a rate lower than 200 beats/min (Fig. 59.6). Sometimes the P waves have an abnormal upward or rightward axis, or the onset of tachycardia is abrupt. These characteristics would distinguish the rhythm from sinus tachycardia. Finally, as discussed later, unlike reentrant atrial rhythms that involve the AV node, AT would not be expected to terminate with agents that slow AV nodal conduction. As with atrial flutter, decreasing AV nodal conduction dynamics might slow the ventricular response to the rhythm and facilitate the diagnosis. It would not generally terminate the rhythm because the origin of the tachycardia is contained entirely within the atria.

Fig. 59.6 Electrocardiogram showing atrial tachycardia at a rate of 163 beats/min with a first-degree heart block and mostly 1 : 1 atrioventricular (AV) conduction with a single nonconducted beat (see lead V₁).

The abnormal rightward P-wave axis in lead I is not consistent with sinus rhythm. The rhythm is too slow for atrial flutter, and dropped beats would not be expected with a reentrant rhythm involving the AV node and ventricles.

Treatment of AT begins with assessment of the underlying causes. Digoxin toxicity should be suspected if AT is accompanied by high-grade AV block. Tachycardia in patients with digoxin toxicity results from altered intracellular calcium dynamics and increased excitability, whereas high-grade AV block results from enhanced vagal tone. When there is no evidence of underlying toxicity, ventricular rate control and electrical or chemical cardioversion for AT should be approached as for AF and flutter. If the patient shows evidence of drug toxicity or uncontrolled pulmonary disease or has new tachycardia, admission for further treatment should be considered.

Reentrant Supraventricular Tachycardia

The nomenclature of reentrant SVTs can be confusing. They are often termed paroxysmal because of their abrupt onset, or they may simply be called SVT. More precisely, they consist of two major subtypes of SVT, AV reentrant tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Reentrant SVTs are moderately common in both children and adults and most frequently are not associated with other cardiopulmonary disease.

Mechanistically, the two major subtypes of reentrant SVT are distinguished by the route of the reentrant pathway. AVRT uses a macroreentrant circuit with atrial and ventricular segments and connecting segments that involve the AV node and an accessory conducting tract, or rarely, two accessory conducting tracts (see Fig. 59.2, B and C). The AV nodal segment usually serves as the necessary slow-conducting portion of the reentrant circuit.

Many patients have at least two discrete segments that can conduct the input wave of excitability from the right atrium into the AV node. The conducting properties of these inputs may differ, and frequently both a fast-conducting input or pathway and a relatively slow-conducting one are present. Usually, conduction to the AV node is via the fast pathway. AVNRT uses a small macroreentrant circuit consisting of the AV node, right atrial tissue, and connecting fast and slow pathway segments to form a full circle of conduction (see Fig. 59.2, A).

Within each subtype of reentrant SVT, the direction of the wave of excitation can vary. In AVRT, the wave of excitation most commonly proceeds down the AV node and normally through the His-Purkinje system, and it returns in a retrograde direction up the accessory tract to the atria to complete the circuit; this pathway is termed orthodromic conduction (see Fig. 59.2, B). Antidromic conduction occurs when the wave of excitation proceeds in the opposite direction, down the accessory pathway, and returns in retrograde fashion up the AV node (see Fig. 59.2, C). In this case, conduction down the His-Purkinje system and normal, nearly simultaneous excitation of the ventricles do not occur. Rather, the ventricles are activated from the terminus of the accessory tract, and the wave of excitation must propagate across the ventricular myocardium similar to excitation from a premature ventricular contraction (PVC). Consequently, it takes longer to excite the entire ventricular muscle mass, and the corresponding QRS wave is widened with antidromic conduction.

Reentrant SVTs are usually easily diagnosed from the ECG. The most common finding is a narrow QRS complex tachycardia at rate of 120 to 250 beats/min. The atria are activated in a retrograde direction from the AV node or an accessory tract. In AVRT, retrograde P waves that are inverted in V₁ and the inferior leads may be observed just after the QRS complex (Fig. 59.7). In AVNRT, retrograde excitation of the atria is often simultaneous with ventricular excitation, and retrograde P waves are not observed because they are hidden or buried within the QRS complex (Fig. 59.8). In this case, P waves appear to be absent.

Fig. 59.7 Electrocardiogram showing atrioventricular reentrant tachycardia (AVRT) with retrograde P waves (inverted in the inferior leads) following the QRS complexes.

