Specific Arrhythmias

Diagnosis and Treatment

Jeffrey E. Olgin, Douglas P. Zipes

Normal Sinus Rhythm

Normal sinus rhythm is arbitrarily limited to impulse formation beginning in the sinus node at rates between 60 and 100 beats/minute. Infants and children generally have faster heart rates than adults do, both at rest and during exercise. The P wave is upright in electrocardiographic leads I, II, and aVF and negative in lead aVR, with a vector in the frontal plane of between 0 and +90 degrees. In the horizontal plane, the P vector is directed anteriorly and slightly leftward and can therefore be negative in leads V₁ and V₂ but positive in V₃ to V₆. The PR interval exceeds 120 milliseconds (msec) and can vary slightly with the rate. If the pacemaker site (site of impulse origin) shifts, a change in morphology of the P wave can occur. The rate of sinus rhythm varies significantly and depends on many factors, including age, sex, and physical activity.

The sinus nodal discharge rate responds readily to autonomic stimuli. Steady vagal (parasympathetic) stimulation decreases the spontaneous sinus nodal discharge rate and predominates over steady sympathetic stimulation, which increases the spontaneous sinus nodal discharge rate.

Rates lower than 60 beats/minute are considered to be bradycardia, and rates higher than 100 beats/minute are considered to be tachycardia. As described in Chapter 33, the normal sequence of electrical activation of the heart is from the sinus node through the atria to the atrioventricular (AV) node and His-Purkinje system and to the ventricular myocardium. Arrhythmias resulting in bradycardia or tachycardia can be thought of as specific disorders of each of these components. Specific tachyarrhythmias and bradyarrhythmias presented as disorders of this electrophysiologic (EP) hierarchy and their characteristics are summarized in Table 37-1.

