ELECTROCARDIOGRAPHY 



38. 



Q Pat @ 



QfPt')® 



FIG. 63. Explanation of the genesis of a monophasic action potential at the boundary to an asys- 

 tolic area (right part of the fiber), where two electrodes are put on the ends of the fiber. The shaded 

 area is still (or again) resting. The arrows indicate differences of the membrane potentials along 

 the fiber surface, with their polarities. On the right, the time course of a record is shown. Pai is 

 the potential difference during the accession, Pa2 during the repolarization of the activity. The 

 arrows indicate merely the distances along which the membrane potential varies. [From Schaefer 



(58).] 



Fio. 64. A : resultant vector of an S-T displacement originated by injury potentials at the boundary 

 between normal and damaged tissue. The damaged area is shadowed. The little arrows represent 

 single fibers crossing the boundary and developing an injury potential and, during activity, a mono- 

 phasic action potential and dipole moment according to fig. 63. Their resultant is shown as STj 

 (integrated vector of S-T displacement). This vector projects, like other vectors, on the lead vectors 

 of the electrodes (here on the Einthoven triangle). B- if the damaged area is surrounded on all sides 

 by normal tissue, and if fiber bundles cross the boundary in the direction of the arrows, two re- 

 sultant vectors develop at the two entries of the fibers into the damaged area. The total resultant 

 will be zero (mute infarct). [From Schaefer (58).] 



example, injury to the right ventricle causes an 

 upward deflection of the Ijase line and a depressed 

 ST segment, whereas left ventricular injury does the 

 opposite (354). It makes no difference whether a 

 part of the heart remains inactive (showing an 

 asystolic area) or the inactive part is removed. This 

 could be demonstrated on an isolated surviving 

 human heart (119). How much current may be 

 recorded from a damaged or asystolic area, with a 



certain electrode position, depends to a large extent 

 on how much contact the damaged area has with 

 the optimally conducting parts of the heart's en- 

 vironment, such as the mediastinum and the thoracic 

 wall (284). Moreover, a damaged area may remain 

 "mute," even with optimal contact with conducting 

 surfaces, if the damaged area is surrounded to an 

 equal degree on all sides with normal tissue. In such 

 a case, the vectors from one side of the area are 