This strip demonstrates the more common orthodromic conduction variant of AVRT. The ventricles are depolarized normally, and then the signal travels up through the bypass tract to depolarize the atria from bottom to top.

Fig. 59.8 Electrocardiogram showing atrioventricular nodal reentrant tachycardia at 180 beats/min with spontaneous termination to normal sinus rhythm.

During tachycardia, retrograde atrial depolarization occurs simultaneously with ventricular depolarization. Thus, retrograde P waves are buried within the QRS complexes.

Reentrant SVT may be manifested as a wide QRS complex primarily for two reasons. Normal rapid conduction down the His-Purkinje system leads to nearly simultaneous excitation and depolarization of the ventricular myocardium and a narrow QRS complex on the ECG. If the left or right bundle of the Purkinje system fails to conduct, the QRS complex is widened and displays bundle branch block (BBB) morphology (see Fig. 59.2, F). This can occur as a result of intrinsic conduction system disease and chronic BBB, or the failure may be rate dependent and occur only during tachycardia. The other reason for a widened QRS complex is AVRT with antidromic conduction antegrade down the accessory pathway (see Fig. 59.2, C). This path does not use the His-Purkinje system, and a widened QRS complex without typical BBB morphology would be expected.

Particularly in children, reentrant SVTs are usually well tolerated. Patients with more rapid heart rates are more prone to cardiovascular instability, including hypotension and presyncope. Patients may also feel palpitations, dyspnea, and chest pain, which can be due to myocardial ischemia.

From an ED perspective, it is not usually important to distinguish AVRT from AVNRT. The acute treatment and prognosis for the two conditions are the same. Vagal maneuvers¹³ should be attempted or drugs administered to slow conduction and increase the refractory period through the AV nodal tissue so that the node is refractory to excitation and conduction when the reentrant wave approaches it. Agents such as adenosine and calcium channel blockers act directly on the nodal tissue, whereas other interventions, such as vagal maneuvers, digoxin, and beta-blockers, may alter vagal or adrenergic tone (Box 59.2). Adenosine may be the optimal agent because it is highly effective and safe with an ultrashort (9-second) half-life in serum. Rapid clearing, however, can be a disadvantage if the tachydysrhythmia is recurrent. In this case, the calcium channel blocker verapamil may be useful because it is equally effective for termination and may prevent recurrent episodes.¹⁴ Verapamil should not be used in infants, however, because of the risk for cardiovascular collapse.¹⁵

Physiologic maneuvers that increase vagal tone, such as immersion of the face in iced water, massage of the carotid bulb, and the Valsalva maneuver, may also be effective but have the same potential disadvantage of recurrence of the tachycardia. Iced water immersion may be more effective and better tolerated in children. Carotid massage should not be attempted in adults until a carotid bruit has been ruled out by auscultation. As for other supraventricular tachydysrhythmias, synchronized DCCV should be reserved for patients who demonstrate cardiovascular instability. Most patients can be discharged home after termination of reentrant SVT. Hospitalization should be considered for those whose tachydysrhythmia is recurrent or associated with cardiovascular instability.

Preexcitation (Wolff-Parkinson-White) Syndrome

When a patient has an accessory pathway of myocardial fiber connecting the atria and ventricles with evidence of antegrade conduction down this pathway, the patient has preexcitation, or WPW, syndrome. The syndrome is uncommon, is usually diagnosed in children or young adults, and is most commonly not associated with other cardiopulmonary disease. Patients may be in normal sinus rhythm or have a variety of supraventricular tachydysrhythmias, including AVRT in 80% of cases, AF in 15% to 30%, and atrial flutter in 5%. Approximately 85% of AVRT episodes have an orthodromic direction of activation, and 15% are antidromic.

The diagnosis can be made while the patient is in normal sinus rhythm if the following characteristics are observed on the ECG: (1) shortened PR interval (<120 msec), (2) widened QRS complex beyond 120 msec, and (3) atypical initiation of the QRS complex with a delta-wave morphology (Fig. 59.9). Associated ST-T wave abnormalities are often present, with the T wave inverted with respect to the delta wave and QRS complex. These three diagnostic abnormalities are easily understood from an electrophysiologic perspective (see Fig. 59.2, D).

Fig. 59.9 Electrocardiogram showing Wolff-Parkinson-White (WPW) syndrome with normal sinus rhythm.

Note the shortened PR interval, widened QRS wave with slurred upstroke, and abnormal inverted T wave. These findings in lead V₅ are diagnostic of WPW syndrome with an accessory conduction tract, probably in the left lateral position.

