SHOCK 291 



same organs under normal conditions. Furthermore, severing of the 

 nerve of such an organ causes an increased outflow. 



To these various pieces of evidence of a constricted condition of at 

 least certain of the vessels in shock, may be added the less direct evi- 

 dence furnished by the pallor of the shocked patient and the indications 

 that the sympathetic nervous system, instead of being paralyzed, is 

 in an excited state, as shown by the sweating and the dilated pupils. 



Furthermore, we know from the experiments of Pike, Guthrie and 

 Stewart 30 on the resuscitation of the nerve centers after interference 

 with the circulation to the brain, that the vasomotor center is remark- 

 ably resistant to anemia. It can withstand this condition without losing 

 its tone or reflex activity better than any of the other cardinal centers. 



Those who have maintained that a deficiency in the tone of the vaso- 

 constrictor and other nerve centers is responsible for shock have based 

 their evidence partly on histologic examination of nerve cells of shocked 

 animals, it being assumed that the chromatolysis shown by these cells 

 indicates an exhausted condition. The assumption is, however, entirely 

 unwarranted, and no regard is given to the well-established fact that 

 similar histologic changes may be produced by other conditions. It 

 is certainly safe to conclude that the changes in the nerve cells in shock 

 are the result and not the cause of the low blood pressure of this 

 condition. 



Since the fall in arterial blood pressure occurs with contracted ar- 

 terioles, it must be dependent on a diminished discharge of Hood from 

 the heart. Interference with the heart action itself (independently of 

 the blood carried to this organ), or a deficiency in the filling of the ven- 

 tricles during diastole, that is, a stasis of blood in the venous or cap- 

 illary areas, are the possible causes for the diminished output. The 

 possibility that the heart action itself has been interfered with, as by 

 paralysis of the vagus mechanism, causing a rapid beating of the heart, 

 has been shown to be untenable by various experiments. After stimulat- 

 ing the central end of an uncut vagus nerve in the neck in shock, the 

 reflex vagus mechanism is still operative. Furthermore, when the arte- 

 rial blood pressure is artificially raised, either by epinephrine injection 

 or by cerebral compression, the heart promptly responds to the in- 

 creased blood pressure by contracting more slowly and vigorously. 

 Evidently, therefore, as the cardiac mechanism itself is normal, the de- 

 ficient discharge of blood must be dependent upon improper diastolic 

 filling. After this condition has set in, it becomes progressively worse 

 because of weakening of the heart muscles consequent upon the failing 

 blood supply through the coronary vessels. 



The question therefore narrows itself down to the cause of the ineffi- 



