The evaluationand management of palpitations

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THE EVALUATION AND MANAGEMENT OF PALPITATIONS Elizabeth R. Keeler, MD, Robert K. Morris, Jr., MD, Dolar S. Patolia, MD, and Eugene C. Toy, MD

Palpitations, defined as an awareness of one’s heartbeat, is a common complaint, reported by up to 16% of patients during physician office visits. Although palpitations may be indicative of worrisome arrhythmias and sudden cardiac death, they are usually associated with benign etiologies. A systematic approach with a detailed history and physical examination, an electrocardiogram, and selective testing will reveal the etiology in over 80% of cases. Palpitations associated with chest pain, dyspnea, syncope, or cardiac disease are worrisome. Thus, as a primary care physician, the obstetrician/ gynecologist must be skilled in detecting cardiac pathology and proficient in the evaluation and management of palpitations. (Prim Care Update Ob/Gyns 2002; 9:199 –205. © 2002 Elsevier Science Inc. All rights reserved.)

ten inciting anxiety, palpitations are rarely associated with malignant cardiac arrhythmias. These sensations may be a manifestation of a change in cardiac rhythm or rate or simply a change in the force of the heart’s contraction. Palpitations may be associated with worrisome arrhythmias, but unfortunately, there is no single consistent indicator of pathology.3 Therefore, it is crucial for the obstetriciangynecologist, as a primary care physician, to be proficient in the differential diagnosis, work-up, and treatment of palpitations.

Palpitations, or “an awareness of one’s heartbeat,” is a common complaint reported by up to 16% of patients asked during office visits.1 Patients describe these palpitations as uncomfortable “chest pounding,” “fluttering,” “stopping,” “skipping,” “irregular,” or “rapid” heartbeats. Furthermore, up to one third of affected individuals report accomplishing less work in the home, impaired productivity, and/or missed work.2 Although of-

CARDIAC ARRHYTHMIAS

From the Obstetrics & Gynecology Residency Training Program, CHRISTUS St. Joseph Hospital/CTMF Brackenridge Hospital–Austin, Houston, Texas.

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Differential Diagnosis There are a variety of mechanisms that produce perceived palpitations, including cardiac arrhythmias, psychiatric disorders, medications, and catecholamine stimulation.1

The primary goal when evaluating individuals with palpitations is to uncover an underlying arrhythmia, that is, a cardiac rhythm that deviates from the normal sinus rhythm. Cardiac arrhythmias are due to faulty formation and/or conduction of the cardiac impulse. Twentyfour– hour ambulatory electrocardiac monitoring of patients with palpitations reveals that a disturbance in cardiac rhythm occurs in 39 – 85% of patients; however, only 15% of the arrhythmias seem to correlate with the symptoms of spe-

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cific palpitations.1 One investigator showed that palpitations were twice as likely to be associated with cardiac arrhythmias if the patients reported that the palpitations occurred regularly.4 NORMAL CARDIAC CONDUCTION. Normal sinus rhythm is characterized by the spontaneous electrical discharge of the sinoatrial (SA) node, which conducts the electrical impulse from the right atrial wall to the atrioventricular (AV) node (located between the atria and the ventricles), and then to the ventricles. Electrical conduction is accomplished by depolarization of each myocardial cell, whereupon the cell enters an absolute refractory period and cannot be excitable. Once the entire myocardium is depolarized, the impulse cannot propagate further, and therefore dies out. The next cardiac cycle begins with the impulse generated in the SA node and the process repeats itself.5 TYPES OF ARRHYTHMIAS. Arrhythmias are divided into categories based on the location of origin. Supraventricular arrhythmias are due to faulty impulse formation in the upper part of the heart, above the bifurcation of the bundle of His. In contrast, ventricular arrhythmias are characterized by electrical charges originating distal to the bifurcation of the bundle of His (i.e., in the Purkinje fibers or in the non– conduction–specific myocardium of the ventricle). All tachyarrythmias are dependent on three electrophysiological mechanisms:

