The only EKG book. 9th Ed

Chapter 7. Finishing Touches

In this chapter you will learn:


that the EKG can be changed by a whole variety of other cardiac and noncardiac disorders. We will discuss the most important of these as well as several other settings where the role of the EKG is perhaps more controversial:

A. electrolyte disturbances

B. hypothermia

C. digitalis effects, both therapeutic and toxic

D. medications that prolong the QT interval

E. other cardiac disorders (pericarditis, cardiomyopathy, myocarditis, and atrial septal defect)

F. pulmonary disorders

G. central nervous system disease

H. sudden cardiac death in persons without coronary artery disease

I. the athlete’s heart

J. screening young athletes before participating in sports

K. sleep disorders

L. the preoperative evaluation


about the cases of Amos T., whose EKG proves to be the key to unraveling an emergent, life-threatening noncardiac condition, and that of Ursula U., almost done in by some very common medications

Many medications, electrolyte disturbances, and other disorders can substantially alter the normal pattern of the EKG. It is not always obvious why the EKG is so sensitive to such a seemingly diffuse array of conditions, but it is, and you should know about them.

In some of these instances, the EKG may actually be the most sensitive indicator of impending catastrophe. In others, subtle electrocardiographic changes may be an early clue to a previously unsuspected problem.

Electrolyte Disturbances

Alterations in the serum levels of potassium and calcium can profoundly alter the EKG.


Hyperkalemia is the great imitator. It can do almost anything to the EKG. This shouldn’t surprise you, since potassium is so critical to the electrical activity of all heart cells.

In its most classic—but by no means only—presentation, hyperkalemia produces a progressive evolution of changes in the EKG that can culminate in ventricular fibrillation and death. The presence of electrocardiographic changes is a better measure of clinically significant potassium toxicity than is the serum potassium level.

As the potassium begins to rise, the T waves across the entire 12-lead EKG begin to peak. This effect can easily be confused with the peaked T waves of an acute myocardial infarction. One difference is that the changes in an infarction are confined to those leads overlying the area of the infarct, whereas in hyperkalemia, the changes are diffuse, seen in most if not all leads.

The peaked, symmetric T waves of hyperkalemia.

With a further increase in the serum potassium, the PR interval becomes prolonged, and the P wave gradually flattens and then disappears.

Ultimately, the QRS complex widens until it merges with the T wave, forming a sine wave pattern. We’re already seen several causes of a widened QRS complex, so—to help you sort them out—here is a little EKG pearl: the presence of a rightward axis (a negative QRS complex in lead I, a positive QRS in aVF) may be an important clue that the wide QRS complexes are the result of hyperkalemia.

Progressive hyperkalemia leads to the classic sine wave pattern. The widened QRS complexes and peaked T waves are almost indistinguishable.

Conduction blocks—high-degree AV blocks and bundle branch blocks—can also appear as the serum potassium rises. Asystole or ventricular fibrillation may eventually develop.

Leads I and aVF in a patient with hyperkalemia. The QRS complexes are wide, and there is a rightward axis. The rhythm is a slow junctional escape rhythm.

It is important to note that whereas these changes frequently do occur in the order described as the serum potassium rises, they do not always do so. Progression to ventricular fibrillation can occur with devastating suddenness. Any change in the EKG due to hyperkalemia mandates immediate clinical attention!


With hypokalemia, the EKG may again be a better measure of serious toxicity than the serum potassium level. Several changes can be seen, occurring in no particular order:

 ST-segment depression

 Flattening of the T wave with prolongation of the QT interval

 Appearance of a U wave

Hypokalemia. The U waves are even more prominent than the T waves. Slight ST- segment depression can also be seen.

The term U wave is given to a wave appearing after the T wave in the cardiac cycle. It usually has the same axis as the T wave and is often best seen in the anterior leads. Its precise physiologic meaning is not fully understood. U waves can sometimes be surprisingly difficult to recognize; at first glance, you may think you are looking at a biphasic T wave. Although U waves are the most characteristic feature of hypokalemia, they are not in and of themselves diagnostic. Other conditions can produce prominent U waves (e.g., central nervous system disease and certain antiarrhythmic drugs), and U waves can sometimes be seen in patients with normal hearts and normal serum potassium levels.

Rarely, severe hypokalemia can cause ST-segment elevation. Whenever you see ST-segment elevation or depression on an EKG, your first instinct should always be to suspect some form of cardiac ischemia, but always keep hypokalemia in your differential diagnosis.

Severe hypokalemia can also cause prolongation of the QT interval as well as supraventricular and ventricular tachyarrhythmias.

Calcium Disorders

Alterations in the serum calcium primarily affect the QT interval.

