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


Chapter 20. Bradycardias and Tachycardias

Review and differential diagnosis

The preceding chapters described the major arrhythmias and atrioventricular (AV) conduction disturbances. These abnormalities can be classified in numerous ways. This “review and overview” chapter simply divides them into two major clinical groups—bradycardias and tachycardias—and discusses the differential diagnosis of each group ( Box 20-1 ).

BOX 20-1 

Major Tachyarrhythmias: Simplified Classification

Narrow QRS Complexes

Wide QRS Complexes

Sinus tachycardia

Ventricular tachycardia

Paroxysmal supraventricular tachycardias (PSVTs)[*]

Supraventricular tachycardia with aberration caused by a bundle branch block– type or Wolff-Parkinson-White pattern

Atrial flutter


Atrial fibrillation preexcitation syndrome



The three most common types of PSVTs are AV nodal reentrant tachycardias (AVNRT), atrioventricular reentrant tachycardia (AVRT) involving a bypass tract, and atrial tachycardia (AT) including unifocal and multifocal atrial tachycardia, as discussed in Chapter 14 . Other nonparoxysmal supraventricular tachycardias may also occur, including types of so-called incessant atrial, junctional, and bypass-tract tachycardias. (For further details of this advanced topic, see selected references cited in the Bibliography .)


A number of arrhythmias and conduction disturbances associated with a slow heart rate have been described. The term bradycardia (or bradyarrhythmia) refers to arrhythmias and conduction abnormalities that produce a heart rate of less than 60 beats per minute. Fortunately, the differential diagnosis of a slow pulse is relatively simple in that only a few causes must be considered. Bradyarrhythmias fall into five general classes ( Box 20-2 ).

BOX 20-2 

Bradycardias: Simplified Classification

Sinus bradycardia, including sinoatrial block

Atrioventricular (AV) junctional (nodal) escape rhythm

AV heart block (second or third degree) or AV dissociation

Atrial fibrillation or flutter with a slow ventricular response

Idioventricular escape rhythm


Sinus bradycardia is sinus rhythm with a rate less than 60 beats/min ( Fig. 20-1 ).[*] Each QRS complex is preceded by a P wave; the P wave is negative in lead aVR and positive in lead II, indicating that the sinoatrial (SA) node is the pacemaker. Some patients may have a sinus bradycardia of 40 beats/min or less.

FIGURE 20-1  Sinus bradycardia with a slight sinus arrhythmia.

Sinus bradycardia may be related to a decreased firing rate of the sinus node pacemaker cells or to actual SA block.[†] The most extreme example is SA node arrest (see Chapter 13 ).

*  Some cardiologists reserve the term sinus bradycardia for rates less than 50 beats/min.
†  SA block refers to situations in which impulses formed in the sinus node fail to depolarize the atria.

With a slow AV junctional escape rhythm ( Fig. 20-2 ), either the P waves (seen immediately before or just after the QRS complexes) are retrograde (inverted in lead II and upright in lead aVR), or no P waves are apparent if the atria and ventricles are stimulated simultaneously.

FIGURE 20-2  The heart rate is about 43 beats/min. The baseline between the QRS complexes is perfectly flat (i.e., no P waves are evident).


A slow ventricular rate of 60 beats/min or less (even as low as 20 beats/min) is the rule with complete heart block because of the slow intrinsic rate of the junctional or idioventricular pacemaker ( Fig. 20-3 ). In addition, patients with second-degree AV block (either Mobitz type I [Wenckebach] or Mobitz type II) sometimes have a bradycardia because of the dropped beats (see Fig. 17-3 and Table 17-1).

FIGURE 20-3  The atrial (P wave) rate is about 80 beats/min. The ventricular (QRS) rate is about 43 beats/min. Because the atria and ventricles are beating independently, the PR intervals are variable. The QRS complex is wide because the ventricles are being paced by an idioventricular pacemaker.

Isorhythmic AV dissociation, which may be confused with complete heart block, is also frequently associated with a heart rate of less than 60 beats/min (see Chapter 17 ).


