Electrophysiologic Testing in Perspective: The Evaluation and Treatment of Cardiac Arrhythmias

The Three Steps in Evaluating and Treating Cardiac Arrhythmias


The appropriate management of cardiac arrhythmias involves following a predetermined plan of therapy aimed at achieving specific goals. Those goals, in turn, are determined by the severity of the arrhythmia being treated. Thus, in evaluating and treating cardiac arrhythmias, three discrete steps are implicit:



Step 1. Assess the severity of the arrhythmia to be treated. The physician decides whether the arrhythmia is benign, potentially harmful, or lethal, and whether the symptoms associated with the arrhythmia require treatment.

Step 2. Decide on the therapeutic end point. The physician decides whether the primary goal of treatment is to prevent death, to minimize harm, or merely to relieve symptoms.

Step 3. Design the treatment plan. The physician devises a treatment plan that is directly aimed at achieving the primary therapeutic end point.

Step 1. Assess the Severity of the Arrhythmia to be Treated


As already stated, the most common and most serious mistake made in the management of cardiac arrhythmias is to institute therapy that is inappropriate for the arrhythmia being treated. This error most often results from the propensity of physicians to assign specific treatments to specific arrhythmias, without considering the setting in which the arrhythmia occurs.


Example: Dr X uses flecainide or encainide to treat all patients with premature ventricular contractions (PVCs; prior to 1990, this was an extremely common practice). For Patient A, who has a normal heart and asymptomatic complex ventricular ectopy, this therapy is too aggressive. Patient A has a normal risk of sudden death, and antiarrhythmic drugs cannot be expected to improve that normal risk (they may, on the other hand, increase it). For Patient B, who is a survivor of sudden cardiac death with PVCs, this therapy is not aggressive enough. Patient B has an extremely high risk of sudden death and empiric therapy with flecainide is not likely to help—indeed, the risk of proarrhythmia is especially high in such a patient.


Physicians who treat a specific arrhythmia the same way in every patient will eventually cause serious problems because the appropriate treatment for an arrhythmia depends on more than just the arrhythmia itself. The appropriate level of aggressiveness in treating an arrhythmia can be judged only when considering the setting in which the arrhythmia occurs. In assessing the severity of a patient’s arrhythmia, the physician must consider at least three factors: (1) What is the arrhythmia? (2) What symptoms are associated with the arrhythmia? (3) What is the nature and the extent of any underlying cardiac disease?


Several specialized laboratory studies are available to help assess these three factors. The studies most often used are those that help to assess the arrhythmia itself (the electrophysiology study and ambulatory monitoring) and those that help to assess underlying cardiac disease (cardiac catheterization, stress testing, echocardiography, and nuclear angiography).


The electrophysiology study, as helpful as it is in guiding the therapy of many cardiac arrhythmias, is only modestly helpful in assessing the severity of arrhythmias. Because the arrhythmias induced in the electrophysiology laboratory are produced under unnatural circumstances, the electrophysiology study is poor at helping to correlate symptoms with arrhythmias. Observing symptoms with spontaneously occurring arrhythmias is far more helpful. On the other hand, in circumstances where an arrhythmia is suspected but not documented, the electrophysiology study can be helpful in diagnosing the arrhythmia itself. The most common example would be in a patient with syncope of unknown origin (see Chapter 10). In such patients, the electrophysiology study can help to diagnose sinus node disease, distal conducting system disease, and ventricular tachyarrhythmias. It bears repeating, however, that both sinus node disease and conducting system disease can most often be diagnosed noninvasively. Regarding ventricular tachyarrhythmias, the sensitivity and specificity of induced ventricular arrhythmias in patients with syncope of unknown origin are strongly related to the presence and the extent of underlying heart disease. In general, electrophysiologic testing should be done in patients with syncope of unknown origin only when they have significant heart disease or when there is a particular reason to suspect an arrhythmic etiology for syncope. The electrophysiology study, in addition, can help to assess the potential for developing severe arrhythmias in patients with atrioventricular bypass tracts (see Chapter 6). Except in patients with syncope of unknown origin or with bypass tracts, however, the electrophysiology study is of limited usefulness in assessing the severity of arrhythmias.


