Assessment of the Patient With a Cardiac Arrhythmia

Published on 20/06/2015 by admin

Filed under Cardiovascular

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1670 times

58

Assessment of the Patient With a Cardiac Arrhythmia

The evaluation of a patient with a suspected cardiac rhythm disturbance is fundamental to the role of the clinical cardiac electrophysiologist. The approach followed for this evaluation varies from patient to patient and is influenced by the patient’s clinical status and symptoms, but a general outline can be established, as presented in this chapter. As always, the initial evaluation begins with a careful history and physical examination.

History Taking

Significant overlap exists among the clinical features of various rhythm disturbances, imparting a degree of imprecision to the interpretation of the patient’s history. Despite this drawback, the history often can provide direction and diagnostic clues as the first step in assessing the patient with, or suspected of having, a cardiac arrhythmia. It often is the most important source of information about the arrhythmia.

Symptoms and Signs

Major symptoms and signs of cardiac arrhythmias are palpitations, presyncope, syncope, and sudden cardiac death (SCD). In this setting, nonspecific symptoms such as shortness of breath, weakness, and fatigue can be due to compromise in cardiac output and prolonged duration of the arrhythmia or its rate, either very fast or very slow. Older patients with bradycardia owing to sinus node dysfunction or atrioventricular (AV) nodal block can present with altered mental status and dementia.

Palpitations

Awareness of an irregular heartbeat varies greatly from patient to patient. Patients who complain of symptoms most commonly note palpitations, defined as sensations experienced as an unpleasant awareness of forceful, irregular, or rapid beating of the heart. Many patients are acutely aware of any cardiac irregularity, whereas others are oblivious even to long runs of a rapid ventricular tachycardia or atrial fibrillation with rapid ventricular rate. Often the asymptomatic patients are those referred for evaluation of an arrhythmia noted incidentally during assessment for another reason, such as a preathletic physical examination in a child or adolescent, a preinsurance physical examination in an adult, or a routine preoperative assessment. Patients describe these symptoms in various ways. Most frequently, they use terms such as a thumping or flip-flopping sensation in the chest; a fullness in the throat, neck, or chest; or a pause in the heart beat, “as if my heart stopped or skipped a beat.” The last is most likely caused by the compensatory pause after a premature ventricular complex (PVC) or the resetting of sinus rhythm after a premature atrial complex. Presumably, the premature beat, particularly if it is a ventricular extrasystole, occurs too early to permit sufficient ventricular filling to cause a sensation when the ventricle contracts. The ventricular systole that ends the compensatory pause may be responsible for the actual palpitation and is caused by a more forceful contraction from prolonged ventricular filling or increased motion of the heart in the chest. Anxiety over such symptoms is commonly the complaint that brings the patient to the physician’s office.

Skipped Beats Versus Sustained Palpitation

Premature atrial or ventricular complexes probably constitute the most common cause of palpitations, and patients often use the term skipped beat or dropped beat to describe them. If the premature complexes are frequent or particularly if a sustained tachycardia is present, patients are more likely to complain of lightheadedness, syncope or near-syncope, chest pain, fatigue, or shortness of breath. The presence of associated cardiovascular problems influences the nature of the symptoms. For example, a supraventricular tachycardia at a rate of 180 beats/min can provoke chest pain in a patient with coronary artery disease or syncope in a patient with aortic stenosis, but result in only a breathless feeling in an otherwise healthy young person.

An important point is that patients with ventricular tachycardia (VT), particularly young, otherwise healthy persons, can be completely asymptomatic or experience minimal symptoms during the arrhythmic episode. The lack of significant symptoms should not exclude the diagnosis of VT. Bradyarrhythmias have their own constellation of symptoms that usually includes syncope, near-syncope, and fatigue.