TABLE 37-1

Characteristics of Arrhythmias *

TYPE OF ARRHYTHMIA	P WAVES			QRS COMPLEXES			VENTRICULAR RESPONSE TO CAROTID SINUS MASSAGE	PHYSICAL EXAMINATION			TREATMENT
TYPE OF ARRHYTHMIA	Rate (Beats/min)	Rhythm	Contour	Rate (Beats/min)	Rhythm	Contour	VENTRICULAR RESPONSE TO CAROTID SINUS MASSAGE	Intensity of S₁	Splitting of S₂	A Waves	TREATMENT
Sinus rhythm	60-100	Regular^†	Normal	60-100	Regular	Normal	Gradual slowing and return to former rate	Constant	Normal	Normal	None
Sinus bradycardia	<60	Regular	Normal	<60	Regular	Normal	Gradual slowing and return to former rate	Constant	Normal	Normal	None, unless symptomatic; atropine
Sinus tachycardia	100-180	Regular	May be peaked	100-180	Regular	Normal	Gradual slowing^‡ and return to former rate	Constant	Normal	Normal	None, unless symptomatic; treat underlying disease
AV nodal reentry	150-250	Very regular except at onset and termination	Retrograde; difficult to see; lost in QRS complex	150-250	Very regular except at onset and termination	Normal	Abrupt slowing caused by termination of tachycardia or no effect	Constant	Normal	Constant cannon a waves	Vagal stimulation, adenosine, verapamil, digitalis, propranolol, DC shock, pacing
Atrial flutter	250-350	Regular	Sawtooth	75-175	Generally regular in absence of drugs or disease	Normal	Abrupt slowing and return to former rate; flutter remains	Constant; variable if AV block changing	Normal	Flutter waves	DC shock, digitalis, quinidine, propranolol, verapamil, adenosine
Atrial fibrillation	400-600	Grossly irregular	Baseline undulation, no P waves	100-160	Grossly irregular	Normal	Slowing; gross irregularity remains	Variable	Normal	No a waves	Digitalis, quinidine, DC shock, verapamil, adenosine
Atrial tachycardia with block	150-250	Regular; may be irregular	Abnormal	75-200	Generally regular in absence of drugs or disease	Normal	Abrupt slowing and return to normal rate; tachycardia remains	Constant; variable if AV block changing	Normal	More a waves than c-v waves	Stop digitalis if toxic; digitalis if not toxic; possibly verapamil
AV junctional rhythm	40-100^§	Regular	Normal	40-60	Fairly regular	Normal	None; may be slight slowing	Variable^‖	Normal	Intermittent cannon waves	None, unless symptomatic; atropine
Reciprocating tachycardias using an accessory (WPW) pathway	150-250	Very regular except at onset and termination	Retrograde; difficult to see; monitor the QRS complex	150-250	Very regular except at onset and termination	Normal	Abrupt slowing caused by termination of tachycardia or no effect	Constant but decreased	Normal	Constant cannon waves	See AV nodal reentry earlier
Nonparoxysmal AV junctional tachycardia	60-100^‖	Regular	Normal	70-130	Fairly regular	Normal	None; may be slight slowing	Variable^‖	Normal	Intermittent cannon waves^‖	None, unless symptomatic; stop digitalis if toxic
Ventricular tachycardia	60-100^‖	Regular	Normal	110-250	Fairly regular; may be irregular	Abnormal, >0.12 sec	None	Variable^‖	Abnormal	Intermittent cannon waves^‖	Lidocaine, procainamide, DC shock, quinidine, amiodarone
Accelerated idioventricular rhythm	60-100^‖	Regular	Normal	50-110	Fairly regular; may be irregular	Abnormal, >0.12 sec	None	Variable^‖	Abnormal	Intermittent cannon waves^‖	None, unless symptomatic; lidocaine, atropine
Ventricular flutter	60-100^‖	Regular	Normal; difficult to see	150-300	Regular	Sine wave	None	Soft or absent	Soft or absent	Cannon waves	DC shock
Ventricular fibrillation	60-100^‖	Regular	Normal; difficult to see	400-600	Grossly irregular	Baseline undulations; no QRS	None	None	None	Cannon waves	DC shock
First-degree AV block	60-100^¶	Regular	Normal	60-100	Regular	Normal	Gradual slowing caused by sinus	Constant, diminished	Normal	Normal	None
Type I second-degree AV block	60-100^¶	Regular	Normal	30-100	Irregular**	Normal	Slowing caused by sinus slowing and an increase in AV block	Cyclical decrease, then increase after pause	Normal	Normal; increasing a-c interval; a waves without c waves	None, unless symptomatic; atropine
Type II second-degree AV block	60-100^¶	Regular	Normal	30-100	Irregular^¶	Abnormal, >0.12 sec	Gradual slowing caused by sinus slowing	Constant	Abnormal	Normal; constant a-c interval; a waves	Pacemaker
Complete AV block	60-100^‖	Regular	Normal	<40	Fairly regular	Abnormal, 0.12 sec	None	Variable^¶	Abnormal	Intermittent cannon waves^¶	Pacemaker
Right bundle branch block	60-100	Regular	Normal	60-100	Regular	Abnormal, 0.12 sec	Gradual slowing and return to former rate	Constant	Wide	Normal	None
Left bundle branch block	60-100	Regular	Normal	60-100	Regular	Abnormal, >0.12 sec	Gradual slowing and return to former rate	Constant	Paradoxical	Normal	None

^* In an effort to summarize these arrhythmias in tabular form, generalizations have to be made. For example, the response to carotid sinus massage may be slightly different from what is listed. Acute therapy to terminate a tachycardia may be different from chronic therapy to prevent recurrence. Some of the exceptions are indicated in the footnotes; the reader is referred to text for a complete discussion.

^† P waves initiated by sinus node discharge may not be precisely regular because of sinus arrhythmia.

^‡ Frequently, carotid sinus massage fails to slow a sinus tachycardia.

^§ Any independent atrial arrhythmia may exit or the atria may be captured retrogradely.

^‖ Constant if the atria are captured retrogradely.

^¶ Atrial rhythm and rate may vary, depending on whether sinus bradycardia, sinus tachycardia, or another abnormality is the atrial mechanism.

^** Regular or constant if block is unchanging.

Modified from Zipes DP: Arrhythmias. In Andreoli K, Zipes DP, Wallace AG, et al (eds): Comprehensive Cardiac Care. 6th ed. St. Louis, CV Mosby, 1987.