In normal sinus rhythm, the wave of excitation can propagate down both the AV node and the accessory pathway. Because the accessory pathway does not contain slow-conducting tissue, the wave traverses the accessory pathway and reaches the ventricular myocardium before traversing the AV node. The shortened PR interval and early delta wave upstroke of the QRS wave are due to preexcitation of the ventricle via the accessory pathway. Eventually, the atrial excitation wave also traverses the AV node, and once this occurs, it will move rapidly through the specialized rapid-conducting His-Purkinje system. In the meantime, the wave that has traversed the accessory pathway propagates slowly through the ventricular myocardium because it does not use the Purkinje fibers for rapid transmission. Consequently, the QRS deflection arrives early with a delta wave, but the latter portion normalizes as a result of the influence of normal AV nodal conduction. Because of the atypical pattern of ventricular depolarization, repolarization changes in the form of ST-T abnormalities are expected.

Patients with WPW syndrome are predisposed to AVRT, as well as to AF and atrial flutter, which often demonstrates a rapid ventricular response. The pathway of conduction of the AF wavelets from the atria to the ventricles depends on the relative refractory period of the accessory pathway with respect to the AV node. The slow-conducting cells of the AV node have a long refractory period, and the refractory period of the accessory conducting tissue is usually shorter. Consequently, the AV node remains refractory when the accessory pathway tissue is repolarized and ready for conduction. In WPW syndrome, AF usually conducts down the accessory pathway with a rapid ventricular response rate that is determined by the refractory period of the accessory conducting tissue (Fig. 59.10; also see Fig. 59.2, E). Similar to the situation with normal sinus rhythm, the ventricles are activated from the ectopic accessory pathway terminus, and an irregularly irregular tachycardia with a wide QRS complex results.

Fig. 59.10 Electrocardiogram showing atrial fibrillation with wide QRS complexes and a rapid variable ventricular response rate consistent with Wolff-Parkinson-White syndrome.

The grossly irregularly irregular rhythm distinguishes this condition from ventricular tachycardia. This is a dangerous condition that requires immediate attention and treatment. The risk for conversion to ventricular fibrillation and cardiovascular collapse is inversely associated with the length of the shortest R-R interval.

Perhaps the greatest concern regarding patients with WPW syndrome is their higher risk for sudden cardiac death. This risk is inversely associated with the minimum refractory period of the accessory conducting tissue.² The mechanism of sudden cardiac death is thought to most commonly be AF with accessory tract conduction and a dangerously high ventricular response rate that causes ischemia and electrical instability and degenerates to VF.

It is important to remember that like the AV node and other cardiac tissue, accessory pathways have dynamic electrophysiologic properties that may vary with the hormonal, physiologic, or pharmacologic milieu. However, in this respect, accessory pathway tissue behaves more like myocardium and less like AV nodal tissue, which is highly sensitive to vagal stimulation. Depending on the current milieu, conduction in many patients with WPW syndrome may variably occur primarily down the accessory pathway or the AV node in normal sinus rhythm, and this variation even occasionally occurs in AF (Fig. 59.11).

Fig. 59.11 Electrocardiogram showing atrial fibrillation in a patient with Wolff-Parkinson-White syndrome and variable conduction down the atrioventricular node and His-Purkinje system with a resulting narrow QRS complex, as well as down the accessory pathway with a slurred upstroke, wide QRS complex.

The slow ventricular response rate suggests that this accessory pathway has a relatively long refractory period and a more benign prognosis.

Treatment of AF with rapid ventricular response in patients with WPW syndrome must be approached differently. The usual treatment of AF is to administer agents that increase the refractory period of the AV node and slow AV nodal conduction. Because conduction is primarily down the accessory pathway in WPW syndrome, treatment must be directed toward lengthening the refractory period of the accessory pathway tissue, not the AV node. Paradoxically, agents that block AV nodal conduction, such as beta-blockers, calcium channel blockers, adenosine, and digoxin, may also cause vasodilation, decrease contractility, or have other effects that reflexively increase adrenergic tone or stimulate and enhance accessory pathway conduction. For this reason, these agents should not be used.

