1. 1
    Current Diagnosis

    • Premature beats are identified by their occurrence at times considerably shorter than the regular sinus rhythm cycles.

    • The origin of the premature beats is determined by the presence or absence of P waves, morphology of the P wave (when present), QRS configuration, and the presence or absence of a compensatory period.

    • The presence of frequent PVCs (≥10 per hour) during the postdischarge evaluation of survivors of acute MI predicts increased risk of arrhythmic death and overall cardiac mortality.

  2. 2
    Current Therapy

    • In general, premature beats in patients without evidence of organic heart disease do not require any specific antiarrhythmic therapy because generally there is no significant increased risk of life- threatening arrhythmia.

    • Correction of any underlying structural cardiopulmonary disorder and other precipitating factors (e.g., electrolyte or metabolic abnormalities).

    • Suppression of PVCs using currently available antiarrhythmic drugs (except for amiodarone) is not advisable for most patients, primarily because of the increased risk of proarrhythmic effects of these drugs.

    • In the occasional patient who is disabled by annoying symptoms due to PVCs, a trial of β-blocker therapy should be considered and often is effective in many patients.

    Premature beats are the most common form of cardiac arrhythmia encountered in clinical practice. Premature beats are one of the most common causes of irregular pulse and palpitations. In many instances, premature beats are not associated with any symptoms. They result from electrical depolarization of myocardium that occurs earlier than the sinus impulse. Premature beats have been referred to by a variety of names, including premature contractions, premature complexes, ectopic beats, and early depolarizations. Although no single term is ideal, most electrophysiologists refer to them as premature complexes because although the term ectopic beat denotes the abnormal site of origin of the depolarization, it does not necessarily require the beat to be premature, and, in some cases, ectopic rhythm indeed occurs as an escape phenomenon.

    Although premature beats generally occur in patients with organic heart disease, they frequently can be seen in the absence of any structural heart disease, especially in elderly patients. Premature beats can be triggered by, or increase in frequency with, myocardial ischemia and heart failure. Premature beats can be provoked by, or occur in association with, a variety of systemic abnormalities, including electrolyte disturbances, acid-base imbalance, toxins from recreational drug and/or alcohol abuse, metabolic perturbations, systemic illnesses such as thyroid disorders, pulmonary disease, infections, and febrile illnesses, and any condition associated with increased catecholamine levels.

    Most premature beats occur as a result of enhanced automaticity, but other electrophysiologic mechanisms, including reentry and triggered activity, might play a role. Based on the corresponding site of origin, premature electrical depolarizations are called premature atrial complexes (PACs), premature junctional complexes (PJCs), and premature ventricular complexes (PVCs). Morphologic features and timing of the premature beat on electrocardiographic (ECG) recording(s) help determine the site of origin and the nature of premature complexes. Premature beats can occur in a repetitive fashion as bigeminy (after every other normal beat), trigeminy (after each sequence of two normal beats), or quadrigeminy (after each sequence of three normal beats). They also can occur as two or three successive premature beats, defined as couplets and triplets, respectively. In this article, the primary focus is on single premature beats.

  3. 3
    Premature Atrial Complexes

    PACs are the most common form of atrial arrhythmias that can originate at any site in the atria. The exact morphology of the atrial activation (P wave) varies depending on the site of origin of the PAC. Careful and systematic examination of the ECG features of PACs usually can distinguish them from PVCs.

    Electrocardiographic Features

    The cardinal features of PACs include their prematurity with reference to sinus beats, abnormal P wave morphology, and, in most cases, QRS morphology that is similar to that of sinus beats. The P wave morphology of the PAC generally differs from the sinus P wave unless the premature complex originates in the high right atrial area adjacent to the sinus node, in which case distinguishing PACs from sinus arrhythmia may be difficult. Although sinus arrhythmias are generally phasic in nature, being influenced by the respiratory cycle, this feature would be helpful in differentiating from high right atrial

    PACs only when the PACs are frequent and repetitive. When the PAC occurs quite early in the diastolic phase, the P wave may not be obvious on surface ECG because it is often hidden in the preceding T wave and would be evident only by watching carefully for the notched or peaked T wave.

    If the PAC is too premature, it might fail to conduct to the ventricles if the atrioventricular (AV) node is refractory owing to conduction of the preceding sinus impulse. Such nonconducted PACs are called blocked PACs, and they are important because they can be confused with instances of AV block. Such erroneous interpretation can be avoided by simply remembering a common rule of thumb that requires normal successive P-P intervals for all sinus beats, including the interval for a blocked P wave, before considering the diagnosis of AV block. Although most PACs have a normal or prolonged PR interval, the relationship of the PAC to the subsequent QRS complex depends on the site of origin of the PAC and the prematurity index. For example, a PAC originating in the lower atrial area near the AV node generally has a shorter PR interval, whereas a PAC that is quite premature and originates in the upper left atrial area might have a longer than usual PR interval. In general, the PR interval of a PAC is inversely related to its prematurity.