Tachyarrhythmias

Tachyarrhythmias are broadly characterized as supraventricular tachycardia (SVT), defined as a tachycardia in which the driving circuit or focus originates, at least in part, in tissue above the level of the ventricle (i.e., sinus node, atria, AV node, or His bundle), and ventricular tachycardia (VT), defined as a tachycardia in which the driving circuit or focus originates solely in ventricular tissue or Purkinje fibers. Because of differences in prognosis and management, distinction between SVT and VT is critical early in the acute management of a tachyarrhythmia.¹ In general (with the exception of idiopathic VT, described later), VT often carries a much graver prognosis, usually implies the presence of significant heart disease, results in more profound hemodynamic compromise, and therefore requires immediate attention and measures to revert to sinus rhythm. SVT is not usually lethal and often does not result in hemodynamic collapse; therefore, more conservative measures can be applied initially to convert to sinus rhythm.²^,³

Distinction between SVT and VT can generally be made on the basis of the electrocardiogram (ECG) obtained during tachycardia (see Chapter 34).⁴ It is important to obtain a 12-lead ECG during tachycardia if possible and to obtain 12-lead (or at least multilead) rhythm strips during any intervention aimed at termination of the tachycardia because examining the termination (and initiation) can help identify the specific arrhythmia.⁵ In general, if the QRS is narrow (duration <120 msec, often referred to as narrow-complex tachycardias), the ventricle is being activated via the normal His-Purkinje system, and thus the origin of the tachycardia is supraventricular (Fig. 37-1). In contrast, a wide QRS (duration >120 msec) during tachycardia suggests VT; however, in some common scenarios SVT can produce a wide QRS complex. Therefore a more descriptive term, wide-complex tachycardia (WCT), is often used when the precise arrhythmia mechanism cannot be determined. For example, SVT with a concurrent bundle branch block or intraventricular conduction defect can produce WCTs despite a supraventricular origin. In addition, preexcited tachycardias (tachycardias in which the ventricle is activated in whole or in part over an accessory pathway) produce wide QRS complexes despite being supraventricular in origin. Therefore, although a narrow-complex tachycardia almost always makes the diagnosis of SVT, a WCT can be supraventricular or ventricular. Fusion or capture beats and AV dissociation are diagnostic of VT (discussed later, see Ventricular Tachycardia, Electrocardiographic Recognition) but are often not present or are difficult to detect. Criteria and algorithms have been developed to determine whether a WCT is more likely to be SVT or VT (see Differentiation between Ventricular and Supraventricular Tachycardia below).⁴ The general principles behind these algorithms rest on the assumption that the closer the QRS morphology is to a typical bundle branch block pattern, the more likely that it is an SVT and assumes that the septum is still rapidly activated in a WCT because of SVT.

FIGURE 37-1 Algorithm for the diagnosis of a narrow-QRS tachycardia. AVRT = atrioventricular reentrant tachycardia; AVNRT = atrioventricular nodal reentrant tachycardia; MAT = multifocal atrial tachycardia; PJRT = permanent form of AV junctional reciprocating tachycardia. (From Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines [Writing Committee to Develop Guidelines for the Management of Patients With Supraventricular Arrhythmias]. Circulation 108:1871, 2003.)

Supraventricular Rhythm Disturbances

Sinus Tachycardia

Electrocardiographic Recognition

During sinus tachycardia (Fig. 37-2), the sinus node exhibits a discharge frequency between 100 and 180 beats/minute, but it can be higher with extreme exertion and in young individuals. The maximum heart rate achieved during strenuous physical activity varies widely but decreases with age. Sinus tachycardia generally has a gradual onset and termination. The P-P interval can vary slightly from cycle to cycle, especially at slower rates. P waves have a normal contour, a larger amplitude can develop, and the wave can become peaked. They appear before each QRS complex with a stable PR interval unless concomitant AV block ensues.

FIGURE 37-2 Sinus tachycardia (150 beats/min) in a patient during acute myocardial ischemia; note the ST-segment depression. P waves are indicated by arrowheads.

Accelerated phase 4 diastolic depolarization of sinus nodal cells (see Chapter 33) is generally responsible for sinus tachycardia and is usually caused by elevated adrenergic tone or withdrawal of parasympathetic tone. Carotid sinus massage and Valsalva or other vagal maneuvers gradually slow sinus tachycardia, which then accelerates to its previous rate on cessation of the enhanced vagal tone. More rapid sinus rates can fail to slow in response to a vagal maneuver, particularly those driven by high adrenergic tone.

