Palpitations
Palpitations are disconcerting and often incite fear, although most cases seen in the office occur among persons with no serious underlying heart disease. The patient with palpitations reports a disquieting awareness of one’s heartbeat, which may be described as a pounding, racing, skipping, flopping, or fluttering sensation. The primary physician must be able to differentiate the high-risk person in need of an intensive evaluation from the low-risk individual who can be reassured after a screening assessment. Ambulatory monitoring techniques and electrophysiological study have improved detection of arrhythmias; their indications and limitations need to be understood.
Most healthy individuals are unaware of their resting heartbeat. Sudden change in rate or rhythm, increase in stroke volume or contractility, and unusual cardiac movement within the thorax may cause awareness of the heartbeat. Acute changes in heart rate or rhythm may be noted, but chronic dysrhythmias often go unnoticed. Patients with depression and other somatization disorders have excessive health concerns and a heightened awareness of normal bodily sensations that can make even the normally imperceptible heartbeat of daily life an unpleasant experience that they report as palpitations. For most other patients, palpitations represent an acute disturbance of the heartbeat.
Premature Atrial or Ventricular Contractions. Awareness of a premature beat derives from the pause and vigorous beat that follows the premature contraction. The delay allows for prolonged ventricular filling, which triggers an increase in contractility and stroke volume. The excessive motion of the heart may be felt as a “turning over” or “flopping.” The sensations are isolated and tend to be most noticeable when the heart rate is slow and the patient is lying in bed supine or in the left lateral decubitus position. If there is atrioventricular dissociation and atrial contraction against a closed arterioventricular valve (as may occur in ventricular premature contractions), then a “pounding in the neck” or a sudden bulging of the neck veins (jugular cannon venous A waves) may be the presentation. Some patients with frequent jugular cannon A waves may report inability to catch one’s breath, although they deny frank dyspnea.
In the absence of underlying heart disease, ventricular premature beats (even when frequent or complex) have no adverse effect on prognosis. Only in the context of heart disease does the presence of PVCs connote an unfavorable prognosis (see below). Similarly, atrial premature beats are harmless in the absence of heart disease, but may be a harbinger of more compromising atrial dysrhythmias when they occur in the setting of cardiac pathology.
Sinus Tachycardia. Excess adrenergic stimulation results in increased contractility and sinus tachycardia, which may present as palpitations with a fast regular rhythm. Onset can be abrupt; resolution is usually more gradual. A constant rapid pounding at rest is felt by patients with hyperkinetic states (e.g., fever, severe anemia, hyperthyroidism, anxiety, agitated depression) due to the catecholamine-induced increase in contractility and stroke volume. Patients with anxiety-induced palpitations often have an underlying panic disorder; typically, they have difficulty telling whether the palpitations or the anxiety came first. Unappreciated is the high frequency of other supraventricular dysrhythmias in this group of patients (see below). An uncommon variant of sinus tachycardia, inappropriate sinus tachycardia, is believed to represent a hypersensitivity to catecholamine stimulation. Hyperthyroidism may have a palpitation presentation similar to that of anxiety; it may also cause atrial fibrillation (see below). In rare instances, the source of adrenergic outpouring is a pheochromocytoma. Its incidence is less than 0.1%, with about half of cases presenting as paroxysms of palpitations, hypertension, perspiration, tremor, nervousness, and other signs of adrenergic stimulation. Episodes are often spontaneous in origin but may be triggered by emotion and thus mimic an anxiety attack. An insulin reaction can produce a similar clinical picture, driven by an outpouring of catecholamines. A regular rhythm without tachycardia is noted in cases of valvular disease accompanied by large stroke volumes, as in aortic regurgitation.
