![]() The intraventricular conduction system is composed of the His-Purkinje system. ![]() ![]() Normal and abnormal intraventricular impulse conduction Note that the terms intranventricular conduction delay and intranventricular conduction defect are used interchangeably. These concepts will be discussed in detail in this and the subsequent articles. The primary ECG manifestations of conduction defects are prolonged QRS complexes and altered QRS appearance. 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. In general, a conduction defect in the left ventricle is more significant, as compared with a defect affecting the right ventricle. The significance of this will depend on the severity of the conduction defect and the affected ventricle. 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). General Introduction to ST, T, and U wave abnormalitiesīasic Concept: the specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances General Introduction to ST-T and U Wave Abnormalities.Intraventricular conduction delay (defect): constellations of bundle branch blocks and fascicular blocks (hemiblocks) In which the ECG changes are found than by the particular changes themselves. Thisĭoes not mean that the ECG changes are unimportant! It is the responsibility of the clinician providing care for the Thus the term, nonspecific ST-T waveĪbnormalities, is frequently used when the clinical data are not available to correlate with the ECG findings. Drug effects (e.g., digoxin, quinidine, etc)."Primary" ST-T Wave Abnormalities (ST-T wave changes that are independent of changes in ventricular activation and that may be the result of global or segmental pathologic processes that affect ventricular repolarization): ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced beats.ST-T changes seen in bundle branch blocks (generally the ST-T polarity is opposite to the major or terminal deflection of the QRS)."Secondary" ST-T Wave changes (these are normal ST-T wave changes solely due to alterations in the sequence of ventricular activation): Ventricular conduction abnormalities and rhythms originating in the ventricles.Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment).Metabolic factors (e.g., hypoglycemia, hyperventilation).Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.).Electrolyte abnormalities of potassium, magnesium, calcium.Drugs (e.g., digoxin, quinidine, tricyclics, and many others).Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction, infiltrative or myopathic processes).Patient to ascertain the importance of the ECG findings.įactors affecting the ST-T and U wave configuration include:
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