In this fashion, the clinician can obtain information about the nature of the beginning and end of the tachycardia, whether the ventricular rhythm is regular or irregular, and the rate of the tachycardia. Knowledge about the typical onset and termination of the tachycardia is helpful. Abrupt, paroxysmal onset is consistent with a tachycardia such as AV nodal reentrant tachycardia (AVNRT; see Chapter 77), whereas gradual speeding and slowing are more in keeping with a sinus tachycardia (see Chapter 72). Termination by Valsalva maneuver or carotid sinus massage suggests a tachycardia incorporating nodal tissue in the reentrant pathway, such as sinus node reentry, AVNRT, or AV reentrant tachycardia (AVRT; see Chapters 77 and 76), and idiopathic right ventricular outflow tract tachycardia. It often is helpful to have the patient tap out the cadence of the perceived palpitations, from onset to termination.

The rate of the untreated tachycardia often narrows diagnostic possibilities, and patients should be taught to count their radial or carotid pulse rate. Ventricular rates of 150 beats/minute (bpm) should always suggest the potential diagnosis of atrial flutter with 2 : 1 AV block (see Chapter 74), whereas most supraventricular tachycardias, such as those caused by AVNRT or AVRT, usually occur at rates exceeding 150 bpm. The rates of VTs overlap those of the supraventricular tachycardias. Palpitations, hot flashes, and sweating in middle-aged women suggest perimenopausal syndrome. Palpitations, dizziness, and shortness of breath on mild exertion, typically in young women with structurally normal hearts, suggest the syndrome of inappropriate sinus tachycardia. Palpitations owing to sinus tachycardia on standing should point toward postural hypotension. Palpitations and presyncope on standing can be symptoms of postural orthostatic tachycardia syndrome. Various possible causes of palpitations are listed in Box 58-1.

Box 58-1   Differential Diagnosis of Palpitations

Junctional Tachycardia

Ventricular tachycardia

Conduction system disease

Familial arrhythmia syndrome

Metabolic syndromes

Structural heart disease

Associated Cardiac or Systemic Diseases

It also is important to establish whether the patient has structural heart disease and, if so, the diagnosis and extent of disease. Certain clinical diagnoses are linked to the presence of specific arrhythmias. For example, the occurrence of mitral stenosis should suggest the possibility of atrial fibrillation, whereas a history of a myocardial infarction or tetralogy of Fallot repair invokes VT as a distinct prospect. Thyrotoxicosis should suggest atrial arrhythmias, including sinus tachycardia. At times it is useful to search for a family history of similar problems and to obtain electrocardiograms (ECGs) of close family members, such as parents, siblings, or children. Family history of palpitations, syncope, or SCD should be investigated carefully for inherited cardiac arrhythmias, including atrial fibrillation, long QT syndrome, short QT syndrome, catecholaminergic polymorphic VT, arrhythmogenic right ventricular dysplasia or cardiomyopathy (ARVD/C), and inherited cardiomyopathy with arrhythmia.

Presyncope and Syncope

The diagnosis of presyncope and syncope and its cause requires comprehensive history taking from the patient and witness. The differential diagnosis of syncope is lengthy and can be a warning sign of SCD (Chapter 99, Table 99-1). It is important to differentiate cardiac versus noncardiac causes of syncope. It is more important to differentiate a benign cause of syncope from a malignant cause. Of the reflex syncopes (neurocardiogenic, carotid hypersensitivity, and situational), neurocardiogenic is the most common. It should be differentiated from syncope owing to orthostasis, which is commonly seen in autonomic failure (e.g., due to diabetes), and from syncope resulting from other cardiac causes.

When caused by a cardiac arrhythmia, onset of syncope is rapid and duration is brief, with or without preceding aura, and usually is not followed by a postictal confusional state. It can be associated with bodily injury if the patient falls while unconscious. Palpitations preceding syncope also support an arrhythmic cause of syncope. Seizure activity is uncommon and occurs mostly after a prolonged asystole. Therefore, the seizure does not begin with the syncope. However, in epileptic seizures, convulsive movements start within seconds of the onset of syncope. Tongue biting or incontinence is also uncommon in cardiac syncope. The history of syncope should be elicited and interpreted carefully because older people who have fallen might deny loss of consciousness during the event because of brief retrograde amnesia.

