The only EKG book. 9th Ed

Chapter 3. Arrhythmias

In this chapter, you will learn:

1

what an arrhythmia is, and what it does (and doesn’t) do to people

2

about rhythm strips and ambulatory monitors

3

how to determine the heart rate from the EKG

4

the five basic types of arrhythmias

5

how to recognize the four common sinus arrhythmias

6

how arrhythmias develop in the first place to ask The Four Questions that will let you recognize and diagnose the

7

common arrhythmias that originate in the sinus node, atria, the atrioventricular (AV) node, and the ventricles

8

how to distinguish supraventricular arrhythmias from ventricular arrhythmias, both clinically and on the EKG

9

how programmed electrical stimulation and other techniques have revolutionized the diagnosis and treatment of certain arrhythmias

10

about the cases of Lola de B., George M., and Frederick van Z., which will leave you feeling astonished by how easily you have mastered material that has cowed even the high and mighty

The resting heart normally beats with a regular rhythm, 60 to 100 times per minute. Because each beat originates with depolarization of the sinus node, the usual, everyday cardiac rhythm is called normal sinus rhythm. Anything else is called an arrhythmia (or, more accurately, a dysrhythmia, but we will stick to the conventional terminology in the discussion to follow). The term arrhythmia refers to any disturbance in the rate, regularity, site of origin, or conduction of the cardiac electrical impulse. An arrhythmia can be a single aberrant beat (or even a prolonged pause between beats) or a sustained rhythm disturbance that can persist for the lifetime of the patient.

Not every arrhythmia is abnormal or dangerous. For example, heart rates as low as 35 to 40 beats per minute are common and quite normal in well-trained athletes. Single aberrant beats, originating elsewhere in the heart than the sinus node, frequently occur in the majority of healthy individuals.

Some arrhythmias, however, can be dangerous and may even require immediate clinical intervention to prevent sudden death. The diagnosis of an arrhythmia is one of the most important things an EKG can do, and nothing yet has been found that can do it better.

The Clinical Manifestations of Arrhythmias

When should you suspect that someone had or is having an arrhythmia?

Many arrhythmias go unnoticed by the patient and are picked up incidentally on a routine physical examination or EKG. Frequently, however, arrhythmias elicit one of several characteristic symptoms.

First and foremost are palpitations, an awareness of one’s own heartbeat. Patients may describe intermittent accelerations or decelerations of their heartbeat, a long pause between heartbeats, or a sustained rapid heartbeat that may be regular or irregular. The sensation may be no more than a mild nuisance or a truly terrifying experience.

More serious are symptoms of decreased cardiac output, which can occur when the arrhythmia compromises the heart’s ability to pump blood effectively. Among these are light-headedness and syncope (a sudden faint).

Rapid arrhythmias can increase the oxygen demands of the myocardium and cause angina (chest pain). The sudden onset of an arrhythmia in a patient with underlying cardiac disease can also precipitate congestive heart failure.

Sometimes, the first clinical manifestation of an arrhythmia is sudden death.

Patients in the throes of an acute myocardial infarction are at a greatly increased risk for arrhythmic sudden death, which is why they are hospitalized in cardiac care units (CCUs) where their heart rate and rhythm can be continuously monitored.

Increasingly, the EKG has become helpful in identifying conditions that predispose to malignant arrhythmias and sudden death and thereby allow the initiation of lifesaving intervention before the catastrophic event. These conditions can be inherited or acquired. Most common among these are repolarization abnormalities that prolong the QT interval, a dangerous substrate for potentially lethal arrhythmias (much more on this later in this chapter and in Chapter 7).

Why Arrhythmias Happen

It is often impossible to identify the underlying cause of an arrhythmia, but a careful search for treatable precipitating factors must always be made. The mnemonic HIS DEBS should help you remember those arrhythmogenic factors that should be considered whenever you encounter a patient with an arrhythmia:

H—Hypoxia: A myocardium deprived of oxygen is an irritable myocardium. Pulmonary disorders, whether severe chronic lung disease or an acute pulmonary embolus, are major precipitants of cardiac arrhythmias.

I—Ischemia and Irritability: We have already mentioned that myocardial infarctions are a common setting for arrhythmias. Angina, even without the actual death of myocardial cells that occurs with infarction, is also a major precipitant. Occasionally, myocarditis, an inflammation of the heart muscle often caused by routine viral infections, can induce an arrhythmia.

S—Sympathetic Stimulation: Enhanced sympathetic tone from any cause (e.g., hyperthyroidism, congestive heart failure, nervousness, exercise) can elicit arrhythmias.

D—Drugs: Many drugs can cause arrhythmias. They do so by a variety of mechanisms. Ironically, the antiarrhythmic drugs are among the leading culprits.

E—Electrolyte Disturbances: Hypokalemia and hyperkalemia are notorious for their ability to induce arrhythmias, but imbalances of calcium and magnesium can also be responsible.

B—Bradycardia: A very slow heart rate seems to predispose to arrhythmias. One could include the bradytachycardia syndrome (also called the sick sinus syndrome) in this category.

S—Stretch: Enlargement and hypertrophy of the atria and ventricles can produce arrhythmias. This is one way in which congestive heart failure, cardiomyopathies, and valvular disease can cause arrhythmias.

Rhythm Strips

In order to identify an arrhythmia correctly, it is often necessary to view the heart rhythm over a much longer period of time than the few complexes present on the standard 12-lead EKG. When an arrhythmia is suspected, either clinically or electrocardiographically, it is standard practice to run a rhythm strip, a long tracing of a single lead or multiple leads. Any lead can be chosen, but it obviously makes sense to choose the lead that provides you with the most information. One or more leads are preprogrammed to run automatically when you hit the Rhythm button on modern EKG machines. The rhythm strip makes it much easier to identify any irregularities or intermittent bursts of unusual electrical activity.

A typical rhythm strip. It can be as short or as long as you need to decipher the rhythm. This particular strip represents a continuous recording of lead II in a patient with normal sinus rhythm, the normal rhythm of the heart.

Ambulatory Monitors and Event Monitors

The ultimate rhythm strips are provided by ambulatory monitors. They are essentially portable EKG machines with a memory. The original ambulatory monitor, the Holter monitor, is a small box containing the recorder that is hooked onto the patient’s belt with wires running up to electrode patches attached to the chest wall. It is worn for 24 to 48 hours. Newer monitors are patches—all the recording technology, one lead included, is contained within the patch—that are attached directly to the chest wall by an adhesive and worn for up to 2 weeks. The patient then goes about his or her normal daily activities—working, showering, exercising, sleeping—while the monitor records every single heartbeat.1 A complete record of the patient’s heart rhythm is stored and later analyzed for any arrhythmic activity.

Ambulatory monitoring is especially valuable when the suspected arrhythmia is an infrequent occurrence and is therefore unlikely to be captured on a random 12-lead EKG. Clearly, the longer one can monitor the patient, the better the chance that the arrhythmia will be detected. Further information can be obtained if the patient is instructed to write down the precise times when he or she experiences symptoms. The patient’s diary can then be compared with the ambulatory recording to determine whether there is a correlation between the patient’s symptoms and any underlying cardiac arrhythmia. The patches frequently have a button that patients can press if they feel palpitations, thereby noting the time of their symptoms on the EKG tracing, and some devices include cell phones that allow the patients to type in their symptoms when they occur.

Some rhythm disturbances or symptoms suspicious for arrhythmias happen so infrequently that even an ambulatory monitor is likely to miss them. For these patients, an event monitor may provide a solution. An event monitor is initiated by the patient whenever he or she experiences palpitations. Some of these monitors are constantly running—they are never “off”—and they are able to go back and make a record of the rhythm from a short period before the patient activates it to several minutes after activation. The resultant EKG recording is sent out over the phone lines for evaluation. In this manner, multiple recordings can be made over the course of the several months during which the patient has rented the monitor. Other monitors are only activated by the patient, who holds the monitor up to his or her chest when symptoms occur. There are also monitors that attach to a typical cell phone and are used in the same way; these can be purchased by the patient and are remarkably inexpensive.

Still other abnormal rhythms are so short-lived or infrequent that they are missed by any standard type of patient-activated mechanism. For these situations, a surgically implanted event recorder can be inserted under the skin of the patient with a small (1-inch) incision. These event recorders can be safely left in place for over a year and can automatically record and store in their memory rapid or slow heart rates (the rates that trigger the recorder are programmable). The patient can also activate the recorder whenever symptoms occur. The recorded data can be easily downloaded, typically every few months, by telemetry communication.

A surgically implanted event monitor recording in a patient with syncope. The small vertical dashes mark off intervals of 1 second. The 3-second pause near the bottom of the strip activates the monitor, which then stores the EKG tracing from several minutes before to several minutes after the activation point. The stored recording is then downloaded and printed at a later time. In this patient, the long pause was associated with a near-syncopal episode.

