RESUMO
The analysis of the common bundle and of the ventrical filtered electrograms has incrased our knowledge of the intraventricular conduction following the simulation of the PVS as well as the different types or reciprocating that can be produced by premature beats. 2. The positive QRS complexes in V1 produced from PVD by St2 can be explained as a greater degree of incomplete recuperation of the right ventricular wall than in the interventricular septum. In contrast with what happened in the basal beats, where the front took longer to reach the TSVD than the VI. 3. The refractarines of the transitional tissues that serve as the phisiological banier was longer than the banal myocardium. The intraventricular propagation, and therefore the morphology and direction of QRS, depended of this one; while the moment of arrival of activation retrogradly to the common bundle was conditioned by the transitional tissues. 4. Episodes of ventricular taquicardies with QRS positive complexes in V1 can be due to a re-entry throught the bundle branches or in (or around) an area that has been recently injured.
Assuntos
Fascículo Atrioventricular/fisiologia , Eletrocardiografia , Sistema de Condução Cardíaco/fisiologia , Função Ventricular , Estimulação Elétrica , Humanos , Taquicardia/diagnósticoRESUMO
His bundle electrograms recorded during atrial stimulation with the extrastimulus technique permitted the analysis of the so called gaps in bundle branch conduction. Three different types of gaps were identified each with a distinct electrophysiological mechanism. In type I gap a CLBBB pattern disappeared at shorter coupling (A1-A2) intervals because the more premature impulses encountered a greater degree of the delay at the A-V node therefore reaching the left bundle branch after its effective refractory period had ended. During this part of the cycle the H1-H2 were longer and H2-V2 intervals shorter than when CRBBB was present. In type II gap a CRBBB pattern disappeared at shorter coupling intervals because the premature impulses met a greater delay in the proximal portions of the His-Purkinje system. In consequence, they arrived at the right bundle branch when its effective refractory period had expired. When this occurred the H1-H2 interval were shorter and the H2-V2 longer than those at which CRBBB had been present. The patient with type III gap had CLBBB. A-V conduction was possible through the right bundle branch very late in the cycle. However, it could not occur at shorter coupling intervals finally reappearing at even shorter coupling intervals. True supernormal conduction or vagal pulsatile discharges could have been present. Yet, we favor, as the most likely possibility, the existence of 2:1 phase 4 block with latent or abortive escapes not recorded in the surface leads.