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1) automatism, 2) triggered activity, and 3) reentry. Of note, the same cardiac pathology can result in a variety of arrhythmias, and one type of specific arrhythmia can be caused by several different types of cardiac pathologies.5,6 PREMATURE ATRIAL OR VENTRICULAR CONTRACTIONS. Premature ventricular contractions (PVCs) are commonly found in patients with and without palpitations. In fact, 40 –75% of normal healthy persons studied for 24 – 48 hours with continuous ambulatory monitoring have documented PVCs. Ectopic foci in the atria or ventricles are primary causes of premature contractions. After a premature contraction, there is typically a pause before the onset of the next cardiac cycle, which allows for prolonged ventricular filling. This triggers an increase in the contractility and stroke volume, resulting in the awareness of one’s heartbeat or palpitation. The sensation is usually isolated and is more noticeable when the heart rate is slow. If the atria contract against a closed valve, then the patient often experiences a bulging of the neck veins associated with an inability to catch one’s breath. In the absence of underlying cardiac disease, PVCs have no adverse effect or prognosis, and atrial premature beats, too, are harmless without cardiac pathology.6,7 SUPRAVENTRICULAR TACHYCARDIAS. A supraventricular tachycardia (SVT) is characterized by a regular rhythm with a rapid rate, and is often associated with palpitations. The two most common types of SVTs are atrioventricular (AV) nodal tachycardia and AV-reciprocating tachycardia. AV nodal tachycardia occurs when two functionally distinct pathways enable a reentrant circuit to develop in the AV node, producing ventricular rates of 160 –180 beats/min. If there is AV dissociation, the patient will report a pounding sensation in the neck be-

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cause the atria are pumping against closed AV valves, causing a reflux of blood to the jugular veins. This condition is more common in women than in men and is associated with sick sinus syndrome, mitral valve prolapse and other valvular disease, coronary artery disease, and cardiomyopathy.1,6,7 In AV-reciprocating tachycardia, there is a large reentrant circuit involving the atria, the AV node, and an accessory pathway. WolffParkinson-White (WPW) syndrome is a type of AV reciprocating tachycardia, and it is complicated by a very rapid ventricular response rate. Because of the potential for decreased cardiac output by the shortening of the ventricular filling time, these arrhythmias are potentially dangerous. Affected patients will frequently report chest pain, weakness, and syncope. Of note, these individuals can often arrest the paroxysmal beats with a Valsalva maneuver, because the increased vagal tone may affect the conducting properties of the reentrant circuit.1,6 – 8 PAROXYSMAL ATRIAL FIBRILLATION.

Paroxysmal atrial fibrillation is associated with an irregularly irregular rhythm and a rapid ventricular rate. This condition can occur in young healthy individuals (“lone” atrial fibrillation), or in association with acute alcohol excess, infection, hyperthyroidism, sick sinus syndrome, cardiomyopathy, ischemia, WPW syndrome, or congestive heart failure. In patients with underlying heart disease, triggers for atrial fibrillation include increased catecholamines (such as during exercise) or the increase of vagal tone (immediately after exercise).6,7

VENTRICULAR TACHYCARDIA.

Ventricular tachycardia, because of its association with sudden cardiac death, is generally the most worrisome of all causes of palpitations. However, not all types of ventricular tachycardias are associated with life-

threatening disease. In nonsustained ventricular tachycardia, onset is usually from the left ventricular outflow tract, and the heart is usually normal. This type of arrhythmia usually presents in the 2nd or 3rd decades of life as palpitations, near-syncope, or syncope. Nonsustained ventricular tachycardia occurring in patients with normal cardiac status is not associated with an increased risk of sudden death.1,6 Ventricular tachycardia occurring in individuals with underlying heart disease is associated with sudden cardiac death. Those at greatest risk have ischemia, prior myocardial infarction, dilated cardiomyopathy, hypertension-associated heart disease with left ventricular enlargement, or hemodynamically significant valvular disease.7 Two particularly worrisome heart conditions are hypertrophic cardiomyopathy and the prolonged QT syndrome. Hypertrophic cardiomyopathy is a hereditary condition associated with asymptomatic hypertrophy, right ventricular involvement, outflow tract obstruction, and a wall thickness of ⱖ13 mm on ultrasound. The electrocardiogram shows prominent septal Q waves in the anterior-apical leads. On physical exam, there is often a systolic ejection murmur along the left sternal border that intensifies with the Valsalva maneuver and decreases with passive leg elevation. Hypertrophic cardiomyopathy is worrisome, because syncope and sudden death have been associated with competitive sports and exertion.1,2,6 PROLONGED QT SYNDROME.