    Because most PACs are able to depolarize the sinus node, they usually can reset the sinus automaticity; therefore, the subsequent pause following most PACs is generally less than compensatory because the sinus node fires earlier than expected. In this case, measurement of the P-P interval between the sinus P wave preceding the PAC and the P wave following the PAC is generally less than twice the basic sinus cycle length. This is in contrast to the full compensatory pause often observed in conjunction with PVCs. In some cases, the PAC collides with the sinus impulse in the perinodal tissue and thus fails to reset the sinus node, thereby resulting in a full compensatory pause.

    In general, electrical depolarization below the AV node is normal with PAC and results in an unchanged (baseline) QRS complex.

    Aberrant conduction, however, may be encountered when the PAC reaches the infranodal tissue during the period when it is still partially refractory. Most frequently, the aberrant conduction usually occurs when a short coupled PAC follows a long pause in patients with sinus bradycardia (long-short cycle). This usually results in a right bundle- branch block pattern and is commonly referred to as the Ashman phenomenon.

    Clinical Features

    Although PACs can occur in normal individuals of all ages, they are quite infrequent except in the elderly. Their frequency increases with age; as many as 50% to 70% of the elderly may have occasional PACs. Some elderly individuals without organic heart disease have frequent PACs and occasionally atrial bigeminy or two to three PACs in a row. Whether the increased frequency of PACs in these individuals is secondary to senile amyloidosis, myocardial fibrosis, or diastolic dysfunction secondary to aging-related changes in the heart is not known. PACs are extremely common in patients with heart disease and in patients with acute as well as chronic respiratory failure. The frequency of PACs can increase markedly during periods of acute febrile illness, shock states, and metabolic disorders, especially in patients with hyperthyroidism and conditions associated with increased catecholamine levels. Use of excessive caffeine, alcohol, tobacco, and recreational drugs can increase the frequency of PACs. In patients with acute myocardial infarction (MI), frequent PACs usually are precursors of atrial fibrillation and occur in association with ventricular failure. In general, the presence of frequent PACs in the setting of acute MI is an indicator of poor prognosis.

    In general, PACs are benign except when they are a marker of an underlying cardiopulmonary disorder(s). The major clinical importance of PACs is related to the increased risk of atrial tachyarrhythmias in patients with an established history of such arrhythmias as well as in the elderly who are generally at high risk for atrial fibrillation. As indicated earlier, in rare instances the blocked PACs may be confused with episodes of AV nodal block; however, careful examination of the ECG features described previously easily establishes the correct diagnosis and avoids unnecessary pacemaker implantation.


    The correction of an underlying structural cardiopulmonary disorder and other precipitating factors (e.g., electrolyte or metabolic abnormalities) usually is all the treatment that is needed. No specific treatment is generally required in most patients because PACs usually are benign except in patients with a history of recurrent atrial tachyarrhythmias, for example, atrial flutter/fibrillation. In such patients, specific treatment may be indicated and could include a β- blocker or a heart rate-modulating calcium channel blocking agent such as verapamil (Calan) or diltiazem (Cardizem). Recent studies have shown that verapamil is quite effective in patients with frequent PACs and multifocal atrial tachycardia in the setting of acute or chronic ventilatory insufficiency. In patients who are at risk for recurrent atrial fibrillation, treatment with a specific antiarrhythmic agent, such as propafenone (Rythmol) or flecainide (Tambocor), may be beneficial; however, these drugs should be used only when the patient has a history of recurrent atrial flutter/fibrillation because of the increased risk of proarrhythmia, especially in the presence of organic heart disease such as recurrent ischemia or heart failure.

  4. 4
    Premature Junctional Complexes

    PJCs are rarely seen in normal individuals and are infrequently encountered even in patients with organic heart disease. When present, PJCs can occur due to abnormal automaticity or reentry phenomenon. Although digitalis toxicity is cited as a common etiologic factor, PJCs also can occur in the setting of MI, myocarditis, and electrolyte/metabolic disturbances.

    Electrocardiographic Features

    The ECG characteristics of PJCs are distinct from those of PACs in that the P wave usually is inverted in the inferior leads (II, III, and aVF) because of retrograde conduction to the atria from the ectopic foci in the junctional area. The second feature of PJCs is that the PR interval almost always is shorter than the normal PR interval because of the proximity of ectopic foci to the AV node and bundle of His. In most cases, the P wave might not even be visible on surface ECGs because it lies hidden within the QRS complex. Rarely, the P wave precedes the QRS complex when the ectopic impulse traverses to the atria before traveling down to depolarize the ventricle. In general, the infranodal conduction of PJCs is normal, and thus the QRS morphology of the conducted PJCs is similar to that noted during sinus rhythm. When the PJC is closely coupled to the preceding sinus beat, aberrant conduction might occur if the impulse traverses down the bundle branch during the relative refractory period (most frequently manifesting as a right bundle-branch block pattern). Because in many instances no obvious P wave accompanies a PJC, aberrantly conducted PJCs may be hard to differentiate from PVCs.

