Intraventricular conduction systems

As it happens with all types of arrhythmias the incidence in the acute MI phase, of RBBBs and LBBBs, has decreased very much since the introduction of reperfusion therapy, because this treatment improves intraventricular conduction system perfusion. Furthermore, the prognosis is better, as in general the ventricular function is also more preserved (Roth et al, 1993). 

May be conducted or nonconducted (blocked) through AV node and heart depending on status of the AV node and intraventricular conduction system. 

Conduction system abnormalities are common in chronic heart failure, occurring in 15-30% of the population with low left ventricular ejection fraction (LVEF) [1-3]. The prevalence in ischemic heart disease is roughly similar to that seen in other forms of dilated cardiomyopathy. Conduction system disease can occur both at the time of an acute myocardial infarction as well as slowly progressing in chronic ischemic heart disease. Intraventricular conduction delays are associated with a poor prognosis in heart failure, with up to a 70% increase in the risk of death, and are also more prevalent in patients with advanced symptoms [2,4]. In ischemic heart disease, all components of the conduction system are at risk of ischemic injury, from the sinoatrial node to the His-Pukinje system. These conduction system abnormalities have the potential to impair cardiac function by a number of mechanisms. Since conduction abnormalities impair cardiac function, it is logical that pacing therapies to correct or improve these conduction abnormalities may improve cardiac function. 

Cardiac toxicity is generally the result of drug-induced depression of cardiac conduction (e.g., atrioventricular block, intraventricular conduction block) and systemic vasodilation. These effects may progress to severe hypotension and cardiac arrest. 

In a series of ten paediatric castor bean ingestions, seven had transient ECG abnormalities, including QT interval prolongation (in five cases), intraventricular conduction disturbance and repolarization changes. The authors suggested that these changes were probably secondary to metabolic disturbances (Kaszds and Papp, 1960). It is possible that these abnormalities may have resulted from ricin-induced apoptosis of key elements of the cardiac conduction system. Such an effect of ricin has been noted in vivo in rats (Leek, 1989). 

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