With vasodepressor and cardioinhibitory syncope, the episode usually unfolds more slowly and can be preceded by manifestations of autonomic hyperactivity such as nausea, abdominal cramping, diarrhea, sweating, or yawning. On recovery, the patient may be bradycardic, pale, sweaty, and fatigued, in contrast with the patient recovering from a Stokes-Adams attack or an episode of VT, who could be flushed and have a sinus tachycardia. Common arrhythmic causes of syncope include bradyarrhythmias caused by sinus node dysfunction or AV block and tachyarrhythmias, most often ventricular but also supraventricular on occasion. Bradycardia can follow tachycardia in patients with the bradycardia-tachycardia syndrome, and treatment of both may be necessary.

Drug-induced (orthostatic hypotension, bradyarrhythmia) and nonarrhythmic cardiac causes such as aortic stenosis, hypertrophic cardiomyopathy, pulmonary stenosis, pulmonary hypertension, and acute myocardial infarction can be excluded by the history, physical examination, ECG, echocardiography, and other laboratory tests. Noncardiac causes of syncope such as hypoglycemia, transient ischemic attack, and psychogenic often can be excluded by a careful history.

Sudden Cardiac Death

Sudden cardiac death (SCD) causes approximately 350,000 to 450,000 deaths annually in the United States. It is responsible for nearly 50% of all cardiovascular-related deaths worldwide. SCD has an incidence of 0.1% to 0.2% per year among adults older than 35 years. Therefore, careful evaluation of patients who are resuscitated from SCD is mandatory. SCD occurs in a majority of patients without known heart disease as the first manifestation of underlying coronary artery disease. The life-threatening ventricular arrhythmias, such as sustained VT and ventricular fibrillation, are responsible for two thirds of SCDs. These arrhythmias occur unpredictably, even in high-risk patients. Structural heart disease, such as coronary artery disease, cardiomyopathy, and congenital heart disease, is responsible for up to 65% to 80% cases of SCD. Approximately 5% to 10% of SCDs occur in people with primary electrical abnormalities of the heart, such as long QT syndrome, Brugada syndrome, idiopathic ventricular fibrillation, and Wolff-Parkinson-White syndrome. The remaining sudden deaths (15% to 20%) are due to noncardiac causes such as pulmonary embolism, drugs, drowning, and sudden infant death syndrome. Therefore, careful questioning to uncover or elucidate a family history of SCD is indicated, and family screening for the suspected cardiac condition should be performed.

Precipitating Factors

Physical Examination

The physical examination offers the opportunity to gain important information about the presence of associated structural heart disease, if any, and the nature of the arrhythmia, if present. Although it is well known that patients with normal hearts can have supraventricular tachycardias, it is less commonly appreciated that patients without recognizable structural heart disease can also have VTs that on occasion are life threatening. Thus, normal results of a physical examination do not preclude the diagnosis of VT, even in a young person. It is likely that at least some of these patients have structural heart disease that is not recognized.

The sex of the patient can be a clue to the nature of the tachycardia. For example, a young woman who complains of episodes of a regular tachycardia over many years is likely to have AVNRT. In contrast, a young man with a similar history is more likely to have AVRT associated with the Wolff-Parkinson-White syndrome. Symptomatic long QT syndrome is more common in females, whereas Brugada syndrome is more common in males.

