In addition to documenting the patient’s description of his or her symptoms (Table 3.1), it is important for the physician to define certain characteristic features of the palpitations.

As discussed previously, arrhythmias may also give rise to symptoms of dyspnea, lightheadedness, weakness, dizziness, and near-syncope or syncope, depending on the extent of hemodynamic embarrassment. Conversely, palpitations preceded by symptoms of angina or dyspnea might suggest that an arrhythmia or sinus tachycardia is occurring on a secondary basis (owing to ischemia, left-sided heart failure, pulmonary hypertension, or pulmonary embolism).

When patients describe symptoms suggestive of tachycardia, inquiries should be made regarding the occurrence of polyuria during a protracted spell, a phenomenon that may result from an atrial neurohormonal response to supraventricular tachyarrhythmias (5). Anxiety-type responses may accompany palpitations. For some patients, the frightening nature of PSVT symptoms may so dominate their subjective experience as to contribute to a misdiagnosis of “panic attacks,” especially when episodes are selfterminating in the absence of organic heart disease (6).

Central to the evaluation and management of patients with palpitations is the determination of the presence or absence of underlying heart disease. This assessment begins during the history with inquiries regarding any known current or prior cardiac conditions. The presence of ischemic heart disease (especially prior myocardial infarction) should certainly prompt suspicion of premature ventricular beats or ventricular tachyarrhythmias. Such arrhythmias may also be considered in the setting of congestive heart failure (either known or suspected on the basis of predisposing conditions such as hypertension). At the same time, it is important to appreciate that patients with sustained supraventricular (especially atrial) tachyarrhythmias, even at relatively low rates of 110 to 140 beats per minute, may over time secondarily acquire symptoms of congestive heart failure—so-called tachycardia-induced cardiomyopathy (7). Careful questioning may help to distinguish between these different cause-and-effect scenarios. Atrial dilatation, in the setting of left or right ventricular dysfunction or both, or resulting from mitral valve disease, can lead to symptomatic atrial tachyarrhythmias. In the absence of organic heart disease, isolated palpitations may be either atrial or ventricular in origin, but sustained rapid-rhythm episodes may well represent reentrant PSVT (especially in younger or middle-aged adults) or paroxysmal atrial fibrillation or flutter (more so in middle-aged and elderly patients).

Knowing that a patient has a history of a specific arrhythmia increases the likelihood that recurrent symptoms represent more of the same. Of course, the physician must always be open to the possibility that a new arrhythmia has developed [e.g., paroxysmal atrial fibrillation in a patient with known left ventricular systolic dysfunction and prior symptomatic premature ventricular complexes (PVCs)]. A history of recent (within a few weeks to months) radiofrequency ablation should prompt consideration of recurrence of the treated tachyarrhythmia, although palpitations are common after even successful procedures (8).

It also is important to determine whether the patient has a pacemaker or implantable cardioverter defibrillator. Ventricular pacing through either of these devices is capable of giving rise to PVC-like symptoms, especially with 1:1 retrograde (ventriculoatrial) conduction; the attendant
palpitations and other symptoms reflecting a reversed AV sequence are collectively referred to as pacemaker syndrome. In patients with dual-chamber pacemakers or defibrillators, palpitations may reflect the occurrence of pacemaker-mediated “endless-loop tachycardias.” When these devices use internal sensors to modulate pacing rate, overly sensitive rate-responsive ventricular pacing during minimal activity may produce a sensation of inappropriately rapid heart beating.

For patients with a family history of sudden death, the physician should maintain a high index of suspicion that palpitations may be caused by an inherited arrhythmogenic disorder, such as long-QT syndrome (Chapter 18), Brugada syndrome (Chapter 18), or familial catecholamine-mediated polymorphic ventricular tachycardia (9). With these conditions, palpitations may reflect the occurrence of nonsustained ventricular tachycardia. Clinical concern deepens with ancillary symptoms of lightheadedness, near-syncope, or syncope. Growing recognition exists of the existence of certain families that harbor an inherited predisposition to atrial fibrillation (10); inquiries about such a family history may prove informative.