Hypocalcemia prolongs it; hypercalcemia shortens it. Do you remember a potentially lethal arrhythmia associated with a prolonged QT interval?

Torsade de pointes, a variant of ventricular tachycardia, can occur in patients with prolonged QT intervals.

Hypocalcemia. The QT interval is slightly prolonged. A premature ventricular contraction (PVC) falls on the prolonged T wave and sets off a run of torsade de pointes.

Other electrolyte disorders can also prolong the QT interval. These include hypokalemia (just discussed) and hypomagnesemia.


As the body temperature dips below normal, several changes occur on the EKG:

1. Everything slows down. Sinus bradycardia is common, and all the segments and intervals—PR, QRS, QT, etc.—become prolonged.

2. A distinctive and virtually diagnostic type of ST-segment elevation may be seen. It consists of an abrupt ascent right at the J point and then an equally sudden plunge back to baseline. The resultant configuration is called a J wave or Osborn wave. J waves will disappear as the patient is rewarmed.

3. Various arrhythmias may appear, including sinus bradycardia, a slow junctional rhythm and slow atrial fibrillation.

4. A muscle tremor artifact due to shivering may complicate the tracing. A similar artifact may be seen in patients with Parkinson disease. The tremor of Parkinson disease can be easily mistaken for atrial flutter, since both tend to cycle at about 5 Hz, or 300 times per minute.

A muscle tremor artifact resembles atrial flutter.



We don’t use digitalis all that much anymore, but EKG books love the stuff because it can do so many interesting things to the EKG. We will continue in that glorious tradition. There are two distinct categories of electrocardiographic alterations caused by digitalis: those associated with therapeutic blood levels of the drug and those seen with toxic blood levels.

EKG Changes Associated With Therapeutic Blood Levels

Therapeutic levels of digitalis produce characteristic ST-segment and T-wave changes. These changes are known as the digitalis effect and consist of ST- segment depression with flattening or inversion of the T wave. The depressed ST segments have a very gradual downslope, emerging almost imperceptibly from the preceding R wave. This distinctive appearance usually permits differentiation of the digitalis effect from the more symmetric ST-segment depression of ischemia; differentiation from ventricular hypertrophy with repolarization abnormalities can sometimes be more problematic, especially because digitalis is still sometimes used in patients with congestive heart failure who often have left ventricular hypertrophy.

The digitalis effect usually is most prominent in leads with tall R waves. Remember: the digitalis effect is normal and predictable and does not necessitate discontinuing the drug.

EKG Changes Associated With Toxic Blood Levels

The toxic manifestations of digitalis, on the other hand, may require clinical intervention. Digitalis intoxication can elicit conduction blocks and tachyarrhythmias, alone or in combination.

Sinus node suppression

Even at therapeutic blood levels of digitalis, the sinus node can be slowed, particularly in patients with the sick sinus syndrome (aka bradytachycardia syndrome, see page 171). At toxic blood levels, sinus exit block or complete sinus node suppression can occur.

Conduction blocks

Digitalis slows conduction through the AV node and can therefore cause first-, second-, and even third-degree AV block.

Wenckebach block caused by digitalis intoxication.

The ability of digitalis to slow AV conduction can be useful in the treatment of supraventricular tachycardias. For example, digitalis can slow the ventricular rate in patients with atrial fibrillation; however, the ability of digitalis to slow the heart rate, best seen when patients are sitting or lying quietly for their EKG recording, is commonly lost during exertion. Beta-blockers, such as atenolol or metoprolol, have a similar effect on AV conduction and may control the rate better when there is increased adrenergic tone (e.g., during exercise or stress).


Because digitalis enhances the automatic behavior of all cardiac conducting cells, causing them to act more like pacemakers, there is no tachyarrhythmia that digitalis cannot cause. Paroxysmal atrial tachycardia (PAT) and PVCs are the most common, junctional rhythms are fairly common, and atrial flutter and fibrillation are the least common.


The combination of PAT with second-degree AV block is the most characteristic rhythm disturbance of digitalis intoxication. The conduction block is usually 2:1 but may vary unpredictably. Digitalis is the most common, but not the only, cause of PAT with block.

Medications That Prolong the QT Interval

We have already seen that hypocalcemia, hypomagnesemia, and severe hypokalemia can prolong the QT interval. Many medications can also prolong the QT interval and increase the risk for a serious ventricular tachyarrhythmia. Most prominent among them are many antiarrhythmic agents (e.g., sotalol, quinidine, procainamide, disopyramide, amiodarone, dofetilide, and dronedarone). These agents are used to treat arrhythmias, but by increasing the QT interval they can paradoxically increase the risk for serious ventricular tachyarrhythmias. The QT interval must be carefully monitored in all patients taking these medications, especially if more than one is being used, and the drug(s) should be stopped if substantial prolongation occurs.

