When is the interventricular septum incomplete

Normal intraventricular conduction requires only two sequential 0. The minimal contribution of the normal right-ventricular myocardium is completely subtracted from the early portion of the QRS complex and then added later, when the right ventricle is activated after the spread of impulses from the left ventricle through the interventricular septum to the right ventricle.

In Figure 6. Normal activation of the left-ventricular free wall spreads simultaneously from two sites near the insertions of the papillary muscles of the mitral valve. Wavefronts of activation spread from these endocardial sites to the overlying epicardium. Because the cancellation is removed, the waveforms of the QRS complex change, as described below Tables 6. A schematic diagram of the left ventricle viewed from its apex upward toward its base is illustrated in Figure 6.

Activation spreading from endocardium to the epicardium in this region is directed inferiorly and rightward. Because the block in the LAF has removed the initial superior and leftward activation, a Q wave appears in leads that have their positive electrodes in a superior-leftward position i.

Following this initial period, the activation wave spreads over the remainder of the left-ventricular free wall in a superior-leftward direction, producing a prominent R wave in lead I and a prominent S wave in lead aVF.

The overall duration of the QRS complex may be within the normal range but is usually prolonged by 0. Activation spreading from the endocardium to the epicardium in this region is directed superiorly and leftward. Because the block in the LPF has removed the initial inferior and rightward activation, a Q wave appears in leads with their positive electrodes in an inferior-rightward position i.

The consideration that LPFB may be present requires that there be no evidence of right-ventricular hypertrophy RVH from either the precordial leads see Fig. Intraventricular Conduction Abnormalities. Isolated absence of septum pellucidum: prenatal diagnosis and outcome. Fetal Diagnosis and Therapy. M Sarwar. The Septum Pellucidum: Normal and Abnormal. American Journal of Neuroradiology. October ; C Traggiai and R Stanhope. Body mass index and hypothalamic morphology on MRI in children with congenital midline cerebral abnormalities.

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Caring for Your Patient with a Rare Disease. FindZebra Diagnosis Assist Tool. Finding Funding Opportunities. Teaching Resources. In this chapter we will discuss intraventricular conduction delays defects , which are caused by functional or anatomical defects in the components of the intraventricular conduction system. Because the conduction system is crucial for rapid and synchronized activation of the ventricles, conduction defects will typically cause abnormal ventricular activation contraction.

The significance of this will depend on the severity of the conduction defect and the affected ventricle. In general, a conduction defect in the left ventricle is more significant, as compared with a defect affecting the right ventricle. This is due to the fact that the left ventricle pumps against greater resistance and any disturbance in ventricular activation will reduce the efficiency of the pumping function.

These concepts will be discussed in detail in this and the subsequent articles. Note that the terms intranventricular conduction delay and intranventricular conduction defect are used interchangeably.

The intraventricular conduction system is composed of the His-Purkinje system. More precisely this system consists of the bundle of His, the left and right bundle branch and the fascicles of the left bundle branch Figure 1. The interventricular septum obtains Purkinje fibers from the left bundle branch. The right bundle branch does not give off any Purkinje fibers during its passage through the septum.

Purkinje fibers are branched off from the right bundle branch at the level of the origin of the anterior papillary muscle. A network of Purkinje fibers sprouts out from the bundle branches an fascicles and spread through the ventricular endocardium. Figure 1 shows the components of the conduction system. Note that conduction defects in the atrioventricular AV node and the bundle of His have been discussed in the previous chapter.

The current chapters discuss conduction defects located in the bundle branches and in the fascicles. The type of ECG changes that occur are as follows:. Anatomical or functional block in the left bundle branch causes left bundle branch block LBBB. Similarly, block in the right bundle branch causes right bundle branch block RBBB. The ventricles whose bundle branch is defect will be depolarized from impulses spreading from the opposite ventricle. This results in characteristic ECG changes depicted in Figure 2.

In lead V6 a broad and deep S wave is noted. In left bundle branch block lead V1 shows a deep S-wave and in V6 a broad and clumsy R-wave is noted Figure 2, panel B. Importantly, in both bundle branch blocks, the QRS duration is at least 0. Consequently, ST-segment elevations and ST-segment depressions are expected in bundle branch blocks.

However, incomplete bundle branch blocks are of significance because they tend to progress to complete blocks. Right bundle branch block in asymptomatic individuals is not correlated with adverse outcomes. On the other hand, new right bundle branch block in patients with chest pain may indicate occlusion in the left anterior descending artery. Finally, new right bundle branch block in patients experiencing dyspnea particularly if acute may indicate pulmonary embolism. In the vast majority of cases, however, right bundle branch block is a benign finding with little if any impact of cardiovascular prognosis.