Ambulatory monitoring is often more helpful than electrophysiologic testing in assessing the severity of cardiac arrhythmias. In patients who are having reasonably frequent spontaneous arrhythmias, ambulatory monitoring is excellent in helping to correlate the arrhythmia with symptoms. Further, the specificity of spontaneous arrhythmias (as opposed to induced arrhythmias) is 100%. There are four general varieties of ambulatory monitoring. The Holter monitor study typically records the cardiac electrogram for 24 hours. If patients are having arrhythmias that occur at least daily, the Holter study is often ideal for assessing the severity of these arrhythmias, because it gives information on the frequency of occurrence, potential exacerbating influences, and related symptoms. The second variety of ambulatory monitor, the cardiac event recorder, records the cardiac electrogram on a continuous tape, so that at any time only the last 30–90 seconds are available for playback. When a symptomatic arrhythmia occurs, the patient can stop the tape by pressing a button and then transmit the contents of the tape by telephone. Such a monitor is usually worn for extended periods of time, until a symptomatic episode is captured on tape. This type of monitor is best suited for a patient who has relatively infrequent symptomatic arrhythmias that have been difficult to document. The third type of ambulatory monitoring is mobile cardiac outpatient telemetry—a device that continuously monitors the heart rhythm for up to several weeks at a time, and automatically transmits arrhythmic “events” to a centralized monitoring center. Physicians are contacted whenever an important arrhythmia is identified. Finally, there is the implantable rhythm monitor. This is a tiny microprocessor-based device that is placed under the skin and records a patient’s ECG for weeks or months at a time. Rhythm strips from inside the device can be downloaded periodically and reviewed. Some electrophysiologists have found this device helpful in assessing the frequency and severity of benign (but symptomatic) cardiac arrhythmias. The implantable rhythm monitor has also been used to help diagnose syncope of unknown origin—but it must be stressed that it is inappropriate to rely on this form of ambulatory monitoring (or any ambulatory monitoring) to reveal arrhythmia-induced syncope, at least until ventricular arrhythmias either have been ruled out as the cause of syncope by electrophysiologic testing or have been deemed extremely unlikely after a noninvasive cardiac workup (see Chapter 10).


The studies used to assess underlying heart disease will vary from patient to patient. Nuclear angiography and echocardiography are often used because these relatively noninvasive tests give excellent information on ventricular wall motion and left ventricular ejection fraction. The echocardiogram is especially useful when significant valvular heart disease or hypertrophic cardiomyopathy are suspected. If cardiac ischemia is suspected, stress/thallium testing and cardiac catheterization are commonly used.


What is the Arrhythmia?


Diagnosing the arrhythmia of concern is an important first step. Once the arrhythmia in question is known, some attempt should be made to classify the risk for sudden death imposed by the arrhythmia as low, moderate, or high. Such a classification, based on the arrhythmia itself, is listed in Table 12.1. Note that some arrhythmias, by their very nature, should automatically be considered as imposing a high risk—namely, sustained ventricular tachycardia, ventricular fibrillation, and complete heart block with an inadequate escape mechanism. The presence of atrial fibrillation itself produces an increased risk of embolic stroke. Most other arrhythmias usually impose low or moderate risk, depending on the underlying heart disease.


Table 12.1 Classification of the risk for sudden death imposed by arrhythmias.




























High risk Moderate risk Low risk
Ventricular tachycardia Complex ventricular ectopy with underlying heart disease Premature atrial complexes
Ventricular fibrillation Second-degree AV block Premature ventricular complexes
Third-degree AV block with an inadequate escape Third-degree AV block with adequate escape Sinus node dysfunction
Wolff–Parkinson– White syndrome with rapid antegrade conduction in atrial fibrillation Atrial fibrillation Supraventricular tachycardias


Complex ventricular ectopy with no underlying heart disease


First-degree AV block

What Symptoms are Associated with the Arrhythmia?


