Sinoatrial arrest

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Sinoatrial arrest
ICD-10 I45.5
ICD-9 426.6
MeSH D012848

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

Under certain circumstances, the SA node fails to initiate an impulse at the expected time in the cardiac cycle. In the absence of an impulse from the SA Node neither the atria nor the ventricles are stimulated and thus an entire PQRST complex drops out for 1 beat(or more). This is called Sinoatrial(SA) Arrest. In other instances the impulse is initiated normally but is blocked within the SA Node and never reaches the atria and ventricles. This is called sinus exit block or sinoatrial block. Sinus arrest is one of several variants of sinus node dysfunction. The word sinus pause is used to indicate a pause in the generation of QRS complexes for 3 seconds or less. If the delay is longer than this, then the term sinus arrest is used. If there is a markedly prolonged or permanent cessation of P wave and QRS complexes, then the term asystole is applied.

Epidemiology

Sinus arrest is fairly uncommon. It is more likely to be observed in elderly patients with a senescent rhythm system. It can be observed in the setting of myocardial disease (myocarditis) and ischemia or infarction (particularly acute inferior or posterior ST segment elevation MI). It can be a manifestation of digitalis or lidocaine toxicity.

Pathophysiology

If there is absence of a P wave or a dropped P wave, it is difficult to determine from the surface EKG if this is 1) a loss of sinus node automaticity (sinus arrest) or 2) if this is a block of sinus node conduction (sinus exit block). This being said, there are some clinical observations that help distinguish sinus arrest from sinus exit block. In sinus arrest, there is a suppression of other potential escape pacemakers in the atrium so that an atrial escape rhythm is rare. In patients with complete sinus exit block, the block is more frequently associated with either an atrial or an AV junctional escape rhythm.

Sinus arrest=

There is no longer generation of pacemaker activity from the sinoatrial node. There is a failure of automaticity in the sinoatrial mode.

Sinoatrial block

In this disorder, the sinoatrial node is generating electrical complexes, but the electrical activity fails to conduct in the atrium. Sinoatrial automaticity is preserved, and the p waves are generated at a regular rate in a regular pattern which are a multiple of the basic sinus cycle.

Type I (Wenckebach phenomenon) sinoatrial exit block

The PP cycle is progressively shortened until there is a pause and the cycle is repeated. The pause is due to the dropped P wave and measures less than twice the PP cycle. It is similar to the behavior of the RR intervals in type I second-degree AV block.

Type II second-degree sinoatrial exit block

There is an unexpected drop of the P wave. Following this drop, there is a pause in the sinus cycle which is a multiple of the basic sinus cycle. Blocked atrial premature beats sometimes mimic second-degree sinoatrial block. Third-degree sinoatrial exit block cannot be distinguished from sinus arrest when the sinus node ceases to fire. Under such circumstances, subsidiary pacemakers in the AV junction or ventricles may take over.

Symptoms

If the AV junctional or ectopic ventricular pacemaker is not sufficiently rapid to generate an adequate cardiac output, then end organ hypoperfusion may result with some of the following symptoms:

Differential diagnosis of underlying causes of sinus arrest

  • Decreased P wave amplitude occurs when the K is > 7.0 meq/li
  • P waves may be absent when the K is > 8.8 meq/li
  • The impulses are still being generated in the SA node and are conducted to the ventricles through specialized atrial fibers without depolarizing the atrial muscle
  • Moderate or sever hyperkalemia can cause sinus arrest [1]
  • Lidocaine
  • Myocarditis
  • Percutaneous coronary intervention of the proximal right coronary artery can obstruct the origin of the SA nodal artery in about 17% of patients (14 of 80 in one series). [2] Sinus arrest with junctional escape rhythm went on to develop in 4 of the 14 patients and one patient required a temporary ventricular pacing. There was resolution of the the junctional escape rhythm in all patients within 3 days of the sinus node artery occlusion.
  • ST elevation myocardial infarction particularly inferior myocardial infarctions and posterior infarctions.
  • Vagal tone

Diagnosis

Laboratory studies

Serum K+, Ca+ and Na+ should be checked as should thyroid function tests to rule out hypothyroidism.


Treatment

Acute

  • Discontinue the agent that may be causing sinus arrest and treat hyperkalemia.
  • Isoproterenol can be used to increase the rate of the escape pacemaker.
  • Atropine can be given if the block may be due to heightened vagal tone
  • Finally, a temporary pacemaker wire can be placed if the patient is symptomatic with end organ hypoperfusion as a result of the AV nodal or ventricular escape rhythm.

Chronic

References

  1. Bonvini RF, Hendiri T, Anwar A (2006). "Sinus arrest and moderate hyperkalemia". Annales De Cardiologie Et D'angéiologie. 55 (3): 161–3. PMID 16792034. Unknown parameter |month= ignored (help)
  2. Munenori Kotoku, Akira Tamura, Shigeru Naono and Junichi Kadota.Sinus arrest caused by occlusion of the sinus node artery during percutaneous coronary intervention for lesions of the proximal right coronary artery. Heart and vessels,2007, p.389-392

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