The normal intraventricular system starts at the AV node as bundle of His that divides into right and left bundle branches which after giving of the fascicular branches ends in the complex Purkinje system. Intraventricular conduction delay are due to abnormalities in the specialized conduction system in the ventricles that transmit impulses arising from the SA node transmitted through the AV node to the ventricles. Abnormalities of local myocardial activation can further alter the specific pattern of venticular activation. An IVCD is the result of abnormal activation of the ventricles caused by conduction delay or block in one or more parts of the specialized conduction system ( bundle of His, bundle branch or purkinje conduction system) resulting in widening of QRS complex. The QRS complex represents electrical activation of the ventricle and normally the entire process of ventricular depolarization in adults is completed within about 0.1 sec (100 msec). The term intraventricular conduction delay or intraventricular conduction disturbances ( IVCDs) refers to disturbances in the intraventricular propagation of supraventricular impulses resulting in changes in the QRS complex either in morphology or duration, or both. Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S Overview Risk calculators and risk factors for Intraventricular conduction delay overviewĮditor-In-Chief: C. To Hospitals Treating Intraventricular conduction delay overview Intraventricular conduction delay overview in the newsīlogs on Intraventricular conduction delay overview Intraventricular conduction delay overview On the WebįDA on Intraventricular conduction delay overviewĬDC onIntraventricular conduction delay overview Natural History, Complications and Prognosis Intraventricular conduction delay Microchaptersĭifferentiating Intraventricular conduction delay from other Disorders This has better correlation a very poor voltage < 5 mm( the largest qrs ) in the limb leads predicts a very badly scarred LV. What is the correlation of low voltage to LV muscle mass ? Because, these conduction defects are very common in cardiomyopathy, there is very poor correlation of LV mass verses high voltage qrs. This happens due to LAFB,LBBB, non specific IVCD. It should be realised conduction defects can cause an increase in qrs voltage irrespective of the status of the muscle. When can limb leads record high voltage in cardiomyopathy ? Note : In spite of this, a dilated LV records high voltage in precardial leads as explained above The limb leads are bi polar leads hence as a rule, they record a smaller voltage than chest leads.In many patients with cardiomyopathy, the muscle mass is replaced by fibrotic tissue (Interstitial fibrosis ) and this brings down the net electrical energy draining from the heart. Why limb leads do not show this high voltage ? The same phenomenon occurs in physiological conditions as in stress testing where excercise increases the qrs voltage due to increased This is some times called as Brody effect. The enlarged LV increases the residual end systolic and end diastolic volume, this increase in blood volume independently increases the electrical conductivity and inscribes a high voltage complex. This increases the electromotive forces reaching the lead.Ģ. In dilated cardiomyopathy the enlarged heart (Usually more than 6 cm in diastole, may reach 9cm ) brings the myocardium closer to chest. We know, chest leads are unipolar and picks up the electrical activity directly beneath the lead. classically patients with severe forms of dilated cardiomyopathy show high voltage qrs complex in V1 to V6 and significantly low voltage in limb leads.ġ. A combination of low voltage qrs and high voltage qrs is a well known marker of dilated cardiomyopathy .
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