Other commonly used drugs can also prolong the QT interval. For most of these, especially in conventional doses, the risk of a potentially fatal arrhythmia is very small. Among them are the following:

Antibiotics: macrolides (e.g., erythromycin, clarithromycin, azithromycin) and fluoroquinolones (e.g., levofloxacin and ciprofloxacin)

Antifungals (e.g., ketoconazole)

Nonsedating antihistamines (e.g., astemizole, terfenadine)

Psychotropic drugs: antipsychotics (e.g., haloperidol, phenothiazines), tricyclic antidepressants (e.g., amitriptyline), selective serotonin reuptake inhibitors (e.g., citalopram, fluoxetine), and methadone

Plus some gastrointestinal medications, antineoplastic agents, and diuretics (the last by causing hypokalemia or hypomagnesemia)

The risk of torsade des pointes is increased in patients who take more than one of these drugs. It is also enhanced when their metabolism is compromised, leading to higher blood levels. Grapefruit juice, for example, inhibits the activity of the cytochrome P450 enzyme system, which is responsible for metabolizing many of these drugs, and the resulting higher serum drug levels can lead to QT prolongation.

The prolonged QT interval on this tracing mandated reducing the patient’s sotalol dosage.

More on the QT Interval

Several inherited disorders of cardiac repolarization associated with long QT intervals have been identified and linked to specific chromosomal abnormalities. The cause in almost half of genotyped individuals is one of various mutations in a gene that encodes pore-forming subunits of the membrane channels that generate a slow K+ current that is adrenergic sensitive. All individuals in these families need to be screened for the presence of the genetic defect with resting and stress EKGs. If the abnormality is found, beta-blocking drugs and sometimes implantable defibrillators are recommended because the risk for sudden death from a lethal arrhythmia is greatly increased, especially when the patient is in childhood or early adulthood. These patients must also be restricted from competitive sports (although modest exercise without “adrenalin bursts” can be encouraged and guided by the results of an exercise stress test) and must never take any drugs that can prolong the QT interval.

How to Measure the QT Interval Accurately

Because the QT interval varies with the heart rate, a corrected QT interval, or QTc, is used to assess absolute QT prolongation. The QTc adjusts for differences in the heart rate by dividing the QT interval by the square root of the R-R interval—that is, the square root of one cardiac cycle:

The QTc should not exceed 500 ms during therapy with any medication that can prolong the QT interval (550 ms if there is an underlying bundle branch block); adhering to this rule will reduce the risk for ventricular arrhythmias. This simple formula for determining the QTc is most accurate at heart rates between 50 and 120 beats per minute; at the extremes of heart rate, its usefulness is limited.

Can the QT interval ever be too short? The answer is yes. A short QT interval is generally defined—not everyone agrees on this—as a QT interval less than 360 ms. Congenital short QT syndrome is far less common than its more lengthy compatriot. It can be caused by any number of inherited “channelopathies.” Most patients appear to have no complications, but there is an increased risk of atrial and ventricular arrhythmias. The differential diagnosis of a short QT interval includes hyperkalemia and hypercalcemia.

Other Cardiac Disorders


Acute pericarditis can cause ST-segment elevation and T-wave flattening or inversion. These changes can easily be confused with an evolving infarction, as can the clinical picture. Certain features of the EKG can be helpful in differentiating pericarditis from infarction:

1. The ST-segment and T-wave changes in pericarditis tend to be diffuse, involving more leads than the localized effect of an infarction. The ST segment is typically concave upward (saddle shaped), unlike the ST elevation seen with an infarction.

2. In pericarditis, T-wave inversion usually occurs only after the ST segments have returned to baseline. In infarction, T-wave inversion usually precedes normalization of the ST segments.

3. In pericarditis, Q-wave formation does not occur.

4. The PR interval is often depressed, usually in many leads (aside from aVR). However, do not overrely on this criterion. It is not specific to pericarditis

(A) Lead V3 shows the ST-segment elevation of acute pericarditis. (B) The same lead several days later shows that the ST segments have returned to baseline and the T waves have inverted. There are no Q waves.

The EKG is only one part of the puzzle when differentiating the chest pain of pericarditis from the chest pain of cardiac ischemia. Recognizing the clinical presentation of pericarditis is essential. If your patient is a young adult with no risk factors for ischemic heart disease, then pericarditis is more likely, but be careful—keep in mind that more than 100,000 myocardial infarctions are diagnosed each year in the United States in patients aged 29 to 44. Unlike angina, the pain is usually sharp, exacerbated by inspirations and coughing, and felt diffusely across the entire anterior chest wall, often radiating to the upper back. The pain usually eases when the patient sits and leans forward. On exam, you may be able to hear a pericardial friction rub over the left sternal border.