How to Determine the Heart Rate From the EKG

The first step in determining the heart’s rhythm is to determine the heart rate. It is easily calculated from the EKG.

The horizontal axis on an EKG represents time. The distance between each

light line (one small square or 1 mm) equals 0.04 seconds, and the distance between each heavy line (one large square or 5 mm) equals 0.2 seconds. Five large squares therefore constitute 1 second. A cycle that repeats itself every five large squares represents 1 beat per second, or a heart rate of 60 beats per minute.

Every QRS complex is separated by five large squares (1 second). A rhythm occurring once every second occurs 60 times every minute.

Of course, not everyone’s heart beats at precisely 60 beats per minute. Fortunately, whatever the heart rate, calculating it is easy.

A Simple Three-Step Method for Calculating the Heart Rate

1. Find an R wave that falls on, or nearly on, one of the heavy lines.

2. Count the number of large squares until the next R wave.

3. Determine the rate in beats per minute as follows:

 If there is one large square between successive R waves, then each R wave is separated by 0.2 seconds. Therefore, over the course of 1 full second, there will be five cycles of cardiac activity (1 second divided by 0.2 seconds), and over 1 minute, 300 cycles (5 x 60 seconds). The heart rate is therefore 300 beats per minute.

 If there are two large squares between successive R waves, then each R wave is separated by 0.4 seconds. Therefore, over the course of 1 full second, there will be 2.5 cycles of cardiac activity (1 second divided by 0.4 seconds), and over 1 minute, 150 cycles (2.5 x 60 seconds). The heart rate is therefore 150 beats per minute.

By similar logic:

 Three large squares = 100 beats per minute

 Four large squares = 75 beats per minute

 Five large squares = 60 beats per minute

 Six large squares = 50 beats per minute

Notice that you can get the same answers by dividing 300 by the number of large squares between R waves (e.g., 300 divided by 4 squares = 75). Even greater accuracy can be achieved by counting the total number of small squares between R waves and dividing 1500 by this total.

What is the heart rate of the following strips?

(A) About 75 beats per minute. (B) About 60 beats per minute. (C) About 150 beats per minute.

If the second R wave falls between heavy lines, that is, if the R waves from each cycle don’t conveniently fall a precise whole number of large boxes from each other, you can estimate that the rate lies between the two extremes on either side.

What is the rate of the following strip?

The R waves are slightly more than four squares apart—let’s say four and one- quarter. The rate must therefore be between 60 and 75 beats per minute. If you guess 70, you’ll be close. Alternatively, divide 300 by four and one-quarter and get 70.6 beats per minute.

If the heart rate is very slow, you can still use this system; simply divide 300 by the number of large squares between complexes to get your answer. However, there is another method that some prefer. Every EKG rhythm strip is marked at 3-second intervals, usually with a series of little lines (or slashes or dots) at the top or bottom of the strip. Count the number of cycles within two of these intervals (6 seconds) and multiply by 10 (10 x 6 seconds = 60 seconds) to get the heart rate in beats per minute. Try it both ways on the example below:

Note the small pink slashes at the top of the rhythm strip marking off 3-second intervals. There are about five and one-half cycles within two of the 3-second intervals. The rate is therefore about 55 beats per minute.

The Five Basic Types of Arrhythmias

Of all of the subjects in electrocardiography, none is guaranteed to cause more anxiety (and palpitations) than the study of arrhythmias. There is no reason for this. First, once you have learned to recognize the basic patterns, nothing is easier than recognizing a classic arrhythmia. Second, the difficult arrhythmias are difficult for everyone, including expert electrocardiographers. Sometimes, in fact, it is impossible to identify what a particular rhythm is. Nothing gladdens one’s heart more than the sight of two venerable cardiologists going at it over a baffling rhythm disturbance.

The heart is capable of five basic types of rhythm disturbances:

1. The electrical activity follows the usual conduction pathways we have already outlined, starting with depolarization of the sinus node, but it is too fast, too slow, or irregular. These are arrhythmias of sinus origin.

2. The electrical activity originates from a focus other than the sinus node. These are called ectopic rhythms.

3. The electrical activity is trapped within an electrical racetrack whose shape and boundaries are determined by various anatomic or electrical myocardial configurations. These are called reentrant arrhythmias. They can occur anywhere in the heart.

4. The electrical activity originates in the sinus node and follows the usual pathways but encounters unexpected blocks and delays. These conduction blocks are discussed in Chapter 4.

5. The electrical activity follows anomalous accessory conduction pathways that bypass the normal ones, providing an electrical shortcut, or short circuit. These arrhythmias are termed preexcitation syndromes, and they are discussed in Chapter 5.

Arrhythmias of Sinus Origin

Sinus Tachycardia and Sinus Bradycardia

Normal sinus rhythm is the normal rhythm of the heart. Depolarization originates spontaneously within the sinus node. The rate is regular and between 60 and 100 beats per minute. If the rhythm speeds up beyond 100, it is called sinus tachycardia; if it slows down below 60, it is called sinus bradycardia.

Sinus tachycardia and sinus bradycardia can be normal or pathologic. Strenuous exercise, for example, can accelerate the heart rate well over 100 beats per minute, whereas resting heart rates below 60 beats per minute are typical in well-conditioned athletes. On the other hand, alterations in the rate at which the sinus node fires can accompany significant heart disease. Sinus tachycardia can occur in patients with congestive heart failure or severe lung disease, or it can be the only presenting sign of hyperthyroidism in the elderly. Sinus bradycardia can be caused by medications, most commonly beta-blockers, calcium channel blockers, and opioids, and is the most common rhythm disturbance seen in the early stages of an acute myocardial infarction; in otherwise healthy individuals, it can result from enhanced vagal tone and cause fainting.

(A) Sinus tachycardia. Each beat is separated by two and one-half large squares for a rate of 120 beats per minute. (B) Sinus bradycardia. More than seven large squares separate each beat, and the rate is 40 to 45 beats per minute.

Sinus Arrhythmia

Often, the EKG will reveal a rhythm that appears in all respects to be normal sinus rhythm except that it is slightly irregular. This is called sinus arrhythmia. This is a normal phenomenon, reflecting the variation in heart rate that accompanies inspiration and expiration. The effect may be so small as to be virtually undetectable or (rarely) large enough to mimic more serious causes of an irregular heartbeat. Inspiration accelerates the heart rate, and expiration slows it down.

A beautiful example of sinus arrhythmia. You may have also noticed the prolonged separation of each P wave from its ensuing QRS complex (i.e., a prolonged PR interval). This represents a conduction delay called first-degree AV block; it is discussed in Chapter 4.

A loss of sinus arrhythmia may be caused by diminished autonomic feedback to the sinus node. It is therefore often seen in patients with diabetes mellitus, which over time can cause an autonomic neuropathy. Sinus arrhythmia can also be diminished with aging, with obesity, and in patients with long-standing hypertension.

Sinus Arrest, Asystole, and Escape Beats

Sinus arrest occurs when the sinus node stops firing. If nothing else were to happen, the EKG would show a flat line without any electrical activity, and the patient would die. Prolonged electrical inactivity is called asystole.

Fortunately, virtually all myocardial cells have the ability to behave as pacemakers. Ordinarily, the fastest pacemaker drives the heart, and under normal circumstances, the fastest pacemaker is the sinus node. The sinus node overdrives the other pacemaker cells by delivering its wave of depolarization throughout the myocardium before its potential competitors can complete their own, more leisurely, spontaneous depolarization. With sinus arrest, however, these other pacemakers can spring into action in a kind of rescue mission. These rescuing beats, originating outside the sinus node, are called escape beats.

Sinus arrest occurs after the second beat—note the long pause. The third beat, restoring electrical activity, has no P wave. This beat is called a junctional escape beat, which we will explain in the very next section.

Nonsinus Pacemakers

Like the sinus node, which typically fires between 60 and 100 times each minute, the other potential pacemaker cells of the heart have their own intrinsic rhythm. Atrial pacemakers usually discharge at a rate of 60 to 75 beats per minute. Pacemaker cells located near the AV node, called junctional pacemakers, typically discharge at 40 to 60 beats per minute. Ventricular pacemaker cells usually discharge at 30 to 45 beats per minute.

Each of these nonsinus pacemakers can rescue an inadequate sinus node by providing just one or a continual series of escape beats. Of all of the available escape mechanisms, junctional escape is by far the most common.

With junctional escape, depolarization originates near the AV node, and the usual pattern of atrial depolarization does not occur. As a result, a normal P wave is not seen. Most often, there is no P wave at all. Occasionally, however, a retrograde P wave may be seen, representing atrial depolarization moving backward from the AV node into the atria. The mean electrical axis of this retrograde P wave is reversed 180° from that of the normal P wave. Thus, whereas the normal P wave is upright in lead II and inverted in lead aVR, the retrograde P wave is inverted in lead II and upright in lead aVR.