Prolonged QT syndrome is a disorder of abnormal length of time for repolarization, leading to an increased susceptibility to lethal ventricular tachycardia, especially torsades de pointes. The hereditary form is characterized by a strong family history of sudden death at an age of Prim Care Update Ob/Gyns

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cerns and heightened awareness of normal body sensations that can make even the normal imperceptible heartbeat of daily life an unpleasant experience. Individuals who somatize and have more health-related anxiety, or have more psychiatric distress, are significantly less likely to have demonstrable cardiac arrhythmias than are other patients who have palpitations.8 One study shows that palpitations in a patient with psychiatric disorder were more likely to last longer than 15 minutes and were accompanied by other psychosomatic symptoms.3 Furthermore, several medications ingested by patients with psychiatric disorders can produce arrhythmias, including phenothiazines and tricyclic antidepressants.2,3,8 Figure 1. Prolonged QT interval. The QT interval depicted in lead II is prolonged, measuring 480 ms (A). The same patient developed spontaneous supraventricular tachycardia, with a heart rate of 180 bpm (B).

⬍30 years and congenital deafness. Up to one half of affected individuals will die within 10 years after a syncopal episode.6 This fatal syndrome is precipitated by severe emotional stress and vigorous exercise (see Figure 1). On the EKG, there is typically QT interval prolongation (⬎0.46 seconds in men and ⬎0.47 seconds in women), bradycardia, T-wave alterations, and notched T waves. Acquired prolonged QT syndrome is more common and is usually a result of medications or clinical conditions. Commonly used antihistamines (like terfenadine and astemizole), usually when taken in excess or with a drug that inhibits their metabolism or causes QT prolongation itself, have this potential. Hypokalemia, hypomagnesemia, hypocalcemia, hypothyroidism, starvation, and liquid protein diets may also produce this potentially deadly arrhythmia (see Table 1).5–7 Volume 9, Number 6, 2002

PSYCHIATRIC DISORDERS Approximately one third of palpitations are due to psychiatric disorders, the most common being panic disorder, generalized anxiety disorder, somatization, and depression.2 Patients with psychiatric disorders often have excessive health con-

Table 1. Etiologies of Prolonged QT Interval5 Antiarrhythmics Quinidine Procainamide Disopyramide Sotalol Psychoactive drugs Phenothiazines Tricyclic antidepressants Antihistamines Terfenadine Astemazole Metabolic causes Hypokalemia Hypomagnesemia Liquid protein diet Hypothyroidism

MEDICATIONS AND ILLICIT SUBSTANCES Caffeine, by inducing tachycardia or arrhythmias, is a commonly cited causative agent of palpitations. Though not well understood, some theories about caffeine-induced palpitations include the following: increased cytosolic calcium concentration by blocking the uptake of calcium into the sarcoplasmic reticulum; inhibition of phosphodiesterase, resulting in a sympathomimetic-like effect; and adenosine receptor antagonistic effect, disrupting cardiac regulation.9 Electrophysiologic clinical studies have not consistently shown cardiac arrhythmias with moderate doses of caffeine (300 mg/d), equivalent to about three cups of coffee or tea. Several randomized controlled studies indicate that moderate ingestion of caffeine does not increase the frequency or severity of ventricular arrhythmias in healthy patients, patients with ischemic heart disease, or those with preexisting serious ventricular ectopy. The effects of higher amounts of caffeine 201

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(900 mg/d) are still being investigated.9 Other stimulants such as cocaine or amphetamines may trigger palpitations. Cocaine causes sympathetic stimulation, hypertension, tachypnea, mydriasis, and tachycardia and may produce lethal arrhythmias. Amphetamine intoxication is characterized by hyperactivity, irritability, delirium, vomiting, diarrhea, mydriasis, and hypertension and may also lead to dysrrhythmias. Finally, ma huang is a dietary supplement containing ephedra alkaloids that is used as a weight reduction agent and energy booster; it has been clinically shown to cause palpitations in ⬎10% of its users.10

CATECHOLAMINE STIMULATION Excessive adrenergic stimulation results in increased contractility and sinus tachycardia. Often the onset is abrupt, with a gradual resolution. Increased catecholamine states are associated with fever, severe anemia, hyperthyroidism, anxiety, and pheochromocytomas.6