Clinical Features

Sinus tachycardia is common in infancy and early childhood and is the normal reaction to various physiologic or pathophysiologic stress, such as fever, hypotension, thyrotoxicosis, anemia, anxiety, exertion, hypovolemia, pulmonary emboli, myocardial ischemia, congestive heart failure, and shock. Drugs such as atropine, catecholamines, and thyroid medications, as well as alcohol, nicotine, caffeine, and amphetamines or other stimulants, can produce sinus tachycardia. Persistent sinus tachycardia can be a manifestation of heart failure.

In patients with structural heart disease, sinus tachycardia can result in reduced cardiac output or angina or can precipitate another arrhythmia, in part related to the abbreviated ventricular filling time and compromised coronary blood flow. Sinus tachycardia can be a cause of inappropriate defibrillator discharge in patients with an implantable cardioverter-defibrillator (ICD; see Chapter 36). Chronic inappropriate sinus tachycardia (also known as the syndrome of inappropriate sinus tachycardia) has been described in otherwise healthy persons, possibly secondary to increased automaticity of the sinus node or an automatic atrial focus near the sinus node.⁶ The abnormality can result from a defect in either sympathetic or vagal nerve control of sinoatrial (SA) automaticity or from an abnormality of the intrinsic heart rate. In postural orthostatic tachycardia syndrome, a related syndrome consisting of orthostatic hypotension and sinus tachycardia, the cause of the orthostatic decrease in blood pressure is not hypovolemia or drugs. Both syndromes can result from autonomic neuropathy (either peripheral, as in diabetic patients, or central, from spinal cord injury). Sinus node reentry (Fig. e37-1) is an atrial tachycardia originating from tissue near the sinus node and thus has a P wave morphology similar to sinus rhythm (see the section Focal Atrial Tachycardias).

FIGURE e37-1 Sinus node reentry. After three spontaneous sinus-initiated beats, premature stimulation of the high right atrium (S₂, S₃) initiates a sustained tachycardia at a cycle length of 450 milliseconds that has the identical high-low atrial activation sequence characteristic of sinus node discharge. This is sinus node reentry. Leads I, II, III, and V₁ are scalar leads. H = His electrogram; HBE = His bundle electrogram; HRA = high right atrial electrogram; RV = right ventricular electrogram. Numbers are milliseconds.

Management

Management should focus on the cause of the sinus tachycardia. In the hospital inpatient setting, the cause is usually obvious (e.g., hemorrhage, sepsis, agitation), whereas in the outpatient setting, it may be more elusive. The most common reversible causes include hyperthyroidism, anemia, infection or inflammation, and hypovolemia. Diabetic neuropathy is also common but not reversible. Elimination of tobacco, alcohol, caffeine, or other stimulants, such as the sympathomimetic agents in nose drops and cold medications, may be helpful. Beta blockers and nondihydropyridine calcium channel blockers (verapamil and diltiazem), fluid replacement in a hypovolemic patient, or fever reduction in a febrile patient can help slow the sinus nodal discharge rate. Treatment of inappropriate sinus tachycardia requires beta blockers or calcium channel blockers, alone or in combination. In severe cases, sinus node radiofrequency (RF) or surgical ablation may be indicated; however, these approaches are usually only temporarily palliative (see Chapter 35). A specific blocker of the pacemaker current (I_f), ivabradine, has been useful in some patients with inappropriate or refractory sinus tachycardia.

Premature Atrial Complexes

Premature complexes are among the most common causes of an irregular pulse and palpitations. They can originate from any area in the heart—most frequently from the ventricles, less often from the atria and the AV junctional area, and rarely from the sinus node. Premature complexes are common in normal hearts and increase in frequency with age.

