Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 15. Supraventricular Arrhythmias

Section II Atrial flutter and atrial fibrillation

Atrial flutter and atrial fibrillation (AF) ( Fig. 15-1 ) are two distinct but closely related tachyarrhythmias (“electrophysiologic cousins”). Like paroxysmal supraventricular tachycardia (PSVT), they areectopic rhythms. In other words, with all three types of arrhythmias the atria are being stimulated not from the sinus node but from an ectopic site or sites. With PSVTs, the atria (or atrioventricular [AV] node) are stimulated at a rate generally between 140 and 250 cycles per minute. With atrial flutter, the atrial rate is even faster, generally 250 to 350 cycles/min. With AF, the atrial depolarization rate is typically between 350 and 600 cycles/min.[*]

FIGURE 15-1  Atrial flutter and fibrillation. Notice the “sawtooth” waves (F waves) with atrial flutter and the irregular fibrillatory waves (f waves) with atrial fibrillation.

With both atrial flutter and AF, no discrete P waves are seen on the ECG. Instead, characteristic flutter (F) waves and fibrillation (f) waves represent continuous atrial electrical activity. Notice the pronounced “sawtooth” shape of the F waves and the more rapid “tremulous” f waves in Figure 15-1 . In some patients, atrial fibrillation and atrial flutter can both occur, so that the ECG may show alternating patterns.

*  The atrial depolarization rate with atrial flutter may be substantially less than 250 beats/min, especially in patients taking certain antiarrhythmic drugs such as flecainide, amiodarone, and quinidine.

Atrial flutter, as introduced in Chapter 14 , is an example of a reentrant type arrhythmia. Reentry is the term used to describe arrhythmias due to a traveling wave of excitation that circulates over a well-defined loop, “chasing its own tail.” With typical atrial flutter, this wave originates in the right atrium, generally traveling in a counterclockwise direction from top to bottom to top ( Fig. 15-2 ).

FIGURE 15-2  Comparison of mechanisms of atrial flutter and atrial fibrillation (AF). Atrial flutter is typically due to a large reentrant wave originating in the right atrium. With typical atrial flutter, the wave spreads in counterclockwise direction. AF is attributed to either multiple reentrant wavelets and/or to multiple sites of atrial automaticity. AV, atrioventricular; LV, left ventricle; RV, right ventricle; SA, sinoatrial.

With atrial flutter, the atrial stimulation (depolarization) rate is about 300/min ( Fig. 15-3 ). What happens to the ventricles during this rapid bombardment of the atria? The answer is that with atrial flutter (and atrial fibrillation) the ventricular (QRS) rate varies, depending on the ability of the atrioventricular (AV) junction to transmit stimuli from the atria to the ventricles. If the ventricles respond to each flutter wave, the ventricular rate is about 300 beats/min, a very unusual occurrence. Most commonly, the ventricular rate with atrial flutter is about 150, 100, or 75 beats/min. Atrial flutter with aventricular response of about 150 beats/min is called 2:1 flutter because the ratio of the atrial rate (300) to the ventricular rate (150) is 2 to 1. Atrial flutter with a ventricular rate of about 100 beats/min is usually 3:1 flutter; with 75 beats/min, it is usually 4:1 flutter.

FIGURE 15-3  A, Notice the variable appearance of flutter waves in different leads. In lead I, the waves are barely apparent, whereas, in leads II and III, the classic “sawtooth” waves appear. The ventricular rate is about 160 beats/min, and the flutter rate is about 320 beats/min; thus 2:1 conduction is present. B, Carotid sinus massage produces marked slowing of the ventricular rate by increasing vagal tone.

Characteristically, patients with atrial flutter increase or decrease their ventricular rate by stepwise fractions of the atrial rate (see Fig. 15-1 ). Thus a patient's ECG may change abruptly from showing atrial flutter with a ventricular response of 75-100 beats/min to 150 beats/min. In some patients the ventricular response with atrial flutter is more variable.[*]

*  The QRS pattern of “group beating” is not uncommon with atrial flutter and represents a Wenckebach-type variant associated with bombardment of the AV node by frequent atrial depolarization waves (e.g., at 300 cycles/min) (see Chapter 17 ).

