PACs may be seen with lung disease and structural heart disease of any type they may be a precursor to paroxysmal AF. Frequent PACs are uncommon in the general population ( 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. Occasional patients have palpitations, but only rarely are these intolerable. PACs occurring in the presence of pericarditis may represent inflammatory irritation of specific foci. 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. They are rarely caused by an MI unless atrial infarction or pericarditis occurs. PACs are common after cardioversion of AF and may be a predictor of its early recurrence. Frequent PACs, especially if multiform, can mimic AF and may constitute a risk for its development. 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.Ītrial 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). A PAC can occasionally initiate a sustained supraventricular tachycardia, such as AF. 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. 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. 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. PACs are extremely common and probably occur in all people, whether or not structural heart disease is present. PACs may also occur as couplets or as bursts of nonsustained atrial tachycardia. The second PAC conducts normally with a narrow QRS complex (seventh QRS complex), but the first PAC conducts aberrantly with a wide QRS complex (fourth QRS complex) that is due to right bundle branch block with left posterior fascicular block. This lead V1 and II rhythm strip shows sinus rhythm with two PACs. 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 pattern) can resemble a premature ventricular complex (PVC) but is differentiated by the premature P wave preceding the QRS complex ( Fig. 3.2 ) are a common cause of brief pauses. 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. 3.1 ), trigeminal, or quadrigeminal fashion. They may be isolated and unifocal or multiform in a bigeminal ( Fig. 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). 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.
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