Cheyne-Stokes Respiration

CHEYNE-STOKES RESPIRATION (Cheyne, Stokes) was first described by Cheyne in 1816 and studied in more detail by Stokes in 1854. This type of breathing is characterized by the fact that respiratory movements, initially shallow and short, gradually become deeper and longer, then, reaching a maximum, decrease again in depth and duration and pass into a prolonged pause. After the pause the cycle repeats again (see Pneumograph, Fig. 4). Simultaneously with the change in breathing, b. ch. are cyclic fluctuations on the part of other organs and systems: the width of the pupils, the pulse rate and the height of the arterial pressure change; fluctuations are observed in the activity of the intestine, bladder, etc. Often during the respiratory pause the patient loses consciousness and comes to with the onset of breathing. Besides the pronounced Cheyne-Stokes breathing and more often its forms of cyclic breathing are observed, when the fluctuations in the depth of respiratory movements do not reach such magnitude as in true Cheyne-Stokes breathing. This is the so-called "trembling" or "wavy" breathing. It can pass into Cheyne-Stokes breathing or develop from it and then gradually disappear. It should be obvious to recognize the unity of the pathogenesis of these two types of disturbance of the respiratory rhythm. In physiological conditions Cheyne-Stokes breathing is sometimes observed during sleep in healthy people. At reduced atmospheric pressure, for example at great heights, Cheyne-Stokes breathing is observed as a rule during sleep, and often also in the waking state in healthy subjects. In pathological conditions Cheyne-Stokes breathing occurs with various diseases: diseases of the brain (hemorrhages, meningitis, tumors, etc.), exogenous and auto-intoxications (morphine poisoning, nicotine, other narcotics, in precomatose state of diabetes, in kidney diseases, etc.) and most often with diseases of the cardiovascular system with impaired compensation. During graphic registration of breathing in such cases, long before the onset of Cheyne-Stokes breathing, the appearance of "wavy breathing" can be noted. In cardiovascular diseases Cheyne-Stokes breathing sometimes can appear even before the onset of clinically distinct signs of decompensation. Having appeared, Cheyne-Stokes breathing in such cases often does not differ in stability and, even having held on for a long time, can completely disappear with improvement of the patient's condition. Cheyne-Stokes breathing often accompanies attacks of Adams-Stokes syndrome (see Adams-Stokes symptom complex). The cause of the onset of Cheyne-Stokes breathing was sought by the old theory of Traube in a decrease in the excitability of the respiratory center. In this case, ordinary irritation is no longer sufficient to cause deep breathing, and deepening of breathing occurs only at higher irritation, only at increased venosity of the blood. After several deep inspirations the venosity of the blood decreases, and the respiratory center again comes into a state of rest. This theory b. or m. satisfactorily explained the onset of Cheyne-Stokes breathing in brain diseases or in narcotic poisonings. In some similar cases, indeed, an increase in the content of CO₂ in arterial blood was observed. However, this theory could not explain Cheyne-Stokes breathing in cardiovascular diseases, when this phenomenon is often very labile and easily disappears. Straub and Meyer found in such states a decrease in alveolar tension of CO₂ and alkalosis of the blood. Klein found that the content of O₂ of arterial blood at the moment of maximum breathing is the lowest. Haldane and his pupils reproduced Cheyne-Stokes breathing experimentally, placing the organism in conditions of oxygen starvation while simultaneously impoverishing it with CO₂. Haldane advances the theory that Cheyne-Stokes breathing occurs because of the impoverishment of the organism with CO₂ (see Acapnia), in which the regulator of breathing becomes the lack of oxygen, and this regulation is less perfect than the regulation via CO₂. Besides general oxygen starvation of the organism, many authors, starting from Filehne, put forward the assumption of the presence of local disturbances of gas exchange of the respiratory center due to vascular spasms in this area (Straub, Ebstein, Guggenheimer). It should be mentioned that some authors (Douglas, Brauer) assumed primary disturbance of O₂ diffusion in the pulmonary alveoli. It is very probable that in various diseases the mechanism of Cheyne-Stokes breathing is different. Prognostically Cheyne-Stokes breathing is a formidable symptom in brain diseases, infectious diseases, and in severe intoxications. In cardiovascular diseases Cheyne-Stokes breathing does not necessarily have an unfavorable prognostic significance and can disappear together with decompensation for many years. Treatment consists in the treatment of the underlying ailment. In cardiovascular decompensation digitalis and strophanthus often stop both Cheyne-Stokes breathing and "wavy breathing" very quickly. A rapid but unstable effect is given by inhaling a mixture of CO₂ and O₂ (Pembrey, Allen). Lobelia and T-ra Lobeliae are also recommended. In recent years, intravenous infusions of aminophylline (0.48 in a 24% solution, preferably with the addition of 10 cm³ of glucose solution) are applied with great success. Vogl recommends alternating administration of ¹/₂ cm³ before the onset of the apnea phase. The action of aminophylline, according to Guggenheimer, is twofold: improvement of heart work due to expansion of its vessels and improvement of gas exchange of the respiratory center due to central vascular expansion. A sharp intensification of Cheyne-Stokes breathing is observed after injecting such patients with morphine.