Atrial flutter is rarely seen in people with normal hearts. This finding is in contrast to AF, which may occur in the absence of apparent organic heart disease. Atrial flutter, like atrial fibrillation, is not specific for any particular type of heart disease but occurs, for example, in patients with valvular (especially mitral) disease, chronic ischemic heart disease, cardiomyopathy, hypertensive heart disease, acute myocardial infarction (MI), chronic obstructive lung disease, and pulmonary emboli. Atrial flutter may also occur after cardiac surgery. Arial flutter and atrial fibrillation often occur in the same patient at different times.

Atrial flutter can lead to cardiac symptoms due to loss of normal atrial contraction and a fast or irregular heart rate. (Occasionally, an excessively slow ventricular response occurs with atrial flutter.) As a consequence, patients with atrial flutter (or atrial fibrillation) may complain of palpitations, light-headness, or even syncope. They may also develop angina due to the rapid heart rate, especially in the presence of coronary disease, or symptoms of congestive heart failure, including shortness of breath and fatigue.

Atrial flutter is also clinically important because it may predispose to the formation of thrombi in the atria, leading to systemic embolization. This complication is most likely in patients who have both atrial fibrillation and atrial flutter and those with under-lying rheumatic mitral valve disease or cardiomyopathy.


The treatment of atrial flutter depends on the clinical condition. In some patients, atrial flutter may revert spontaneously to normal sinus rhythm. In patients who are hypoxemic, oxygen therapy may help restore normal sinus rhythm.

Patients who have atrial flutter with a rapid ventricular response are usually treated initially with one drug or a combination of drugs (beta blockers, calcium channel blockers, digitalis) to slow impulse conduction through the AV node. Occasionally, the arrhythmia converts to normal sinus rhythm spontaneously in the course of this initial therapy. In some cases, an antiarrhythmic drug (e.g., ibutilide, dofetilide, amiodarone, procainamide) is used to help directly convert the flutter to normal sinus rhythm. Such drugs must be used with extreme care as they can cause life-threatening adverse effects, including cardiac arrest due to torsades de pointes (see Chapter 16 ).

Despite initial therapy, atrial flutter persists or recurs in many patients. Fortunately, it is one of the arrhythmias most easily treated with DC electrical cardioversion. As described in Chapter 14 , asynchronized DC shock is given with the patient properly premedicated. Anticoagulation may also be indicated to decrease the risk of systemic embolization.

Another way of attempting to convert atrial flutter is with very rapid pacing of the atria by means of a temporary pacing wire. This therapy may be particularly useful shortly after cardiac surgery when electrical pacing wires are still in place.

In recent years, radiofrequency (RF) catheter ablation has emerged as a major modality to treat patients with atrial flutter. This method, briefly described in Chapter 14 , is based on carefully burning out a small area of tissue involved in initiating or maintaining an arrhythmia. In treating atrial flutter, ablation therapy is usually directed to an area near the tricuspid valve, in the lower part of the right atrium.

In summary, atrial flutter is a tachyarrhythmia in which the atria are stimulated (depolarized) at a rate of usually 250 to 350 cycles/min, with a ventricular response that is often some fraction of the atrial rate (e.g., ½, ¼). Atrial flutter may be treated with special drugs, synchronized DC shock, rapid atrial pacing, or RF ablation technology.



With atrial fibrillation (AF), one of the most common arrhythmias, the atria are stimulated (depolarized) at a very rapid rate, usually between 350 and 600 times/min. This fibrillatory activity produces a characteristically irregular wavy pattern in place of the normal P waves. The irregular waves are called fibrillatory or f waves ( Fig. 15-4 ). In some cases, the f waves are relatively “coarse” ( Fig. 15-5 ); in others, a faster “fine” pattern of fibrillation is seen ( Fig. 15-6 ). Therefore AF is characterized by rapid depolarizations of the atria that produce irregular undulations of the ECG baseline without discrete (true) P waves.

FIGURE 15-4  Rapid oscillation of the baseline due to fibrillatory (f) waves. No true P waves are present, and the ventricular rate is irregular.

