Assessment of the Patient With a Cardiac Arrhythmia

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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.

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