Paroxysmal atrial fibrillation (AF), prior to treatment, is generally associated with a rapid ventricular rate. The rate may become excessively slow (less than 50 to 60 beats/min), however, because of drug effects or toxicity (beta blockers, calcium channel blockers, digitalis) or because of underlying disease of the AV junction ( Fig. 20-4 ). In such cases, the ECG shows the characteristic atrial fibrillatory (f) waves with a slow ventricular (QRS) rate. The f waves may be very fine and easily overlooked. (A very slow, regularized ventricular response in AF suggests the presence of underlying complete AV heart block; see Chapter 17 .)

FIGURE 20-4  Regularization and excessive slowing of the ventricular rate with atrial fibrillation are usually a sign of drug toxicity (especially digitalis) or intrinsic AV node disease (see Chapter 18 ).


When the SA nodal and AV junctional escape pacemakers fail to function, a very slow pacemaker in the ventricular conduction (His-Purkinje) system may take over. This rhythm is referred to as anidioventricular escape rhythm. The rate is usually very slow (less than 45 beats/min), and the QRS complexes are wide without any preceding P wave (see Fig. 17-6 ). In such cases, hyperkalemia should always be excluded.


With the exception of sinus bradycardia, which is a common normal variant, the other bradycardias are often abnormal.[*] The possible causes of AV junctional rhythms, heart block, and AF were described in earlier chapters.

Digitalis excess or other drug toxicity (e.g., beta blockers, calcium channel blockers, lithium carbonate) must always be considered in any patient with a bradycardia. Hyperkalemia is another important, reversible, life-threatening cause of bradyarrhythmias (see Chapter 10 ). Prominent intermittent sinus bradycardia and sinus pauses at night may occur with obstructive sleep apnea syndrome.

Patients with any of the bradycardias just discussed may have no symptoms, or they may complain of light-headedness or fainting because of decreased cardiac output. The treatment depends on the particular arrhythmia and the clinical setting.

In summary, most patients with an ECG heart rate of less than 60 beats/min have one of the five following classes of arrhythmia: sinus bradycardia (including SA block), AV junctional escape rhythm, AV heart block (or AV dissociation), AF or atrial flutter with a very slow ventricular rate, or idioventricular escape rhythm.[†]

*  Normal persons (in particular, athletes with increased vagal tone at rest) occasionally show a slow junctional rhythm or even Wenckebach AV block.
†  Bradycardia can also be due to a wandering atrial pacemaker (see Fig. 20-15 ) or isorhythmic AV dissociation (see Fig. 17-10 ).



At the opposite end of the spectrum from bradyarrhythmias are the tachycardias. These rhythm disturbances produce a heart rate faster than 100 beats/min. The tachyarrhythmias can be usefully divided into two general groups: those with a “narrow” (normal) QRS duration and those with a “wide” QRS duration. Narrow-complex tachycardias are almost invariably supraventricular (i.e., the focus of stimulation is within or above the AV junction). Wide-complex tachycardias, by contrast, are either ventricular or supraventricular with aberrant ventricular conduction (supraventricular tachycardia [SVT] with aberrancy).

The four major classes of supraventricular tachyarrhythmia[‡] are sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and AF. With each class, cardiac activation occurs at one or more sites in the atria or AV junction (node), above the ventricles (hence supraventricular). This is in contrast to ventricular tachycardia (VT), in which the stimulus starts in the ventricles themselves. VT is defined as a rapid run of three or more consecutive premature ventricular depolarizations (see Fig. 16-5 ). The QRS complexes are always wide because the ventricles are not being stimulated simultaneously. The rate of VT is usually between 100 and 200 beats/min. By contrast, with supraventricular arrhythmias, the ventricles are stimulated normally (simultaneously), and the QRS complexes are therefore narrow (unless a bundle branch block–type pattern is also present).

The first step in analyzing a tachyarrhythmia is to look at the width of the QRS complex in all 12 leads if possible. If the QRS complex is narrow (0.1 sec or less), you are dealing with some type of supraventricular arrhythmia and not VT. If the QRS complex is very wide (particularly if greater than 0.14 sec), you should consider the rhythm to be VT unless it can be proved otherwise.