Atrioventricular Dissociation

If the tachycardia is present during the physical examination, a 12-lead ECG should be obtained, if time and the patient’s clinical status permit. If an ECG is not possible, a careful physical examination can yield helpful findings. For example, the presence of regular cannon A waves in the jugular venous pulse would be consistent with a 1 : 1 retrograde ventriculoatrial relation, as in tachycardias such as AVRT, AVNRT, and some junctional tachycardias and VTs. In contrast, the patient can have physical features indicative of AV dissociation, such as intermittent cannon A waves in the neck, variable intensity of the first heart sound, and variable peak systolic blood pressure. Common arrhythmic causes of AV dissociation include VT and nonparoxysmal AV junctional tachycardia, without retrograde capture of the atria. Ventricular or junctional tachycardias that produce retrograde 2 : 1 or Wenckebach block cause intermittent cannon A waves that recur at regular intervals.

Carotid Sinus Massage

Modulating autonomic tone by carotid sinus massage during the physical examination can be useful to expose the patient with the hypersensitive carotid sinus reflex. The clinician first needs to listen carefully over both carotids to be certain that no bruit is present, palpate lightly to determine that a normal carotid pulse is present, and then gently depress or rub the carotid sinus. Gentle massage for approximately 10 to 15 seconds or less usually is all that is necessary to produce significant periods of sinus arrest or AV block in susceptible patients.

The response to carotid sinus massage or other vagal maneuvers can be helpful in differentiating one tachycardia from another. In the most definitive responses, carotid sinus massage acutely terminates tachycardias such as AVRT, AVNRT, sinus node reentry, adenosine-sensitive atrial tachycardia, and idiopathic right ventricular outflow tract tachycardia. Carotid sinus massage can gradually slow a sinus tachycardia without termination and will decrease the ventricular response to atrial tachycardia, atrial flutter, and atrial fibrillation without termination, thereby exposing atrial activity. Carotid sinus massage transiently terminates the permanent form of AV junctional reciprocating tachycardia, which then restarts when carotid massage ceases. Carotid sinus massage does not affect reentrant ventricular or junctional tachycardias. Unfortunately, not all presentations of these tachycardias behave in such a predictable fashion, and intermediate or overlapping responses can occur.

Laboratory Tests

As indicated earlier, the initial assessment of the patient begins with a careful history and physical examination. Several noninvasive and invasive tests add to the physician’s ability to obtain information about the arrhythmia. Before any test is ordered, however, it is imperative to decide whether the information provided by the test is sufficiently important to justify its risk or expense. Whenever possible, tests with maximal sensitivity, specificity, and predictive accuracy are chosen. A 12-lead ECG is obtained in all patients, and frequently a 24-hour ECG or 30-day event recording and stress test is helpful in exposing the arrhythmia. A chest roentgenogram and an echocardiogram provide information about the presence of structural heart disease. The hierarchy of steps taken to evaluate and treat a patient suspected of having an arrhythmia generally proceeds from simple, noninvasive, and inexpensive tests to more complex, expensive, and invasive studies.

The nature of the rhythm disturbance and its effects on the patient determine the order in which the tests are performed. Some rhythm disturbances, such as sustained VT or ventricular fibrillation, are hazardous in and of themselves, whereas others, such as AVRT or AVNRT, must be evaluated according to the context in which they occur. AVRT or AVNRT occurring at a rate of 180  bpm in a young patient who complains only of palpitations or mild anxiety is approached differently from such arrhythmias precipitating angina in a patient with coronary artery disease, syncope in a patient with aortic stenosis, or claudication in a patient with peripheral vascular disease. It is imperative to remember that clinical decision making must be founded on the ECG interpretation of the arrhythmia in concert with the assessment of the patient. Thus, the physician evaluates and determines treatment for a patient who has a rhythm disturbance, rather than a rhythm disturbance in isolation.

The principle in diagnosing and treating symptomatic patients with an undocumented cardiac rhythm disturbance is simple and obvious. One needs merely to record the ECG during a symptomatic episode and then document a causal relation between arrhythmia and symptoms. This often is easier said than done, however, and a variety of approaches are used to achieve that result.