FIGURE 15-5  Atrial fibrillation with a rapid ventricular response. This patient has hyperthyroidism. (The commonly used term rapid atrial fibrillation is actually a misnomer, because “rapid” is intended to refer to the ventricular rate rather than the atrial rate. The same is true for the term slow atrial fibrillation.) The atrial fibrillation waves here have a “coarse” appearance.

FIGURE 15-6  Fibrillatory waves may be hard to find. In this tachyarrhythmia, no atrial waves are evident. The ventricular rate is about 140 beats/min and is irregular. No clear fibrillatory waves are visible; nevertheless, the rhythm is atrial fibrillation.

The detailed electrophysiologic mechanism of AF is a subject of active study. Current analysis favors the view that the rapid atrial depolarization is related to multiple reentrant wavelets in the atria or to multiple foci of atrial automaticity. Figure 15-2 compares the atrial activation patterns in AF and atrial flutter.

Because of the rapid atrial depolarization rate, the AV junction in patients with AF is bombarded by innumerable stimuli from the atria. If every stimulus (each f wave) penetrated the AV junction, the ventricles would beat at a rate of up to 600 times per minute, with obvious catastrophic consequences. Fortunately, the AV junction is refractory to most of these impulses and allows only a fraction to reach the ventricles.

In patients with a normal AV junction in whom AF suddenly develops, the mean ventricular rate is generally between 110 and 180 beats/min. Figure 15-6 shows an example of AF with an average ventricular rate of about 140 beats/min. Characteristically, the ventricular rate with AF is haphazardly irregular because the AV junction is being stimulated in an apparently random fashion by the rapidly fibrillating atria.

In summary, AF has two ECG characteristics:



An irregular wavy baseline produced by the rapid f waves



A ventricular (QRS) rate that is usually quite irregular 
When the ventricular rate is very fast ( Fig. 15-7 ), the f waves may be difficult to distinguish. In such cases, the diagnosis of AF can usually be suspected by finding a very irregular ventricular rate in the absence of distinct P waves.

FIGURE 15-7  Relatively subtle fibrillation waves give the baseline between irregularly spaced R waves a wrinkly appearance.


AF is the most common arrhythmia causing hospital admissions. Over 2 million Americans have intermittent or chronic AF, and the incidence rises with age.

In some patients, AF occurs paroxysmally and may last only minutes, hours, or days. Some patients may experience only one episode or occasional episodes, whereas others have multiple recurrences. In other patients, AF is more persistent and may become permanent (chronic), lasting indefinitely, even if cardioversion is attempted ( Box 15-1 ). With these fibrillatory episodes, some patients are quite symptomatic (typically complaining of palpitations, fatigue, dyspnea, light-headedness, and even syncope, or chest pain), whereas others have no specific complaints. In the asymptomatic patient, AF may first be discovered during a routine examination or when the patient presents with heart failure or stroke. AF can occur in people with no detectable heart disease and in patients with a variety of cardiac diseases (see Chapter 24 ). The term lone atrial fibrillation is sometimes used to describe recurrent or chronic AF in patients without other clinical evidence of heart disease. Paroxysmal AF may occur spontaneously, or it may be associated with excessive alcohol consumption in otherwise healthy individuals (“holiday heart syndrome”). In such cases, the arrhythmia often spontaneously reverts to normal sinus rhythm or is converted easily with pharmacologic therapy alone.

BOX 15-1 

Classification of Clinical Atrial Fibrillation (AF) Patterns




Stops spontaneously within 7 days and usually within 48 hours


Lasts for more than 7 days and usually requires cardioversion

Permanent (Established or Chronic)

Lasts indefinitely or fails to terminate (or recurs) even if cardioversion is attempted

Note: AF of any pattern may be symptomatic (palpitations, chest discomfort, weakness, dyspnea, lightheadedness) or asymptomatic.


Episodes are typically recurrent.

Changes in autonomic tone may provoke AF in susceptible individuals. Sometimes the arrhythmia is related to increased sympathetic tone (e.g., occurring during exercise or with emotional excitement). At other times, AF may occur in the context of high vagal tone (e.g., with sinus bradycardia during sleep).

