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