A history of symptoms consistent with hyperthyroidism (on an endogenous or iatrogenic basis) may imply that sinus tachycardia or paroxysmal atrial fibrillation is responsible for the palpitations. Patients with pheochromocytoma may come to attention because of palpitations secondary to sinus tachycardia; this diagnosis may be suspected with associated symptoms of headache, diaphoresis, and pallor.

Supraventricular and ventricular tachyarrhythmias may be precipitated by bronchodilator therapy or various over-thecounter sympathomimetic agents taken for cold symptoms. It is important to determine whether patients are taking cardiac or noncardiac QT-prolonging medications, which would raise the possibility of life-threatening polymorphic ventricular tachycardia (torsades de pointes). (A list of the most common QT-prolonging drugs may be found in Chapter 18, Table 18.3; a more complete listing is available on the Internet at www.qtdrugs.org). The examiner should inquire about possible excessive consumption of caffeine or alcohol, certain herbal agents (e.g., ephedra), or other stimulatory substances (e.g., cocaine and amphetamines), all of which are capable of causing supraventricular and ventricular arrhythmias. Symptomatic arrhythmias associated with hyperthyroidism may occur in patients taking thyroid-replacement medication on a therapeutic or surreptitious basis.

This test should be performed in all patients. Obviously, a palpitation is not likely to be “caught” during the brief recording period of an electrocardiogram (ECG). However, the resting ECG provides important clues as to the presence or absence of underlying structural heart disease, which can provide a substrate for arrhythmias. A completely normal ECG cannot absolutely exclude coronary artery disease, but it tends to imply preserved left ventricular systolic function (11). Impaired left ventricular systolic function may be suspected in middle-aged and older patients who exhibit left bundle-branch block, nonspecific intraventricular block, or prior myocardial infarction (especially when multiple). ECG evidence of left ventricular hypertrophy, whether associated with abnormal left ventricular systolic function or not, raises the possibility not only of PVCs but also of atrial tachyarrhythmias, secondary to elevated mean left atrial filling pressure. Increased susceptibility to atrial tachyarrhythmias can also be suspected in patients in whom the ECG shows signs consistent with chronic obstructive pulmonary disease or mitral stenosis.

In the absence of stigmata of organic heart disease, the ECG should be scrutinized for the possible presence of a delta wave (slurred QRS upstroke with short PR interval). The latter indicates ventricular preexcitation (Wolff-Parkinson-White syndrome) and suggests the possibility that palpitations are being caused by AV reentrant tachycardias and/or paroxysmal atrial fibrillation with rapid conduction via an accessory pathway. Delta waves on an ECG can thus be a useful clue to the origin of palpitations; when this ECG sign is overlooked, misdiagnosis can result (6). In this regard, it should be noted that the delta wave may be quite subtle (and with PR interval sometimes greater than 0.12 seconds) in patients with a left lateral accessory pathway, owing to the relatively long intraatrial conduction time from sinus node to the accessory pathway, in comparison with sinus impulse propagation to the ventricles via the normal AV conduction system.

An ECG lacking the aforementioned abnormalities should also be examined for the possible presence of a prolonged rate-corrected QT interval (longer than 0.45 seconds in men and longer than 0.46 seconds in women) and/or “bifid” or “notched” T waves or other ST-T-wave morphologic abnormalities, which may suggest long-QT syndrome (12). “Coved”-type ST elevation in the right precordial leads, with concomitant T-wave inversion, and often incomplete or complete bundle-branch block pattern in V₁, points to a diagnosis of Brugada syndrome (Chapter 18, Fig. 18.1) (13). Finally, low-amplitude notching early in the ST segment of the right precordial leads, with associated T-wave inversions, suggests a diagnosis of arrhythmogenic right ventricular dysplasia (13).

If the history, physical examination, or ECG raises any question about possible cardiac pathology, an echocardiogram can be very useful in ruling in or ruling out overt structural heart disease. For several decades, a widely held belief has existed in some association between mitral valve prolapse and various cardiac symptoms, including palpitations. According to more recent echocardiographic observations, however, the prevalence of this valvular abnormality in a community-based population is low (1% to 2% range), and frequencies of various cardiac symptoms and arrhythmias are no different from those found in individuals without evidence of mitral valve prolapse (14). Thus, except perhaps in patients with significant attendant mitral regurgitation, mitral valve prolapse, per se, should not be considered a likely explanation for palpitations.