Electrocardiographic Recognition

The diagnosis of premature atrial complexes (PACs) is made on the ECG (Fig. 37-3) by the presence of a premature P wave with a PR interval exceeding 120 milliseconds (except in Wolff-Parkinson-White [WPW] syndrome, in which case the PR interval is generally shorter than 120 msec). Although the contour of a premature P wave can resemble that of a normal sinus P wave, it generally differs. Even though variations in the basic sinus rate can at times make the diagnosis of prematurity difficult, differences in the contour of the P waves are usually apparent and indicate a different focus of origin. When a PAC occurs early in diastole, conduction may not be completely normal. The AV junction may still be refractory from the preceding beat and prevent propagation of the impulse (blocked or nonconducted PAC; Fig. 37-3A) or cause conduction to be slowed (PAC with a prolonged PR interval). As a general rule, the RP interval is inversely related to the PR interval; thus, a short RP interval produced by an early PAC occurring close to the preceding QRS complex is followed by a long PR interval. When PACs occur early in the cardiac cycle, the premature P waves can be difficult to discern because they are superimposed on T waves. Careful examination of tracings from several leads may be necessary before the PAC is recognized as a slight deformity of the T wave. Frequently, such PACs are blocked before reaching the ventricle and can be misinterpreted as a sinus pause or sinus exit block (see Fig. 37-3A).

The length of the pause that follows any premature complex or series of premature complexes is determined by the interaction of several factors. If the PAC occurs when the sinus node and perinodal tissue are not refractory, the impulse can be conducted into the sinus node, discharge it prematurely, and cause the next sinus cycle to begin from that time. The interval between the two normal P waves flanking a PAC that has reset the timing of the basic sinus rhythm is less than twice the normal P-P interval, and the pause after the PAC is said to be noncompensatory (Fig. 37-3E, F). Reset (noncompensatory pause) occurs when the A₁-A₂ interval plus the A₂-A₃ interval is less than two times the A₁-A₁ interval and the A₂-A₃ interval is greater than the A₁-A₁ interval. The interval between the PAC (A₂) and the following sinus-initiated P wave (A₃) exceeds one sinus cycle but is less than fully compensatory (see later) because the A₂-A₃ interval is lengthened by the time that it takes the ectopic atrial impulse to be conducted to the sinus node and depolarize it and then for the sinus impulse to return to the atrium. These factors lengthen the return cycle, that is, the interval between the PAC (A₂) and the following sinus-initiated P wave (A₃) (see Fig. 37-3E, F). Premature discharge of the sinus node by an early PAC can temporarily depress sinus nodal automatic activity and cause the sinus node to beat more slowly initially (Fig. 37-3D). Often when this happens, the interval between the A₃ and the next sinus-initiated P wave exceeds the A₁-A₁ interval.

FIGURE 37-3 A, PACs that block conduction entirely or conduct with a functional right or functional left bundle branch block. Depending on the preceding cycle length and coupling interval of the PAC, the PAC blocks conduction entirely in the AV node (arrowhead ↑) or conducts with a functional left bundle branch block (arrowhead ↓) or functional right bundle branch block (arrowhead →). B, A PAC on the left (arrowhead) initiates AV nodal reentry that is caused by reentry anterogradely and retrogradely over two slow AV nodal pathways, with a retrograde P wave produced midway in the cardiac cycle. On the right, a PAC (arrowhead) initiates AV nodal reentry as a result of anterograde conduction over the slow pathway and retrograde conduction over the fast pathway (see Fig. 37-8A), which produces a retrograde P wave in the terminal portion of the QRS complex that simulates an r′ wave. C, D, A PAC (arrowhead ↓) initiating a short run of atrial flutter (C) and a PAC (arrowhead ↑) depressing return of the next sinus nodal discharge (D). A slightly later PAC (arrowhead ↓) in D does not depress sinus nodal automaticity. B-D, Monitor leads. E, Diagrammatic example of the effects of a PAC. The sinus interval (A₁-A₁) equals X. The third P wave represents a PAC (A₂) that reaches and discharges the SA node, which causes the next sinus cycle to begin at that time. Therefore the P-P (A₂-A₃) interval equals X + 2Y milliseconds, assuming no depression of SA nodal automaticity. F, Diagram of the interactions of a PAC (yellow circles indicate origin; QRS complexes omitted) with the sinus node (SN) depending on the degree of prematurity. The top represents spontaneous sinus rhythm. The bottom is a late coupled PAC that collides with the exiting sinus impulse and therefore does not affect (or reset) the sinus pacemaker. The next sinus impulse (S₃) occurs at exactly twice the sinus interval. An early coupled PAC in the next diagram is able to penetrate the SN and resets the pacemaker, thereby resulting in resetting of the SN (as depicted in E). An even earlier coupled PAC in the lower part of the figure reaches refractory tissue around the SN and is thus unable to penetrate it (SN entrance block); therefore, it does not affect SN discharge. The next spontaneous sinus beat (S₃) arrives exactly at the sinus interval. (E, Modified from Zipes DP, Fisch C: Premature atrial contraction. Arch Intern Med 128:453, 1971.)