Junctional escape. The first two beats are normal sinus beats with a normal P wave preceding each QRS complex. There is then a long pause followed by a series of three junctional escape beats occurring at a rate of 40 to 45 beats per minute. Retrograde P waves can be seen buried in the early portion of the T waves (can you see the little downward notches?). Retrograde P waves can occur before, after, or during the QRS complex, depending on the relative timing of atrial and ventricular depolarization. If atrial and ventricular depolarizations occur simultaneously, the much larger QRS complexes can completely mask the retrograde P waves.

Sinus Arrest Versus Sinus Exit Block

Because sinus node depolarization is not recorded on the EKG, it is impossible to determine whether a prolonged sinus pause is due to sinus arrest or to failure of sinus depolarization to be transmitted out of the node and into the atria, a situation called sinus exit block. You may hear these different terms bandied about from time to time, but for all intents and purposes, sinus arrest and sinus exit block mean the same thing: There is a failure of the sinus mechanism to deliver its current into the surrounding tissue.

(A) Normal sinus rhythm. The sinus node fires repeatedly, and waves of depolarization spread out into the atria. (B) Sinus arrest. The sinus node falls silent. No current is generated, and the EKG shows no electrical activity. (C) Sinus exit block. The sinus node continues to fire, but the wave of depolarization fails to exit the sinus node into the atrial myocardium. Again, the EKG shows no electrical activity; there is not sufficient voltage to generate a detectable P wave.

SUMMARY

Arrhythmias of Sinus Origin

Normal sinus rhythm

Sinus tachycardia

Sinus bradycardia

Sinus arrest or exit block

Sinus arrest or exit block with junctional escape

Special note for the electrically infatuated: There is a way in which transient sinus arrest and sinus exit block can sometimes be distinguished on the EKG. With sinus arrest, resumption of sinus electrical activity occurs at any random time (the sinus node simply resumes firing). However, with sinus exit block, the sinus node has continued to fire silently, so when the block is lifted, the sinus node resumes depolarizing the atria after a pause that is some integer multiple of the normal cycle (e.g., exactly one missed P wave, or exactly two missed P waves, or more).

Ectopic Rhythms

The two major causes of nonsinus arrhythmias are ectopic rhythms and reentrant rhythms. Ectopic rhythms are abnormal rhythms that arise from elsewhere than the sinus node. They can consist of single, isolated beats or sustained arrhythmias. Ectopic rhythms can be caused by any of the precipitating factors described previously.

At the cellular level, they arise from enhanced automaticity (i.e., intrinsic pacemaker activity) of a nonsinus node site, either a single focus or a roving one. As we have already stressed, the fastest pacemaker usually drives the heart, and under normal circumstances, the fastest pacemaker is the sinus node. Under abnormal circumstances, however, any of the other pacemakers scattered throughout the heart can be accelerated, that is, stimulated to depolarize faster and faster until they can overdrive the normal sinus mechanism and establish their own transient or sustained ectopic rhythm. Among the common causes of enhanced automaticity are digitalis toxicity, beta adrenergic stimulation from inhaler therapies used to treat asthma and chronic obstructive lung disease, caffeine, alcohol, and stimulant drugs such as cocaine and amphetamines. We will see examples of ectopic rhythms in the pages to come.

(A) Normally, the sinus node drives the heart. (B) If another potential pacemaker (e.g., the AV junction) is accelerated, it can take over the heart and overdrive the sinus node.

Reentrant Rhythms

The second major cause of nonsinus arrhythmias is called reentry. Whereas enhanced automaticity represents a disorder of impulse formation (i.e., new impulses that are formed elsewhere than the sinus node take over the heart), reentry represents a disorder of impulse transmission. The results, however, are similar: creation of a focus of abnormal electrical activity. Here is how reentry works:

Picture a wave of depolarization arriving at two adjacent regions of myocardium, A and B, as shown in part 1 of the figure on the next page. A and B conduct the current at the same rate, and the wave of depolarization rushes past, unperturbed, on its way to new destinations. This is the way things usually operate.

Suppose, however, that pathway B transmits the wave of depolarization more slowly than does pathway A. This can result, for example, if pathway B has been damaged by ischemic disease or fibrosis, or if the two pathways are receiving different degrees of input from the autonomic nervous system. This situation is depicted in part 2 of the figure. The wave of depolarization now rushes through pathway A but is held up in pathway B. The impulse emerging from pathway A can now return back through pathway B, setting up an uninterrupted revolving circuit along the two pathways (see figure, part 3). As the electrical impulse spins in this loop, waves of depolarization are sent out in all directions. This is called a re-entry loop, and it behaves like an electrical racetrack, providing a source of electrical activation that can overdrive the sinus mechanism and run the heart.

A model showing how a reentrant circuit becomes established. (1) Normally, pathways A and B (any two adjacent regions of cardiac function) conduct current equally well. (2) Here, however, conduction through pathway B is temporarily slowed. Current passing down A can then turn back and conduct in a retrograde fashion through B. (3) The reentry loop is established.

A reentry loop can vary greatly in size. It can be limited to a small loop within a single anatomic site (e.g., the AV node), it can loop through an entire chamber (either an atrium or ventricle), or it can even involve both an atrium and ventricle if there is an accessory pathway of conduction connecting the two chambers (this last point will be made more obvious in Chapter 5).

The Four Questions

As you will see in just a moment, all of the clinically important nonsinus arrhythmias—the ones you have probably heard of—are either ectopic or reentrant in origin. It is therefore critical to be able to identify them, and you will spend the rest of this chapter learning exactly how to do that. This may sound like a tall order, but to assess any rhythm disturbance on the EKG, you only need to answer four questions:

 Are Normal P Waves Present? The emphasis here is on the word normal. If the answer is yes, if there are normal-appearing P waves with a normal P- wave axis (positive in lead II and negative in lead aVR), then the origin of the arrhythmia is almost certainly within the atria. If no P waves are present, then the rhythm must have originated below the atria, in the AV node or the ventricles. The presence of P waves with an abnormal axis may reflect (1) activation of the atria from impulses originating from an atrial focus other than the sinus node or (2) retrograde activation from a site within the AV node or the ventricles, that is, from current flowing backward into the atria through the AV node or through an accessory pathway connecting the atria and ventricles (more on all of this later).

 Are the QRS Complexes Narrow (<0.12 Seconds in Duration) or Wide (>0.12 Seconds in Duration)? A narrow normal QRS complex implies that ventricular depolarization is proceeding along the usual pathways (AV node to His bundle to bundle branches to Purkinje cells). This is the most efficient means of conduction, requiring the least amount of time, so the resulting QRS complex is of short duration (narrow). A narrow QRS complex, therefore, indicates that the origin of the rhythm must be at or above the AV node. A wide QRS complex usually implies that the origin of ventricular depolarization lies within the ventricles themselves. Depolarization is initiated within the ventricular myocardium, not the conduction system, and therefore spreads much more slowly. Conduction does not follow the most efficient pathway, and the QRS complex is of long duration (wide). (The distinction between wide and narrow QRS complexes, although very useful, cannot, unfortunately, be fully relied on to assess the origin of an arrhythmia. We’ll see why shortly.)

Questions 1 and 2 thus help to make the important distinction of whether an arrhythmia is ventricular or supraventricular (atrial or junctional) in origin.

 What Is the Relationship Between the P Waves and the QRS Complexes? If the P wave and QRS complexes correlate in the usual one-to- one fashion, with a single P wave preceding each QRS complex, then the rhythm almost certainly has a sinus or other atrial origin. Sometimes, however, the atria and ventricles depolarize and contract independently of each other. This will be manifested on the EKG by a lack of correlation between the P waves and QRS complexes, a dangerous situation termed AV dissociation.

 Is the Rhythm Regular or Irregular? This is often the most immediately obvious characteristic of a particular rhythm and is sometimes the most critical.

Whenever you look at an EKG, you will need to assess the rhythm. These four questions should become an intrinsic part of your thinking:

1. Are normal P waves present?

2. Are the QRS complexes narrow or wide?

3. What is the relationship between the P waves and the QRS complexes?

4. Is the rhythm regular or irregular (remember, though, that a sinus arrhythmia is normal)?

For the normal EKG (normal sinus rhythm), the answers are easy:

1. Yes, there are normal P waves.

2. The QRS complexes are narrow.

3. There is one P wave for every QRS complex.

4. The rhythm is essentially regular.

We will now see what happens when the answers are different.

Normal sinus rhythm and “The Four Questions” answered.

Supraventricular Arrhythmias

Let us look first at the arrhythmias that originate in the atria or the AV node, the supraventricular arrhythmias.

Atrial arrhythmias can consist of a single beat or a sustained rhythm disturbance lasting for a few seconds or many years.

Atrial and Junctional Premature Beats

Single ectopic supraventricular beats can originate in the atria or in the vicinity of the AV node. The former are called atrial premature beats (or premature atrial contractions, PACs) and the latter, junctional premature beats. These are common phenomena, neither indicating underlying cardiac disease nor requiring treatment. They can, however, initiate more sustained arrhythmias.

