Premature atrial complexes
Premature atrial complexes (PACs) are supraventricular ectopic depolarizations originating in or near the atria or in the pulmonary veins that supersede activation from the sinus node. The most common sites of origin appear to be in or around the pulmonary vein ostia, especially in patients who are at risk for atrial fibrillation (AF). They may be isolated and unifocal or multiform in a bigeminal ( Fig. 3.1 ), trigeminal, or quadrigeminal fashion. PACs that are very early may not conduct to the ventricle due to block in the atrioventricular (AV) node or the His-Purkinje system; these blocked PACs ( Fig. 3.2 ) are a common cause of brief pauses. At times, when the heart rhythm is more irregular, an early PAC following a longer R-R interval can conduct aberrantly; the resultant wide QRS (typically a right bundle branch block [RBBB] pattern) can resemble a premature ventricular complex (PVC) but is differentiated by the premature P wave preceding the QRS complex ( Fig. 3.3 ).
PACs may also occur as couplets or as bursts of nonsustained atrial tachycardia. PACs are extremely common and probably occur in all people, whether or not structural heart disease is present. Most of the time they do not cause symptoms, but if they are not conducted to the ventricles and result in a low effective heart rate, symptoms can be present. Early-coupled PACs, in which atrial systole occurs in close temporal relationship to ventricular contraction and thus against closed AV valves, can produce symptoms because of an inability of the atria to empty, producing loss of stroke volume, as well as atrial stretch and increased atrial pressure (seen as cannon A waves), that can cause a sense of palpitations. Unlike many PVCs, most PACs do not encounter entrance block at the sinoatrial (SA) node and thus will reset the sinus node, resulting in a postextrasystolic pause that is less than fully compensatory; however, the type of postextrasystolic pause is not a good criterion of the origin of a premature depolarization. A PAC can occasionally initiate a sustained supraventricular tachycardia, such as AF. PACs can be confused with PVCs if the P wave is buried (hidden) in the preceding T wave, especially if intraventricular aberration of the conducted beat is present.
Atrial ectopy can be exacerbated by alcohol, caffeine, theobromine (chocolate), methylxanthines, catecholamines, smoking, stress, lack of sleep, fatigue, hypoxia, transient or chronic elevations in atrial pressure, or mechanical stimulation (e.g., from a Swan-Ganz catheter). Frequent PACs, especially if multiform, can mimic AF and may constitute a risk for its development. PACs are common after cardioversion of AF and may be a predictor of its early recurrence. They are rarely caused by an MI unless atrial infarction or pericarditis occurs. The underlying mechanism of PAC production during atrial infarction is unknown but may be due in some cases to focally discharging sites or microreentry located in or around the pulmonary vein ostia. PACs occurring in the presence of pericarditis may represent inflammatory irritation of specific foci.
Clinical Symptoms and Presentation
Occasional patients have palpitations, but only rarely are these intolerable. Frequent PACs are uncommon in the general population (< 2% of healthy subjects have > 100 PACs per 24-hour period), but their prevalence increases with age, especially when there is an associated atrial conduction abnormality, elevated atrial pressures, or atrial enlargement. PACs may be seen with lung disease and structural heart disease of any type; they may be a precursor to paroxysmal AF.
Approach to Management
Suppression is rarely indicated. The patient should be reassured and therapy discouraged unless severe or intolerable symptoms are present because the treatments to suppress these ectopic beats may be worse (e.g., side effects, proarrhythmia) than the rhythm itself. Patient education often helps in this regard. Suppression of PACs may be required early after DC cardioversion of AF because they may presage early AF recurrence. If PACs induce AF or are highly symptomatic, antiarrhythmic drug suppression or even ablation may be required ( Table 3.1 ).
|Mild or no symptoms|
|Triggers atrial fibrillation|
|Nonconducted (“blocked”) PACs|
Premature junctional complexes
Premature junctional complexes (PJCs) originate in the AV junction. Postextrasystolic pauses may be fully compensatory or noncompensatory, depending on whether the junctional impulse encounters entrance block at the SA node (which does not disturb the rate of the sinus impulse, a fully compensatory pause) or penetrates it (depolarizing the sinus pacemaker cells and resetting the sinus rate). PJCs ( Fig. 3.4 ) have a narrow QRS complex unless BBB is present. A PJC is often characterized as a premature beat with no P wave or with a retrograde P (inverted in leads II, III, and aVF) occurring just before, during, or after QRS complex. P waves may also be dissociated from the junctional complexes.