Arrhythmias generally cause only a few types of symptom: palpitations, lightheadedness or dizziness, and loss of consciousness. Palpitations are the most common symptom and are commonly associated with ectopic beats. Most patients can tolerate palpitations if this is the only symptom they experience, especially if they can be reassured that their arrhythmia is benign. Lightheadedness and dizziness, which occur with various levels of severity, tend to be associated either with bradyarrhythmias or with tachyarrhythmias that consist of more than isolated extra beats. Although many patients can tolerate occasional mild episodes of lightheadedness, others find these symptoms to be extremely disturbing. Loss of consciousness from an arrhythmia indicates extreme hemodynamic compromise, and any bradyarrhythmia or tachyarrhythmia that produces this symptom should be considered to imply a high risk of sudden death. (An important exception to this rule: syncope accompanied by bradycardias is most often vasoactive in nature. In such cases, the bradycardia itself is usually not the cause of syncope (instead, vasodilation is the cause) and should not be considered a lethal arrhythmia.)


Some arrhythmias cause symptoms by producing or worsening symptoms of congestive heart failure. Any form of tachycardia that persists for weeks or months (such as persistent reentrant supraventricular tachycardia, inappropriate sinus tachycardia, or atrial fibrillation with a rapid ventricular response) can ultimately produce ventricular remodeling and dilation and thus congestive heart failure. In patients with diastolic dysfunction, whose noncompliant ventricles are dependent on atrial contraction to achieve a high end-diastolic pressure while maintaining a relatively normal mean atrial pressure, loss of that atrial contraction with the onset of atrial fibrillation can produce pulmonary congestion quite acutely.


When a patient has symptoms compatible with an arrhythmia, determining whether those symptoms are actually due to an arrhythmia is not always straightforward. Quite often, a Holter-monitor study will show arrhythmias and symptoms but will fail to show a correlation between the two. In these instances, the arrhythmia should not be construed as the cause of the symptoms. Because the appropriate treatment of many nonlethal arrhythmias depends on the symptoms they produce, every attempt should be made to document a correlation between the arrhythmia and the symptoms before any potentially toxic therapy is initiated. Further, several symptoms are often attributed to arrhythmias but in fact are only rarely due to arrhythmias. These symptoms include dyspnea, nonspecific fatigue, and seizures or localizing neurologic symptoms. Any of these symptoms, even if accompanied by cardiac arrhythmias, should prompt a thorough search for other causes.


Once it is determined that symptoms are due to the arrhythmia in question, those symptoms should be categorized in terms of their severity. The classification of the severity of symptoms described in Table 12.2 includes three categories: life-threatening symptoms, severely disruptive symptoms, and minor or no symptoms.


Table 12.2 Classification of the severity of arrhythmic symptoms.












Life-threatening Presyncope, syncope, aborted sudden death
Severely disruptive Significant lightheadedness or dizziness, severe palpitations, worsening congestive heart failure (such as in atrial fibrillation with rapid ventricular response)
Minor/none Mild lightheadedness, palpitations

What is the Underlying Heart Disease?


In general, any arrhythmia is more severe in the face of significant underlying heart disease than in a normal heart. In particular, as described in Chapter 7, underlying heart disease is the primary determinant of lethal ventricular arrhythmias. Thus, complex ventricular ectopy that has only minimal significance in a patient with no heart disease has significant implications in patients with severe left ventricular dysfunction.


By considering these three factors, one can accurately judge the severity of the arrhythmia in question. The next step is to use this information to decide on a specific goal of therapy.