Formation of a substantial pericardial effusion dampens the electrical output of the heart, resulting in low voltage in all leads. The ST-segment and T-wave changes of pericarditis may still be evident.

How do we define low voltage? Well, to no one’s surprise, there are criteria. The most sensitive are either (1) the sum of the total QRS voltage in leads I, II, and III is less than 15 mV or (2) the sum of the total QRS voltage in leads V1, V2, and V3 is less than 30 mV. More specific criteria are (1) the QRS voltage in all limb leads is less than 5 mV or (2) the QRS voltage in all precordial leads is less than 10 mV.

A pericardial effusion is not the only cause of low voltage. Anything that dampens the ability of the surface electrodes to detect the electricity generated by the heart can be responsible, such as the expanded, air-filled lungs of chronic lung disease; a pneumothorax; a large pleural effusion; or the marked adiposity of someone who is very obese. Also, anything that reduces the heart’s ability to generate normal voltage can be the culprit, for example, infiltrative diseases of the heart (such as amyloidosis), severe hypothyroidism, and end-stage cardiomyopathy caused by multiple infarctions.

Lead I before (A) and after (B) the development of a pericardial effusion. Decreased voltage is the only significant change.

If an effusion is sufficiently large, the heart may actually rotate freely within the fluid-filled sac. This produces the phenomenon of electrical alternans in which the electrical axis of the heart varies with each beat. This can affect not only the axis of the QRS complex but also that of the P and T waves. A varying axis is most easily recognized on the EKG by the varying amplitude of each waveform from beat to beat.

Electrical alternans. The arrows point to each QRS complex.

Hypertrophic Obstructive Cardiomyopathy

We have already discussed hypertrophic obstructive cardiomyopathy (HOCM), also known as idiopathic hypertrophic subaortic stenosis, in the case of Tom L. (page 100). Many patients with HOCM have normal EKGs, but left ventricular hypertrophy and left axis deviation are not uncommon. Deep, narrow, daggerlike Q waves may also be seen laterally and inferiorly. These do not represent infarction.

Hypertrophic obstructive cardiomyopathy. Deep Q waves can be seen in both lateral and inferior leads.


Any diffuse inflammatory process involving the myocardium can produce a number of changes on the EKG. Most common are conduction blocks, especially bundle branch blocks and hemiblocks.

Right bundle branch block in a patient with active myocarditis following a viral infection.

Atrial Septal Defect

An atrial septal defect (ASD) is a small opening between the left and right atria. It is often first diagnosed in adulthood. Symptoms arise from the prolonged shunting of blood from the high pressure left atrium into the right atrium, and typically include fatigue and shortness of breath. Complications include atrial arrhythmias, pulmonary hypertension, and paradoxical embolization, in which an embolus from a deep venous thrombosis in the extremities travels to the heart, is shunted to the left side of the heart through the ASD, and enters the systemic circulation where it can cause a stroke. Closure of the ASD is indicated for patients with symptoms or evidence of right heart enlargement.

The EKG may be normal. With enlargement of the right atrium and right ventricle, however, you can see first-degree AV block, atrial tachyarrhythmias, incomplete right bundle branch block, and, with the more common secundum ASD, right axis deviation (you may see left axis deviation with a primum ASD). The most characteristic finding, however, is what has been termed the crochetage pattern, a small notch in the QRS complexes in the inferior leads. It can occur early or late in the QRS complex. Interestingly, the size of the notch is proportional to the size of the ASD and the size of the shunt. Crochetage can also be seen in patients with a patent foramen ovale and sometimes in perfectly normal hearts.

The small notch in the terminal portion of these QRS complexes is the crochetage pattern of an atrial septal defect.

Pulmonary Disorders

Chronic Obstructive Pulmonary Disease (COPD)

The EKG of a patient with long-standing emphysema may show low voltage, right axis deviation, and poor R-wave progression in the precordial leads. The low voltage is caused by the dampening effects of the large residual volume of air trapped in the lungs. Right axis deviation is caused by the expanded lungs forcing the heart into a vertical or even rightward-oriented position, as well as by the pressure overload hypertrophy from pulmonary hypertension.

COPD can lead to chronic cor pulmonale and right-sided congestive heart failure. The EKG may then show right atrial enlargement (P pulmonale) and right ventricular hypertrophy with repolarization abnormalities.

Chronic obstructive pulmonary disease. Note the low voltage, extreme right axis deviation, right atrial enlargement (in lead II), and precordial criteria for right ventricular hypertrophy.