    In some instances when PJCs occur during the period when the AV node as well as the infranodal conduction systems both are refractory, the PJC may encounter both retrograde and antegrade blocks for impulse propagation. In such situations, no P wave or QRS complex is related to the PJC. Although the ectopic impulse would be invisible on a surface ECG, it would penetrate a portion of the conduction system and thus make it partially or completely refractory to conduction of the subsequent sinus impulse. This would be manifested as a sudden prolongation of subsequent PR interval in case of partial refractoriness or as an episode of “pseudo AV nodal block” due to the blocked sinus beat if the infranodal tissue were unable to conduct the sinus impulse. Thus, even though some PJCs might not have any surface ECG complexes, their presence can be suspected based on their influence on the conduction of the following sinus beat, owing to the electrophysiologic phenomenon described as “concealed conduction.”

    Clinical Features

    PJCs usually are not seen in normal persons and are rarely encountered in cardiac patients except in the setting of digitalis intoxication and infrequently in the setting of MI or myocarditis. In patients with digitalis toxicity, PJCs may lead to junctional tachycardia, occasionally resulting in palpitation, but are rarely associated with hemodynamic compromise. Because in some cases concealed conduction of PJCs might result in periods of varying degrees of pseudo AV blocks, it is clinically important to recognize their presence in order to prevent undue concern and avoid inappropriate pacemaker implantation.

  5. 5
    Premature Ventricular Complexes

    PVCs are the most common form of arrhythmia and can be encountered frequently in healthy individuals as well as in patients with a variety of cardiac disorders. PVCs are often triggered by electrolyte abnormalities, acid-base imbalance, metabolic perturbations, hypoxia, and ischemia.

    Electrocardiographic Features

    PVCs occur as a result of premature depolarization of the ventricles due to ectopic foci in the ventricular myocardium or Purkinje fibers.

    In general, PVCs result in wide QRS complexes with the T wave axis usually opposite to that of the QRS. In the vast majority of cases, PVCs do not conduct retrogradely and thus do not result in a distinct P wave. The sinus beats may, however, continue uninterrupted and thus manifest as an instance of AV dissociation in conjunction with PVCs. For the same reason, because PVCs usually do not conduct retrogradely and depolarize the atrium and the sinus node, there usually is a full compensatory pause in contrast to the partial compensatory pause generally seen with PACs. In patients with slow sinus rates, however, interpolated PVCs might occur. If the ectopic foci for PVCs are located high in the His-Purkinje system, the resulting premature complexes may have a narrow QRS morphology quite similar to that seen during sinus rhythm. Additionally, if the PVCs occur rather late, in close proximity to the sinus impulse, there may also be a narrow complex QRS because of fusion between the normal depolarization due to sinus impulse and the abnormal activation sequence from the ectopic foci. In the instance of fusion beats, a normal P wave precedes the QRS. The PR interval is shorter, and the QRS morphology may be only partially altered. In some cases, this might give the appearance of an intermittent bundle-branch block or preexcitation (Wolff-Parkinson-White syndrome) pattern.

    Based on the morphologic features of PVCs, they have been classified as uniform or multiform; they also have been referred to as unifocal or multifocal. Also recommended is classification of PVCs based on their coupling interval with the preceding sinus beat. PVCs with a short coupling interval near or on the previous T wave have been described as showing R-on-T phenomenon; alternatively PVCs may have long coupling intervals. Based on the underlying electrophysiologic mechanism responsible for PVCs, the coupling interval may be fixed, as in reentrant beats, or variable, as seen with ventricular parasystole. PVCs may have a repetitive pattern, for example, bigeminy or trigeminy, or they may occur in pairs. It is now thought that repetitive PVCs, such as couplets and triplets, are prognostically more important than just the frequency of isolated PVCs.

    Clinical Features

    PVCs can be recorded frequently in normal individuals, and, similar to PACs, their frequency increases with age. In patients without organic heart disease or without prior evidence of sustained ventricular tachyarrhythmias, the mere presence of frequent PVCs is not considered prognostically important. However, individual exceptions do exist, and the clinician is advised to evaluate each given patient accordingly. In patients with organic heart disease, PVCs are the most common form of arrhythmia and carry significant prognostic importance, especially in survivors of acute MI and patients with recurrent ischemia and advanced heart failure. It has been well established during the past two decades that frequent PVCs occurring during the acute phase of MI are associated with an increased risk of sustained ventricular arrhythmias in the initial 48 hours, but they do not predict long-term outcome or risk of arrhythmic events. More recently, it has been shown in patients receiving thrombolytic therapy that PVCs, particularly episodes of nonsustained ventricular tachycardia, increase in frequency but are generally short-lived and represent a sign of myocardial reperfusion. However, the presence of frequent PVCs during the postdischarge evaluation of survivors of MI is indicative of a poor prognosis.