Supraventricular Tachycardias. Attacks of palpitations that are regular in rhythm and rapid in rate may also be due to paroxysmal supraventricular tachycardia (SVT), sometimes referred to as paroxysmal atrial tachycardia. There are two basic mechanisms. In atrioventricular nodal tachycardia, the most common SVT, there are two functionally distinct conduction pathways in the nodal area that enable a reentrant circuit to develop, producing ventricular response rates as high as 160 to 180 beats/min. If the atria in this rhythm disturbance are unaffected by the nodal rhythm disturbance, there can be arterioventricular nodal dissociation manifested as rapid regular pounding in the neck. The condition is considerably more common in women than men and occurs in a wide variety of patients, including those with normal hearts, sick-sinus syndrome, mitral valve prolapse and other forms of valvular disease, coronary artery disease, and cardiomyopathy. Onset may occur in the setting of emotional stress (e.g., panic attack). Some patients note that standing up after bending over may bring on an episode that can be terminated by lying down.
In the second form of SVT with a regular rhythm, atrioventricular reciprocating tachycardia, there is a large macrorentrant circuit that involves the atrium, the arterioventricular node, an accessory pathway (e.g., Bundle of Kent or James), and the ventricle. The preexcitation syndromes (so-called because of their short electrocardiographic PR intervals), Wolff-Parkinson-White (WPW) and Lown-Ganong-Lown, operate by the reciprocating mechanism. An electrocardiographic hallmark of WPW is the delta wave at the beginning of the QRS, indicative of aberrant conduction through the accessory bundle; the QRS may be widened considerably during a run of SVT and mimic a ventricular dysrhythmia, especially when WPW is complicated by a very rapid ventricular response rate, as in atrial flutter or atrial fibrillation (see below). Any SVT with a very rapid ventricular response rate may seriously compromise cardiac output in a patient with underlying heart disease and cause chest pain, dyspnea, profound weakness, or even loss of consciousness.
Onset of SVT is characteristically sudden and may be precipitated by excess alcohol, emotional upset, or strenuous exertion. Caffeinated beverages are less of a risk factor. SVTs may be initiated by the occurrence of premature beats that alter conduction in the normal pathway. Paroxysms cease when the conducting properties of the reentrant circuit are disturbed by changes in vagal tone, hence the report by patients of ability to terminate attacks by Valsalva. Resolution is typically abrupt. Syncope is uncommon, but may occur at the outset if the rate is very rapid and/or there is acute vasodilation.
Some of the conditions associated with SVT are responsible for other dysrhythmias as well. For example, almost half of patients with sick sinus syndrome experience heart block or marked bradycardia in addition to bouts of SVT.
Paroxysmal Atrial Fibrillation. Sudden onset of palpitations with an irregularly irregular rhythm and rapid rate typifies paroxysmal atrial fibrillation, which occurs in a host of settings including acute alcohol excess (“holiday heart”), infection, hyperthyroidism, sick-sinus syndrome, WPW syndrome, cardiomyopathy, and acute worsening of ischemia or congestive heart failure; the condition is also found among otherwise healthy young people (“lone” atrial fibrillation). High levels of circulating catecholamines may trigger atrial fibrillation, especially in someone with underlying organic heart disease. A common precipitant is exercise or the termination of exercise with its surge of vagal tone. Chronic atrial fibrillation usually does not produce palpitations. An irregularly irregular tachycardia may also be seen if there are runs of multifocal atrial tachycardia (MAT), which takes place in the context of severe pulmonary disease, particularly when there is an acute fall in PO2 or pH. Frequent atrial or ventricular premature contractions can lead to a similarly irregular rhythm and rapid rate.
Ventricular Tachycardia. Ventricular tachycardia is among the most worrisome of dysrhythmias related to palpitations, being associated in some instances with risk of sudden death. Nonetheless, not all ventricular tachycardia represents life-threatening disease. Nonsustained ventricular tachycardia (NSVT) may occur in otherwise normal persons (idiopathic ventricular tachycardia) and in those with underlying heart disease. In idiopathic disease, the ventricular arrhythmia most often arises from the right ventricular outflow tract; the heart appears structurally normal. Onset is typically in the second or third decades of life and may present as palpitations, near-syncope, or even true loss of consciousness. In normal subjects, NSVT is not associated with an increased risk of sudden death; however, any NSVT that compromises cardiac output may lead to dizziness, near syncope, or loss of consciousness.