The preferred pharmacologic agents for patients with WPW syndrome and AF with a rapid ventricular response are the class IA antidysrhythmic agent procainamide¹⁶ and, possibly, class III medications such as amiodarone and sotalol. These antidysrhythmics are used to decrease the ventricular response rate, and they may also terminate AF. Nevertheless, they have multiple potential dangers and must be used with caution. All these antidysrhythmic agents can decrease blood pressure. When administered intravenously, amiodarone blocks AV nodal conduction, so the concerns already described with other AV nodal blocking agents may be applicable.¹⁷ The safest and most effective treatment for patients with WPW syndrome and AF with a rapid ventricular response is synchronized DCCV. The EP should consider using DCCV with sedation before administering antidysrhythmics to patients with a ventricular response greater than 150 beats/min or borderline low blood pressure.

For patients with WPW syndrome, the principles of treatment of AVRT are similar to those for AF. AV nodal blocking agents should not be used to treat presumed antidromic wide QRS complex AVRT because the underlying rhythm could be misdiagnosed as atrial flutter or tachycardia with accessory pathway conduction. AV nodal blocking agents could be used to treat orthodromic AVRT with a narrow QRS complex, but subsequent AF with rapid accessory pathway conduction remains a potential concern. It may be wiser to use the class IA or class III antidysrhythmics described previously or to proceed directly to DCCV.

Patients with WPW syndrome and rapid antegrade bypass tract conduction are at higher risk than other patients with SVT for cardiovascular decompensation. In particular, patients with recurrent unstable tachycardias should be admitted to the hospital. Nevertheless, the decision to admit or discharge most patients should be made individually in consultation with the cardiologist.

Junctional Tachycardia

Junctional tachycardia is an uncommon dysrhythmia associated with toxic stimulation of the AV node by digoxin, methylxanthines, or other stimulants or with cardiac disease such as inferior MI, acute rheumatic fever, or myocarditis. The most common mechanism is enhanced automaticity of the nodal tissue. The heart sounds are usually regular. In patients with simultaneous antegrade ventricular and retrograde atrial activation, the right atrium may contract against a closed tricuspid valve and thereby lead to large cannon jugular venous waves. The ECG appearance is a narrow complex tachycardia up to a rate of approximately 130 beats/min without synchronous preceding P waves. P waves may be present with evidence of AV dissociation. Alternatively, retrograde nodal-to-atrial conduction with abnormal P waves and a superior axis occurring after the QRS deflection may be seen. P waves may be absent if atrial depolarization occurs simultaneously with ventricular depolarization.

Digoxin toxicity is an important cause of junctional tachycardia. In particular, digoxin toxicity should be suspected when the rapid ventricular response to AF becomes regular during digoxin treatment. Diagnosis and treatment should focus on identifying and addressing the underlying cause, including reversal of toxicity, if any. Digoxin immune Fab fragments (Digibind) may be necessary for the cardiovascular instability associated with digoxin toxicity, and DCCV should be avoided if possible. Most patients require admission until the underlying disease or toxicity is resolved.

Wide QRS Complex Tachycardia: Differentiating Supraventricular From Ventricular Tachycardia

Wide QRS complex tachycardia may be due to an SVT with aberrant His-Purkinje conduction or antegrade conduction down an accessory pathway or be due to VT. Diagnosis of the underlying mechanism is important for a number of reasons. The optimal short- and long-term treatment and prognosis may vary considerably, depending on the mechanism involved. The history, physical examination, and ECG findings can be used to make the diagnosis (Box 59.3). In the ED, the pretest probability favors VT by a ratio of 2 : 1 to 3 : 1.

No single historical factor has been found to be both sensitive and specific for diagnosing VT. Nevertheless, age older than 35 years and male sex are sensitive for VT, and a previous history of MI or coronary artery bypass graft surgery, recent angina, or CHF is a specific predictor of VT.²³ The primary underlying theme for all these predictors is a greater likelihood of coronary artery disease and previous infarction with scar formation. In fact, the strongest single historical predictor of VT is a history of MI, which has a positive likelihood ratio of 13 : 1 to 20 : 1 and a negative likelihood ratio of 0.36.^23,24

A number of approaches may be used to diagnose wide QRS complex tachycardia from the physical examination. Perhaps the first and most important principle to remember is that apparent hemodynamic stability does not rule out VT. AV dissociation is present about half the time in patients with VT.²⁵ When it is present, the atria are contracting independently of the ventricles, so the atria may either contract during ventricular diastole and assist cardiac output or contract against closed valves during ventricular systole with a large retrograde venous pulsation. The EP can assess for beat-to-beat variation of the first heart sound or systolic blood pressure or for large cannon jugular venous waves. Unfortunately, even under controlled experimental conditions, none of these findings are both sensitive and specific.²⁶ In clinical conditions in which about half the patients have some form of retrograde ventricular-atrial conduction, these tests for physical evidence of AV dissociation can approach a sensitivity for VT of only approximately 50% at best.