(A) The third beat is an atrial premature beat. Note how the P-wave contour of the premature beat differs from that of the normal sinus beat. (B) The fourth beat is a junctional premature beat. There is no P wave preceding the premature QRS complex.

An atrial premature beat can be distinguished from a normal sinus beat by the contour of the P wave and by the timing of the beat.

Contour. Because an atrial premature beat originates at an atrial site distant from the sinus node, atrial depolarization does not occur in the usual manner, and the configuration of the resultant P wave differs from that of the sinus P waves. If the site of origin of the atrial premature beat is far from the sinus node, the axis of the atrial premature beat will also differ from that of the normal P waves.

Timing. An atrial premature beat comes too early; that is, it intrudes itself before the next anticipated sinus wave.

The third beat is an atrial premature beat. The P wave is shaped differently from the other, somewhat unusual-looking P waves, and the beat is clearly premature.

With junctional premature beats, there is usually no visible P wave, but sometimes, a retrograde P wave may be seen. This is just like the case with the junctional escape beats seen with sinus arrest.

What is the difference between a junctional premature beat and a junctional escape beat? They look exactly alike, but the junctional premature beat occurs early, prematurely, interposing itself into the normal sinus rhythm. An escape beat occurs late, following a pause when the sinus node has failed to fire.

(A) A junctional premature beat. The third beat is obviously premature, and there is no 

P wave preceding the QRS complex. (B) The third beat is a junctional escape beat, establishing a sustained junctional rhythm. It looks just like a junctional premature beat, but it occurs late, following a prolonged pause, rather than prematurely.

Both atrial and junctional premature beats are usually conducted normally to the ventricles, and the resultant QRS complex is therefore narrow.

Sometimes, an atrial premature beat may occur sufficiently early that the AV node will not have recovered (i.e., repolarized) from the previous conducted beat and will therefore be unable to conduct the atrial premature beat into the ventricles. The ECG may then show only a P wave without an ensuing QRS complex. This beat is then termed a blocked atrial premature contraction.

Look at the second beat. The T wave looks deformed, clearly different from the preceding T wave. Why? There is a PAC buried within it. At the time of the PAC, the AV node is still repolarizing and is therefore unable to conduct the PAC into the ventricles. This kind of PAC is called a blocked PAC. There is therefore a pause—no QRS complex or T wave can be generated before the next normal P wave at last comes along and reestablishes normal conduction.

There are several types of sustained supraventricular arrhythmias that you must learn to recognize:

1. AV nodal reentrant tachycardia (AVNRT), still referred to by some old school (and some not-so-old-school) cardiologists as paroxysmal supraventricular tachycardia

2. Atrial flutter

3. Atrial fibrillation

4. Multifocal atrial tachycardia (MAT)

5. Paroxysmal atrial tachycardia (PAT), also called ectopic atrial tachycardia

6. AV reciprocating tachycardia (we’ll hold on discussing this one until Chapter 5, since it is uniquely associated with a particular kind of cardiac condition called preexcitation)

AV Nodal Reentrant Tachycardia

AVNRT is a very common arrhythmia. Its onset is sudden, usually initiated by a premature supraventricular beat (atrial or junctional), and its termination is just as abrupt. It can occur in perfectly normal hearts; there may be no underlying cardiac disease at all. Persons with AVNRT typically present with palpitations, shortness of breath, dizziness, or syncope. Not uncommonly, alcohol, coffee, or just sheer excitement can elicit this rhythm disturbance.

AVNRT is an absolutely regular rhythm, with a rate usually between 150 and 250 beats per minute. It is most often driven by a reentrant circuit looping within the AV node. Retrograde P waves may sometimes be seen in leads II or III, but your best bet would be to look in lead V1 for what is called a pseudo-R', a little blip in the QRS complex that represents the superimposed retrograde P wave. More often than not, however, the P waves are so buried within the much larger QRS complexes that they cannot be identified with any confidence. As with most supraventricular arrhythmias, the QRS complex is usually narrow.

(A-C) AVNRT in four different patients. A shows simultaneous activation of the atria and ventricles; therefore, the retrograde P waves are lost in the QRS complexes. B shows a supraventricular tachycardia mimicking a more serious rhythm called ventricular tachycardia (see Page 154 for a discussion of how this happens, or better yet don’t—you’ll get there shortly). In C, retrograde P waves can be seen. (D) A good example of the pseudo-R' configuration in lead V1 representing the retrograde P waves (arrows) of AVNRT. (E) The AV node is usually the site of the reentrant circuit that causes the arrhythmia. Atrial depolarization therefore occurs in reverse, and if P waves can be seen, their axis will be shifted nearly 180° from normal (that is why these are called retrograde P waves).

Carotid Massage

Massaging the carotid artery can help to diagnose and terminate an episode of AVNRT. Baroreceptors that sense changes in the blood pressure are located at the angle of the jaw where the common carotid artery bifurcates. When the blood pressure rises, these baroreceptors cause reflex responses from the brain to be sent along the vagus nerve to the heart. Vagal input decreases the rate at which the sinus node fires and, more importantly, slows conduction through the AV node.

These carotid baroreceptors are not particularly shrewd, and they can be fooled into thinking that the blood pressure is rising by gentle pressure applied externally to the carotid artery. (For that matter, anything that raises the blood pressure, such as a Valsalva maneuver or squatting, will stimulate vagal input to the heart, but carotid massage is the simplest and most widely used maneuver.) Because, in most cases, the underlying mechanism of AVNRT is a reentrant circuit involving the AV node, carotid massage may accomplish the following:

Interrupt the reentrant circuit and thereby terminate the arrhythmia

At the very least, slow the arrhythmia so that the presence or absence of P waves can be more easily determined and the arrhythmia diagnosed

The carotid sinus contains baroreceptors that influence vagal input to the heart, primarily affecting the sinus node and AV node. Stimulation of the right carotid baroreceptors primarily stimulates sinus node vagal input, whereas stimulation of the left carotid baroreceptors is more likely to affect the vagal input to the AV node.

How to Do Carotid Massage

Carotid massage must be done with great care.

1. Auscultate for carotid bruits. You do not want to cut off the last remaining trickle of blood to the brain nor dislodge an atherosclerotic plaque. If there is evidence of significant carotid disease, do not perform carotid massage.

2. With the patient lying flat, extend the neck and rotate the head slightly away from you.

3. Palpate the carotid artery at the angle of the jaw and apply gentle pressure for 10 to 15 seconds. Press as firmly as would be required to compress a tennis ball.

4. Never compress both carotid arteries simultaneously!

5. Try the right carotid first because the rate of success is somewhat better on this side. If it fails, however, go ahead and try the left carotid next.

6. Have a rhythm strip running during the entire procedure so that you can see what is happening. Always have equipment for resuscitation available; in rare instances, carotid massage may induce sinus arrest.

An episode of AVNRT is broken almost at once by carotid massage. The new rhythm is a sinus bradycardia with a rate of 50 beats per minute.

For patients with an acute episode of AVNRT that does not respond to carotid massage or other vagal maneuvers, pharmacologic intervention will usually terminate the arrhythmia. A bolus injection of adenosine, a short-acting AV nodal blocking agent, is almost always effective (avoid this drug in patients with bronchospastic lung disease). Second-line therapies include beta-blockers, calcium channel blockers, and—rarely—electrical cardioversion.

Atrial Flutter

Atrial flutter is less common than AVNRT. It can occur in normal hearts or, more often, in patients with underlying cardiac pathology. The atrial activation in atrial flutter, as in AVNRT, is absolutely regular but is even more rapid. P waves appear at a rate of 250 to 350 beats per minute. In its most common form, it is generated by a reentrant circuit that runs largely around the annulus of the tricuspid valve.

In atrial flutter, atrial depolarization occurs at such a rapid rate that discrete P waves separated by a flat baseline are not seen. Instead, the baseline continually rises and falls, producing so-called flutter waves. In some leads, usually leads II and III, these may be quite prominent and may create what has been termed a saw-toothed pattern.

The AV node cannot handle the extraordinary number of atrial impulses bombarding it—it simply doesn’t have time to repolarize in time for each ensuing wave—and therefore not all of the atrial impulses pass through the AV node to generate QRS complexes. Some just bump into a refractory node, and that is as far as they get. This phenomenon is called AV block. A 2:1 block is most common. This means that for every two visible flutter waves, one passes through the AV node to generate a QRS complex, and one does not. Blocks of 3:1 and 4:1 are also frequently seen. Carotid massage may increase the degree of block (e.g., changing a 2:1 block to a 4:1 block), making it easier to identify the saw-toothed pattern. Because atrial flutter originates above the AV node, carotid massage will not result in termination of the rhythm.