    Although as many as 80% to 90% of patients with chronic heart failure have frequent PVCs, the results of several recent studies have shown that only the presence of nonsustained ventricular tachycardia (defined as three or more PVCs in a row) at a rate greater than 100 bpm is strongly predictive of an increased risk of sudden cardiac death in these patients. This is in clear contrast to the findings of several large clinical trials, which showed that more than 10 PVCs per hour in post-MI patients are predictive of a poor prognosis and an increased risk of arrhythmic death.

    Overall, the association between PVCs and an increased risk of ventricular tachyarrhythmias and sudden cardiac death appears to be related not only to the frequency and complexity of PVCs but also to the severity of underlying structural heart disease. For example, a patient with mitral valve prolapse and frequent PVCs would be at relatively low risk for arrhythmic events compared to a patient with advanced heart failure who has repetitive PVCs and episodes of nonsustained ventricular tachycardia. Proper evaluation of the risk of PVCs has become more crucial than ever because most currently available antiarrhythmic drugs have the potential for causing serious adverse reactions, including proarrhythmias, in patients with advanced cardiac disorders.


    In general, PVCs in patients without evidence of organic heart disease do not require any specific antiarrhythmic therapy because generally there is no significantly increased risk of life-threatening arrhythmia. However, when PVCs are associated with disabling palpitations, reassurance and treatment with β-blockers (atenolol [Tenormin], metoprolol [Toprol-XL]) may help in relieving symptoms. In patients with systemic illness or other provoking factors (e.g., electrolyte abnormalities or acid-base imbalance), immediate correction of the underlying abnormality usually is associated with beneficial effects.

    Because of the associated poor prognosis with PVCs in the setting of acute MI, common practice in the past consisted of routine administration of intravenous lidocaine (Xylocaine) in an effort to suppress PVCs during the initial phase of acute MI. However, because recent data suggest that the routine use of lidocaine is not necessary and often can be harmful, lidocaine should be avoided because of the risk of serious adverse reactions, especially central nervous system side effects such as seizures in the elderly. With the ready availability of cardiac monitoring, it now is possible to accurately identify a harbinger of ventricular tachyarrhythmias early in the coronary care unit, so prophylactic use of lidocaine is generally not recommended.

    Furthermore, results from several studies and their meta-analyses have demonstrated that routine use of prophylactic lidocaine during the acute or healing phase of MI does not alter the overall mortality in patients with acute MI.

    In contrast, it is well established that the presence of frequent PVCs (≥10 per hour) during the postdischarge evaluation of survivors of acute MI predicts an increased risk of arrhythmic death and overall cardiac mortality. Numerous trials have been conducted with a variety of different antiarrhythmic drugs. Many of the studies demonstrated that suppression of PVCs with most currently available antiarrhythmic drugs is not beneficial in reducing the increased risk associated with PVCs. The Cardiac Arrhythmia Suppression Trials (CAST I and II) clearly demonstrated that, compared to placebo, treatment with class Ic antiarrhythmic drugs (which primarily work by slowing conduction) was associated with an increased risk of arrhythmic death despite adequate suppression of PVCs. The findings from CAST I and II, as well as several other clinical trials, indicate that although frequent PVCs may be a marker for an adverse event, suppression of PVCs with type I antiarrhythmic agents does not favorably influence the associated increased risk of death. Results from the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT) and the European Myocardial Infarct Amiodarone Trial (EMIAT) suggest that in patients with frequent PVCs in the post- MI setting, use of amiodarone (Cordarone), a complex drug with predominantly class III antiarrhythmic properties, in combination with β-blockers is associated with improved outcome. However, because of the associated drug toxicity with long-term amiodarone use, it is generally considered suitable only for the high-risk cohort (although many patients with low left ventricular ejection fraction now undergo implantation of an automatic internal cardiac defibrillator).

    In general, suppression of PVCs using currently available antiarrhythmic drugs (except for amiodarone) is not advisable for most patients, primarily because of the increased risk of proarrhythmic effects of these drugs. In the occasional patient who is disabled by annoying symptoms due to PVCs, an initial trial of β- blocker therapy should be considered and is effective in many patients. Correction of the provoking factors and appropriate management of any underlying heart disease often are beneficial in managing patients with frequent PVCs.

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