Vagal maneuvers, such as carotid sinus massage or the Valsalva maneuver, can be performed to increase vagal tone and alter AV nodal conduction. Depending on the type of SVT, vagal maneuvers could terminate a reentrant rhythm involving the AV node or temporarily decrease the ventricular response to a purely atrial rhythm such as atrial flutter. Termination of wide QRS complex tachycardia with vagal maneuvers would suggest a supraventricular rhythm because most forms of VT are not responsive. Temporary slowing of the ventricular response to an atrial tachydysrhythmia could be diagnostic.

A similar principle of brief increased refractoriness of the AV node underlies the use of adenosine to diagnose and treat wide QRS complex tachycardia. The combined response to a 12-mg bolus of adenosine—either termination of the tachycardia or transient ventricular slowing—has a sensitivity of 90% and a specificity of 98% for an underlying SVT.²⁷ Considered in reverse fashion, “nonresponse” to a 12-mg bolus of adenosine would have a positive likelihood ratio of about 9 and a negative likelihood ratio of 0.03 for VT. This test is useful for diagnosis, but is it safe?

The primary safety concern is the administration of adenosine to patients with atrial flutter and antegrade accessory pathway conduction, which might cause subsequent transient acceleration of this conduction and the ventricular response. This and other destabilizing scenarios have been reported after the administration of adenosine to patients with wide QRS complex tachycardia secondary to SVT and VT. Adenosine should never be given to patients with a rapid, irregularly irregular wide QRS complex tachycardia because it may actually be AF with accessory pathway conduction, and acceleration of the ventricular response has been reported in this situation as well. Nonetheless, the adverse affects previously described after adenosine administration to patients with regular wide QRS complex tachycardia are rare. Multiple consecutive case series have found no greater rate of adverse effects with adenosine than with other antidysrhythmic medications.^27,28 Adenosine should be used as a diagnostic and therapeutic agent for regular wide QRS complex tachycardia when the history, physical examination, and ECG findings suggest a supraventricular origin. The EP should ensure that the adenosine is used properly—administered as a 12-mg rapid bolus dose followed immediately by a normal saline bolus flush, with a cardioverter-defibrillator immediately available in the event of destabilization.

A number of ECG findings can be used to diagnose wide QRS complex tachycardia. Possible differentiating characteristics include the heart rate, frontal axis of the QRS deflection, concordance across the precordial leads, QRS duration, morphology of the QRS complex, AV dissociation, and capture or fusion beats. On average, wide QRS complex tachycardia secondary to SVT has a faster heart rate than that secondary to VT.²⁵ This difference has been slightly augmented in the recent past with the use of ICDs. A patient with VT may have already received an ICD, which is preferentially programmed to treat rapid VT, usually greater than 160 to 180 beats/min. It cannot be programmed to treat slower VT because of the risk for inappropriate pacing or shocks for sinus tachycardia. Nevertheless, there is still too much overlap in the heart rate of patients with SVT and VT to use it as a firm differentiating factor. Regardless of the underlying rhythm, higher heart rates are associated with compromised cardiac output because of inadequate diastolic filling and greater electrical instability. Immediate DCCV should be considered for patients with rapid wide QRS tachycardia, regardless of the presumed etiology.

Because of the common ectopic left ventricular origin of the rhythm in VT, abnormal upward and rightward propagation of the excitation wave may be seen. In fact, the QRS axis may point to any of the four quadrants in VT, but an upward and rightward QRS axis is highly unusual for SVT. This finding, defined by a negative QRS deflection in leads I and aVF, is insensitive (24%) but highly specific (100%) for VT (Fig. 59.12).²⁹ An abnormal QRS vector that points toward or away from all of the precordial leads simultaneously is also indicative of VT. A QRS deflection that is primarily positive in all of the precordial leads is defined as positive concordance. The finding of primarily negative QRS deflections in all precordial leads is defined as negative concordance. Each of these findings is also insensitive (10%) but specific (85%) for VT.²⁹

Fig. 59.12 Diagram of the chest with the six electrocardiographic limb leads superimposed.

Depolarization of the QRS complex can be viewed as primarily positive in one of four quadrants, and the right upward quadrant is specifically identified in this diagram. Normal QRS depolarization is most commonly in the direction of the left lower quadrant. When the QRS complex points to the right upward quadrant, it is highly abnormal and suggestive of ventricular tachycardia. Sens, Sensitivity; Spec, specificity.