Step 2. Decide on the Therapeutic End Point


Cardiac arrhythmias are treated because they either produce symptoms, pose a threat to health, or have the potential to cause sudden death. Thus, there are three general therapeutic end points in treating cardiac arrhythmias: to relieve symptoms, to maintain health, or to prevent sudden death. Before a treatment plan can be devised, it is vital to decide which of these goals is to be pursued and to keep that goal clearly in mind.


The appropriate goal of therapy should be chosen based on the severity of the arrhythmia, as determined in step 1. The following generalizations can be made. Low-risk arrhythmias, because they do not have the potential to produce death, should be treated only if they are producing symptoms that are disruptive to the patient’s life, in which case the goal of therapy is merely to reduce symptoms. High-risk arrhythmias, on the other hand, should always be treated, and the goal of therapy with these arrhythmias is to prevent sudden death.


Moderate-risk arrhythmias are the most problematic. Two arrhythmias tend to fall in to this category: atrial fibrillation and complex ventricular ectopy in the setting of significant underlying cardiac disease.


Atrial fibrillation presents a problem (aside from the symptoms caused by the arrhythmia itself) because it poses a long-term risk of embolic stroke, and in some patients it can produce or exacerbate heart failure. Furthermore, as we have discussed, “getting rid” of atrial fibrillation (with either antiarrhythmic drugs or ablation) can be extremely difficult and risky. So, in treating this arrhythmia the clinician must decide whether to use a “conservative” approach (controlling the rate response and anticoagulating) or an “aggressive” approach (trying to restore and maintain sinus rhythm). Neither of these approaches is easy or straightforward, and both may require escalating attempts at achieving the therapeutic goal (for instance, advancing from drug-based therapy to ablation-based therapy).


Complex ventricular ectopy, in the setting of significant underlying cardiac disease, has become much less a clinical dilemma than it used to be, for two reasons. First, it is now well established that trying to abolish these arrhythmias with antiarrhythmic drugs merely increases risk, and that treating empirically with amiodarone does not improve outcomes. So the temptation to treat the ectopy itself has become much less compelling. And second, as described in Chapter 7, thanks to the results of several randomized clinical trials, we can now offer implantable defibrillators to many of these patients. So, while treatment still does not entail getting rid of the ectopy itself, we are now able to materially improve the survival of many of the patients who fall into this category.


Step 3. Design the Treatment Plan


The final step in the management of cardiac arrhythmias is to decide on a therapeutic plan aimed at achieving the chosen goal of therapy. Keeping the goal of therapy clearly in mind is vitally important because treatments for similar arrhythmias may vary markedly from patient to patient, depending on whether the aim of therapy is to prevent sudden death or merely to relieve symptoms. (It should be noted that in managing bradyarrhythmias, the basic therapy for both relieving symptoms and preventing sudden death is essentially the same—a permanent pacemaker. The following discussion thus pertains mainly to ectopic beats and tachyarrhythmias.)


Treating to Relieve Symptoms


When the primary goal of therapy is to relieve symptoms, the physician must determine what steps are necessary to achieve that goal. For most patients in whom symptom relief is the therapeutic end point, the arrhythmia being treated is benign. Thus, therapy aimed at relieving symptoms is often (and appropriately) less aggressive than therapy aimed at preventing sudden death. Empiric trial-and-error therapeutic attempts are often appropriate and are frequently performed on an outpatient basis. Generally, milder therapies are tried first, moving progressively and as necessary to more aggressive treatments. Before each escalation of therapy, careful consideration is given as to whether the symptom being treated warrants yet more aggressive therapy. Although serial ambulatory monitoring is often helpful, it should be remembered that, when the goal is merely to relieve symptoms, this goal has already been met if monitoring is necessary to tell whether the arrhythmia is still present.