Acute Pulmonary Embolism

A sudden massive pulmonary embolus can profoundly alter the EKG. Findings may include the following:

1. A pattern of right ventricular hypertrophy with repolarization changes, presumably due to right ventricular dilatation, although it takes time for the right ventricle to enlarge, so criteria for right ventricular hypertrophy may not be seen acutely.

2. Right bundle branch block.

3. A large S wave in lead I and a deep Q wave in lead III. This is called the S1Q3 pattern. The T wave in lead III may also be inverted (S1Q3T3 pattern). Unlike an inferior infarction, in which Q waves are usually seen in at least two of the inferior leads, the Q waves in an acute pulmonary embolus are generally limited to lead III.

4. T-wave inversion may be seen over the right precordial leads.

5. A number of arrhythmias may be produced; most common are sinus tachycardia and atrial fibrillation.

The S1Q3T3 pattern of a massive pulmonary embolus.

The EKG in a nonmassive pulmonary embolism is normal in most patients, or it may show only a sinus tachycardia.

Central Nervous System Disease

Central nervous system (CNS) catastrophes, such as a subarachnoid bleed or cerebral infarction, can produce diffuse T-wave inversion and prominent U waves. The T waves are typically very deep and very wide, and their contour is usually symmetrical (unlike the asymmetrical inverted T waves of secondary repolarization associated with ventricular hypertrophy). Sinus bradycardia also is commonly seen. These changes are believed to be due to involvement of the autonomic nervous system.

Deeply inverted, wide T waves in lead V4 in a patient with a central nervous system bleed.

Sudden Cardiac Death

By far the most common cause of sudden cardiac death is underlying atherosclerosis (coronary artery disease) triggering infarction and/or arrhythmia. However, there are many other causes as well, some of which we have discussed. These include the following:

 Hypertrophic cardiomyopathy.

 Long QT interval syndrome, acquired or congenital (and very rarely, short QT syndrome).

 Wolff-Parkinson-White syndrome.

 Viral myocarditis.

 Infiltrative diseases of the myocardium (e.g., amyloidosis and sarcoidosis).

 Valvular heart disease.

 Drug abuse (especially stimulants such as cocaine and amphetamines).

 Commotio cordis, in which blunt force to the chest causes ventricular fibrillation.

 Anomalous origin of the coronary arteries, in which constriction of a coronary artery by surrounding tissue—exacerbating by the increased myocardial contractions of exercise—can cause ventricular fibrillation.

• Brugada pattern (it is called Brugada syndrome when the EKG changes are accompanied by symptoms) occurs in structurally normal hearts and, in this way, resembles the long QT syndromes. It is inherited as an autosomal dominant trait, yet it is much more common in men (especially those in their 20s and 30s) than in women. The cause in some patients is a genetic mutation affecting voltage-dependent sodium channels during repolarization. Brugada pattern can be identified by a specific set of abnormalities on the EKG: (1) a pattern resembling right bundle branch block with a slow, prolonged downslope of the R' component of the QRS complex, (2) T-wave inversion in leads V1 and/or V2, and (3) ST-segment elevation in leads V1, V2, and V3. The ST-segment elevation is often concave and descends into an inverted T wave, a pattern referred to as coving.

Two examples of Brugada pattern in lead V1. Note the right bundle branch appearance and the inverted T wave in V1. The ST-segment elevation can appear coved (first figure) or saddle-backed (second figure).

The importance of Brugada pattern lies in its propensity to cause ventricular arrhythmias that can lead to sudden death. The most typical of these is a fast polymorphic ventricular tachycardia that looks just like torsade de pointes. Sudden death is most likely to occur during sleep or when the patient has a fever. Implantable cardiac defibrillators are a critical component of management. All family members of an affected patient must be screened for this condition.

Polymorphous ventricular tachycardia with unusually narrow QRS complexes in a patient with Brugada syndrome.

• Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable disorder characterized by fibrofatty infiltration of the right ventricular myocardium. It has been increasingly recognized as an important cause of ventricular arrhythmias and sudden death. The genetic mutations that cause ARVC affect desmosomal proteins that are involved in cell-to-cell adhesion and thereby compromise the flow of electric current between cells. The most common feature on the EKG is T-wave inversion in leads V1 through V3, but this finding—as with most things T-wave related—is not very specific. The most characteristic feature on the EKG—although present in only about 30% of patients with this condition—is a small positive deflection at the end of the QRS complex called an epsilon wave (Why? It looks like the Greek letter epsilon: e).

The epsilon wave is the small notch at the terminal portion of the QRS complex in lead V1.