Palpitations in Women Palpitations are more commonly reported by women, and hormones likely play a large role. Plasma-level ovarian hormones exhibit a cyclical variation and may be associated with changes in catecholamine and adrenergic activity. In addition, estradiol has been found to have a calcium-antagonistic effect in isolated myocytes. During the follicular phase of the menstrual cycle, estradiol levels are increased, which may be cardioprotective against arrhythmias. During the secretory phase, plasma estradiol levels fall, and this effect is lost. Although little is known about the cardiac effects of progesterone, because progesterone generally counteracts the effects of estrogen, some investigators have assumed that 202

progesterone has a pro-arrhythmogenic effect upon the heart.11

PALPITATIONS DURING THE MENSTRUAL CYCLE A small study of 26 women reporting palpitations who were diagnosed with paroxysmal SVT noted an increase in symptoms and duration of palpitations on day 28 of the cycle as compared with days 7 and 14. Furthermore, serum progesterone levels seem to correlate with the number and duration of paroxysmal SVT, whereas higher serum estradiol levels are associated with fewer arrhythmias. Direct ovarian hormone effect or increased sympathetic activity during the luteal phase are speculated mechanisms. More research is needed in this area.11

PALPITATIONS

AND

PREGNANCY

Pregnancy is associated with many hemodynamic changes, including a 30 –50% increase in cardiac output. The increased cardiac output in the first trimester is a result of the augmented stroke volume, due in part to the decreased vascular resistance. Later in pregnancy, the stroke volume continues to increase because of the increased diastolic filling time. Malignant arrhythmias during the course of normal gestation are rare. Some investigators have suggested that pregnancy is arrhythmogenic; however, many patients report that their palpitations improve with pregnancy. The antiarrhythmic effects may be due to the increased plasma levels of estrogen and their calcium antagonistic effect. Nevertheless, an increased incidence of SVT is generally observed during pregnancy.11 In women without underlying heart disease, these palpitations may be due to sinus tachycardia and related to cardiac adaptations of reduced peripheral vascular resistance. Episodes of SVT may be related to the mechanical effect of the fetus push-

ing up on the mother’s diaphragm, causing mechanically stimulated tachyarrhythmias. Pregnant women with organic heart disease usually have arrhythmias because of the increased hemodynamic burden of pregnancy, and these may be the first manifestation of heart disease.12 Obviously, in patients with underlying heart disease and limited myocardial reserve, the increased burden on the heart with the hemodynamic changes of pregnancy can affect both fetal and maternal well-being.11,12

PALPITATIONS IN THE PERIMENOPAUSAL AND MENOPAUSAL PERIODS Palpitations associated with menopause and the perimenopausal period are usually related to sinus tachycardia or to simple arrhythmias because of increased sympathetic drive. The menopausal state is characterized by a marked decrease in ovarian estradiol production and an associated increase in adrenergic activity. In menopausal women, cardiovascular control shifts toward a sympathetic predominance. Estrogen replacement therapy improves this altered control and can improve the cardiovascular symptoms such as hot flushes and palpitations. Of note, some progestins given in conjunction with estrogen replacement may trigger cardiac arrhythmias in patients; however, this effect is usually remedied by decreasing the progestin dose or by using a natural progestational agent.11

Evaluation of Palpitations The primary goals in the evaluation of palpitations are to establish an etiology and to exclude the possibility of a life-threatening arrhythmia. This can usually be accomplished with a thorough history. In Prim Care Update Ob/Gyns

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one study of 190 patients complaining of palpitations, investigators found that an etiology was established in 84% of the cohort.3

HISTORY Because the palpitations nearly always have ceased by the time that the patient is being evaluated in the office, the history plays a vital role in establishing the etiology. The physician needs to elicit characteristics such as duration, regularity versus irregularity, radiation to the neck, exacerbating factors, and alleviating factors. Certain arrhythmias have distinct presentations. Rapid, regular palpitations that pound into the neck describe AVnodal tachycardia. Fast, regular palpitations that do not radiate to the neck indicate atrial tachycardia, ventricular tachycardia, and arrhythmias associated with accessory pathways. Rapid, irregular palpitations are characteristic of atrial fibrillation, atrial tachycardia, and atrial flutter. Slow, regular palpitations fluttering to the neck region suggest ventricular premature beats, whereas slow, regular palpitations without sensation in the neck are more characteristic of nonspecific premature beats.1,6,7,13 The speed of onset and cessation are important, because an abrupt onset suggests paroxysmal abnormal tachycardia, whereas paroxysmal SVT or VT may be more progressive. Although there are many exceptions, an abrupt ending to a palpitation usually indicates a pathological etiology, whereas a more gradual resolution suggests a nonworrisome sinus tachycardia.1,2,6,7 Questions should assess for symptoms of pheochromocytoma, such as headache, sweating, flushing, anxiety, nausea, fatigue, and weight loss. Questions relating to thyroid dysfunction should be asked such as anxiety, emotional lability, heat intolerance, weight Volume 9, Number 6, 2002