The level of aggressiveness used in controlling symptoms depends on the severity of the symptoms being treated. For instance, therapy to relieve symptoms does not necessarily involve suppressing the culprit arrhythmia. Quite often, the symptoms that a patient experiences with a benign arrhythmia are magnified by the anxiety that often accompanies the knowledge that one has a cardiac arrhythmia (an anxiety that is often provoked by a physician who expresses grave concern over the arrhythmia’s presence). In such cases, the symptoms often can be ameliorated simply by reassuring the patient of the benign nature of the arrhythmia. The therapeutic goal of relieving symptoms, then, can sometimes be achieved without subjecting the patient to potentially toxic drugs, and without affecting the frequency of the offending arrhythmia at all.


On the other hand, a patient may have an arrhythmia that is non-life-threatening but that produces severely disabling symptoms. In such instances, it may be entirely appropriate to attempt very aggressive therapy. As an example, consider a patient with severe cardiomyopathy who has atrial fibrillation with a rapid ventricular response, resulting in moderate decompensation of the patient’s congestive heart failure. With such a patient, one might begin with attempts to control the ventricular response with digitalization, calcium blockers, or β-blockers. If this were unsuccessful, one would have to consider more radical measures, such as His bundle ablation and insertion of a permanent pacemaker. Therefore, one may arrive at aggressive therapy in relieving the symptoms of an arrhythmia, but in general only after less aggressive measures have failed.


The electrophysiology study has only a moderate role in managing arrhythmias when the suppression of symptoms is the primary goal. Although the electrophysiology can help in assessing the presence of various nonlethal arrhythmias (such as sinus node or AV node dysfunction), this study cannot supply much information on the symptoms caused by these arrhythmias.


For several types of arrhythmia, however, the electrophysiology study can be helpful in abolishing symptoms. This is especially true for most reentrant supraventricular tachycardias, which usually can be cured with transcatheter ablation.


Treating to Prevent Sudden Death


Once the physician decides that the primary goal of therapy is to prevent the patient’s sudden death, a treatment plan should be devised that reflects the urgency of the therapeutic end point. By its nature, sudden death occurs instantaneously and unexpectedly. Thus, when a patient is judged to be a candidate for sudden death, immediate and aggressive efforts should be made to prevent this event. Ideally, these efforts should include placing the patient in the hospital and on a monitor until adequate therapy is derived. Trial-and-error (empiric) methods of treatment are inappropriate. When the goal of therapy is to prevent sudden death, the initial therapy must be effective because the physician is unlikely to have a second chance should therapy prove ineffective.


With regard to patients who are at high risk for sudden death from ventricular arrhythmias, the treatment “plan” has been greatly simplified over the past few years. In contrast to the days when the electrophysiology study was used as the cornerstone of a complex therapy-selection strategy, today the “baseline” treatment strategy is almost always the same: to insert an implantable defibrillator. The electrophysiology study, when done at all, is generally used to help determine how to optimally program the implantable defibrillator—for instance, in optimizing antitachycardia pacing.


For the other major variety of arrhythmia that poses an increased risk of sudden death—a bypass tract with rapid antegrade conduction—the electrophysiology study with ablation remains the mainstay of effective treatment.


Conclusion


This final chapter outlines a general approach to, and a perspective on, the use of the electrophysiology study in the management of cardiac arrhythmias. Devising a reasonable treatment plan depends on defining the goals of therapy. Those goals, in turn, depend on the severity of the arrhythmia and of the symptoms caused by the arrhythmia. The electrophysiology study can be of moderate help in assessing the severity of cardiac arrhythmias and can be extremely helpful in abolishing both the symptoms and the risk caused by several cardiac arrhythmias.


Most fatal mistakes in treating cardiac arrhythmias stem from failing to match the aggressiveness of therapy to the severity of the arrhythmia being treated. Using a logical, stepwise approach to the evaluation and treatment of cardiac arrhythmias allows one to avoid this critical error.


Stay updated, free articles. Join our Telegram channel

Aug 12, 2016 | Posted by in CARDIOLOGY | Comments Off on Electrophysiologic Testing in Perspective: The Evaluation and Treatment of Cardiac Arrhythmias

Full access? Get Clinical Tree

Get Clinical Tree app for offline access