The EKG is a critical tool in evaluating any young person following an unexplained episode of sudden cardiac death (from which, of course, he or she was successfully resuscitated) or loss of consciousness (syncope). You may get lucky and capture an underlying arrhythmia, but even if the EKG shows normal sinus rhythm, you may see evidence of a congenital, drug-induced, or other type of heart condition that predisposes to a potentially lethal arrhythmia. The most common congenital predisposing conditions that you might see on the EKG are hypertrophic cardiomyopathy, long QT syndrome, Wolff-Parkinson-White, Brugada pattern, and arrhythmogenic right ventricular cardiomyopathy.

The Athlete’s Heart

Marathon runners and other athletes involved in endurance training that demands maximal aerobic capacity can develop alterations in their EKGs that can be quite unnerving if you are unfamiliar with them but are in fact benign. These changes may include the following:

1. A resting sinus bradycardia, sometimes even below 30 beats per minute! Rather than a cause for concern, this profound sinus bradycardia is a testimony to the efficiency of their cardiovascular system.

2. Nonspecific ST-segment and T-wave changes. Typically, these consist of ST- segment elevation in the precordial leads with T-wave flattening or inversion. T-wave inversion in leads V1 through V4 is especially common in African American athletes.

3. Criteria for left ventricular hypertrophy and sometimes right ventricular hypertrophy.

4. Incomplete right bundle branch block.

5. Various arrhythmias, including junctional rhythms and a wandering atrial pacemaker.

6. First-degree or Wenckebach AV block.

7. A notched QRS complex in lead V1.

Sinus bradycardia and first-degree AV block in a triathlete.

None of these conditions is cause for concern, nor do they require treatment. More than one endurance athlete, undergoing a routine EKG, has been admitted to the cardiac care unit (CCU) because of unfamiliarity with these changes.

Preparticipation Screening for Athletes

During exercise, athletes are at an increased risk of sudden death compared to age-matched populations of nonathletes. Fortunately, the number of cases of sudden death in young athletes is very low, estimated as 1 out of 50,000 to 300,000 athletes. The most common causes are disorders of the heart muscle and sudden ventricular arrhythmias. This raises the obvious question: Should young athletes be screened for congenital abnormalities of the heart before participating in sports?

This is a very controversial area fraught with heated debate and disagreement. For young individuals with worrisome symptoms—dizziness, syncope, chest pain, shortness of breath, and palpitations—or a family history of congenital heart disease, a complete evaluation with a history, physical, EKG, and additional testing (e.g., an echocardiogram, stress test, or ambulatory monitor) is appropriate. But most young athletes have no family history of problems and feel just fine. In these youngsters, there is little evidence that preparticipation screening makes much difference. False positives are common; for example, a small percentage of young athletes will have at least one abnormality on their EKG, such as nonspecific T-wave inversions, first-degree AV block, and J-point elevation. The presence of even an insignificant abnormality may lead to costly, unnecessary testing; anxiety in the patient and family members; and pointless disqualification from further athletic activities. The majority of false positives, however, have been found to stem from EKGs that are read and interpreted by inadequately trained health care personnel, a problem that you have solved by reading this book!

Findings that mandate further evaluation include:

 T-wave inversion beyond lead V2 in white athletes or beyond V4 in African American or Caribbean athletes

 T-wave inversion in the lateral leads

 ST-segment depression in any lead

 Any of the findings we described in the preceding section on sudden cardiac death, such as evidence of hypertrophic cardiomyopathy, long QT syndrome, Wolff-Parkinson-White syndrome, Brugada pattern, or arrhythmogenic right ventricular cardiomyopathy

Evaluation starts with a careful history, family history, physical exam, and echocardiogram and may include genetic testing and a cardiac MRI, which can detect some abnormalities that the echocardiogram may miss.

Sleep Disorders

Many of us are tired during the day, and most often the cause is simple—we don’t get enough sleep! However, there is an increased awareness that many people with daytime sleepiness have one of various sleep disorders, such as sleep apnea or restless legs syndrome.

Patients with sleep apnea are at increased risk of atrial and ventricular arrhythmias and heart block, as well as nocturnal angina, myocardial infarction, systemic and pulmonary hypertension, and right heart failure. Disrupted sleep causes transient hypoxia and altered autonomic function that probably underlie these problems.

Part of a rhythm strip obtained during sleep in a patient with sleep apnea. Note the sinus bradycardia (~50 beats per minute) and first-degree AV block (prolonged PR interval).

The patient’s bedroom partner is typically the first to suspect the disorder, complaining about the patient’s incessant snoring. Most people who snore do not have sleep apnea, whereas those with sleep apnea typically demonstrate periods of apnea lasting several seconds (often occurring many times an hour) interrupted by bursts of arousal accompanied by loud snoring and sometimes frantic breathing.