‡  Be aware of possible confusion in terminology. Cardiologists use the term supraventricular tachycardia (SVT) in two related, but different ways. First, SVT refers most generally to any arrhythmia originating in area of the AV junction, atria, or SA node, above the ventricular conduction system (hence supraventricular). Second, SVT is also used more specifically to refer to a class of paroxysmal supraventricular tachycardias (PSVTs) originating in the region of the atria or AV junction (node) or involving an atrioventricular bypass tract. These PSVTs, caused by reentry or automaticity, are distinct from sinus tachycardia, AF, or atrial flutter (see Chapters 14 and 15 ). DIFFERENTIAL DIAGNOSIS OF NARROW-COMPLEX TACHYARRHYTHMIAS

The characteristics of sinus tachycardia, PSVTs, AF, and atrial flutter have been described in previous chapters. Sinus tachycardia in adults generally produces a heart rate between 100 and 180 beats/min, with the higher rates (150 to 180 beats/min) generally occurring in association with exercise. If you find a narrow-complex tachycardia with a rate of 150 beats/min or more in a resting adult, you are most likely dealing with one of the other three types of (nonsinus) arrhythmias mentioned previously.

PSVT and AF can generally be distinguished on the basis of their regularity. PSVT resulting from AV nodal reentry or a concealed bypass tract is usually an almost perfectly regular tachycardia with a ventricular rate between 140 and 250 beats/min (see Chapter 14 ). AF, on the other hand, is distinguished by its irregularity. Remember that with rapid AF ( Fig. 20-5 ) the f waves may not be clearly visible, but the diagnosis can be made in almost every case by noting the absence of P waves and the haphazardly irregular QRS complexes.

FIGURE 20-5  The ventricular rate is about 130 beats/min (13 QRS cycles in 6 sec). Notice the characteristic haphazardly irregular rhythm.

Atrial flutter is characterized by “sawtooth” flutter (F) waves between QRS complexes ( Fig. 20-6 ). When atrial flutter is present with 2:1 block (e.g., the atrial rate is 300 beats/min and the ventricular response is 150 beats/min), however, the F waves are often hidden. Therefore atrial flutter at 150 beats/min can be confused with sinus tachycardia, PSVT, or AF ( Fig. 20-7 ). AF can be excluded because atrial flutter with 2:1 conduction is generally very regular.

FIGURE 20-6  Atrial flutter with 2:1 conduction.

FIGURE 20-7  Four “look-alike” narrow-complex tachyarrhythmias (lead II). A, Sinus tachycardia. B, Atrial fibrillation. C, Paroxysmal supraventricular tachycardia (PSVT) resulting from AV nodal reentrant tachycardia (AVNRT). D, Atrial flutter with 2:1 block. When the ventricular rate is about 150 beats/min, these four arrhythmias may be difficult if not impossible to tell apart on the standard ECG, particularly from a single lead. In the example of sinus tachycardia, the P waves can barely be seen in this case. Next, notice that the irregularity of the atrial fibrillation here is very subtle. In the example of PSVT, the rate is quite regular without evident P waves. In the strip illustrating atrial flutter, the flutter waves cannot be seen clearly in this lead.

Nevertheless, the differential diagnosis of sinus tachycardia, PSVT with a ventricular rate of about 150 beats/min, AF, and atrial flutter can be a problem (see Fig. 20-7 ). One measure often used to help separate these arrhythmias is carotid sinus massage (CSM).[*] Pressure on the carotid sinus produces a reflex increase in vagal tone. The effects of CSM on sinus tachycardia, reentrant-types of PSVT, and atrial flutter are described next.

*  CSM is not without risks, particularly in elderly patients. Consult texts cited in the Bibliography for details on this maneuver and the use of adenosine in the differential diagnosis of tachycardias.
Sinus Tachycardia

Sinus tachycardia generally slows slightly with CSM. No abrupt change in heart rate usually occurs, however. Slowing of sinus tachycardia may make the P waves more evident. Sinus tachycardia generally begins and ends gradually, not abruptly.