loss, and proximal muscle weakness.6,7 The patient should be asked about symptoms that may point to an anxiety disorder, such as intense feelings of doom or fear; fear of death; or sweating, nausea, numbness, or a tingling sensation. Anxiety-related etiologies should be considered when symptoms develop abruptly and reach a peak within 10 minutes. Depressive symptoms should also be elicited by asking about feelings of sadness, hopelessness, and/or misery and about sleep or appetite disorders. These types of questions will help the physician distinguish between a psychiatric disorder and a physiologic disorder.2,3,11 Perhaps the most important aspect of the history is the presence of associated symptoms. Palpitations are more likely to reflect a serious arrhythmia if they are associated with hemodynamic compromise like syncope, lightheadedness, dizziness, or shortness of breath. It has been well established that syncope in patients with ventricular arrhythmias carries a poor prognosis. Chest pain and the presence of congestive heart failure also are worrisome symptoms.1– 8 The patient’s medical history should be obtained, with care to note preexisting coronary artery disease, cardiac structural abnormalities, thyroid disorders, and psychiatric disorders. A list of medications, both prescribed and over-the-counter, is mandatory. The patient should be asked in a nonjudgmental manner about illicit drug and alcohol use, because these agents may be the sole trigger of the palpitations. A family history should also be obtained, noting family members with heart disease, cardiomyopathy, pheochromocytoma, or sudden cardiac death.1–3,5–7 Information about the initiating factors, frequency of episodes, effects on the quality of life, and success of previous treatment are

also important parts of the history because they can assist in guiding the treatment. Finally, any previous electrocardiographic or echocardiographic examination must be vigorously sought.

THE PHYSICAL EXAM Even if the physician is not fortunate enough to examine a patient experiencing palpitations during the actual office visit, the cardiovascular exam is invaluable. The blood pressure must be obtained to determine elevation, marked postural changes, and a widened pulse pressure. The pulse should be determined apically because arrhythmias may cause a discrepancy between the peripheral pulse and the heart rate. The arterial and jugular pulses should also be noted.6,7 Heart sounds can provide clues to the presence of atrial flutter, atrial fibrillation, or underlying valvular disease. The cardiac exam should be done in a quiet room, and attention should focus on the presence of murmurs and on location within the phase of the cardiac cycle. There are several murmurs that a primary care physician should be able to identify. The murmur of pulmonary stenosis and hypertrophic obstructive cardiomyopathy (HOCM) are both harsh systolic crescendo– decrescendo murmurs. Holosystolic murmurs include mitral regurgitation, tricuspid regurgitation, and ventricular septal defects. The murmur of mitral valve prolapse (MVP) occurs late in systole, often preceded by a nonejection click. A diastolic decrescendo murmur is typical of pulmonic or aortic regurgitation. With mitral stenosis, auscultation reveals a mid-diastolic murmur that is associated with an opening snap. The continuous “machinery-like murmur” is nearly diagnostic of patent ductus arteriosus.5–7 The cardiac examination should be performed with the patient in 203

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various positions. The patient should be asked to breathe deeply since left-sided murmurs tend to become louder with expiration. The Valsalva maneuver will cause most murmurs to decrease in length and intensity; however, the murmurs associated with MVP and hypertrophic obstructive cardiomyopathy usually become louder. The patient should be placed in the left lateral decubitus and then the sitting positions. The standing position again will accentuate the murmurs of HOCM and MVP, whereas squatting will cause other murmurs such as mitral regurgitation to become louder.5–7 The head and neck examination should include inspection of the nasal septum to detect erosions possibly caused by cocaine use. The thyroid gland should be palpated for a goiter, masses, or nodules. The presence of proptosis, hyperreflexia, or a fine tremor should be sought. In addition, a thorough yet efficient mental status exam should be performed. This valuable exam provides an assessment about the patient’s attention span, orientation, memory, insight, and judgment. The patient is asked his or her name, the current date, and present location to establish orientation. A patient’s concentration can be assessed by having the patient serially subtract numbers, such as 7 from 100, then 7 from 93, then 7 from 86, and so on. Immediate recall is tested by asking the patient to remember three distinct objects and having the patient repeat them within 5 minutes. Remote memory can be evaluated by having the patient recount the history of the palpitations or the names of some famous historical figures. Finally, the patient should be asked to interpret proverbs such as, “People who live in glass houses shouldn’t throw stones” to assess insight and abstract thinking. Patients with anxiety or depressive disorders are less likely able to maintain concentration, and their 204

short-term memory will likely also be affected. The remainder of the mental status exam should be normal in these patients.1–7