The axis of the P waves (flutter waves) in atrial flutter depends upon whether the reentrant circuit rotates counterclockwise (the more common form, producing negative saw-toothed deflections in the inferior leads) or clockwise (positive deflections in the inferior leads) around the tricuspid valve.

Atrial flutter. Lead II shows classic negative deflections.

Approximately 200,000 cases of atrial flutter are diagnosed each year in the United States. Common conditions associated with atrial flutter include the following:

 Hypertension

 Obesity

 Diabetes mellitus

 Electrolyte imbalances

 Alcohol intoxication

 Drug abuse, particularly cocaine and amphetamines

 Pulmonary disease (e.g., chronic obstructive pulmonary disease and pulmonary embolism)

 Thyrotoxicosis

 Various underlying cardiac conditions, both congenital (e.g., atrial septal defect) and acquired (e.g., rheumatic valvular disease, coronary artery disease, and congestive heart failure)

Although atrial flutter is rarely life threatening, the rapid ventricular response may cause shortness of breath or angina or precipitate or worsen congestive heart failure, which may mandate urgent clinical intervention. Electrical cardioversion is usually effective at restoring normal sinus rhythm, although pharmacologic cardioversion is sometimes first attempted in patients who are hemodynamically stable. Long-term control with antiarrhythmic drugs can be difficult. Definitive treatment can now be accomplished in most patients with typical atrial flutter using a technique called catheter ablation, in which radiofrequency energy is delivered to the myocardium via a catheter to create small lesions that disrupt the reentry pathway.

Atrial Fibrillation

In atrial fibrillation, atrial activity is completely chaotic, and the AV node may be bombarded with more than 500 impulses per minute! Whereas in atrial flutter a single constant reentrant circuit is responsible for the regular saw-toothed pattern on the EKG, in atrial fibrillation, multiple tiny reentrant circuits whirl around in totally unpredictable fashion. No true P waves can be seen. Instead, the baseline appears flat or undulates slightly. The AV node, faced with this extraordinary blitz of atrial impulses, allows only occasional impulses to pass through at variable intervals, generating an irregularly irregular ventricular rate, usually between 120 and 180 beats per minute. However, slower or faster ventricular responses (see figures A and B below) can often be seen.

This irregularly irregular appearance of QRS complexes in the absence of discrete P waves is the key to identifying atrial fibrillation. The wavelike forms that may often be seen on close inspection of the undulating baseline are called fibrillation waves.

(A) Atrial fibrillation with a slow, irregular ventricular rate. (B) Another example of atrial fibrillation. In the absence of a clearly fibrillating baseline, the only clue that this rhythm is atrial fibrillation is the irregularly irregular appearance of the QRS complexes.

Atrial fibrillation is not the only tachyarrhythmia that can cause an irregularly irregular rhythm, but it is by far the most common. Other possibilities include (1) atrial flutter with variable block (although the appearance of the QRS complexes will appear irregular, they are not truly chaotic), and (2) an arrhythmia we will be discussing shortly, multifocal atrial tachycardia. In addition, perfectly healthy people with normal hearts can have a marked sinus arrhythmia as they inhale and exhale; if you check their pulse, it may appear irregularly irregular. In the vast majority of cases, however, an irregularly irregular rhythm means the patient has atrial fibrillation.

Carotid massage may slow the ventricular rate in atrial fibrillation, but it is rarely used in this setting because the diagnosis is usually obvious.

ATRIAL FIBRILLATION: CLINICAL STUFF YOU SHOULD KNOW:

Atrial fibrillation is the most common and clinically significant sustained arrhythmia in the general population. It is especially common in the elderly. Underlying causes are similar to those for atrial flutter, but there is an especially high incidence of underlying cardiovascular disorders, notably hypertension, metabolic syndrome, mitral valve disease, and coronary artery disease. Other common risk factors include obesity and alcoholism. An important cause that should not be overlooked, particularly in patients with nocturnal atrial fibrillation, is obstructive sleep apnea. You often won’t be able to identify an acute precipitant in patients with atrial fibrillation, but keep in mind the possibility of a pulmonary embolism, thyrotoxicosis, and pericarditis.

Atrial fibrillation can cause palpitations, chest pain, shortness of breath, or dizziness. A significant number of patients, particularly the elderly, may have no symptoms at all and may not even be aware they are in atrial fibrillation until you feel their pulse and give them the news.

Patients can be managed initially with a strategy of either rhythm control, in which efforts are made to return their heart to normal sinus rhythm, or rate control, in which the atrial fibrillation is allowed to persist but the heart rate (i.e. the rate at which QRS complexes appear) is limited by medications, such that the patient - although remaining in atrial fibrillation - experiences no symptoms at all. Although there appears to be no significant difference in patient outcomes, such as heart attack and stroke, between patients treated with rhythm control versus rate control, many patients feel better when they are back in normal sinus rhythm.

Rhythm control can be attempted with either antiarrhythmic medications or catheter ablation. The latter is becoming more and more popular. In most patients, atrial fibrillation is triggered by electrical activity in the pulmonary veins where they enter the left atrium. The cornerstone of ablative therapy is to electrically isolate the pulmonary veins from the rest of the heart by burning a firewall around the source of the problem, thereby preventing the abnormal electrical impulses from spreading into the heart.

Catheter ablation therapy for atrial fibrillation. A catheter is advanced into the right atrium, through the intra-atrial septum and into the left atrium. The site where the atrial fibrillation originates—where the pulmonary veins join the left atrium—is then electrically isolated from the rest of the heart by bursts of radiofrequency energy that create an electrical firewall.

Patients with new-onset, recurrent, or persistent atrial fibrillation are at risk of systemic embolization. The fibrillating atria (the chambers quiver rather than contract, and have been compared in appearance to a bag of worms) provide an excellent substrate for blood clots to form. Pieces of these clots can break off—embolize—and travel through the systemic circulation and cause a stroke or vascular occlusion elsewhere in the body. Patients at risk for embolization are treated with anticoagulants. For patients at high risk of forming a blood clot but also at high risk of bleeding from an anticoagulant, the insertion of a left atrial appendage device can prevent clots from forming in the left atrium.

A blood clot formed in a fibrillating left atrium can come loose and travel to the brain and cause a stroke.

Multifocal Atrial Tachycardia and Wandering Atrial Pacemakers

MAT is an irregular rhythm occurring at a rate of 100 to 200 beats per minute. It probably results from the random firing of several different ectopic atrial foci. Sometimes, the rate is less than 100 beats per minute, in which case the arrhythmia is often called a wandering atrial pacemaker.

MAT is very common in patients with severe lung disease. It rarely requires treatment. Carotid massage has no effect on MAT. A wandering atrial pacemaker can be seen in normal, healthy hearts.

Like atrial fibrillation, MAT is an irregular rhythm. It can be distinguished from atrial fibrillation by the easily identifiable P waves occurring before each QRS complex. The P waves, originating from multiple sites in the atria, will vary in shape, and the interval between the different P waves and the QRS complexes may vary as well. In order to make the diagnosis of MAT, you need to identify at least three different P-wave morphologies.

Multifocal atrial tachycardia. Note that (1) the P waves vary dramatically in shape, (2) the PR intervals vary, and (3) the ventricular rate is irregular.

An arrhythmia called a wandering atrial pacemaker is very similar to MAT. Again, at least three different P-wave morphologies can be seen, but there will be at least two or three beats of each P-wave morphology before the site moves on and creates the next morphology. Technically it is not a tachyarrhythmia, since the rate is between 60 and 100 beats per minute.

Paroxysmal Atrial Tachycardia

The last of our supraventricular arrhythmias, PAT, is a regular rhythm with a rate of 100 to 200 beats per minute. It can result either from the enhanced automaticity of an ectopic atrial focus or from a reentrant circuit within the atria. The automatic type typically displays a warm-up period when it starts, during which the rhythm appears somewhat irregular, and a similar cool-down period when it terminates. The less common reentrant form starts abruptly with an atrial premature beat; this form of PAT has also been termed atypical atrial flutter.

PAT is most commonly seen in otherwise normal hearts. It can also be caused by digitalis toxicity (see Chapter 7).

How can you tell PAT from AVNRT? Many times, you can’t. However, if you see a warm-up or cool-down period on the EKG, the rhythm is likely to be PAT. In addition, carotid massage can be very helpful: Carotid massage will slow or terminate AVNRT, whereas it has virtually no effect on PAT (other than some mild slowing).

PAT. P waves are not always visible, but here they can be seen fairly easily. You may also notice the varying distance between the P waves and the ensuing QRS complexes; this reflects a varying conduction delay between the atria and ventricles that often accompanies PAT (but we are getting way ahead of ourselves; conduction delays are discussed in Chapter 4).