Paroxysmal Supraventricular Tachycardias

PSVT resulting from AV nodal reentry (AVNRT) or atrioventricular reentry (AVRT) involving a concealed bypass tract usually has an all-or-none response to CSM. In successful cases, it breaks suddenly, and sinus rhythm resumes during the CSM (see Fig. 14-7 ). At other times, CSM has no effect, and the tachycardia continues at the same rate. In cases of PSVT caused by atrial tachycardia (AT), CSM may have no effect or may increase the degree of block, resulting in a rapid sequence of one or more nonconducted P waves.

Atrial Flutter

CSM often increases the degree of block in atrial flutter, converting flutter with a 2:1 response to 3:1 or 4:1 flutter with a ventricular rate of 100 or 75 beats/min. Slowing of the ventricular rate unmasks the characteristic F waves (see Fig. 15-2 ).


Another variant of PSVT that has not yet been specifically discussed is multifocal atrial tachycardia (MAT). An example is shown in Figure 20-8 . This tachyarrhythmia is characterized by multiple ectopic foci stimulating the atria. The diagnosis of MAT requires the presence of three or more (nonsinus) P waves with different shapes at a rate of 100 or more per minute. The PR intervals often vary. MAT is usually seen in patients with chronic lung disease. Because the ventricular rate is irregular and rapid, this arrhythmia is most likely to be mistaken for AF. MAT is caused by multiple atrial pacemakers firing in an unpredictable fashion. This is in contrast to classic (unifocal) atrial tachycardia, which typically involves only a single ectopic pacemaker in the atrium (see Chapter 14 ).

FIGURE 20-8  Note the rapidly occurring P waves showing variable shapes, variable PR intervals, or both.


Tachycardias are divided into SVTs and ventricular tachycardia (VT). This section briefly describes the differential diagnosis of VT. A tachycardia with widened (broad) QRS complexes indicates two possible diagnostic considerations. The first and more important is VT, a potentially life-threatening arrhythmia.[*] As noted, VT is a consecutive run of three or more ventricular premature beats at a rate generally between 100 and 200 or more beats/min. It is usually very regular. The second possible cause of a tachycardia with widened QRS complexes is so-called SVT with aberration. The termaberration simply means that some abnormality in ventricular activation is present, causing widened QRS complexes.

*  Most cases of VT are associated with a very wide QRS complex. More rarely, VT may occur with a QRS complex that is only mildly prolonged, particularly if the arrhythmia originates in the upper part of the ventricular septum or in the proximal part of the fascicles.

Aberrancy with an SVT has two major mechanisms: bundle branch block and, much more rarely, Wolff-Parkinson-White (WPW) preexcitation.

Supraventricular Tachycardia with Bundle Branch Block

If any of the SVTs just discussed occurs in association with a bundle branch block (or related pattern), the ECG shows a wide-complex tachycardia that may be mistaken for VT. For example, a patient with sinus tachycardia, AF, atrial flutter, or PSVT and concomitant right bundle branch block (RBBB) or left bundle branch block (LBBB) has a wide-complex tachycardia.

Figure 20-9 A shows AF with a rapid ventricular response occurring in conjunction with LBBB. Figure 20-9 B shows an example of VT. Because the arrhythmias look so similar, it can be difficult to tell them apart. The major distinguishing feature is the irregularity of the AF as opposed to the regularity of the VT. VT can sometimes be irregular, however.

FIGURE 20-9  A, Atrial fibrillation with a left bundle branch block pattern. B, Ventricular tachycardia. Based on the ECG appearance, differentiating supraventricular tachycardia with bundle branch block from actual ventricular tachycardia may be difficult and sometimes impossible.

You need to remember that in some cases of SVT with aberration, the bundle branch block is seen only during the episodes of tachycardia. Such rate-related bundle branch blocks are said to betachycardia (or acceleration) dependent.

Supraventricular Tachycardias with Wolff-Parkinson-White Preexcitation

The second mechanism responsible for a wide-complex tachycardia is SVT with a Wolff-Parkinson-White (WPW) pattern. As noted, patients with WPW preexcitation have an accessory pathway connecting the atria and ventricles, thus bypassing the AV node. Such patients are especially prone to a reentrant type of PSVT with narrow (normal) QRS complexes. Sometimes, however, particularly if AF or atrial flutter develops, a wide-complex tachycardia may result from conduction down the bypass tract at very high rates. This kind of wide-complex tachycardia obviously mimics VT. An example of WPW with AF is shown in Figure 20-10 .*

FIGURE 20-10  A, Atrial fibrillation with the Wolff-Parkinson-White preexcitation syndrome may lead to a wide-complex tachycardia that has a very rapid rate. Notice that some of the RR intervals are less than 0.20 sec. Irregularity is due to the underlying atrial fibrillation. B, After the arrhythmia has been converted to sinus rhythm, the classic triad of the Wolff-Parkinson-White syndrome is visible but subtle: relatively short PR interval, wide QRS complex, and delta wave (arrow in lead V3).