Short-Term and Long-Term Continuous Ambulatory Electrocardiographic Monitoring

The duration of electrocardiographic monitoring depends on the frequency of symptoms. Rhythm disturbances occurring with great frequency are naturally easier to document than those that occur sporadically. Long-term ECG recordings in the outpatient setting usually constitute one of the early diagnostic choices in the patient without a life-threatening cardiac arrhythmia. The patient with a life-threatening arrhythmia may need to be hospitalized to allow for these recordings. A long-term ECG recording provides the most direct documentation of an infrequent cardiac arrhythmia. Prolonged ECG recordings in patients engaged in normal daily activity provide the methodology to quantitate the frequency and complexity of the rhythm disturbance, to correlate these alterations with symptoms, and to evaluate the effect of appropriate pharmacologic therapy on the arrhythmia. In addition, such recordings can document alterations in the QRS-ST and T contour. A 30-day event recorder often is helpful if arrhythmia occurs at least once in a month. The patient can activate these latter devices when symptoms occur, store 30 seconds or more of the ECG rhythm (a memory loop provides ECG information about the arrhythmia that transpired for some seconds before device activation), and transmit it to a central monitoring station over the telephone. Alternatively, some devices automatically record rhythms that exceed preset limits. The automatic recorder is useful in patients who fail to perceive all symptoms associated with the arrhythmia or are unable to activate the recording system because of rapidly progressing syncope or other problems.

1. 24- to 48-hour ambulatory Holter monitoring. Short-term continuous Holter monitoring may be sufficient for patients with daily symptoms related to arrhythmia such as palpitation, presyncope, or syncope. If the arrhythmia does not occur with sufficient frequency, then a simple 24-hour, or even 48-hour, recording will not be useful. Newer Holter monitors also record a 12-channel ECG. Such studies are helpful in arrhythmia characterization including atrial fibrillation, as well as ST-T wave changes related to ischemia and Brugada syndrome.

2. Long-term (15-day) Holter monitoring system. These systems are used for diagnosing arrhythmias occurring once or twice in a week. With these devices, cardiac activity is continuously recorded by chest electrodes that are attached to a pager-sized sensor. The sensor of the pager wirelessly transmits collected data to a portable monitor that analyzes the rhythm data. If an arrhythmia is detected by an arrhythmia algorithm, the monitor automatically transmits recorded data wirelessly via the internet to a central monitoring station for subsequent analysis. Patient activated data is also transmitted.

3. Event recorders (with and without loop):

a. Trans-telephonic monitoring (TTM) systems are external event recorders without loop; they are noncontinuous ambulatory recording system.1 After activation by the patient, an ECG is recorded and directly transmitted by telephone to a receiving center.

b. Event recorders with looping memory (continuous event recorders [CERs]) make a continuous one-lead recording, but the rhythm strip will only be saved when a patient activates the device. Most devices can be programmed to save preactivation and postactivation rhythm strips.

c. Autotriggered event monitors with looping memory (autotriggered CER) devices automatically recognize prespecified high and low heart rates. One such device performs a continuous ECG analysis combined with automatic storage of abnormal events detected in a 20-minute solid-state memory with continuous loop analysis up to 7 days. In addition, it also records patient-trigger events. The most recent advancement in ambulatory arrhythmia monitoring is mobile cardiac outpatient telemetry in which a portable sensor continuously detects asymptomatic, prespecified arrhythmias and transmits the ECG data in real-time to a pocket-sized monitor at the patient’s home. If the algorithms in the monitor detect an abnormal heartbeat, the monitor automatically transmits the patient’s ECG data to the monitoring center using wireless communications.

4. Implantable autotriggered and patient-triggered loop recorders. An implantable loop recorder placed beneath the skin can be used for monitoring of the cardiac rhythm for as long as 12 to 24 months. Therefore, it is useful in patients with infrequent symptoms. The device has both autotriggered and patient-activated arrhythmia recording facilities. The devices are also available for recording a specific arrhythmia, such as atrial fibrillation. Use of such devices has been successful in recording tachyarrhythmias and, more commonly, bradyarrhythmias. Arrhythmia recordings can be sent to the analyzing center via the telephone and then to physicians via the Internet.