The diagnosis is made by monitoring the patient’s sleep, either at home or in a sleep lab. The treatment of choice for obese individuals, who are at greatly increased risk for sleep apnea, is weight loss. If that fails, and for everyone else, continuous positive airway pressure (CPAP) can be very effective and lowers the risks of arrhythmias, ischemic heart disease, and hypertension.

A patient with sleep apnea sleeps peacefully (and soundly!) wearing his CPAP apparatus.

The Preoperative Evaluation

The overall risk of a surgical procedure depends upon the particular procedure, the type of anesthesia, the experience of the surgeon and the hospital staff, and the patient’s overall health. Most serious perioperative complications are either cardiac or pulmonary in nature, the former including ischemic episodes and arrhythmias. In an effort to reduce the risks, many surgeons request preoperative assessments from a patient’s primary health care provider. However, for most patients there is little evidence to support this practice.

All patients, no matter how tenuous their cardiac status, can proceed to low-risk surgical procedures (e.g., cataract surgery, dermatologic surgery, and ambulatory procedures such as many arthroscopic procedures) without any evaluation. At the other extreme, patients who require urgent surgery should go right to the operating room without any pause for preoperative evaluation.

What, though, about patients who may have one or more risk factors for a cardiac complication (e.g., a history of ischemic heart disease or diabetes) who are undergoing a procedure with moderate (e.g., abdominal surgery) to high (cardiac or vascular surgery) risk? A resting EKG will rarely be helpful, but a stress test can more closely mimic the stress of surgery. A stress test appears to be appropriate and sometimes helpful for high-risk patients undergoing high-risk procedures. However, for everyone else, the information gleaned from stress testing has not been consistently proven to lead to preoperative interventions that improve surgical outcomes.

For now, the jury is still out. Remember, however, that no patient has zero surgical risk. It is therefore never appropriate to “clear” a patient for surgery; instead, one should state that, based on whatever evaluation has been carried out, there are no contraindications to the planned procedure.


Miscellaneous Conditions

Electrolyte Disturbances

 Hyperkalemia: The great imitator. Evolution of (1) peaked T waves, (2) PR prolongation and P-wave flattening, and (3) QRS widening. Ultimately, the QRS complexes and T waves merge to form a sine wave, and ventricular fibrillation may develop.

 Hypokalemia: ST depression, T-wave flattening, U waves. When severe, prolonged QT interval.

 Hypocalcemia: Prolonged QT interval.

 Hypercalcemia: Shortened QT interval.

Differential Diagnosis of a Prolonged QT Interval



 Severe hypokalemia

 Congenital heart disorders

 Many medications (see page 295)


Differential Diagnosis of a Shortened QT Interval



 Congenital heart disorders


 Osborn waves, prolonged intervals, sinus bradycardia, slow junctional rhythms, and slow atrial fibrillation. Beware of muscle tremor artifact.


 Digitalis: Therapeutic levels are associated with ST-segment and T-wave changes in leads with tall R waves; toxic levels are associated with tachyarrhythmias and conduction blocks; PAT with block is most characteristic.

 Antiarrhythmic agents (and numerous other drugs; see page 295): Prolonged QT interval.

Other Cardiac Disorders

 Pericarditis: Diffuse ST-segment and T-wave changes, PR depression. A large effusion can cause low voltage and electrical alternans.

 Hypertrophic cardiomyopathy: Ventricular hypertrophy, left axis deviation, inferior and lateral Q waves.

 Myocarditis: Conduction blocks.

 Atrial septal defect: First-degree AV block, atrial tachyarrhythmias, incomplete right bundle branch block, right axis deviation, QRS complex crochetage.

Pulmonary Disorders

 COPD: Low voltage, right axis deviation, and poor R-wave progression. Chronic cor pulmonale can produce P pulmonale and right ventricular hypertrophy with repolarization abnormalities.

 Acute pulmonary embolism: Right ventricular hypertrophy with repolarization abnormalities, right bundle branch block, S1Q3 or S1Q3T3. Sinus tachycardia and atrial fibrillation are the most common arrhythmias.

CNS Disease

 Diffuse T-wave inversion, with T waves typically wide and deep; U waves

Causes of Sudden Cardiac Death

 Coronary artery disease

 Hypertrophic cardiomyopathy

 Long QT syndrome

 Wolff-Parkinson-White syndrome

 Viral pericarditis/myocarditis

 Infiltrative diseases of the myocardium

 Valvular heart disease

 Drug abuse (especially stimulants)

 Trauma (commotio cordis)

 Anomalous origin of the coronary arteries

 Brugada syndrome—right bundle branch pattern with ST elevation in V1V3

 Arrhythmogenic right ventricular cardiomyopathy—may see an epsilon wave in terminal portion of QRS

The Athlete’s Heart

 Nonpathologic findings can include sinus bradycardia, junctional rhythms and a wandering atrial pacemaker, nonspecific ST-segment and T-wave changes, left and right ventricular hypertrophy, incomplete right bundle branch block, first-degree or Wenckebach AV block, and a notched QRS complex in lead V1.