WPW with AF should be strongly suspected if you encounter a wide-complex tachycardia that is (1) irregular, and (2) has a very high rate (very short RR intervals). In particular, RR intervals of 0.20 second or less are rarely seen with conventional AF, and very rapid VT is usually quite regular. These very short RR intervals are related to the ability of the bypass tract (in contrast to the AV node) to conduct impulses in extremely rapid succession (see Fig. 20-10 A).

The recognition of WPW with AF is of considerable clinical importance because digitalis may paradoxically enhance conduction down the bypass tract. As a result, the ventricular response may increase, leading to possible myocardial ischemia and, in some cases, to ventricular fibrillation. A similar hazardous effect has been reported with intravenous verapamil.

VT vs. SVT: Diagnostic Clues

Differentiating VT from SVT (e.g., PSVT, atrial flutter, or atrial fibrillation) with bundle branch block–type aberrancy can be very challenging. Three clues may be especially helpful in favoring VT.



AV dissociation is an important clue that may be helpful in differentiating SVT with aberrancy from VT. Recall from Chapter 17 that, with AV dissociation, the atria and ventricles are paced from separate sites. Some patients with VT also have AV dissociation; in other words, the ventricles are stimulated from an ectopic site at a rapid rate, while the atria continue to be paced independently by the SA node. In such cases, you may be able to see P waves occurring at a slower rate than the rapid wide QRS complexes, as shown in Figure 20-11 . Some of the P waves may be buried in the QRS complexes and therefore difficult to discern. 
Unfortunately, only a minority of patients with VT clearly show ECG evidence of AV dissociation. Therefore the absence of AV dissociation does not exclude VT. The presence of AV dissociation in a patient with wide QRS complexes at a rapid rate, however, is virtually diagnostic of VT. Furthermore, in some cases of VT with AV dissociation, the SA node may transiently “capture” the ventricles, producing a capture beat, which has a normal QRS duration, or a fusion beat, in which the sinus and ventricular beats coincide to produce a hybrid complex. Figure 20-12 illustrates capture and fusion beats occurring with VT.



The shape of the QRS in V1/V2 and V6. When the QRS shape resembles an RBBB pattern, a typical rSR′ shape in lead V1 suggests SVT and a single broad R wave or a qR, QR, or RS complex in that lead strongly suggests VT ( Fig. 20-13 ). When the QRS shape resembles an LBBB pattern, a broad (0.04 sec or longer) initial R wave in lead V1 or V2 or a QR complex in lead V6 strongly suggests VT.



The QRS duration. A QRS width of greater than 0.14 sec with an RBBB morphology or greater than 0.16 sec with an LBBB morphology suggests VT. (This criterion is not reliable if the patient is on a drug that widens the QRS, or in the presence of hyperkalemia.)

FIGURE 20-11  Sustained monomorphic ventricular tachycardia with atrioventricular (AV) dissociation. Note the independence of the atrial (sinus) rate (75 beats/min) and ventricular (QRS) rate (140 beats/min). The visible sinus P waves are indicated by &z.cirf;, and the hidden P waves are indicated by ○.

FIGURE 20-12  Sustained monomorphic ventricular tachycardia with atrioventricular dissociation producing fusion (F) and capture (C) beats. Leads I and II were recorded simultaneously.