More worrisome are runs of nonsustained or sustained ventricular tachycardia occurring in the context of underlying heart disease. Patients with such a presentation have an increased risk of sudden death, especially those with ischemia, prior myocardial infarction with scar formation, dilated cardiomyopathy, hypertensive heart disease with left ventricular remodeling, or hemodynamically significant valvular disease. The clinical picture may be dominated by manifestations of the underlying heart disease, but more subtle forms of heart disease (e.g., hypertrophic cardiomyopathy and prolonged QT syndrome) also may trigger ventricular tachycardia and result in sudden death.
Hypertrophic cardiomyopathy is a hereditary condition featuring asymmetric hypertrophy, right ventricular involvement, outflow tract obstruction, prominent septal Q waves in the anteroapical leads of the electrocardiogram (ECG), and a wall thickness on ultrasound of more than 13 mm. A characteristic finding on physical examination is a systolic ejection murmur along the left sternal border that increases with Valsalva and decreases with passive leg elevation.
Prolonged QT syndrome is a disorder of repolarization that increases susceptibility to potentially lethal polymorphic ventricular tachycardias (“torsades de pointes”). Hereditary and acquired forms have been described. In the hereditary form, there is a strong family history of sudden death below the age of 30 and congenital deafness. Ten-year mortality rates after onset of syncope approach 50%. Precipitants include severe emotional stress and very vigorous exercise. On ECG, prolongation of the QT interval, bradycardia, T-wave alternans, and notched T waves are characteristic. In the much more common acquired form, QT prolongation occurs as a result of medications or clinical conditions. Medications with this potential include the commonly used antihistamines such as terfenadine and astemizole, usually when taken in excess or concurrently with a drug that inhibits its metabolism (e.g., cimetidine) or causes QT prolongation itself (e.g., the macrolide antibiotics, ketoconazole, itraconazole). Other pharmacologic precipitants include the class IA antiarrhythmics (e.g., quinidine, procainamide, disopyramide), class III antiarrhythmics (e.g., sotalol), tricyclic antidepressants, and phenothiazines. Clinical conditions that prolong the QT interval include hypokalemia, hypomagnesemia, hypocalcemia, hypothyroidism, starvation and liquid protein diets.
Patients with underlying heart disease have a lowered threshold for ventricular tachycardia. In addition to the factors associated with prolonged QT interval, digitalis toxicity is an important precipitant of ventricular tachycardia. Digitalis toxicity is associated with ventricular tachycardia, atrial fibrillation, ventricular bigeminy, and junctional tachycardias. Concurrent hypokalemia and hypomagnesemia lower the threshold for development of “dig-toxic” rhythm disturbances. The methylxanthines (e.g., theophylline) have a narrow therapeutic range, which when exceeded increases the risk of serious rhythm disturbances, including ventricular tachycardia, especially in persons with underlying heart disease.
Although determining the nature of the heartbeat disturbance helps to identify etiology and prognosis, the key determinant of prognosis is the presence, type, and severity of underlying heart disease. Consequently, a search for cardiac pathology is a high priority.
History. Eliciting a complete description of the patient’s palpitations is essential, including its mode of onset, frequency, rate, rhythm, duration, termination, associated symptoms, and precipitants and alleviating factors. Unfortunately, many patients are unable to give an accurate or detailed account of their symptoms. The relation of the onset of symptoms to exertion can aid in separating the anxious individual, whose symptoms may occur at rest and are usually not worsened by exertion, from the patient with heart disease and impaired exercise tolerance. Identification of precipitants such as emotional upset, stimulant intake, fever, pregnancy, volume depletion, and severe anemia is essential, because their recognition can contribute to design of proper therapy. Inquiry into symptoms of an insulin reaction and hyperthyroidism may also prove productive.