Preparticipation Screening for Athletes

Findings that require further evaluation:

 T-wave inversion beyond lead V2 in white athletes or beyond V4 in African American or Caribbean athletes

 T-wave inversion in the lateral leads

 ST-segment depression in any lead

 Evidence of a congenital heart condition such as hypertrophic cardiomyopathy, long QT syndrome, Wolff-Parkinson-White syndrome, Brugada syndrome, and arrhythmogenic right ventricular cardiomyopathy

CASE 12.

Amos T., a 25-year-old graduate student, is brought by ambulance to the emergency room, clutching his chest and looking not at all well. Vital signs show a blood pressure of 90/40 mm Hg and an irregular pulse. His rhythm strip looks like this.

Do you recognize the arrhythmia?

The patient is in atrial fibrillation. There are no P waves, the baseline undulates, and the QRS complexes appear irregularly and are narrow.

Appropriate measures are taken, and Amos is converted back to sinus rhythm, although his rate remains fast at around 100 beats per minute. His blood pressure rises to 130/60 mm Hg. Despite successful conversion of his rhythm, he still complains of severe chest pain and shortness of breath. The emergency room physician wants to send him to the catheterization lab to evaluate him for acute coronary syndrome, but you insist on a good 12- lead EKG first—not an unreasonable request because, except for his tachycardia, his vital signs are stable. The EKG is obtained.

Do you now agree with the emergency room physician’s assessment?

Of course you don’t. Hopefully, you noticed some of the following features:

1. The patient now has a rate of 100 beats per minute.

2. A pattern of right ventricular hypertrophy with repolarization abnormalities is present.

3. A deep Q wave is seen in lead III and a deep S wave in lead I, the classic S1Q3T3 of an acute pulmonary embolus.

Do you now start jumping up and down and scream that the patient has an acute pulmonary embolus? No. You start jumping up and down and scream that the patient may have a pulmonary embolus. These EKG findings are suggestive but hardly conclusive. You have done your job well just by raising the issue; appropriate diagnostic steps can now be taken.

Amos is placed on heparin while awaiting his chest CT scan. This is done within the hour, and the diagnosis of a pulmonary embolism is confirmed. Amos remains in the hospital for several days on heparin therapy and is discharged home on oral anticoagulant therapy. There is no recurrence of his pulmonary embolism.

By the way, in case you were wondering why Amos developed a pulmonary embolism, you should know that he had a strong family history of deep venous thrombophlebitis, and a careful hematologic workup found that he had an inherited deficiency of protein S, a normal inhibitor of the coagulation cascade. Now, try to find that in other EKG books!

CASE 13.

Ursula U. was recently seen at your local hospital for pyelonephritis (a urinary tract infection involving the kidney) and discharged home on the antibiotic, trimethoprimsulfamethoxazole. She seeks routine follow-up care with you. She is fairly new in town and new to your practice. Her infection certainly seems to be responding well to the antibiotic, but you note that her blood pressure is a little elevated at 145/95. She tells you that she is currently taking the blood pressure medication, lisinopril, an angiotensin-converting enzyme inhibitor, but has not seen a physician since the drug was prescribed. Something clicks in your head, and you obtain an EKG. Here are the tracings from just her augmented limb leads. What do you see?

This looks like pretty wild stuff. But analyze this slowly: the QRS complexes are clearly very wide, and there are no visible P waves. Although the QRS complexes and T waves are distinct, they certainly seem to be merging into a single configuration (note particularly lead aVR). Could this be some kind of idioventricular rhythm (see page 151)? Well, perhaps, but the clinical context argues for another interpretation. Both trimethoprim-methoxazole and lisinopril can each cause hyperkalemia that is usually mild, but combined, they can cause severe, even life-threatening elevations in the serum potassium. And that’s what you are seeing here—EKG manifestations of hyperkalemia.

Because of the risk of ventricular fibrillation in this setting, you send Ursula right to the emergency room where she is treated aggressively for hyperkalemia, taken off her medications, and monitored in the CCU until her EKG returns to normal. Eventually, she is discharged on a different antibiotic and a different class of medication for her blood pressure. She does very well and declares that you are the best clinician she has ever met and will recommend you to all her new friends.

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