EXCITATION OF THE HEART 



3'7 



mM 

 WO- 



90- 



80- 



msec 



WO 



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0% 95% 



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[Aktionspot-} ' Amplitude 

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msec 



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60 



Pla *feaur\Dauer 



ISO 



ZOO 



220 



_1_ 



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^Wmin 260 



FIG. 40. The effects of oxygen lack on the action potential 

 of heart muscle. Transition from 95*: c to 0*^7 oxygen leads to 

 decrease of amplitude and duration of the action potential. 

 [From Trautwein & Dudel (133).] 



PHASE II. When a blood vessel supplying the ven- 

 tricular myocardium is completely occluded by a 

 thrombus or the deposition of atheromatous plaques 

 in the vessel wall, and when no collateral circulation 

 exists, the cells previously supplied by this vessel 

 will be completely deprived of oxygen. A compli- 

 cated series of events will ensue, all of them causing 

 the same change in the relationship between the 

 S-T and T-Q segments. 



The first change which takes place is a shortening 

 of the intracellular action potential. This occurs 

 within a few seconds after the tying of a ligature in an 

 experimental animal, as has been demonstrated by 

 several investigators (105, 133, fig. 40). When the 

 action potential is shortened, the injured cells de- 

 polarize normally but repolarize more rapidly than 

 do adjacent normal cells. For this reason, during the 

 period of repolarization, i.e., during the S-T segment 

 of the electrocardiogram, current flows from the 

 injured cells to the adjacent normal cells (since, by 

 definition, current flow is from positive to negative). 

 This flow then leads to a change in the S-T segment, 

 which becomes elevated in unipolar leads facing the 

 area of the infarct. This elevation is a primary change 

 in the S-T segment; it is transient, however, and re- 

 covery from this phase occurs within a few minutes 

 (figs. 40, 41). 



While this change is still in eff'ect (and during the 

 period of recovery), a second change takes place: a 



\ 



FIG- 41 . Three possible mechanisms for S-T segment changes. 

 In the top drawing, the base line is depressed at rest, i.e., during 

 the T-Q interval. Since the injured cells are partially depo- 

 larized during this period, current flows into them. When all 

 cells are uniformly depolarized during the S-T interval, the 

 base line is at true zero. In the second case, the base line is 

 normal at rest but elevated during the S-T interval due to a 

 shortening of the action potential duration in the injured cells. 

 In the third case, the injured cells cannot depolarize. A wave 

 of activity reaches the border of the injured region but cannot 

 invade it, so that the S-T segment is elevated. The second of 

 these states occurs early in experimental infarction and is 

 followed by the first. 



decrease in the steady potential of the injured cells. 

 Since the steady potential of the injured cells is now 

 lower than that of the adjacent uninjured cells, cur- 

 rent flows from the normal cells into the injured ones 

 during electrical diastole. (This current is frequently 

 referred to as the "current of injury.") This condition 

 produces a depression of the T-Q segment of the 

 electrocardiogram in unipolar electrodes facing the 

 area of injury. At first this depression adds to the 

 true S-T segment shift mentioned previously, but it 

 continues after the initial change disappears. The 