The more hypochondriacal or somatizing the patient, the poorer the correlation between symptoms and Holter monitoring results; however, reports of fluttering, stopping, or beating irregularly are predictive of finding an arrhythmia. Any isolated thumping or flip-flopping in the chest suggests an atrial or ventricular premature beat. Associated pounding in the neck is indicative of arterioventricular dissociation, as seen with ventricular premature beats or arterioventricular nodal tachycardia. Sudden onset and sudden cessation of rapid regular heartbeats are characteristic of nodal and reentrant SVT and NSVT, whereas more gradual onset and cessation characterize sinus tachycardia. Palpitations brought on by exercise or emotional stress point to idiopathic ventricular tachycardia, atrial fibrillation, other SVTs, prolonged QT interval, and inappropriate sinus tachycardia. Onset in conjunction with a panic attack is indicative not only of sinus tachycardia but also of nodal reentrant tachycardia, as is onset with standing up after bending over and cessation with lying down.
Inquiries into concurrent dyspnea, chest pain, lightheadedness, near-syncope, and syncope are essential both for etiology and assessment of hemodynamic severity. Syncope suggests ventricular tachycardia or a very fast SVT with vasodilatation. Chest pain and dyspnea may also be signs of marked hemodynamic compromise. Additionally useful are questions about risk factors for coronary disease (smoking, diabetes, hypertension, hyperlipidemia, positive family history of early onset syncope or sudden death before age 30) and prior cardiac history (heart murmur, rheumatic fever, myocardial infarction, other forms of cardiac illness, family history of heart disease). Although one should not mistake symptoms of anxiety, such as chest tightness and air hunger at rest, for evidence of organic heart disease, the presence of anxiety symptoms does not rule out an arterioventricular nodal tachycardia. Nonetheless, assessment is not complete without specific inquiry into symptoms of panic and somatization disorders.
Use of all cardiotonic drugs should be detailed, including antiarrhythmics, digitalis preparations, theophylline compounds, sympathomimetics, and anticholinergics. Also to review are drugs associated with QT prolongation: antiarrhythmics, terfenadine, astemizole, macrolide antibiotics, ketoconazole, itraconazole, phenothiazines, and tricyclic antidepressants. Many over-the-counter decongestants and diet pills contain catecholamines or theophylline derivatives; their abuse may be responsible for symptoms. The history should include inquiry into alcohol abuse, a common precipitant of paroxysmal SVT. Family history of early-onset syncope can be a clue to hereditary prolonged QT syndrome or hypertrophic cardiomyopathy.
Physical Examination. Important observations include determination of the blood pressure for elevation, marked postural change, and widened pulse pressure. The apical pulse is noted for rate and rhythm disturbances; relying on the peripheral pulse may be misleading when there is a pulse deficit, as occurs in atrial fibrillation or premature beats. The temperature should be recorded. The skin is examined for pallor and signs of hyperthyroidism and anemia; the eyes for exophthalmos; the neck for goiter; the carotid pulse for upstroke; the jugular venous pulse for distention and cannon A waves; the chest for rales, rhonchi, wheezes, and dullness; the heart for heaves, thrills, clicks, murmurs, rubs, and third heart sound; and extremities for edema and calf tenderness. The finding of a systolic ejection murmur along the left sternal border should be followed by examining its response to Valsalva maneuver; an increase in intensity suggests hypertrophic cardiomyopathy. Response to modest exercise should also be noted, because a number of dysrhythmias may be triggered by it. Finally, the mental status examination should include checking for manifestations of anxiety, depression, panic disorder, and substance abuse. In addition to possibly providing important diagnostic information, the careful unhurried physical examination can be of considerable use in reassuring the worried patient.