Although described by patients in a myriad of ways, guiding the patient through a careful description of their palpitations may indicate a mechanism and narrow the differential diagnosis. Pertinent questions include the age at first episode; precipitants; and rate, duration, and degree of regularity of the heartbeat during the subjective palpitations. Palpitations lasting less than 5 minutes and a family history of panic disorder reduce the likelihood of an arrhythmic cause (LR = 0.38 and LR = 0.26, respectively). To better understand the symptom, the examiner can ask the patient to “tap out” the rhythm with his or her fingers. The circumstances associated with onset and termination can also be helpful in determining the cause. Palpitations that start and stop abruptly suggest supraventricular or ventricular tachycardias. Termination of palpitations using vagal maneuvers (eg, Valsalva maneuver) suggests supraventricular tachycardia.
Three common descriptions of palpitations are (1) “flip-flopping” (or “stop and start”), often caused by premature contraction of the atrium or ventricle, with the perceived “stop” from the pause following the contraction, and the “start” from the subsequent forceful contraction; (2) rapid “fluttering in the chest,” with regular “fluttering” suggesting supraventricular or ventricular arrhythmias (including sinus tachycardia) and irregular “fluttering” suggesting atrial fibrillation, atrial flutter, or tachycardia with variable block; and (3) “pounding in the neck” or neck pulsations, often due to “cannon” A waves in the jugular venous pulsations that occur when the right atrium contracts against a closed tricuspid valve.
Palpitations associated with chest pain suggest ischemic heart disease, or if the chest pain is relieved by leaning forward, pericardial disease. Palpitations associated with light-headedness, presyncope, or syncope suggest hypotension and may signify a life-threatening cardiac arrhythmia. Palpitations that occur regularly with exertion suggest a rate-dependent bypass tract or hypertrophic cardiomyopathy. If a benign etiology for these concerning symptoms cannot be ascertained at the initial visit, then ambulatory monitoring or prolonged cardiac monitoring in the hospital might be warranted.
Noncardiac symptoms should also be elicited since the palpitations may be caused by a normal heart responding to a metabolic or inflammatory condition. Weight loss suggests hyperthyroidism. Palpitations can be precipitated by vomiting or diarrhea that leads to electrolyte disorders and hypovolemia. Hyperventilation, hand tingling, and nervousness are common when anxiety or panic disorder is the cause of the palpitations. Palpitations associated with flushing, episodic hypertension, headaches, anxiety, and diaphoresis may be caused by a pheochromocytoma or paraganglioma. In patients with suspected pheochromocytoma or paraganglioma, a 24-hour urine collection for fractionated plasma or urinary metanephrines and catecholamines has a sensitivity and specificity of 98%.
A family history of palpitations or sudden death suggests an inherited etiology such as long QT syndrome or Brugada syndrome. Chagas disease may cause palpitations and acute myocarditis. Younger patients should be asked about consumption of “energy drinks.” Finally, dual use of cigarettes and e-cigarettes may cause palpitations.
Rarely does the clinician have the opportunity to examine a patient during an episode of palpitations. However, careful cardiovascular examination can find abnormalities that can increase the likelihood of specific cardiac arrhythmias. The midsystolic click of mitral valve prolapse can suggest the diagnosis of a supraventricular arrhythmia. The harsh holosystolic murmur of hypertrophic cardiomyopathy, which occurs along the left sternal border and increases with the Valsalva maneuver, suggests atrial fibrillation or ventricular tachycardia. A crescendo mid-diastolic murmur may be caused by an atrial myxoma. The presence of dilated cardiomyopathy, suggested on examination by a displaced and enlarged cardiac point-of-maximal impulse, increases the likelihood of ventricular tachycardia and atrial fibrillation. In patients with chronic atrial fibrillation, in-office exercise (eg, a brisk walk in the hallway) may reveal an intermittent accelerated ventricular response as the cause of the palpitations. The clinician should also look for signs of hyperthyroidism (eg, tremulousness, brisk deep tendon reflexes, or fine hand tremor), or signs of stimulant drug use (eg, dilated pupils or skin or nasal septal perforations). Visible neck pulsations (LR, 2.68; 95% CI, 1.25–5.78) in association with palpitations increases the likelihood of atrioventricular nodal reentry tachycardia.
Commonly used studies in the initial evaluation of a patient with palpitations are the 12-lead ECG and ambulatory ECG monitoring devices (eg, the Holter monitor or an event recorder).
A 12-lead ECG should be performed on all patients reporting palpitations because it can provide evidence for a wide variety of causes. Although in most instances a specific arrhythmia will not be detected on the tracing, a careful evaluation of the ECG can help the clinician deduce a likely etiology in certain circumstances.
For instance, bradyarrhythmias and heart block can be associated with ventricular ectopy or escape beats that may be experienced as palpitations by the patient. Evidence of prior myocardial infarction on ECG (eg, Q waves) increases the patient’s risk for nonsustained or sustained ventricular tachycardia. Ventricular preexcitation (Wolff-Parkinson-White syndrome) is suggested by a short PR interval (less than 0.20 ms) and delta waves (upsloping PR segments). Left ventricular hypertrophy with deep septal Q waves in I, AVL, and V4 through V6 is seen in patients with hypertrophic obstructive cardiomyopathy. The presence of left atrial enlargement as suggested by a terminal P-wave force in V1 more negative than 0.04 msec and notching in lead II reflects a patient at increased risk for atrial fibrillation. A prolonged QT interval and abnormal T-wave morphology suggest the long QT syndrome, which puts patients at increased risk for ventricular tachycardia. Persistent ST-segment elevations in ECG leads V1–V3 (particularly with a coved or saddle-back pattern) suggest Brugada syndrome.
For high-risk patients (Table 2–3), further diagnostic studies are warranted. A step-wise approach has been suggested—starting with ambulatory monitoring devices (ambulatory ECG [Holter] monitoring if the palpitations are expected to occur within the subsequent 72-hour period, event monitoring if less frequent). An implantable loop recorder can be used for extended monitoring if clinical suspicion is high, especially if there is syncope. A single-lead, lightweight, continuously recording ambulatory adhesive patch monitor (Zio Patch) worn for 14 days has been shown to be superior to 24-hour ambulatory ECG (Holter) monitoring. This is then followed by inpatient continuous monitoring if serious arrhythmias are strongly suspected despite normal findings on the ambulatory monitoring, and by invasive electrophysiologic testing if the ambulatory or inpatient monitor records a worrisome arrhythmia. Validation studies are underway on the use of smartphone-based event recorders.
In patients with a prior myocardial infarction, ambulatory cardiac monitoring or signal-averaged ECG is an appropriate next step to help exclude ventricular tachycardia. ECG exercise testing is appropriate in patients with suspected coronary artery disease and in patients who have palpitations with physical exertion. Frequent premature atrial contractions during exercise may be a predictor of atrial fibrillation. Echocardiography is useful when physical examination or ECG suggests structural abnormalities or decreased ventricular function.