FIGURE 20-13  A, Sustained monomorphic ventricular tachycardia at a rate of about 200 beats/min. Notice the wide QRS complexes with a right bundle branch block morphology. The QRS complex in leads V1 and V2 shows a broad R wave. B, Following conversion to sinus rhythm, the pattern of an underlying anterior wall myocardial infarction and possible ventricular aneurysm becomes evident. Q waves and ST elevations are seen in leads in V1, V2, and V3; ischemic T wave inversions are present in leads V4, V5, and V6. Note also that the QRS complex is wide (0.12 sec) because of an intraventricular conduction delay (IVCD) with left axis deviation (left anterior fascicular block). The prominent negative P waves in lead V1 are due to left atrial abnormality.

Box 20-3 summarizes some of the major findings that favor VT over SVT with bundle branch block aberrancy. For more detailed discussion, consult the Bibliography .

BOX 20-3 

Wide Complex Tachycardia: Selected Criteria Favoring Ventricular Tachycardia



AV dissociation



QRS width: >0.14 s with RBBB configuration[*] 
>0.16 s with LBBB configuration[*]



Shape of the QRS complex 
RBBB: Mono- or biphasic complex in V1 


LBBB: Broad R waves in V1 or V2 ≥ 0.04 s 
Onset of QRS to tip of S wave in V1 or V2 ≥ 0.07 s 
QR complex in V6 


Modified from: Josephson ME, Zimetbaum P: The tachyarrhythmias. In Kasper DL, Braunwald E, Fauci A, et al (eds): Harrison's Principles of Internal Medicine, 16th ed. New York, McGraw-Hill, 2004.


*  QRS duration may also be increased in supraventricular tachycardias in presence of drugs that prolong QRS derivation or with hyperkalemia. 

At times, you may find it impossible to distinguish reliably between VT and SVT with aberration from the 12-lead ECG. In such cases, clinical judgment must be used. For example, if the patient is hypotensive, the tachycardia is generally treated as VT (see Box 20-1 ). On the other hand, remember that not all patients with VT are hypotensive. Indeed, occasional patients may have minimal symptoms at rest when they are in sustained VT.

Remember that intravenously administered verapamil should not be used in undiagnosed wide-complex tachycardias. This drug may cause hemodynamic collapse in patients with VT or AF with WPW preexcitation syndrome that may simulate VT.


As mentioned previously, the first question to ask in looking at any tachyarrhythmia is whether the rhythm is VT. If sustained VT is present, emergency treatment is required (see Chapter 16 ).

The treatment of narrow-complex tachycardias depends on the clinical setting. In patients with sinus tachycardia (see Chapter 13 ), treatment is directed at the underlying cause (e.g., fever, sepsis, congestive heart failure, or hyperthyroidism). Similarly, the treatment of MAT should be directed at the underlying problem (usually decompensated chronic pulmonary disease). Direct-current electrical cardioversion should not be used with MAT because it is unlikely to be helpful and it may induce serious ventricular arrhythmias. A calcium channel blocker (verapamil or diltiazem) can be used to slow the ventricular response in MAT.

In assessing any patient with a narrow-complex tachycardia, you should ask the following three key questions about the effects of the tachycardia on the heart and circulation:



Is the patient's blood pressure abnormally low? In particular, is the patient severely hypotensive or actually in shock?



Is the patient having an acute myocardial infarction or severe ischemia?



Is the patient in severe congestive heart failure (pulmonary edema)?

Patients in any one of these categories who have AF or atrial flutter with a rapid ventricular response or a PSVT require emergency therapy. If they do not respond promptly to initial drug therapy, electrical cardioversion should be considered.

Another major question to ask about any patient with a tachyarrhythmia (or any arrhythmia, for that matter) is whether digitalis or other drugs are part of the therapeutic regimen. Some arrhythmias (e.g., AT with block) may be digitalis-toxic rhythms, disturbances for which electrical cardioversion is contraindicated (see Chapter 18 ). Drug-induced QT prolongation is an important substrate for torsades de pointes type VT as discussed in Chapter 16 .



An interesting group of patients has bradyarrhythmia sometimes alternating with episodes of tachyarrhythmia. The term sick sinus syndrome was coined to describe patients with SA node dysfunction that causes marked sinus bradycardia or sinus arrest, sometimes with junctional escape rhythms, which may lead to symptoms of light-headedness and even syncope.