LABORATORY EVALUATION A few basic hematological and chemistry studies should be performed to assess for anemia, hyperthyroidism, electrolyte disturbances (especially in patients taking digitalis), and hypoglycemia. If there is evidence suggesting a pheochromocytoma, a 24-hour urine assessment for vanillylmandelic acid is helpful.1,2,4,5–7 All patients complaining of palpitations should have an electrocardiogram to distinguish supraventricular from ventricular tachycardias and to help to identify the type of SVT during the arrhythmia. Regular tachycardia with a narrow QRS complex is associated with accessory pathway arrhythmias, AV-nodal reentrant tachycardia, atrial tachycardia or atrial flutter. Regular tachycardia with wide QRS complex characterizes right or left bundle branch block or ventricular tachycardia. SVT conducted to ventricles in a variable way (atrial flutter, atrial tachycardia, and most commonly atrial fibrillation) or VT with an irregular rate creates an irregular tachycardia with a narrow or wide QRS complex. A normal ECG at rest does not exclude an arrhythmia. The patient may still have idiopathic VT or SVT (intranodal tachycardia or a concealed accessory pathway).1–7 If the history, physical examination, and a 12-lead electrocardiogram fail to point to an etiology of the palpitations, further investigation should be performed. If palpitations occur on a daily basis, 24-hour continuous ambulatory electrocardiographic monitoring may be helpful. The patient is instructed to keep a log of the daily activities and note the occurrences of palpitations. The rhythm record

is then analyzed. The Holter monitor is not very helpful unless symptoms are frequent.14 If symptoms occur less frequently, several investigators support using an event recorder to decrease cost and increase findings.15 The device is given to the patient for approximately 30 days; the patient applies the leads to her chest during the symptoms, and the cardiac rhythm is recorded. The recording is then transmitted over the telephone for interpretation. Several studies have found that in general, symptoms of palpitations do not seem to correlate with arrhythmias.1– 6 When palpitations are associated with exertion, an exercise stress testing should be done because ventricular tachycardia may be uncovered, even though they may not appear on Holter monitors or event recorders. An echocardiogram should be done when the history, physical exam, or EKG raise suspicion of valvular disease or cardiomyopathy. Electrophysiological studies (EPS), either via the transesophageal or intracavitary route, are able to identify some arrhythmias. Because this technique is invasive, EPS should be limited to individuals who have asymptomatic nonsustained VT and either evidence of underlying heart disease or a reduced ejection fraction (⬍40%).1

Management The majority of patients who complain of palpitations have no arrhythmia. These individuals should be reassured that their symptoms are not associated with an increased mortality. Other conditions associated with a low risk for sudden death include asymptomatic atrial ectopy and unsustained SVT, asymptomatic ventricular ectopy that is not associated with VT, simple ventricular ectopy in the setting of an acute myocardial infarction, asymptomatic unsustained VT in the Prim Care Update Ob/Gyns

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absence of heart disease, asymptomatic patients with WPW syndrome, and mildly symptomatic patients with simple atrial or ventricular ectopy. These patients should be instructed, however, to be aware of any worrisome accompanying symptoms such as chest pain, syncope, and shortness of breath, and to return if any of these symptoms occur.1,6,11 Implantation of a cardioverterdefibrillator is believed to be the best therapeutic approach for patients with life-threatening ventricular dysrrhythmias, such as those patients with prolonged QT syndrome, or patients with ventricular tachycardia and underlying cardiac disease. A right ventricular lead senses and identifies the cardiac rhythm and sends out a small but adequate electrical shock when an aberrant rhythm is detected. Small studies have shown that the use of these defibrillators leads to a 25% reduction in the relative risk and a 7% reduction in the absolute risk of cardiac or sudden death.6 Medical therapy includes betablockers and anti-arrhythmic drugs. Beta-blockers increase the fibrillatory threshold and decrease the risk of ventricular fibrillation and sudden death. The frequency of PVCs or premature atrial contractions is reduced with beta-blockers such as atenolol, with doses as small as 20 –50 mg/d. When a defibrillator is warranted, beta-blockers are usually prescribed as adjuvant therapy. Anti-arrhythmic drugs are used in patients who present with sustained VT or prior ventricular fibrillation arrest who refuse or cannot receive defibrillator implantation. However, anti-arrhythmic drugs have proven to be disappointing, producing only a slight reduction in mortality in patients with lethal arrhythmias; therefore, the therapy of choice for patients with malignant arrhythmias remains the cardioverter-defibrillator.1,6,7,11 The prognosis for patients reporting palpitations is generally excelVolume 9, Number 6, 2002