Before We Move On

Here is a question to see how well you’ve grasped the material on supraventricular tachycardias. Suppose a patient comes to see you complaining of palpitations and feeling short of breath. You take your patient’s pulse and notice two things—(1) it is very fast and (2) it is regular. Before you get an EKG, based on what you’ve learned so far, what is your differential diagnosis? Exclude for now the possibility of ventricular tachycardia, first because your patient would be unlikely to just come strolling in if he or she had ventricular tachycardia, and second because we won’t discuss it until the next section of this chapter.

No cheating—don’t look at the next page until you have thought this through.

There are only a few possibilities, and you probably figured out that they include sinus tachycardia, AVNRT, paroxysmal atrial tachycardia, and atrial flutter with a regular block. So now when you get your EKG on this patient you know what you are looking for. If you see one normal P wave for every QRS complex, your patient has sinus tachycardia. With atrial flutter and regular block, you should see flutter waves. Finally, with AVNRT or the less common PAT, the rate will usually be faster than your average sinus tachycardia, and you will see either no P waves or retrograde P waves.

SUMMARY

Remember: The key to diagnosing a supraventricular tachyarrhythmia is to look for P waves. They are most likely to be prominent in leads II and V1.

Ventricular Arrhythmias

Ventricular arrhythmias are rhythm disturbances arising below the AV node.

Premature Ventricular Contractions

Premature ventricular contractions (PVCs) are certainly the most common of the ventricular arrhythmias. The QRS complex of a PVC appears wide and bizarre because ventricular depolarization does not follow the normal ventricular conduction pathways. However, the QRS complex may not appear wide in all leads, so scan the entire 12-lead EKG before making your diagnosis. The QRS duration must be at least 0.12 seconds in most leads to make the diagnosis of a PVC. A retrograde P wave may sometimes be seen, but it is more common to see no P wave at all. A PVC is usually followed by a prolonged compensatory pause before the next beat appears. Less commonly, a PVC may occur between two normally conducted beats without a compensatory pause. These are called interpolated PVCs.

Isolated PVCs are common in normal hearts and rarely require treatment. An isolated PVC in the setting of an acute myocardial infarction, however, is more ominous because it can trigger ventricular tachycardia or ventricular fibrillation, both of which are life-threatening arrhythmias.

PVCs typically occur randomly, but they may alternate with normal sinus beats in a regular pattern. If the ratio is one normal sinus beat to one PVC, the rhythm is called bigeminy. Trigeminy refers to two normal sinus beats for every one PVC, and so on.

(A) A PVC. Note the compensatory pause before the next beat. (B) Bigeminy. PVCs and sinus beats alternate in a 1:1 fashion.

When should you worry about PVCs? In most situations, you don’t have to worry at all. However, if PVCs constitute more than 10% of a patient’s heartbeats, this situation can actually lead to remodeling of the myocardium with the development of a dilated cardiomyopathy, so these patients are usually treated with either medications or ablation therapy. In addition, there are certain circumstances in which PVCs pose an increased risk for triggering ventricular tachycardia, ventricular fibrillation, and death. These situations are summarized in the rules of malignancy:

1. Frequent PVCs.

2. Runs of consecutive PVCs, especially three or more in a row.

3. Multiform PVCs, in which the PVCs vary in their site of origin and hence in their appearance.

4. PVCs falling on the T wave of the previous beat, called the “R-on-T” phenomenon. The T wave is a vulnerable period in the cardiac cycle, and a PVC falling there is more likely to set off ventricular tachycardia.

5. Any PVC occurring in the setting of an acute myocardial infarction.

Although PVCs meeting one or several of these criteria are associated with an increased risk for developing a life-threatening arrhythmia, there is no evidence that suppressing these PVCs with antiarrhythmic medication reduces mortality in any setting.

(A) Beats 1 and 4 are sinus in origin. The other three beats are PVCs. The PVCs differ from each other in shape (multiform), and two occur in a row. (B) A PVC falls on the T wave of the second sinus beat, initiating a run of ventricular tachycardia.

Ventricular Tachycardia

A run of three or more consecutive PVCs is called ventricular tachycardia. The rate is usually between 120 and 200 beats per minute and, unlike AVNRT, may be slightly irregular (although it may take a very fine eye to see this). Both sustained ventricular tachycardia—defined as lasting more than 30 seconds—or ventricular tachycardia associated with hemodynamic instability are emergencies, presaging cardiac arrest and requiring immediate treatment.

Ventricular tachycardia. The rate is about 200 beats per minute.

The morphology of ventricular tachycardia may be uniform, with each complex appearing similar to the one before it, as in the picture above, or it may be polymorphic, changing appearance from beat to beat. Polymorphic ventricular tachycardia is more commonly associated with acute coronary ischemia, infarction, profound electrolyte disturbances, and conditions causing prolongation of the QT interval (Why a prolonged QT interval? Hang in there and you will have your answer on page 152). Uniform ventricular tachycardia is more often seen with healed infarctions; the scarred myocardium provides the substrate for the reentrant ventricular tachycardia.

Approximately 3.5% of patients develop ventricular tachycardia after a myocardial infarction, the large majority of these within the first 48 hours. However, an increased risk of ventricular tachycardia persists for weeks beyond the myocardial infarction. The development of sustained ventricular tachycardia within the first 6 weeks postinfarction is associated with a high 1-year mortality rate.

Ventricular Fibrillation

Ventricular fibrillation is a preterminal event. It is seen almost solely in dying hearts. It is the most frequently encountered arrhythmia in adults who experience sudden death. The EKG tracing jerks about spasmodically (coarse ventricular fibrillation) or undulates gently (fine ventricular fibrillation). There are no true QRS complexes.

In ventricular fibrillation, the heart generates no cardiac output, and cardiopulmonary resuscitation and electrical defibrillation must be performed at once.

Ventricular tachycardia degenerates into ventricular fibrillation.

Common precipitants of ventricular fibrillation include

 Myocardial ischemia/infarction

 Heart failure

 Hypoxemia or hypercapnia

 Hypotension or shock

 Electrolyte imbalances

 Overdoses of stimulants, especially when used in combination (e.g., MDMA [e.g., Ecstasy or Molly] plus an amphetamine)

In many cases, ventricular fibrillation is preceded by ventricular tachycardia

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm is a benign rhythm that is sometimes seen during an acute infarction or during the early hours following reperfusion, that is, after an occluded coronary artery has been opened in the catheterization lab. It is a regular rhythm occurring at 50 to 100 beats per minute and probably represents a ventricular escape focus that has accelerated sufficiently to drive the heart. It is rarely sustained, does not progress to ventricular fibrillation, and rarely requires treatment. When the rate falls below 50 beats per minute, it is then simply called an idioventricular rhythm (i.e., the term accelerated is dropped).

Accelerated idioventricular rhythm. There are no P waves, the QRS complexes are wide, and the rate is about 75 beats per minute.

Torsade de Pointes

Torsade depointes, meaning “twisting of the points,” is more than just the most lyrical name in cardiology. It is a unique form of ventricular tachycardia that is usually seen in patients with prolonged QT intervals.

The QT interval, you will recall, encompasses the time from the beginning of ventricular depolarization to the end of ventricular repolarization. It normally constitutes about 40% of the complete cardiac cycle.

A prolonged QT interval can be congenital in origin (resulting from mutations in genes encoding cardiac ion channels), result from various electrolyte disturbances (notably hypocalcemia, hypomagnesemia, and hypokalemia), or develop during an acute myocardial infarction. Numerous pharmacologic agents can also prolong the QT interval. These include antiarrhythmic drugs, tricyclic antidepressants, the phenothiazines, and some antifungal medications and antihistamines when taken concurrently with certain antibiotics, particularly erythromycin, azithromycin, and the quinolones.

A prolonged QT interval is generally the result of prolonged ventricular repolarization (i.e., the T wave is lengthened). A PVC falling during the elongated T wave can initiate torsade de pointes.

Torsade de pointes looks just like ordinary, run-of-the-mill ventricular tachycardia, except that the QRS complexes spiral around the baseline, changing their axis and amplitude. It is important to distinguish torsade de pointes from standard ventricular tachycardia because they are treated very differently.

Torsade de pointes. The QRS complexes seem to spin around the baseline, changing their axis and amplitude.

SUMMARY

Ventricular Arrhythmias

Accelerated idioventricular rhythm Torsades de pointes

Rules of Malignancy for PVCs

Frequent PVCs

Consecutive PVCs

Multiform PVCs

R-on-T phenomenon

Any PVC occurring during an acute myocardial infarction (or in any patient with underlying heart disease)

Supraventricular Versus Ventricular Arrhythmias

The distinction between supraventricular arrhythmias and ventricular arrhythmias is extremely important because the latter generally carry a far more ominous prognosis and the therapy is very different. In most cases, the distinction is simple: Supraventricular arrhythmias are associated with a narrow QRS complex and ventricular arrhythmias with a wide QRS complex.

There is one common circumstance, however, in which supraventricular beats can produce wide QRS complexes and make the distinction considerably more difficult. This occurs when a supraventricular beat is conducted aberrantly through the ventricles, producing a wide, bizarre-looking QRS complex that is indistinguishable from a PVC. Here’s how it happens.

