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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.

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.

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.

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 × 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 × 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?

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?

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 × 6 seconds = 60 seconds) to get the heart rate in beats per minute. Try it both ways on the example below:

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.

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.

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.

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.

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.

SUMMARY

Arrhythmias of Sinus Origin

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.

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 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.

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