PJCs occur in structurally normal hearts, are usually of no clinical importance, and are self-limited. They may be seen in sinus node dysfunction. PJCs are rare during myocardial infarction (MI).
Clinical Symptoms and Presentation
PJCs may cause palpitations.
Approach to Management
Management is the same as for PACs. Treatment is generally not indicated unless the patient is symptomatic. PJCs may be difficult to suppress with an antiarrhythmic drug and are generally difficult or impossible to ablate without risk of complete heart block ( Table 3.2 ).
|Preoperative and Postoperative|
Premature ventricular complexes
PVCs are premature ectopic beats arising from the right ventricle (RV) or left ventricle (LV) that can occur in a variety of patterns and can occasionally cause symptoms. PVCs can occur during sinus rhythm or any other prevailing cardiac rhythm. PVCs can cause a “compensatory pause” if no retrograde atrial activation is present or if retrograde atrial encounters entrance block at the sinus node, thereby producing no disturbance in the sinus firing rate; however, less than fully compensatory pauses will be produced if sinus node reset is produced by the retrograde atrial activation penetrating the node. The type of postextrasystolic pause may not distinguish PVCs from supraventricular complexes. “Interpolated” PVCs ( Fig. 3.5 ) can occur in which the R-R interval enclosing the PVC is not disturbed, even though retrograde (“concealed”) depolarization into the AV node often occurs producing “pseudo first-degree AV block” for one beat.
PVCs can occasionally be confused with other ectopic beats: PACs conducted to the ventricles aberrantly can mimic PVCs; however, a premature P wave is usually evident on close inspection of multiple simultaneously recorded ECG leads. A short burst of PACs can cause concealed conduction and result in perpetuated aberration that resembles multiple consecutive PVCs. PVCs can (1) occur as single unifocal complexes, (2) have multiple morphologies (multifocal or multiform) and fusion complexes ( Fig. 3.6 ) in which the ventricles are depolarized via both the PVC and the antegrade conducted supraventricular impulse, (3) have multiple coupling intervals to the preceding sinus beats, (4) occur as couplets or triplets, or (5) initiate nonsustained or sustained ventricular tachycardia (VT). PVCs can alternate with every other beat (ventricular bigeminy) or every third beat (ventricular trigeminy) or occur every fourth beat (ventricular quadrigeminy) ( Fig. 3.7 ). PVCs can also be a manifestation of a parasystolic focus, in which the focus fires at a constant rate that can be stable over years; the timing of its appearance on an ECG will reflect tissue refractoriness and varying degrees of exit (and entrance) block to depolarize surrounding ventricular tissue, and because it fires independently of surrounding depolarizations, it has no fixed coupled interval to preceding complexes. Ventricular parasystole is benign. Parasystolic tachycardia is extremely rare and difficult to diagnose.
PVCs are extremely common in patients with and without structural heart disease. The frequency of PVCs in normal healthy individuals ranges from 0.77% to 2.8% in a single ECG; on a Holter monitor the prevalence is 17% to 100%. In patients with normal hearts, PVCs (even if frequent) tend to be unifocal and often originate in the outflow tract, most commonly in the RV ( Fig. 3.8 ) and less commonly in the LV outflow tract ( Fig. 3.9 ), including the aortic cusp or other sites in the LV or RV. They may cause anxiety, which may increase their frequency. Complex ventricular ectopy (frequent, multiform complexes or bursts of VT) tends to occur in the older population and those with structural heart disease, with an incidence varying from 7% to 22% (up to 77% of elderly), depending on the population studied. They may occur in a variety of patterns and be exacerbated by exercise, emotional stress, alcohol, ischemia, heart failure, or mechanical stimulation (e.g., Swan-Ganz catheter).