AF is also one of the most frequently observed arrhythmias in patients with organic (structural) heart disease. The prevalence of this arrhythmia rises with advancing age. Common pathologic substrates include coronary artery disease, hypertensive heart disease, and valvular heart disease. Patients with coronary artery disease may experience AF for the first time during an acute MI or, more commonly, as a consequence of chronic ischemic myocardial disease, possibly because of associated atrial dilation or fibrosis. Hypertensive heart disease is often associated with left atrial enlargement. AF is also commonly caused by valvular heart disease, particularly when the mitral valve is involved. For example, severe mitral stenosis or mitral regurgitation produces atrial enlargement, which is a predisposing factor for atrial arrhythmias.

Numerous other conditions can also lead to AF. For example, patients with thyrotoxicosis (hyperthyroidism) may develop AF (see Fig. 15-6 ). AF (or atrial flutter) is quite common after cardiac surgery. It may also occur with pericardial disease (especially chronic disease), lung disease, obstructive sleep apnea, pulmonary emboli, cardiomyopathy, congenital heart disease (e.g., atrial septal defect), and other forms of heart disease. Often, patients have more than one predisposing factor for this arrhythmia.

Chapter 24 presents an “instant review” of the common substrates for AF.


What happens physiologically when AF develops? After the P wave, the atria normally contract and pump blood into the ventricles. With AF, normal atrial depolarization is lost and the atria fibrillate (quiver) instead of contracting synchronously. In these circumstances, the normal atrial “kick” is lost, and the result is decreased cardiac output (since ventricular filling is decreased). Furthermore, the stagnation (stasis) of blood in the atria may lead to thromboembolic complications (discussion to follow).

Decreased Cardiac Output

Hemodynamically the most significant effect of AF is decreased cardiac output, which is especially marked in patients with underlying cardiac impairment and in elderly people, who have stiffer cardiac musculature and are therefore more dependent on atrial contraction for filling of the ventricles. In addition, the amount of this decreased output depends importantly on the ventricular rate with AF. The faster the rate, the less time there is for adequate ventricular filling and the greater the decrease in cardiac output. Thus the patient with AF at a rate of 150 beats/min is more likely to be hypotensive or develop congestive heart failure (CHF) than is the patient with a rate of 100 beats/min. In patients with coronary artery disease, a rapid ventricular rate can also cause myocardial ischemia and even infarction, further reducing cardiac output (see Chapter 8 ).

Atrial Thrombi and Embolization

The second significant effect of AF, resulting from the stagnation of blood, is a tendency in some patients for atrial thrombi to develop and dislodge into the arterial circulation, causing peripheral embolism. The thrombi can produce a cerebrovascular accident, occlusion of the blood supply to the legs, and other complications.

The risk of thrombus formation and embolization is highest in patients with chronic AF related to rheumatic mitral valve disease. Thrombi and embolization also occur, however, in patients with AF from other causes (so-called nonrheumatic atrial fibrillation). Indeed, atrial fibrillation is a major substrate for embolic strokes, particularly in the elderly, as well as those with hypertension or heart failure.


Rather than discussing the details of treating AF, this section focuses on the general clinical approach to patients with this arrhythmia. AF may convert to sinus rhythm in three principal ways. The first is spontaneous conversion in which the AF stops and sinus rhythm resumes without apparent reason. The second occurs with pharmacologic therapy. The third is with electrical cardioversion (as already described for PSVT and atrial flutter).

In approaching patients with AF, you need to address promptly three major clinical questions:



Is the arrhythmia acute and causing a life-threatening decrease in cardiac function, as indicated by severe myocardial ischemia, hypotension, or very severe CHF? As a general rule, patients with very recent–onset AF that is producing severe shock, severe myocardial ischemia, or pulmonary edema should be considered candidates for electrical cardioversion if they do not respond promptly to emergency drug therapy.



Is the AF likely of very recent onset (especially less than 48 hrs) or is it of longer duration?



Is there a specific cause (or causes) of the arrhythmia?