On average, the duration of initial depolarization as recorded by the QRS wave is longer with VT than with wide QRS complex SVT. A QRS duration greater than 140 msec with a right BBB (RBBB) pattern or a QRS duration greater than 160 msec with a left BBB (LBBB) pattern is insensitive but more than 90% specific for VT.²⁹ Brugada et al.³⁰ modified this concept and found that an RS interval greater than 100 msec in the precordial leads has a sensitivity of 66% and a specificity of 98% for VT (Fig. 59.13). Unfortunately, the high specificity of these findings is not applicable if the patient has received a medication that widens the QRS complex, such as a class I antidysrhythmic.

Fig. 59.13 How to measure the RS interval (double arrow).

The RS interval begins with the upstroke of the R wave and ends with the nadir of the S wave.

QRS morphology may be helpful, particularly if an old ECG is available. QRS morphology with tachycardia similar to a previous BBB morphology noted in sinus rhythm may suggest, but does not prove SVT.³¹ The distinction of RBBB versus LBBB is itself not helpful, but various morphologic variants within these two categories can at least be theoretically helpful.^24,25,30

When present, the most definitive evidence of VT is AV dissociation. In SVT an atrial contraction is associated with each ventricular beat. AV dissociation is defined by atrial activity that is separate and independent of ventricular contractions (Fig. 59.14). AV dissociation is present in about half of VT episodes, and it can be seen on the ECG in half of these cases, or about one quarter of all VT episodes. Thus, AV dissociation has a sensitivity of about 25% and specificity approaching 100% for VT. Dissociated P waves should be sought in the V₁ rhythm strip, where they are usually most easily seen. The key is to find two candidate P waves. One can then look an equal distance on each side of these two waves for a third deflection. If three consecutive deflections are found that “march out,” they are probably P waves; such identification can be confirmed by marching out more on the ECG. Fusion beats represent fusion of supraventricular excitation mediated by the His-Purkinje system and local ventricular excitation. Capture beats signify complete ventricular depolarization by a supraventricular signal and usually have a narrow QRS complex. Both these phenomena also suggest AV dissociation and VT (Figs. 59.15 and 59.16).

Fig. 59.14 Electrocardiogram showing ventricular tachycardia with atrioventricular dissociation.

Although the QRS complexes are relatively narrow, there is clear evidence of atrioventricular dissociation in the V₁ rhythm strip.

Fig. 59.15 Electrocardiogram showing ventricular tachycardia with a single capture beat.

Fig. 59.16 Electrocardiogram showing ventricular tachycardia with evidence of atrioventricular dissociation and independent atrial activity (arrowheads).

Note that a single atrial beat partly captures the ventricles (arrow), and there is probably fusion with the ongoing ventricular cycle.

Severe hyperkalemia can also cause wide QRS complex tachycardia. Clues to this diagnosis include a history of renal failure or other medical causes of hyperkalemia and an ECG with very wide and bizarre QRS complexes (Fig. 59.17). Once the condition is diagnosed, it should be confirmed with a serum potassium measurement and treated with intravenous calcium, insulin, glucose, and bicarbonate. Patients who overdose with cyclic antidepressants or other sodium channel blocking agents may have a wide QRS complex tachycardia. An important clue to this diagnosis on the ECG is right axis deviation of the terminal 30 msec of the QRS complex. Patients with suspected overdose should be treated with a continuous intravenous sodium bicarbonate infusion. Patients with acute respiratory distress secondary to pulmonary disease and with an underlying BBB may appear to have a primary tachydysrhythmic condition. Addressing the airway, with intubation if necessary, may slow the heart rate, expose the P waves, and clarify the rhythm.

Fig. 59.17 A 50-year-old man was found lying down with lethargy and shortness of breath. He was a hemodialysis patient who had missed dialysis for a week. His serum potassium level was 8.4 mEq/L. Note the marked wide and bizarre QRS complexes with a right upward frontal plane axis on his electrocardiogram.

Finally, in a significant proportion of cases it may not be possible to make a definitive ED diagnosis. In some cases of VT the bundle branches may be used as part of the reentrant limb, thereby mimicking aberrant conduction, and excitation of the ventricles via an accessory pathway may give an ECG appearance of VT. When the diagnosis is in doubt, the safest approach is to sedate the patient, perform DCCV, and leave the definitive diagnosis for the electrophysiologist.