Less commonly, the PAC encounters a refractory sinus node or perinodal tissue (see Fig. 37-3F), in which case the timing of the basic sinus rhythm is not altered because the sinus node is not reset by the PAC and the interval between the two normal sinus-initiated P waves flanking the PAC is twice the normal P-P interval. The interval that follows this premature atrial discharge is said to be a full compensatory pause, that is, of sufficient duration that the P-P interval bounding the PAC is twice the normal P-P interval. However, sinus arrhythmia can lengthen or shorten this pause. Rarely, an interpolated PAC may occur. In this case the pause after the PAC is very short, and the interval bounded by the normal sinus-initiated P waves on each side of the PAC is equal to one normal P-P cycle length or slightly longer. The interpolated PAC fails to affect the sinus nodal pacemaker, and the sinus impulse that follows the PAC is conducted to the ventricles, often with a slightly lengthened PR interval. An interpolated atrial or ventricular premature complex of any type represents the only type of premature systole that does not actually replace the normally conducted beat. PACs can originate in the sinus node and are identified by premature P waves that have a contour identical to that of the normal sinus P wave.

On occasion, when the AV node has had sufficient time to repolarize and conduct without delay, the supraventricular QRS complex initiated by the PAC can be aberrant in configuration because the His-Purkinje system or ventricular muscle has not completely repolarized and conducts with a functional delay or block (see Fig. 37-3A). The refractory period of cardiac fibers is directly related to cycle length. (In an adult, the effective AV nodal refractory period is prolonged at shorter cycle lengths.) A slow heart rate (long cycle length) produces a longer His-Purkinje refractory period than does a faster heart rate. As a consequence, a PAC that follows a long R-R interval (long refractory period) can result in a functional bundle branch block (aberrant ventricular conduction). Because the right bundle branch at long cycles has a longer refractory period than the left bundle branch does, aberration with a right bundle branch block pattern at slow rates occurs more commonly than aberration with a left bundle branch block pattern. At shorter cycles, the refractory period of the left bundle branch exceeds that of the right bundle branch, and a left bundle branch block pattern may be more likely to occur.

Clinical Features

PACs can occur in various situations, such as during infection, inflammation, or myocardial ischemia, or they can be provoked by various medications, tension states, tobacco, alcohol, or caffeine. PACs can precipitate or presage the occurrence of sustained supraventricular (Fig. 37-3B, C) and, rarely, ventricular tachyarrhythmias. Frequently, PACs occur without any reversible causes and increase in frequency with aging. In general, PACs have a benign prognosis. Most patients do not have significant symptoms with PACs; however, those who do have symptoms most often feel the pauses that occur after the PAC.

Management

PACs generally do not require therapy. In symptomatic patients or when the PACs precipitate tachycardias, treatment with a beta blocker or a calcium antagonist can be attempted. In drug-refractory, highly symptomatic cases, ablation of the PAC focus can be effective when a single focus can be identified.

Atrial Fibrillation

See Chapter 38.

Atrial Tachycardias

Three types of atrial tachycardia have been distinguished experimentally—automatic, triggered, and reentrant. Entrainment, resetting patterns in response to overdrive pacing, the patient’s response to adenosine, recording of monophasic action potentials, and the mode of initiation may suggest the presence of one of these mechanisms. However, in most cases no clear identification of the mechanism can be made clinically because the clinical and EP features can overlap, especially when the reentrant circuit is small (i.e., microreentry). For example, adrenergic stimulation can initiate automatic and triggered atrial tachycardias, and burst pacing may initiate triggered and microreentrant atrial tachycardias. Therefore, because it determines the approach to mapping and management, atrial tachycardias are more broadly characterized clinically as being focal (originating from a small area of the atrium with atrial excitation emanating from this focus) or macroreentrant (a relatively large reentrant circuit using conduction barriers to create the circuit).⁷ Atrial flutter is the most common type of macroreentrant atrial tachycardia.

