CLINICAL AND EXPERIMENTAL OBSERVATIONS UPON CHEYNE-STOKES RESPIRATION

Abstract

In addition to the results brought out in the separate sections I wish to direct especial attention to the following conclusions: (1) In ten cases of Cheyne-Stokes respiration observed clinically, the alternate periods of respiratory activity and apnœa were associated with Traube-Hering waves of blood pressure. These cases may be separated into two groups characterized by the relation of the respiratory changes to the changes of blood pressure. In one group the period of respiratory activity was associated with a rise of blood pressure, the period of apnœa with a fall; in the other group, the reverse relations existed. The former group included two cases of Cheyne-Stokes respiration occurring with increased intracranial tension; the latter contained eight cases with cardiac and arterial disease. (2) By means of cerebral compression, periodic respirations may be produced experimentally, and the relation of the blood pressure changes to the respiratory variations are the same as in the clinical cases with increased intracranial tension, namely, a rise of pressure with each group of respirations and a fall with each period of apnœa. In the experiments, during each respiratory group, the blood pressure rises above the line of intracranial tension and with each period of apnœa it falls below this line. With the disappearance of this relation, the periodicity of the respirations likewise disappears. It is probable that the same relation between the blood pressure and intracranial pressure exists when Cheyne-Stokes respiration occurs clinically in association with increased intracranial tension. (3) Disappearance of the periodic respiratory activity in the clinical cases of both groups is accompanied by disappearance of the waves of blood pressure. (4) The waves of blood pressure cannot be regarded as a mechanical effect of the periodic respiratory activity; on the contrary the latter must be due to the changes of blood pressure, or both phenomena may be referable to a common cause. (5) Cheyne-Stokes respiration in states of increased intracranial tension, with blood pressure waves rising and falling above and below the line of intracranial tension, is due to periodic activity of the respiratory, vasomotor, and cardio-inhibitory centres, the underlying cause of which is an alternate anæmia and blood supply to the medullary centres. The vasomotor centre, as the result of periodic increase and decrease of the stimulus, shows periodic variations in its activity. It is stimulated to greater activity during the periods of anæmia, and partially relaxes with each period of blood supply. During the periods of anæmia, the respiratory centre loses its irritability for the acting stimulus, and is therefore apnœic. It is finally stimulated to activity, either as a result of an increase in its irritability from a preceding rise of blood pressure, or from a great increase in the respiratory stimulus. The cardio-inhibitory centre is stimulated by the periods of anæmia. This stimulation causes slowing of the pulse, which passes off to a considerable extent with the following period of blood supply. (6) Cheyne-Stokes respiration has heretofore been regarded as always the manifestation of the same conditions and capable of the same explanation; the results of this work, on the contrary, show that two distinct groups of cases may be recognized, depending upon the relation of the blood pressure changes to the periodic respiratory activity.19 (7) The medullary centres show great differences in their susceptibility to anæmia. The respiratory centre is very susceptible to a much reduced blood supply; its irritability is rapidly reduced or lost upon the occurrence of marked or complete anæmia, and is rapidly regained when the blood supply is renewed if the anæmia has not been maintained too long. The effect of a considerable anæmia upon this centre is entirely different from that of a normal or somewhat reduced supply of blood which is more venous than normal, that is, contains more carbon dioxide and less oxygen, such as occurs with ordinary asphyxia. The vasomotor and cardio-inhibitory centres are not nearly so susceptible to anæmia. The former centre may, and frequently does, respond when in a condition of complete anæmia. (8) I am able to confirm, as a result of my experiments upon cerebral compression, in all essential details the conclusions of Cushing, and the general law formulated by him, namely that "an increase of intracranial tension occasions a rise of blood pressure which tends to find a level slightly above that of the pressure exerted against the medulla."