390 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



rate (is flattened in increasing rates), though the rate 

 change may be caused by very different agents (463). 

 Metabolism governs the actual effect. Monohalogenic 

 acids act about in the same way. The plateau vanishes 

 completely and the ECG consists therefore only of a 

 diphasic curve like those of the action potential of 

 skeletal muscle (331). How such marked effects are 

 produced remains imperfectly vmderstood, but may 

 involve blocking carbohydrate metabolism, thus 

 blocking the energy sources responsible for the return 

 of potassium. We know that every increase in the ex- 

 ternal potassium concentration accelerates repolariza- 

 tion, without increase in the membrane resistivity, a 

 fact true only of heart fibers and contrasting with the 

 opposite behavior of resistivity in skeletal muscle and 

 nerve. There are still some quantitative difficulties in 

 the explanation of metabolic and other effects, as 

 mentioned previously. 



The energv metabolism has a second effect : the ion 

 pump has to remove the Na from the interior of the 

 fiber. Since the sodium influx into the fiber generates 

 the depolarization potential and therelsy QRS, the 

 QRS complex should be sulyect to a certain degree of 

 metabolic influence. This really is the case to some 

 extent. In general, however, depolarization is ex- 

 tremely stable compared with repolarization and 

 plateau. Changes in T may be elicited by a simple 

 procedure as the intake of 100 to 200 g of glucose, 

 which leads to a flattening or even an inversion of T 

 (495). This action is not identical with the action of a 

 concomitant hypopotassemia (494). The potassium 

 content of the fiber seems therefore not to be the only 

 determinant of metabolic influences. In hypoglycemic 

 shock much more severe alterations occur, such as 

 voltage increase and prolongation of QRS, S-T de- 

 pression, flattening or inversion of T, lengthening of 

 QT, and increase of U (235). Here, conduction seems 

 to be altered together with a change in repolarization. 



The result is that metabolism influences T in a 

 comparatively predictable manner. The effect to be 

 expected in most cases of impaired metabolism would 

 be a flattening of the plateau and a shortening of the 

 potential, as is seen in low oxygen tension. Flattening 

 would lead to a different behavior of the T area, which 

 in its "elementary" part would remain unchanged, 

 but with the potential differences distributed over the 

 whole S-T interval. It is extremely unlikely that the 

 inhomogeneities should remain unchanged. If, at a 

 given time, the potential is reduced, an inhomogeneity 

 of the potential pattern cannot be of the same amount, 

 leading to reduced potential differences and diminu- 

 tion of the ventricular gradient. Small magnitudes of 



the gradient, therefore, may be due to metabolic dis- 

 turbances of an over-all distribution. Any time that a 

 flattening of the plateau happens only in certain parts 

 of the heart, the whole picture is reversed : the in- 

 homogeneities are augmented, the gradient increases, 

 and its axis is shifted. It must be said, however, that 

 these conclusions are true only to a degree of proba- 

 bility, for it may occur that a local process changes 

 the plateau in such a manner that the "normal" in- 

 homogeneity is counterbalanced by the abnormal, and 

 the gradient decreases. The differentiation between 

 localized and general trauma therefore always remains 

 uncertain, but it has Ijecn stated in clinical experience 

 that local e\'ents influence the Q vector so that analysis 

 may re\'eal an additional abnormal vector of inho- 

 inogeneity, which points directly to the site of this 

 disturliance, e.g., an infarct (294, 514). 



The picture of metabolic influences given in the 

 preceding pages is incomplete in one way. In case of 

 local disturbances of blood supply, the ECG changes 

 so that a gradient will he recorded (as after infarcts), 

 the position of which can only be explained by assum- 

 ing that the plateau is lengthened in the damaged 

 region (58, p. 301). We have neither experimental 

 evidence for this assumption, nor any other explana- 

 tion for such ECG patterns. The postextrasystolic T 

 wave changes also raise some unanswered questions 

 (319, 345, 484). T is changed after extrasystolic beats, 

 and its vector is shifted to the left and upward (a be- 

 comes more negative), even if the interval between 

 extrasystole and the following beat is lengthened. 

 Only part of such changes can be interpreted as the 

 consequences of prolongation of the interval. 



Ions 



The influence of ions (47, 103, 254, 259, 384) on 

 the ECG of the whole heart is not fully clarified, in 

 spite of a good understanding of their effects on a 

 single heart fiber and its monophasic action potential. 

 There are several reasons which account for the wideh' 

 differing results, a) In an intact animal or in man, 

 sufficiently large changes in the plasma content of 

 certain ions are difficult to achieve and, if they are 

 present, they influence not only the action potential 

 of the single fiber, but also the conduction, thus lead- 

 ing to a changed pattern of interaction of the various 

 fibers of the heart, b) All changes in ionic concentra- 

 tion produce side effects on other functions, such as 

 liberation of hormones, activation of autonomic 

 nerves, disturbances of the water equilibrium, c) In 

 many clinical cases, not one but several ions changed 