5. Pacemakers and implantable cardioverter defibrillators. Dual-chamber pacemakers can record atrial and ventricular high-rate episodes and can be correlated with the arrhythmia. Apart from diagnosing ventricular arrhythmia, a dual-chamber implantable cardioverter defibrillator also helps in identifying cycle length, duration, and frequency of atrial arrhythmias.

Diagnostic Yield of Electrocardiographic Monitoring

For the recording session to be specific, the patient must have both the arrhythmia and symptoms simultaneously. If symptoms occur without an arrhythmia, the latter can be excluded as a cause. Recording arrhythmias without symptoms precludes a definitive causal relation between symptoms and arrhythmia and reduces the specificity of the test. The sensitivity of the test is highly variable, depending on the prevalence of the arrhythmia.

The diagnostic value of ambulatory monitoring seems to depend on a number of variables, including the frequency and duration of arrhythmia, accurate diary maintenance, and inpatient monitoring versus outpatient monitoring. Approximately 25% to 50% of patients experienced a symptom, but only 2% to 15% record a causal cardiac arrhythmia, and 35% will log a symptom without a corresponding ECG abnormality.

Correlation With Cardiac Arrhythmias on 24-Hour and Long-Term Electrocardiographic Monitoring

Twenty-Four–Hour Holter Recordings

In a study of 518 patients, 24-hour Holter recordings were performed for palpitations and other symptoms related to arrhythmia. Two hundred seventy-four (53 %) had significant arrhythmias (41% ventricular and 20% ventricular, 8% both).2 No presenting complaint or cardiovascular diagnosis correlated closely with any specific cardiac arrhythmia. Major arrhythmias, including supraventricular and ventricular tachycardias, often occurred asymptomatically (in 44 of 54 and 37 of 40 patients, respectively). Among 371 patients with accurate historic logs, only 176 (47%) who had long-term electrocardiographic monitoring had typical symptoms during the monitoring period. Only 50 patients (13%) had concurrence of their presenting complaints with an arrhythmia, whereas 126 patients (34%) had their typical symptoms associated with a normal electrocardiogram, which may be helpful in excluding any cardiac arrhythmia as the primary cause for their complaints.

ILR Versus Noninvasive Testing

Giada et al.4 studied 50 patients for the diagnostic yield of the use of insertable loop recorder (ILR), which was randomly compared with conventional strategy (24-hour Holter recording, a 4-week period of CER, or electrophysiological testing if the previous two strategies yielded negative results).4 The diagnosis was made in only five patients (21%) of 25 patients in the conventional strategy group compared with 19 (73%) of 25 patients in ILR group (with arrhythmia recording up to 1 year).

Electrophysiologic Study

Naturally, in many patients, invasive electrophysiologic testing is required to initiate the electrical abnormality. Such studies provide important information when a particular arrhythmia can be initiated that is responsible for the patient’s symptoms. In some instances, however, a tachyarrhythmia present clinically cannot be induced in the electrophysiology laboratory. An important point is that failure to demonstrate a rhythm abnormality does not exclude the possibility that it is present on another occasion and is still responsible for the patient’s symptoms. Thus, the sensitivity of the electrophysiological study may be low, depending on the nature of the rhythm disturbance. Absence of proof is not the same as proof of absence.

Ideally, the electrophysiologic study would induce only clinically and prognostically important cardiac arrhythmias in all patients who are at risk for a spontaneous arrhythmia and in no patient without such a risk. Unfortunately, this is not the case, and it is clear that such a study, depending on the number of extra stimuli used, can induce nonspecific tachyarrhythmias, in particular flutter and fibrillation in both the atria and ventricles. With certain arrhythmias, the test can be highly specific. For example, it would be uncommon to induce a sustained AVRT or AVNRT in a patient who does not also have this arrhythmia clinically or is at risk of having it. Furthermore, it would not be likely to induce a sustained monomorphic VT in a patient who is not at risk for a clinical occurrence of such an arrhythmia.