In most cases, acute AF does not require immediate electrical cardioversion. Drug therapy alone can be used initially to control the ventricular rate. Beta blockers, calcium channel blockers (verapamil, diltiazem), and digitalis all act by slowing conduction of stimuli through the AV node.[*]

The usual sequence in treating AF pharmacologically is first to control the ventricular response with a beta blocker or a calcium channel blocker, and sometimes with digoxin. Always consider factors such as hypoxemia, severe anemia, fever, severe congestive heart failure, and hyperthyroidism, which can contribute to the rapid ventricular response and which, until addressed, will make rate control much more difficult.

If sinus rhythm is not spontaneously restored in association with rate slowing, the addition of a specific antiarrhythmic drug is often considered. Elective DC cardioversion ( Fig. 15-8 ) is generally reserved for patients who fail to respond to an initial trial of drug therapy and who are felt to have a reasonable likelihood of maintaining sinus rhythm for an extended time. Sometimes, DC cardioversion is used without specific antiarrhythmic drug therapy.

Attempts to convert AF to sinus rhythm with either pharmacologic therapy or DC cardioversion should not be made unless the patient has been sufficiently anticoagulated or atrial thrombus formation has been convincingly excluded (e.g., by transesophageal echocardiography). The reason for this caveat is that restoration of normal atrial contractility during sinus rhythm may cause dislodgment of an atrial thrombus formed while the atria are fibrillating. The longer the duration of the fibrillation, the more likely thrombus formation becomes. Thrombus formation may also occur, however, with fibrillation of relatively short duration.

FIGURE 15-8  Cardioversion of atrial fibrillation to sinus rhythm. With external direct-current (DC) cardioversion, an electric shock is administered to the heart via special electrode paddles placed on the chest wall. In the case depicted here, one electrode is placed on the anterior chest wall, to the left of the sternum, the other (indicated by dashed lines) is placed on the back, under the left scapula. The shock is synchronized with the peak of the QRS complex to avoid inducing ventricular fibrillation if the stimulus is delivered at the peak of the T wave.

Not all patients with AF are candidates for pharmacologic or electrical cardioversion. Patients with persistent or recurrent AF who cannot be converted to or maintained in sinus rhythm are candidates for ventricular rate control along with long-term anticoagulation using warfarin or aspirin, depending on the circumstances. Antiarrhythmic drug therapy of AF has been disappointing because of the high failure rate and the toxicity of the agents, including the risk of potentially fatal ventricular arrhythmias (proarrhythmia) (see also Chapters 16 and 19 ).

Some patients with chronic AF who cannot be converted to sinus rhythm have an uncontrollably fast ventricular response despite maximal drug therapy. A useful approach to this problem is ablation of the AV node with RF current delivered by a special cardiac catheter (see Chapter 14 ). Because this therapy may result in complete heart block, a permanent pacemaker must also be implanted.

The limited efficacy and toxicities of drug therapies for preventing recurrence of atrial fibrillation has prompted major efforts to find new approaches to management. A number of nonpharmacologic therapies to treat recurrent atrial fibrillation are evolving. These include atrial ablation procedures and atrial implanted defibrillators. Atrial ablation therapy is based on the finding that many cases of AF originate with ectopic stimuli from the area around the pulmonary veins in the left atrium. Electrical “isolation” of the pulmonary veins using RF ablation techniques is being used as a new approach to therapy for carefully selected patients with drug-refractory, recurrent AF. Implanted atrial defibrillators may be useful in selected patients as well. These and other emerging approaches have exciting potential, but are not without serious risks. For example, atrial rupture and pulmonary vein thrombosis, among other serious complications, have occurred with ablation procedures. Atrial defibrillation from an implanted device can cause painful shocks, limiting the clinical use of this technology.

At the same time that you are starting to treat a patient with AF, you should be thinking of possible causes for this common arrhythmia. You should search for evidence of excessive chronic or acute alcohol use (holiday heart syndrome), hypertensive heart disease, cardiomyopathy, obstructive sleep apnea, valvular disease, coronary artery disease, or chronic pericardial disease, if indicated. A blood test for thyroid function should be performed in any patient with unexplained AF because thyrotoxicosis is an important treatable cause of this arrhythmia. The approach to the patient with AF in the setting of recent cardiac surgery is a subject of current interest and evolving strategies.