lent, with the 1-year mortality rate being only 1%. Because ⱕ75% of individuals report recurrent palpitations, they must be monitored carefully.1

5.

Referral Individuals with underlying cardiac disease and those with palpitations associated with syncope, nearsyncope, chest pain, or dyspnea should be referred to a specialist, usually a cardiologist. Additionally, the patient with a seemingly benign etiology, but worsening symptoms after conservative therapy of 4 to 8 weeks, should also be referred.1–7

8.

Conclusion

9.

Heart palpitations are a common complaint, occurring more frequently in women and affected by pregnancy, hormonal changes, and the menopause. The etiologies are numerous, yet identification of lifethreatening arrhythmias may increase survival. Palpitations are a source of anxiety and distress for many patients. Although most palpitations have a benign etiology, the obstetrician/gynecologist must be skilled in identifying the prolonged QT syndrome on electrocardiogram and be able to perform an accurate cardiac examination. With these tools, as a primary care physician, the obstetrician/gynecologist would be well positioned to evaluate, treat, and monitor patients with palpitations. References 1. Weitz HH, Weinstock PJ. Approach to patient with palpitations. Med Clin North Am 1995;79:449 –56. 2. Weber BE, Kapoor WN. Evaluation and outcomes of patients with palpitations. Am J Med 1996;100:138 – 48. 3. Barsky AJ, Clearly PD, Barnett MC, et al. The accuracy of symptoms reporting by patients complaining of palpitations. Am J Med 1994;97: 214 –21. 4. Summerton N, Mann S, Rigby A,

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Petkar S, Dhawan J. New-onset palpitations in general practice: assessing the discriminant value of items within the clinical history. Fam Pract 2001;18:383–92. Goldberger AL. Electrocardiography. In Braunwald E, Fauci AS, Kasper DL, eds. Harrison’s principles of internal medicine. 15th ed. New York: McGraw-Hill, 2001: 1262–71. Goroll AH. Evaluation of palpitations. In Goroll AH, Mulley AG, eds. Primary care medicine. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 2000:141–9. Lee TH. Chest discomfort and palpitations. In Braunwald E, Fauci AS, Kasper DL, eds. Harrison’s principles of internal medicine. 15th ed. New York: McGraw-Hill, 2001:60 –6. Barsky AJ. Palpitations, arrhythmias, and awareness of cardiac activity. Ann Intern Med 2001;134: 832–7. Myers MG. Caffeine and cardiac arrhythmias. Ann Intern Med 1991; 114:147–50. Haller CA, Benowitz NL. Adverse cardiovascular and central nervous system events associated with dietary supplements containing ephedra alkaloids. N Engl J Med 2000; 343:1833–88. Rosano GM, Rillo M, Leonardo F, Pappone C, Chierchia SL. Palpitations: what is the mechanism, and when should we treat them? Int J Fertil Womens Med 1997;42:94 – 100. Rotmensch HH, Rotmensch S, Elkayam U. Management of cardiac arrhythmias during pregnancy. Current concepts. Drugs 1987;33:623– 33. Brugada P, Gursoy S, Brugada J, Andries E. Investigation of palpitations. Lancet 1993;341:1254 –8. DiMarco JP, Philbrick JT. Use of ambulatory electrocardiographic (Holter) monitoring. Ann Intern Med 1990;113:53–68. Kinlay S, Leitch JW, Neil A, et al. Cardiac event recorders yield more diagnoses and are more cost-effective than 48-hour Holter monitoring in patients with palpitations: a controlled clinical trial. Ann Intern Med 1996;124:16 –20.

Address correspondence and reprint requests to Eugene C. Toy, MD, CHRISTUS St. Joseph Hospital, 1819 Crawford Street, Suite 1708, Houston, TX 77002. 205