Stress Testing and Other Noninvasive Studies

An exercise stress test can be useful, particularly in patients who experience symptoms when exercising (see Chapter 63). In response to exercise testing, approximately one third of normal subjects have ventricular ectopy, usually in the form of occasional uniform PVCs. These PVCs are more likely to occur at greater heart rates and are not reproducible from one test to the next. Multiform PVCs, pairs of PVCs, and VT infrequently develop in response to exercise in healthy subjects. Because they can be recorded in normal subjects, their presence does not establish the existence of ischemia or heart disease. Ventricular ectopy generally appears at lower heart rates (<130 bpm) in patients with coronary artery disease than in a normal population, and it often occurs in the early recovery period. Ventricular arrhythmias are more reproducible from one test to the next in patients with coronary artery disease, and more frequent PVCs (exceeding 10 per minute), polymorphic PVCs, and VT are more likely to occur in patients with coronary artery disease than in persons with normal hearts. PVCs at rest can be suppressed by exercise in patients with documented coronary disease; therefore, this observation does not necessarily imply a benign prognosis or absence of underlying structural heart disease. In normal subjects, results from consecutive exercise tests might not be reproducible, whereas the test results are more reproducible in patients with coronary artery disease, but not dependably so. Exercise testing may be useful to expose ECG abnormalities in patients with less obvious forms of the long QT syndrome.

A variety of noninvasive tests have been developed in an attempt to identify patients at risk for sudden arrhythmic death. These tests include signal-averaged electrocardiography, heart rate variability QT dispersion testing, T wave alternans assessment, and baroreflex testing. Although these tests can help to identify groups of patients at greater or lower risk for SCD, they all suffer from an inability to predict precisely the occurrence of life-threatening arrhythmias in individual patients (see Chapters 65 to 69).

Tests Indicated for Specific Symptoms

Syncope

The underlying disorder can be determined using standardized clinical evaluation in up to three fourths of patients with syncope. In unselected populations, slightly more than one third of the patients have neurocardiogenic syncope, one fourth have orthostatic hypotension, and the remaining patients have miscellaneous conditions. Evaluation of patients suspected of cardioinhibitory or vasodepressor syncope often includes tilt table testing. The yield from prolonged ECG ambulatory recordings and from electrophysiological studies in patients experiencing syncope who do not have structural cardiac disease is in general low and unrewarding. It is important to establish the cause of the syncope, if possible, because patients who have syncope from a noncardiac cause usually have an excellent prognosis, whereas those who have syncope from a cardiac cause have a greater prevalence of sudden cardiac death.

Electrophysiological testing is recommended for patients who have syncope or near-syncope that remains unexplained after a thorough evaluation, including a complete neurologic evaluation and ambulatory ECG recordings. Because both bradycardia and tachycardia can be responsible for syncope, the diagnosis or exclusion of a specific etiologic disorder should not be based on anything other than an ECG recording during the syncopal event, or replication, during an electrophysiological study or other maneuvers, of a cardiac rhythm disturbance that produces the same or similar symptoms in the patient. For example, in the patient who has first-degree AV block and left bundle branch block, episodes of VT may be responsible for the syncope, rather than episodes of more advanced AV block.

Bradyarrhythmias

Many patients have asymptomatic bradyarrhythmias, and it is important to establish that they produce symptoms in a given patient before assuming that therapy is required. Conversely, if the patient becomes symptomatic when a spontaneous bradyarrhythmia is demonstrated, further diagnostic studies might not be necessary. It is also possible that patients can be minimally symptomatic but have arrhythmias that permit definitive therapeutic decisions. For example, in patients who have type II second-degree AV block, the demonstration of His-Purkinje block, even in the minimally symptomatic or possibly asymptomatic person, can be sufficient evidence to conclude that pacemaker therapy is indicated because of the risk for progression to complete AV block.