Patients with underlying AV nodal disease may develop persistent AF with a slow ventricular response in the absence of drug therapy. If the ventricular rate becomes exceedingly slow, a permanent (ventricular) pacemaker may be required. Atrial-based pacemaker therapy may be helpful in patients with sinus node dysfunction (“sick sinus syndrome”) who develop recurrent episodes of AF.

Guidelines for current therapy of AF are available at the websites of the American Heart Association and the American College of Cardiology (see Bibliography ).

*  Digitalis glycosides act primarily by increasing vagal tone at the AV node. Beta blockers decrease sympathetic tone. Calcium channel blockers directly interfere with conduction by impairing the cellular entry of calciumions, which play a major role in electrical impulse transmission in the AV node.

Atrial fibrillation (or atrial flutter) may occur with other arrhythmias and conduction disturbances, just as sinus rhythm can occur with ventricular premature beats (VPBs), AV heart block, and so on. An example of AF with VPBs is presented in Figure 15-9 . AF or atrial flutter can also occur with complete heart block ( Fig. 15-10 ); in such cases, the ventricular response is very slow and regular. Possible digitalis toxicity should always be considered in the patient who has AF and a very slow or regularized ventricular rate (see Chapter 18 ).

FIGURE 15-9  Atrial fibrillation with ventricular premature beats.

FIGURE 15-10  Atrial fibrillation with complete atrioventricular (AV) block. The ventricular rate is very slow and regular because of the block. (Notice the right bundle branch block morphology of the escape rhythm QRS complexes.)

The special case of AF with the Wolff-Parkinson-White (WPW) syndrome is discussed in Chapter 20 .

Occasionally, it can be difficult to decide whether AF or atrial flutter is present (see Chapter 23 ). The coarse atrial fibrillatory waves may resemble flutter waves (see Fig. 23-3 ). This arrhythmia, which is sometimes referred to as fibrillation-flutter (“fib-flutter”), usually has the same clinical significance and treatment as AF.



With atrial flutter, the ECG shows the following features:



Characteristic “sawtooth” flutter waves instead of discrete P waves



A constant or variable ventricular rate (e.g., one QRS complex with every fourth flutter wave, 4:1 flutter; one QRS with every two flutter waves, 2:1 flutter, and the ventricular rate half the atrial rate; or the rare 1:1 flutter, in which the ventricles contract about 300 times a minute)

Atrial flutter rarely occurs in normal hearts but is most often seen in valvular heart disease, ischemic heart disease, lung disease, cardiomyopathy, or pulmonary emboli. It may also occur after cardiac surgery. Atrial flutter may be treated with a synchronized direct-current (DC) shock (cardioversion), rapid atrial pacing, radiofrequency catheter ablation, or drug therapy.

The ECG of a patient with atrial fibrillation (AF) shows the following:



Rapid irregular undulations of the baseline (fibrillatory waves) instead of P waves



A ventricular rate that is usually grossly irregular

In some patients, AF occurs permanently; in others, it is paroxysmal. Occasionally, AF is seen without evidence of underlying heart disease. Common factors predisposing to AF are coronary artery disease, hypertensive heart disease, and mitral valve disease. This arrhythmia may also occur in many other settings, such as with hyperthyroidism, cardiomyopathy, excessive alcohol use, cardiac surgery, pulmonary emboli, and chronic pericarditis. It may be seen with other arrhythmias (e.g., ventricular ectopy or complete heart block). With an extremely slow or regularized ventricular rate (50 beats/min or less), AF may signify digitalis toxicity. Sustained AF can sometimes be converted to normal sinus rhythm with DC cardioversion or pharmacologic therapy, or controlled with newer approaches using radiofrequency atrial ablation.





Answer the following questions about the monitor lead rhythm strip below:




What is the atrial rate?



What is the ventricular rate?



What is this arrhythmia?



Answer the following questions about this rhythm strip:




What is the average heart rate?



What is this arrhythmia?



The atrial rate with atrial flutter is (faster, slower) than the atrial rate with atrial fibrillation.



The atrial rate with atrial flutter is usually (faster, slower) than that with atrial tachycardia.



True or false: The ventricular rate with atrial fibrillation is always greater than 100 beats/min.



True or false: Systemic embolization causing stroke or vascular occlusion is not a risk with atrial flutter.

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