Aberrancy

Sometimes, an atrial premature beat occurs so early in the next cycle that the Purkinje fibers in the ventricles have not had a chance to repolarize fully in preparation for the next electrical impulse. The right bundle branch, in particular, can be sluggish in this regard, and when the premature atrial impulse reaches the ventricles, the right bundle branch is still refractory. The electrical impulse is therefore prevented from passing down the right bundle branch but is able to pass quite freely down the left bundle branch (figure A). Those areas of the ventricular myocardium ordinarily supplied by the right bundle branch must receive their electrical activation from elsewhere, namely, from those areas already depolarized by the left bundle branch (figure B). The complete process of ventricular depolarization, therefore, takes an unusually long time; the vector of current flow is distorted; and the result is a wide, bizarre QRS complex that looks, for all the world, like a PVC (figure C).

(A) A premature atrial impulse catches the right bundle branch unprepared. Conduction down the right bundle is blocked but proceeds smoothly down the left bundle. (B) Right ventricular depolarization occurs only when the electrical forces can make their way over from the left ventricle—a slow, tedious process. This mode of transmission is very inefficient and results in a wide, bizarre QRS complex. (C) The third P wave is a premature atrial contraction. It is conducted aberrantly through the ventricles, generating a wide, bizarre QRS complex.

A wide QRS complex can therefore signify one of two things:

 A beat originating within the ventricles

 A supraventricular beat conducted aberrantly

How do you tell the two apart? In the case of a single premature atrial contraction, it’s usually easy because there is a P wave preceding the wide QRS complex. Look especially closely at the T wave of the preceding beat to see if a premature P wave is hidden within it. On the other hand, and rather obviously, there is no P wave preceding a PVC.

However, when there are several consecutive beats occurring in rapid succession, or a lengthy, sustained arrhythmia, the distinction can be much more difficult. AVNRT and ventricular tachycardia have about the same rates. Thus, the tracing below is consistent with either ventricular tachycardia or AVNRT conducted aberrantly.

In the tracing above, normal sinus rhythm degenerates into a new rhythm, but is it ventricular tachycardia or supraventricular tachycardia conducted aberrantly? Don’t feel bad if you can’t tell. From this strip alone, as you will see, it is impossible to know for sure.

As you can see from the preceding rhythm strip, it is sometimes impossible to tell these two entities apart. There are, however, several clinical and electrocardiographic clues that can be helpful.

Clinical Clues

1. Ventricular tachycardia is usually seen in diseased hearts (e.g., in a patient with a prior myocardial infarction or congestive heart failure). AVNRT is usually seen in otherwise normal hearts.

2. Carotid massage may terminate AVNRT, whereas it has no effect on ventricular tachycardia.

3. More than 75% of cases of ventricular tachycardia are accompanied by AV dissociation. In AV dissociation, the atria and ventricles beat independently of each other. There is a ventricular pacemaker driving the ventricles and producing ventricular tachycardia on the EKG and an independent sinus (or atrial or nodal) pacemaker driving the atria; the atrial rhythm may sometimes be seen but often is not, hidden on the EKG by the much more prominent ventricular tachycardia. The AV node is kept constantly refractory by the ceaseless bombardment of impulses from above and below, and therefore, no impulse can cross the AV node in either direction. If, as will occur from time to time, the ventricles contract just before the atria, the atria will find themselves contracting against closed mitral and tricuspid valves. This results in a sudden back-flooding of blood into the jugular veins, producing the classic cannon A waves of AV dissociation. Cannon A waves are not seen in AVNRT.

Electrocardiographic Clues

1. AV dissociation accompanying ventricular tachycardia can sometimes be seen on the EKG. The P waves and QRS complexes march along the rhythm strip completely independently of each other. In AVNRT, if P waves are seen, they bear a 1:1 relation to the QRS complexes. And remember, the P waves of AVNRT will be retrograde P waves, with a positive deflection in lead aVR and a negative deflection in lead II.

2. Fusion beats may be seen in ventricular tachycardia only. A fusion beat (or capture beat) occurs when an atrial impulse manages to slip through the AV node at the same time that an impulse of ventricular origin is spreading across the ventricular myocardium. The two impulses jointly depolarize the ventricles, producing a QRS complex that is morphologically part supraventricular and part ventricular.

The second beat is a fusion beat, a composite of an atrial (sinus) beat (beats 1 and 4) and a PVC beat (beat 3).

3. In AVNRT with aberrancy, the initial deflection of the QRS complex is usually in the same direction as that of the normal QRS complex. In ventricular tachycardia, the initial deflection is often in the opposite direction.

None of these criteria is infallible, and sometimes it remains impossible to identify a tachyarrhythmia as ventricular or supraventricular in origin. In patients with recurrent tachycardias whose origin (and, hence, treatment) remains obscure, electrophysiologic testing may be necessary (see Page 162).

The Ashman Phenomenon

We aren’t quite ready to leave the subject of aberrancy. The Ashman phenomenon is another example of aberrant conduction of a supraventricular beat. It is commonly seen in patients with atrial fibrillation.

The Ashman phenomenon describes a wide, aberrantly conducted supraventricular beat occurring after a QRS complex that is preceded by a long pause.

This is why it happens. The bundle branches reset their rate of repolarization according to the length of the preceding beat. If the preceding beat occurred a relatively long time ago, then the bundles repolarize somewhat leisurely. So imagine a normal beat (the second beat on the tracing below) followed by a long pause before the next beat (the third beat on the tracing). The bundle branches anticipate another long pause following this beat and repolarize slowly. If, before repolarization is complete, another supraventricular impulse should pass through the AV node, conduction will be blocked along one of the normal bundle branch pathways, and a wide, bizarre QRS complex will be inscribed (the fourth and obviously abnormal beat).

Atrial fibrillation, with its variable, irregular conduction producing long and short pauses between QRS complexes, is the perfect setting for this to occur.

The Ashman phenomenon. The fourth beat looks like a PVC, but it could also be an aberrantly conducted supraventricular beat. Note the underlying atrial fibrillation, the short interval before the second beat, and the long interval before the third beat—all in all, a perfect substrate for the Ashman phenomenon.

Fortunately, most supraventricular arrhythmias are associated with narrow QRS complexes; aberrancy, although not uncommon, is at least the exception, not the rule. The point to take home is this: A narrow QRS complex virtually always implies a supraventricular origin, whereas a wide QRS complex usually implies a ventricular origin but may reflect aberrant conduction of a supraventricular beat.

SUMMARY

Ventricular Tachycardia Versus Supraventricular Tachycardia With Aberrancy

 

Ventricular Tachycardia

Supraventricular Tachycardias

Clinical Clues

   

Clinical history

Diseased heart

Usually healthy heart

Carotid massage

No response

May terminate

Cannon A waves

May be present

Not seen

EKG Clues

   

AV dissociation

May be seen

Not seen

Fusion beats

May be seen

Not seen

Initial QRS deflection

May differ from normal QRS complex

Same as normal QRS complex

Electrophysiology Studies (EPS)

EPS has added a new dimension to the treatment of arrhythmias. Before the introduction of EPS, a patient with an arrhythmia requiring treatment was given a drug empirically, and after several days, when therapeutic levels had been achieved, a 24-hour Holter monitor would be used to see whether the frequency of the arrhythmia had been reduced. This hit-or-miss approach was timeconsuming and exposed patients to the potential side effects of drugs that might prove of no benefit.

EPS is not necessary for all patients with arrhythmias, and the Holter monitor remains the staple of arrhythmia diagnosis and treatment. EPS is expensive and invasive, but for certain patients it has great value, greatly refining the process of diagnosing a given arrhythmia and choosing the right drug for patients who need rapid and effective therapy.

The patient is taken to the electrophysiology laboratory where the particular arrhythmia is induced with intracardiac electrodes. Tiny catheters are inserted through peripheral veins or arteries and are then advanced to various locations within the chambers of the heart. A catheter placed at the junction of the right atrium and ventricle at the upper posterior portion of the tricuspid ring will record a His bundle potential, which can help to define the electrical relationship of the atria and ventricles during the propagation of an arrhythmia. For example, if with atrial activation a His potential precedes every QRS complex, then a supraventricular origin is likely. In this way, the source of an arrhythmia can be mapped to determine the most appropriate therapy.

(A) A His bundle recording and (B) the corresponding EKG. In A, the small spike (H) between the spikes of atrial (A) and ventricular (V) activation reflects activation of the bundle of His.

EPS has been used most successfully in managing patients who have recurrent ventricular tachycardia or who have experienced a previous episode of sudden death requiring cardiopulmonary resuscitation. It is also used to identify an arrhythmia in patients with syncope of unknown cause.

