The electrical resistivity of intracardiac blood is less than the resistivity of the surrounding tissues. This affects the transmission of cardiac forces to the body surface: the radial forces are enhanced, whereas the transmission of tangential forces is diminished (the Brody effect). Blood resistivity is directly related to haematocrit, hence, haematocrit changes are expected to affect the transmission of cardiac forces, resulting in changes in QRS complex voltage. To assess this hypothesis, a 12-lead electrocardiogram was recorded in 40 patients affected by thalassaemia before and after a transfusion of concentrated red cells. The voltage of each QRS component was carefully measured in every lead, and the sum of all R wave amplitudes (sigma R) was calculated. The post-transfusional electrocardiogram reflected a significant decrease in the R wave amplitude in every lead. sigma R also decreased, whereas S wave amplitude in lead V6 increased. A negative correlation between the ratio of haematocrit pre/post transfusion and that of the corresponding sigma R values was also observed (r = -0.434; P less than 0.01). An increase in haematocrit is therefore associated with a decrease in R wave amplitude. These findings explain why several patients with high haematocrit manifest relatively low voltage QRS complexes.

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This presentation reflects a case of phase-3 left bundle branch block (LBBB). Analysis reveals that relatively early QRS complexes are wide, whereas beats occurring later than a critical time are narrow. There are, however, two unexpected phenomena: (1) an overlap occurs between the range of R-R intervals resulting in normal intraventricular conduction and the range of R-R intervals resulting in LBBB pattern. Complexes that follow a wide beat are often wide although they are associated with relatively long R-R intervals, whereas complexes that follow a normal beat tend to be normal even after relatively short R-R cycles. This is due to concealed retrograde penetration of the bundle branch that is blocked in anterograde direction (the so-called linking phenomenon). (2) Some early supraventricular impulses, paradoxically, resulted in normal intraventricular conduction. The phenomenon is a manifestation of supernormal LBB conduction, and only occurs following a wide QRS complex associated with retrograde activation of the LBB. The linking phenomenon reveals or unmasks the supernormal phase of LBB conduction. Following a retrograde and delayed activation of the LBB, the refractory period of the bundle branch is postponed, in such a way that a supraventricular impulse is allowed to occur during the early phase of supernormal conduction.

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