In some patients with sick sinus syndrome, bradycardia episodes are interspersed with paroxysms of tachycardia (usually AF, atrial flutter, or some type of PSVT). Sometimes the bradycardia occurs immediately after spontaneous termination of the tachycardia. The term brady-tachy syndrome has been used to describe patients with sick sinus syndrome who have both tachyarrhythmias and bradyarrhythmias ( Fig. 20-14 ).

FIGURE 20-14  Brady-tachy (sick sinus) syndrome. This rhythm strip shows a narrow-complex tachycardia (probably atrial flutter) followed by a prominent sinus pause, two sinus beats, an atrioventricular junctional escape beat (J), and then sinus rhythm again.

The diagnosis of sick sinus syndrome and, in particular, the brady-tachy variant often requires monitoring the patient's heartbeat over several hours or even days. A single ECG strip may be normal or may reveal only the bradycardia or tachycardia episode. Treatment generally requires a permanent pacemaker to prevent sinus arrest and radiofrequency ablation therapy or antiarrhythmic drugs to control the tachycardias after the pacemaker has been inserted.



Wandering atrial pacemaker (sometimes abbreviated as WAP) is an arrhythmia that is somewhat difficult to classify. As shown in Figure 20-15 , this rhythm is characterized by multiple P waves of varying configuration with a relatively normal or slow heart rate. This pattern reflects rapid shifting of the pacemaker between the sinus node and different ectopic atrial sites, and sometimes the AV junction. Wandering atrial pacemaker may be seen in a variety of settings. Occasionally, it develops in normal persons (particularly during sleep). It may also occur with digitalis excess or certain other drug toxicity, sick sinus syndrome, and different types of organic heart disease.

FIGURE 20-15  The variability of the P wave configuration in this lead II rhythm strip is caused by shifting of the pacemaker site between the sinus node and ectopic atrial locations.

Wandering atrial pacemaker is quite distinct from MAT, another arrhythmia with multiple different P waves. In wandering atrial pacemaker, the rate is normal or slow. In MAT, it is rapid.



Arrhythmias can be grouped into bradycardias (heart rate slower than 60 beats/min) and tachycardias (heart rate faster than 100 beats/min).

Bradycardias include five major classes of arrhythmias or conduction disturbances:



Sinus bradycardia



Atrioventricular (AV) junctional (nodal) escape rhythm



Second- or third-degree heart block or AV dissociation



Atrial fibrillation or flutter with a slow ventricular rate



Idioventricular escape rhythm.

Digitalis or other drug toxicity, or hyperkalemia, may be responsible for any of these arrhythmias.

Tachycardias can be subdivided into those with narrow QRS complexes and those with wide QRS complexes. The narrow-complex QRS tachycardias are almost always supraventricular in origin and include the following:



Sinus tachycardia



Paroxysmal supraventricular tachycardias (PSVTs), including atrial tachycardia (AT), AV nodal reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT) (see Chapter 14 )



Atrial fibrillation



Atrial flutter

Carotid sinus massage is sometimes helpful in differentiating these arrhythmias at the bedside. Tachycardias with wide QRS complexes may be either ventricular or any of the supraventricular tachycardias associated with a bundle branch block or Wolff-Parkinson-White preexcitation mechanism.

The term sick sinus syndrome describes patients with sinoatrial node dysfunction who have a marked sinus bradycardia, sometimes with sinus arrest or slow junctional rhythms that causes light-headedness or syncope. Some patients with sick sinus syndrome have periods of tachycardia alternating with the bradycardia (brady-tachy syndrome).

Wandering atrial pacemaker is an arrhythmia characterized by multiple P waves of varying configuration, usually with a relatively normal or slow heart rate.





Answer the following questions about the rhythm strip below:




Is the rate regular or irregular?



Are discrete P waves present?



What is this arrhythmia?



What is the most likely diagnosis for the wide complex tachycardia arrhythmia shown below? 




A 40-year-old woman complaining of occasional palpitations with a fast heartbeat is found to have runs of narrow QRS complex tachycardia at a rate of 200 beats/min without evident P waves on her Holter monitor tracing. The rhythm is very regular. What is the most likely diagnosis?



What is the cause of the bradycardia in the rhythm strip shown below? 




Name five reversible pharmacologic or metabolic causes of bradycardia.

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