Atrial Flutter and Other Macroreentrant Atrial Tachycardias

Atrial flutter is the prototypic macroreentrant atrial rhythm. The typical atrial flutter is a reentrant rhythm in the right atrium that is constrained anteriorly by the tricuspid annulus and posteriorly by the crista terminalis and eustachian ridge. The flutter can circulate in a counterclockwise direction around the tricuspid annulus in the frontal plane (typical flutter, counterclockwise flutter) or in a clockwise direction (atypical, clockwise, or reverse flutter). Because both these forms of atrial flutter use the same circuit and are constrained by the same anatomic structures, their rates and flutter wave morphology on the surface ECG are consistent and predictable (see later). Rarely, intra-isthmus flutter can occur when the reentrant circuit is isolated to the cavotricuspid isthmus rather than rotating around the entire tricuspid annulus; this typically occurs after ablation in this region (usually done as treatment of typical flutter). Other forms of atrial flutter are now recognized as distinct types and include atrial macroreentry caused by incisional scars from previous atrial surgery, previous atrial ablation, mitral annular flutter, idiopathic fibrosis in areas of the atrium, or other anatomic or functional barriers to conduction in the atria. Because the barriers that constrain these atrial flutters are variable, the electrocardiographic pattern of these so-called atypical atrial flutters can be varied. Sometimes, flutter wave morphology changes during the same episode of flutter, which indicates multiple circuits or nonfixed conduction barriers.

Electrocardiographic Recognition

The atrial rate during typical atrial flutter is usually 250 to 350 beats/minute, although it is occasionally slower, particularly when the patient is treated with antiarrhythmic drugs, which can reduce the rate to about 200 beats/minute. If such slowing occurs, the ventricles can respond in a 1:1 fashion to the slower atrial rate.

In typical atrial flutter, the ECG reveals identically recurring, regular, sawtooth flutter waves (see Fig. 37-3C) and evidence of continual electrical activity (lack of an isoelectric interval between flutter waves), often best visualized in leads II, III, aVF, or V₁ (Fig. 37-4).⁸ In some cases, transient slowing of the ventricular response, via either carotid sinus massage or adenosine, is necessary to visualize the flutter waves. The flutter waves for the most common form of atrial flutter, counterclockwise typical atrial flutter, are inverted (negative) in these leads because of a counterclockwise reentrant pathway, and sometimes they are upright (positive) when the reentrant loop is clockwise (see Fig. 37-4). When the flutter waves are upright from clockwise rotation, they are often notched. If the AV conduction ratio remains constant, the ventricular rhythm will be regular; if the ratio of conducted beats varies (generally the result of a Wenckebach AV block), the ventricular rhythm will be irregular, although this is rare. Various degrees of penetration into the AV junction by flutter impulses can also influence AV conduction. The ratio of flutter waves to conducted ventricular complexes is most often an even number (e.g., 2:1, 4:1).

FIGURE 37-4 Twelve-lead ECG showing counterclockwise and clockwise atrial flutter. In counterclockwise atrial flutter, the flutter waves are negative in leads II, III, aVF, and V₆ and upright in V₁. In clockwise atrial flutter, the flutter waves are upright in leads II, III, and aVF and often notched.

As mentioned earlier, because the circuits for atypical flutter (not involving the cavotricuspid isthmus) can be variable, the electrocardiographic features of these macroreentrant atrial tachycardias are highly variable, without consistent rates or flutter wave contours (see Fig. e37-2). However, these tachycardias frequently have a flutter rate similar to that of typical flutter (250 to 390 beats/min). Table 37-2 shows common electrocardiographic findings with the different types of macroreentrant atrial flutter. After extensive left atrial ablation for atrial fibrillation, the electrocardiographic pattern of even typical flutter can appear “atypical” (not have the typical appearance described before) because of the altered left atrial activation as a result of altered conduction secondary to the left atrial ablation. In addition, unusual forms of atrial flutter can occur around ablation lines.

