ESSENTIALS OF DIAGNOSIS
Sinus node dysfunction (“sick sinus syndrome”)
Sinus bradycardia: sinus rate less than 50 bpm.
Sinoatrial (SA) exit block.
Sinus pauses: P wave nonoccurrence more than 3 seconds.
Sinus arrest: no evidence of P waves.
Atrioventricular (AV) block
First degree: 1:1 AV conduction ratio and PR interval more than 200 ms.
Type I: failure of AV conduction and QRS complex nonoccurrence preceded by increasing PR intervals.
Type II: failure of AV conduction not preceded by increasing PR intervals.
“2:1”: without consecutive PR intervals, unable to define as either type I or type II block.
Advanced (“high-grade” or “high-degree”): ≥ 3:1 AV conduction ratio.
Third degree (“complete”): independent atrial and ventricular rhythms with failure of AV conduction despite temporal opportunity to occur
The clinical presentation of patients with conduction system disease is determined by two underlying abnormal conditions: the inability to increase or maintain the sinus rate in response to metabolic need and atrioventricular (AV) dyssynchrony (inappropriately timed atrial and ventricular depolarization and contraction sequences).
PATHOPHYSIOLOGY & ETIOLOGY
A. Sinus Node Dysfunction
Sinus node dysfunction (“sick sinus syndrome”) is usually due to age-dependent and progressive degenerative fibrosis of the sinus node and sinoatrial (SA) area (Table 14–1). Often, the degenerative process also involves the approaches to the AV node, the AV node itself, the His bundle, as well as the intraventricular conduction system; as many as 25–30% of patients with sinus node dysfunction have evidence of AV conduction disease.
++ Table Graphic Jump Location Table 14–1.Causes of Sinus Node Dysfunction ||Download (.pdf) Table 14–1. Causes of Sinus Node Dysfunction
Ischemic (inferior wall MI, Bezold-Jarisch reflex)
Inflammatory (pericarditis, collagen vascular diseases)
Infiltrative (amyloidosis, sarcoidosis, hemochromatosis)
Non-dihydropyridine calcium channel blockers (diltiazem, verapamil)
Digoxin (with high prevailing vagal tone)
Class I antiarrhythmic agents (flecainide, propafenone)
Class III antiarrhythmic agents (amiodarone, sotalol)
Other cellular ion channel blockers (ivabradine)
Acetylcholinesterase inhibitors (donepezil)
Sympatholytic drugs (clonidine, methyldopa)
Respiratory sinus arrhythmia, in which the sinus rate increases with inspiration and decreases with expiration, is not an abnormal rhythm and is mostly seen in young healthy persons. Nonrespiratory sinus arrhythmia, in which phasic changes in sinus rate are not due to respiration, may be accentuated by the use of vagotonic agents, such as digoxin and morphine, and is more likely to be observed in older patients who have underlying cardiac disease, although the arrhythmia itself is not a marker for structural heart disease; its mechanism is unknown. Ventriculophasic sinus arrhythmia is an unusual rhythm that occurs during advanced second-degree or complete AV block; it is characterized by shorter P-P intervals ...