Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
An atrial premature beat (APB) is characterized by a nonsinus P wave that occurs before the next anticipated sinus beat. Several electrocardiographic leads may be needed to distinguish P waves originating in the sinus node versus an ectopic focus. In the rare case of sinus nodal premature beats, the P wave will be identical. The post-extrasystolic cycle length is typically less than compensatory because of penetration and resetting of the sinus node by the premature depolarization, but suppression of sinus node automaticity may also occur and result in pauses equal to or longer than the sinus cycle. Intraventricular conduction may be normal or aberrant, whereas the PR interval can be longer than that of the normal sinus beat because of atrioventricular nodal delay. This especially occurs in the rare case of interpolated APBs, which do not depolarize the sinus node and do not affect the sinus rate. Blocked premature beats may masquerade as pauses or bradycardias when P waves are not seen. The T wave of those beats that precede a pause should be carefully inspected to detect any “hidden” premature P wave. Nonconducted APBs are a common cause of unexpected pauses. They can arise anywhere in the atria, including the sinus node.
Sinus tachycardia is defined as a nonparoxysmal increase in sinus rate to more than 100 beats per minute (bpm) in keeping with the level of physical, emotional, pathologic, or pharmacologic stress. ,
It is due to physiologic influences on individual pacemaker cells and from an anatomic shift in the site of origin of atrial depolarization superiorly within the sinus node.
In normal sinus rhythm, the P wave on a 12-lead electrocardiogram (ECG) in adults is positive in leads I, II, and aVF and V 3 to V 6 . It is negative in aVR and V 1 and V 2 . In sinus tachycardia P waves have a normal contour, but a larger amplitude may develop and the wave may become peaked.
Inappropriate sinus tachycardia (IST) is a fast sinus rhythm (>100 bpm) at rest or minimal activity that is out of proportion with the level of physical, emotional, pathologic, or pharmacologic stress. The syndrome of inappropriate sinus tachycardia is also defined as a sinus heart rate greater than 100 bpm at rest (with a mean 24-hour heart rate >90 bpm not a result of primary causes) and is associated with distressing symptoms of palpitations. ,
The underlying mechanism of IST remains poorly understood and is likely to be multifactorial (dysautonomia, neurohormonal dysregulation, intrinsic sinus node hyperactivity). A gain-of-function mutation of the pacemaker hyperpolarization-activated cyclic nucleotide-gated (HCN) 4 channel has been reported in a familial form of IST. There is also evolving evidence that immunoglobulin G anti-β receptor antibodies are found in IST.
Diagnosis is based on the following:
The presence of a persistent sinus tachycardia, greater than 100 bpm at rest or greater than 90 bpm on average over 24 hours, during the day with excessive rate increase in response to activity and nocturnal normalization of rate.
The tachycardia and associated symptoms are usually nonparoxysmal with P-wave morphology and endocardial activation identical to sinus rhythm.
Exclusion of a secondary systemic cause (e.g., hyperthyroidism, physical deconditioning), and postural orthostatic tachycardia syndrome (POTS).
The limited and disappointing experience with catheter ablation reported in small observational studies suggests that catheter ablation should not be considered as part of the routine management of most patients with IST. It may be considered in very symptomatic patients who do not respond to therapy with both a beta blocker and ivabradine. It is aimed at modifying the sinus node with an unavoidable, concomitant risk of iatrogenic sinus nodal disease and the need for permanent pacing. Catheter modification of the sinus node is moderately effective (60%), but the benefits may be short term and can be complicated by the need of permanent pacing in 10% of the patients. Narrowing of the superior vena cava and phrenic nerve palsy may also occur.
Sinus nodal reentrant tachycardia arises from a reentry circuit involving the sinus node and, in contrast to IST, is characterized by paroxysmal episodes of tachycardia. On the ECG, the polarity and configuration of the P waves are similar to the configuration of sinus P waves.
It is unclear whether the reentrant circuit is completely confined to the sinus node or if surrounding atrial tissue is involved.
Diagnosis is based on the following:
The tachycardia is paroxysmal.
P-wave morphology is almost identical to sinus rhythm.
Endocardial atrial activation is similar to that of sinus rhythm.
Induction and/or termination of the arrhythmia occurs with premature atrial stimuli.
Termination occurs with vagal maneuvers or adenosine.
Ιnduction of the arrhythmia is independent of atrial or atrioventricular (AV) nodal conduction time.
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here