EPS mapping techniques have become extremely precise, and combined with the technique of catheter ablation, which we discussed on page 141, is often used to treat atrial fibrillation, atrial flutter, AVNRT, and (to be discussed in Chapter 5) AV reciprocating tachycardia.

Implantable Defibrillators

Even when EPS-guided drug therapies or catheter ablation techniques are used, the recurrence rates for ventricular tachycardia are still unacceptably high. For this reason, implantable cardioverter-defibrillators have become the standard form of protection for most patients with life-threatening arrhythmias. These small devices are surgically implanted, like a pacemaker, under the skin below the clavicle. There they continuously monitor the heart rhythm and, when they sense a dangerous arrhythmia, deliver either a rapid pacing rhythm or an electric shock to the heart through an electrode that rests in the right ventricle.

The heartbeat of a 72-year-old woman is rescued from ventricular tachycardia by a shock delivered by an implantable cardioverter-defibrillator.

External Defibrillators

Automatic external defibrillators are small portable devices that come equipped with patches that attach to the chest wall. Once hooked up, these devices can quickly determine whether the rhythm of an individual who has collapsed is ventricular fibrillation and, if so, can deliver defibrillation shocks that may be lifesaving. Minimal training is required to learn how to operate the defibrillator and place the patches properly. They are now widely available in police cars, on airplanes, and in public venues.

On the following page is an opportunity to review the arrhythmias we have been discussing. For each tracing, use the four-step method discussed previously. Always ask the following questions:

1. Are normal P waves present?

2. Are the QRS complexes narrow or wide?

3. What is the relationship between the P waves and QRS complexes?

4. Is the rhythm regular or irregular?

(A) Atrial fibrillation. (B) Ventricular tachycardia. (C) Sinus bradycardia. (D) Ventricular tachycardia degenerating into ventricular fibrillation. (E) AVNRT.

CASE 3.

Lola de B., predictably, is the life of the party. Never missing a turn on the dance floor nor a round at the bar, she becomes increasingly intoxicated as the evening progresses. Her husband, a young business executive, forces her to drink some coffee to sober her up before they leave. As he is wandering around in search of their coats, he hears a scream and rushes back to find her collapsed on the floor. Everyone is in a panic and all eyes turn to you, word having gotten around that you have recently been reading a well-known and highly regarded EKG book. The terror in the room is palpable, but you grin modestly, toss down a final swig of mineral water, and stride confidently to the patient saying as you go, “Don’t worry. I got this.”

Do you? What has happened to Lola, and just what are you going to do about it?

Of course, a whole host of things could have happened to Lola (they usually do), but you know that the combination of alcohol, coffee, and the excitement of the party can induce AVNRT in anyone, no matter how healthy they are and no matter how normal their heart is. It is likely that this supraventricular rhythm disturbance has caused her to faint.

You bend down over her, assure yourself that she is breathing, and feel her pulse. It is rapid and regular with a rate of about 200 beats per minute. Because she is young and very unlikely to have significant carotid artery disease, you go right ahead and perform carotid massage, and within about 10 seconds, you feel her pulse shift gears and return to normal. Her eyes blink open, and the room erupts in cheers. Your guess was correct.

As you are carried out of the room on everyone’s shoulders, don’t forget to remind them which book you were reading that taught you all this good stuff.

In patients with tachyarrhythmias that result in syncope, further evaluation is usually warranted because of the high likelihood of recurrence. This evaluation usually includes at least appropriate laboratory studies (e.g., to rule out electrolyte imbalances and hyperthyroidism), a baseline EKG, a stress echocardiogram (to look for valvular disease and coronary artery disease; see Page 272 on “Stress Testing”), and an ambulatory monitor to capture any further rhythm disturbances. Seizure activity associated with the syncopal event or any persistent neurologic deficits will necessitate a full neurologic evaluation. In many states and countries, if no treatable cause for the syncopal event is found, the patient will not be permitted to drive for at least several months.

CASE 4.

George M., irascible and older than time, comes to see you late one Friday afternoon (he always comes late on Friday afternoons, probably because he knows you like to get an early start on the weekend). This time, he tells you that he fainted the day before and now is feeling a bit light-headed. He also has a strange fluttering sensation in his chest. George is always complaining of something, and you have yet to find anything the matter with him in the many years you have known him, but just to be careful, you obtain an EKG.

You quickly recognize the arrhythmia and are reaching for your stethoscope when George’s eyes roll back in his head and he drops unconscious to the floor. Fortunately, the EKG is still running, and you see

You drop down to his side, ready, if need be, to begin cardiopulmonary resuscitation, when his eyes pop open and he mutters something under his breath. The EKG now shows

You may not know what’s going on, but at least you can identify the three tracings. Right?

The first and third tracings are the same, showing classic atrial fibrillation. The baseline is undulating, without clear-cut P waves, and the QRS complexes appear irregularly. The second tracing is more interesting. It shows the atrial fibrillation terminating abruptly and then a long pause. (It was during such a pause that George dropped to the floor, a result of brain hypoxia caused by the lack of significant cardiac output.) The beats that you see next are ventricular escape beats. The QRS complexes are wide and bizarre, there are no P waves, and the rate is about 33 beats per minute, exactly what you would expect of a ventricular escape rhythm. The final thing you see on the strip is the sinus node kicking in. The last strip shows him once again in atrial fibrillation.

George has sick sinus syndrome, also called the bradytachycardia syndrome. It is typified by alternating episodes of a supraventricular tachycardia, such as atrial fibrillation, and bradycardia. Often, when the supraventricular arrhythmia terminates, there is a long pause (>4 seconds) before the sinus node fires again (hence, the term sick sinus). Fortunately for George, a few ventricular escape beats came to a timely rescue.

Sick sinus syndrome usually reflects significant underlying disease of the conduction system of the sort that we will be studying in the next chapter. It is one of the leading reasons for pacemaker insertion.

George M. revives in your office and insists on going home. Fortunately, wiser heads prevail and he is taken by ambulance to the hospital. A short stay in the CCU confirms that he has not had a heart attack, but his heart monitor shows numerous episodes of prolonged bradycardia alternating with various supraventricular arrhythmias. It is decided that George should have a pacemaker placed, and he reluctantly agrees. The pacemaker provides a safety net, giving George’s heart an electrical “kick” every time his own electrical mechanism fails him. George is discharged, and no further episodes of symptomatic bradycardia occur.

CASE 5.

Frederick van Z. is a renowned (and highly strung) orchestral conductor whose delusions of grandeur are tempered by a small regular dose of haloperidol, an antipsychotic medication. Late one night, after a triumphant all-Beethoven performance at the large concert hall in your town, he is rushed to the hospital with a high fever, confusion, and blood in his urine (hematuria). In the emergency room, he is found to be hypotensive from urosepsis. He is immediately treated with the intravenous antibiotic, levofloxacin. Here is lead II from his cardiac monitor in the emergency room. Can you identify his rhythm?

You should recognize two different types of beats of very different morphology, alternating with one another. The maestro is in bigeminy, with supraventricular beats (junctional beats, with a narrow QRS complex, and no visible P wave) occurring in a 1:1 ratio with ventricular beats (PVCs, with a wide QRS complex).

He is transferred to the intensive care unit where you confidently take over his case. As soon as you hook him up to the heart monitor, you see this. What has happened?

Let’s read this left to right. The first beat is a junctional beat, the second a PVC, and the third and fourth beats two more junctional beats. He clearly is no longer in strict bigeminy. On the fifth beat, right after the QRS complex, a PVC has landed on the vulnerable QT interval and triggered a short run of a ventricular tachycardia that is fortunately self-terminating.

Moments later, his blood pressure collapses, his body seizes up in bed, and you see the following arrhythmia. In a flash, you recognize it and prepare to swing into action. What does the tracing show?

As in the previous tracing, a PVC has fallen on a QT interval, but now, the resulting ventricular tachycardia persists. The changes in amplitude of the QRS complexes (reflecting a change in axis as the QRS complexes spiral around the baseline) identify the arrhythmia as torsade de pointes, a medical emergency.

The great conductor is successfully treated (urgent temporary cardiac pacing does the trick), and his vital signs return to normal.

Several hours later, his rhythm strip now shows this. What do you see (hint: look closely at the lengths of the various intervals)?

He is in normal sinus rhythm—note the presence of P waves— but take a close look at his QT interval. Normally, it should constitute about 40% of the cardiac cycle, but here, it measures well over 50% of one cardiac cycle. This prolonged QT interval was the perfect substrate for torsade de pointes. The patient was on two drugs that can prolong the QT interval—haloperidol, which he was taking on a chronic basis, and levofloxacin, the antibiotic he was given in the emergency room that acutely lengthened his QT interval even more and set up the great master for the nearly fatal events that followed. You immediately discontinue both medications, and his QT interval normalizes. There will be no more episodes of torsade de pointes on your watch!

1The patches are pretty innocuous and don’t interfere with whatever the patient chooses to do. The adhesive can itch, however.



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