TABLE 37-2

Characteristics of Different Types of Atrial Flutter and Distinguishing Features on Scalar Electrocardiography

TYPE	REENTRANT CIRCUIT	ECG PATTERN	LEAD V₁/V₆
Typical counterclockwise	Tricuspid annulus dependent on the CTI	Sawtooth flutter wave; negative in II, III, and aVF	Positive V₁ Negative V₆
Typical clockwise	Tricuspid annulus dependent on the CTI	“Inverse sawtooth”; positive and often notched in II, III, and aVF	Broad and negative in V₁ (often notched) Positive in V₆
Lower loop reentry	CTI	Usually similar to typical counterclockwise CTI flutter except subtle loss of terminal positive deflection in leads II, III, and aVF	Usually similar to typical counterclockwise
Upper loop reentry	SVC and upper crista terminalis	Similar to typical clockwise flutter	Similar to typical clockwise flutter
Right atrial free wall	Around areas of scar in the lateral or posterior right atrium (caused by previous atrial surgery or spontaneously)	Variable	Typically negative or biphasic with terminal negative deflection in V₁
Septal atrial flutter	Atrial septum, typically after previous surgery	Variable	Usually biphasic or isoelectric in V₁
Mitral annular flutter	Around the mitral annulus, often slow zone of block around the PV interval; frequently occurs in the setting of left atrial surgery or ablation	Variable; I, III, and aVF, often positive but low amplitude	Usually positive in V₁ (or rarely isoelectric) and often broad
Post–atrial fibrillation ablation/MAZE flutter	Variable; the circuit involves previous ablations or scar in the left atrium	Variable	Variable

CTI = cavotricuspid isthmus.

FIGURE e37-2 Macroreentrant atrial tachycardia in a patient who underwent repair of an atrial septal defect 10 years earlier. This tachycardia uses a reentrant circuit established by the atriotomy on the lateral atrial wall. Ablation to extend the scar to the tricuspid annulus eliminated this tachycardia.

Clinical Features

Atrial flutter is less common than atrial fibrillation. It can occur as a result of atrial dilation from septal defects, pulmonary emboli, mitral or tricuspid valve stenosis or regurgitation, heart failure, previous extensive atrial ablation, and aging, but it can also occur without underlying heart disease. Toxic and metabolic conditions that affect the heart, such as thyrotoxicosis, alcoholism, and pericarditis, can cause atrial flutter. It can follow surgical repair of congenital heart disease. When it follows reparative surgery for congenital heart disease, most patients will be able to have both typical flutter and atypical flutter involving the atriotomy, which often occurs years after the surgery.

Atrial flutter usually responds to carotid sinus massage with a decrease in the ventricular rate in stepwise multiples and returns in reverse manner to the former ventricular rate at the termination of carotid massage. Physical examination may reveal rapid flutter waves in the jugular venous pulse. If the relationship of flutter waves to conducted QRS complexes remains constant, the first heart sound will have a constant intensity. Sounds caused by atrial contraction can occasionally be auscultated.

Management

Cardioversion (see Chapter 35) is commonly the initial treatment of choice for atrial flutter because it promptly and effectively restores sinus rhythm. Cardioversion can be accomplished with synchronous direct current (DC), which often requires relatively low energy (≈50 J). If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore sinus rhythm, or depending on clinical circumstances, the atrial fibrillation can be left untreated and can revert to atrial flutter or sinus rhythm. The short-acting antiarrhythmic medication ibutilide can also be given intravenously to convert atrial flutter. Ibutilide appears to successfully cardiovert approximately 60% to 90% of episodes of atrial flutter. However, because this medication prolongs the QT interval, torsades de pointes is a potential complication during and shortly after the infusion. Other medications, such as procainamide or amiodarone, can be given to convert atrial flutter chemically, but they are generally less effective than ibutilide. Rapid atrial pacing with a catheter in the esophagus or the right atrium can effectively terminate typical and some forms of atypical atrial flutter in most patients. Because ablation is highly effective for typical flutter and because of the high relapse rate after cardioversion, ablation is the preferred approach for stable patients who do not require immediate cardioversion. Although the risk for thromboembolism is lower than that for atrial fibrillation, patients with atrial flutter do appear to have a risk for thromboembolism immediately after conversion to sinus rhythm. In general, indications for anticoagulation in patients with atrial flutter are similar to those in patients with atrial fibrillation.

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