For additional ancillary materials related to this chapter. please visit thePoint.
In this chapter you will learn:
1 | 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:
- electrolyte disturbances
- digitalis effects, both therapeutic and toxic
- medications that prolong the QT interval
- other cardiac disorders (pericarditis, cardiomyopathy, myocarditis, and atrial septal defect)
- pulmonary disorders
- central nervous system disease
- sudden cardiac death in persons without coronary artery disease
- the athlete’s heart
- screening young athletes before participating in sports
- sleep disorders
- the preoperative evaluation
2 | 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.
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.
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.
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
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.
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.
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:
- Everything slows down. Sinus bradycardia is common, and all the segments and intervals—PR, QRS, QT, etc.—become prolonged.
- 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.
- Various arrhythmias may appear, including sinus bradycardia, a slow junctional rhythm and slow atrial fibrillation.
- 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.
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.
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.
Digitalis slows conduction through the AV node and can therefore cause first-, second-, and even third-degree AV block.
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.
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.