“Frequent” PVCs (> 10 PVCs per hour) may have prognostic significance for mortality in patients with ischemic heart disease, although arrhythmic mortality is not well predicted. In addition to causing symptoms, PVCs can occasionally have hemodynamic consequences acutely and over the long term can cause ventricular dysfunction. In some patients with very frequent PVCs, especially if a functional left bundle branch block (LBBB) is produced, cardiomyopathy may occur; suppression of the PVCs by medical or ablative approaches may improve the cardiomyopathy. PVCs appear to carry a benign prognosis in patients without structural heart disease and in patients with structural heart disease but normal ventricular function. The presence of frequent PVCs may be associated with a slightly increased risk of sudden cardiac death and total mortality, even in a population without structural heart disease, although this issue remains controversial. On the other hand, there are no data to indicate that treatment of PVCs in otherwise healthy individuals without structural heart disease will improve outcome. In contrast, frequent or complex PVCs are associated with increased total and cardiovascular mortality in patients with systolic ventricular dysfunction or after MI, with prognosis related to their frequency, complexity (couplets, triplets, nonsustained VT), and timing relative to acute clinical events. The incidence of PVCs peaks early after MI and then tapers gradually over time. The prognostic significance and mortality after MI increases if PVCs and complex ventricular ectopy occur 48 to 96 hours after MI, especially if the left ventricular ejection fraction (LVEF) is less than 0.40. PVCs therefore become a predictor of increased mortality similar to LVEF, multivessel coronary disease, abnormal signal-averaged ECG, abnormal heart rate variability, T-wave alternans, and a variety of other noninvasive parameters. The presence of isolated PVCs is not as highly predictive of mortality as some other risk factors, but patients with frequent PVCs (> 10 per hour) occurring greater than 6 days after MI have been reported to have a 7% mortality after MI. The predictive value increases if the LVEF is less than 0.40 with an approximate doubling in mortality. However, much of this information was collected in the pre-percutaneous coronary intervention (pre-PCI) era and may not be applicable to aggressively managed acute MI patients nowadays.
Clinical Symptoms and Presentation
PVCs are usually asymptomatic, but in some patients, including those without structural heart disease, they may be associated with palpitations, dizziness, weakness, fatigue, shortness of breath, or chest discomfort. Most individuals feel the postextrasystolic beat after the PVC and do not feel the PVC itself because its early timing is associated with a lower stroke volume; however, the postextrasystolic (usually) compensatory pause allows a longer time for the ventricle to fill, and thus the sensation often can be described as a “skipped” beat followed by a forceful or strong beat. The sensation may also be due in part to postextrasystolic potentiation from the irregularity in pulse and from atrial contraction against closed AV valves. Pounding, slow palpitations are typical of bigeminal PVCs. In patients with symptoms consistent with PVCs, it is important to try to correlate the symptom with the arrhythmia. There are many symptoms that may mimic those from PVCs, but many PVCs still remain asymptomatic. New-onset PVCs in a patient at risk for or with known heart disease can be a red flag; such patients need to be evaluated carefully for the presence of developing or progressive heart disease.
Approach to Management
No Structural Heart Disease
In patients with no structural heart disease and PVCs, treatment to suppress PVCs has not been shown to improve survival (and mortality is low to begin with in these patients). In most cases no therapy is recommended, and reassuring the patient as to the benign nature of the rhythm is essential. Therapy is directed toward reduction or elimination in symptoms and may include β-adrenergic blockers, calcium channel blockers, or class I, II, or III antiarrhythmic drugs. Fish oil may be effective. Antiarrhythmic drugs should be used only if a patient has frequent and severe symptoms that cannot otherwise be controlled with a β-adrenergic blocker or a calcium channel blocker. There are few if any data to indicate that a β-adrenergic blocker or calcium channel blocker actually is effective in suppressing PVCs. Fish oil may suppress some symptomatic PVCs, but no other supplement is known to have any benefit. It is important to determine whether a patient has structural heart disease. It may be useful to follow the patient long term to determine whether new symptoms develop or whether there is a new onset of or progression in heart disease that was not present initially. For refractory symptoms or frequent PVCs leading to a PVC-associated cardiomyopathy or functional LBBB ventricular dyssynchrony, electrophysiology study with mapping and ablation of the PVC is helpful. This represents the distinct minority of patients without structural heart disease. PVCs can originate from the endocardium or epicardium of either ventricle ( Algorithm 3.1 ).