The patient with sinus node dysfunction can have syncope or near-syncope but also might complain of symptoms consistent with low cardiac output because of persistent bradycardia, such as fatigue or even manifestations of congestive heart failure. Some patients can have associated tachycardia—producing the aforementioned bradycardia-tachycardia syndrome. Electrophysiological studies of sinus node function have low sensitivity but relatively high specificity. Correlation of the presence of the bradycardia with the patient’s symptoms is of utmost importance. Electrophysiological studies are indicated only when a causal relation between the appearance of the bradycardia and the patient’s symptoms cannot be established despite repeated noninvasive evaluations. It is important to keep in mind that asymptomatic sinus bradycardia with heart rates of 35 to 40 bpm, sinus arrhythmia with pauses of 2 to 3 seconds, Wenckebach second-degree AV block (particularly during sleep), wandering atrial pacemaker, and junctional escape complexes can be completely normal, especially in young people and in well-conditioned athletes.

In patients with AV block, the scalar ECG is the most important laboratory test, because the site of block usually dictates the clinical course of the patient and whether a pacemaker is needed, and the site of block usually can be determined from analysis of the scalar ECG. Only infrequently is an electrophysiological study indicated. Autonomic manipulation can be used to help establish the site of block. Atropine or isoproterenol shorten AV nodal conduction time and refractoriness, whereas vagal maneuvers prolong them. Little change occurs in the normal His-Purkinje conduction. Thus, exercise, atropine, or isoproterenol can shorten the PR interval and increase the ratio of conducted P waves during type I (Wenckebach) AV nodal block, whereas these maneuvers can increase the number of blocked P waves in type II second-degree AV block. Of note, however, important overlap between the two responses is possible.

Tachyarrhythmias

As mentioned earlier, a 12-lead ECG should be obtained during tachycardia, as long as the patient’s condition is relatively stable. If the QRS is normal and identical to that present during sinus rhythm, the tachycardia must be supraventricular, and the differential diagnosis now relates to its mechanism (see Chapters 73 77–79). The 12-lead ECG provides many diagnostic clues in this regard. Supraventricular tachycardias can be classified as short RP′ or long RP′ tachycardias, depending on the timing of the P wave in relation to the preceding R wave. When a P wave occurs closer to the preceding R wave (i.e., in the first half of the R-R interval), the tachycardia is called a short RP′ tachycardia, whereas if a P wave occurs in the second half of the RR cycle, the arrhythmia is called a long RP′ tachycardia. Considerations in the differential diagnosis for a short RP′ tachycardia include AVNRT, AVRT, junctional tachycardia, and atrial tachycardia with a markedly prolonged PR interval. If no P waves or other evidence of atrial activity are apparent, and the R-R interval is regular, AVNRT is most likely. If a retrograde P wave is present in the ST segment, AVRT is most probable. Long RP tachycardias include sinus tachycardia, atypical AVNRT, permanent junctional reciprocating tachycardia, and atrial tachycardia. The presence of conduction over an accessory pathway during sinus rhythm or during tachycardia naturally suggests that the Wolff-Parkinson-White syndrome with its associated accessory pathway is responsible for the dysrhythmia. During VT, specific QRS contours and the presence of AV dissociation are useful in making the diagnosis.

Related posts:

Voltage-Gated Sodium Channels and Electrical Excitability of the Heart Exercise-Induced Arrhythmias Genetics of Atrial Fibrillation Inheritable Phenotypes Associated With Altered Intracellular Calcium Regulation Ventricular Arrhythmias in Congenital Heart Disease Cardiac Monitoring: Short- and Long-Term Recording