ELECTROCARDIOGRAPHV 



389 



additional anoxic effect. Besides, most hormones or 

 drugs act in a multifold manner: e.g., noradrenaline 

 constricts vessels and induces a reflex bradycardia via 

 a vagal activity. The only influences strictly referable 

 to the autonomic nerves and their hormones are those 

 on the single cell (see Chapter 12 by Scher). Here 

 adrenaline and the stimulation of the sympathetics 

 lengthen tlic action potential somewhat, although 

 most probably only in damaged fibers, and steepen 

 depolarization; whereas acetylcholine and vagal stim- 

 ulation shorten the action potential, especially the 

 plateau, and slow depolarization. With both effects, 

 however, it is difficult to explain the action on the 

 whole heart. 



There are some additional and comparatively sim- 

 ple effects on the spread of excitation : the vagus de- 

 creases the propagation velocity, and therefore 

 lengthens the P-Q time and the QRS duration. The 

 sympathetic acts antagonistically, though to a com- 

 paratively feeble degree. The relative Q-T duration 

 is unchanged or somewhat lengthened by the sympa- 

 thetic. The vagus is said to shorten Q.T, but only rela- 

 tively and apparen ly indirectly. The amplitude of 

 QRS is increased bty the vagus and decreased by the 

 sympathetic, as a consequence of lower or higher syn- 

 chronization and cancellation of all myocardial 

 fibers, due to changed conduction velocity, \agal in- 

 hibition of conduction results, in strong stimulations, 

 in complete A-V block. In the case of a permanent 

 augmentation of vagal tone, as seen in athletes, the 

 P-Q interval may be markedly lengthened up to 

 0.5 sec. The discrimination between such functional 

 states and abnormality is easy : in functional vago- 

 tonia exercise reduces the interval to normal (102, 

 380). 



The influence on the T wave is rather complicated, 

 because it is difficult to isolate pure effects. Neverthe- 

 less, it is probable that the vagus augments and the 

 sympathetic depresses the T wave. The vagal effect 

 may be imitated by acetylcholine, and in a dog's 

 heart is independent of changes in blood pressure or 

 heart rate (324). These effects remain difficult to 

 understand, because acetylcholine shortens the action 

 and flattens the plateau, which should lead to a de- 

 creased amplitude of T. As the vagus does not enter 

 the ventricular muscle mass with sufficiently numer- 

 ous fibers, the effects of acetylcholine (which may 

 easily penetrate into all parts of the heart) and vagal 

 stimulation should be treated separately. It could be 

 argued that the reflex vagal effects may be associated 

 with a diminution of sympathetic tone. But sympa- 

 thectomy does not imitate the vagal effect. So explana- 



tion of the vagal effects is impossible for the present. 

 Sympathetic effects, however, are most probably due 

 to local metabolic influences, which would explain the 

 similarity between the influences of sympathetic tone 

 and hypoxia on T. In cases of "pheochromocytoma," 

 T may become inverted, as in severe anoxia. 



The influences of adrenaline or noradrenaline are 

 similar if not identical to those of sympathetic ac- 

 tivity. Some details of the action of adrenaline have 

 been mentioned earlier. Adrenaline and acetylcholine 

 are, like their respective nerves, antagonistic and 

 cancel their effects if given in a ratio of 10:1; adrenal- 

 ine exerts the much feebler action (92). Both sympa- 

 thetic (adrenergic) and cholinergic stimuli affect ion 

 exchanges during depolarization and repolarization, 

 as listed above. A peculiar effect of large doses of 

 adrenaline is an augmentation of the U wave, which 

 may be due to strong afterpotentials (152), not yet 

 analyzed in full detail. 



As a paradoxical action of acetylcholine and vagal 

 stimulation, the asystolic atria become active under 

 their influence. This effect is due to the repolarizing 

 action of acetylcholine, so that generator potentials, 

 badly damaged before, are restored (490). 



Ps\(hologi(al Influence 



Much has been written about psychological influ- 

 ences on the ECG. It may briefly be stated that such 

 influences do exist, but can be interpreted as changes 

 in the tonic autonomic innervation. The nature of 

 such influences therefore can be predicted without 

 difficulty and they resemble more or less the action of 

 adrenaline (349). They are found in 40 per cent of all 

 patients lying on an operating table (330) and may- 

 be elicited easily in hypnosis by suggestions of an 

 anxiety-fear situation (107). 



Metabolism 



Metabolism has a decisive influence, especially on 

 the T wave. The reasons are obvious. Repolarization 

 depends heavily upon the ion pump and the velocity 

 of relocating the potassium which passed the cell 

 membrane during depolarization. These processes are 

 brought about by cell metabolism. As a matter of fact, 

 nearly all poisons and enzyme inhibitors shorten the 

 action potential (510), in the same way as hypoxia, 

 and most probably by permitting an augmented ex- 

 ternal potassium concentration (Trautwein, personal 

 communication). Therefore, it is not surprising that 

 the T wave changes rather predictably with heart 



