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The Mechanism of Cheyne-Stokes Respiration THE MECHANISM OF CHEYNE-STOKES RESPIRATION Ramon L. Lange, Hans H. Hecht J Clin Invest. 1962;41(1):42-52. https://doi.org/10.1172/JCI104465. Research Article Find the latest version: https://jci.me/104465/pdf Journal of Clinical Investigation Vol. 41, No. 1, 1962 THE MECHANISM OF CHEYNE-STOKES RESPIRATION * By RAMON L. LANGE t AND HANS H. HECHT (From the Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah) (Submitted for publication June 1, 1961; accepted September 14, 1961) The unusual breathing pattern characterized by on the part of the patient"); d) the crescendo- cycles of hyperventilation and apnea was first de- decrescendo respiratory pattern; e) return to nor- scribed by Cheyne in 1818 (1) but wider attention mal breathing when circulation is improved. was attracted to the phenomenon by Stokes in his Pryor (3) demonstrated a phasic temporal shift work "The Diseases of the Heart and Aorta" in between ventilatory function and arterial blood gas 1854 (2). This pattern is most commonly seen values in individuals with Cheyne-Stokes (C-S) in patients with heart disease. The form of cardiac respiration and heart disease with arterial oxygen dysfunction associated with this respiratory dis- saturation highest during the period of apnea. order is characterized by left ventricular dilatation, This was not true in patients with intracranial pulmonary congestion, and a low cardiac output. hemorrhage or increased intracranial pressure who Hypertensive disease or ischemic heart disease are also exhibited intermittent respiration. He as- the usual etiological factors. sumed that in C-S breathing an increased lung-to- The underlying mechanism of this disorder has brain circulation time caused oscillatory variations been the subject of debate since Cheyne described in arterial saturation resulting from a delayed it in a man with "heart disease and apoplexy." feedback of the ventilatory effects (output) to the Stokes implicated heart disease more specifically respiratory center (input) (Figure 1). This by stating, "But there is a symptom which appears mechanism implies that in a given instance well to belong to a weakened state of the heart, and ventilated blood does not mix well with the poorly which, therefore, may be looked for in many cases ventilated blood and causes the respiratory cen- of fatty degeneration. I have never seen it except ter(s) to be exposed for relatively long periods to in examples of that disease. The symptom in blood which is alternately well or poorly ventilated. question (cyclic respiration) was observed by This concept had been suggested earlier by Klein Dr. Cheyne although he did not connect it with in 1930 (4), but in 1932 Anthony, Cohn and Steele the special lesion of the heart." (5) publishing findings similar to those predicted There is still no general agreement concerning by Klein, did not reach this same conclusion. No the cause of this type of cyclic respiration; some further observations were available until Guyton, consider the altered breathing pattern primarily Crowell and Moore (6) demonstrated that when neurogenic, others inveigh a circulatory disorder. the lung-to-brain circulation time was artificially Any proposed mechanism must be able to ac- increased in an otherwise normal dog, oscillatory, count for the consistent findings seen in this dis- or C-S respiration could be induced. order: a) the long duration, often years, of the More recently, Brown and Plum (7) observed respiratory dysrhythmia, frequently without ob- hypocapnea in patients with cyclic respiration of vious evidence of central nervous system disease; the C-S type and suggested that this type of breath- b) the absence of cyanosis or polycythemia in spite ing is primarily neurogenic in origin. Review of of periods of prolonged apnea; c) mental clarity, or the data of Pryor also shows the relative hypo- absence of altered sensorium during the apneic capnea described by Brown and Plum. The di- phase (described by Stokes as "the long continued vergent conclusions derived from seemingly con- cessation of respiration yet without any suffering sistent observation suggested that both simultane- ous and continuous measurements of respiratory * Supported in part by Grant H-3126 from the United States Public Health Service. and blood gases together with estimates of circu- t Present address: Department of Medicine, Marquette lation times from lung to artery would be desirable University School of Medicine, Milwaukee, Wis. to resolve the differences in interpretation. In 42 CHEYNE-STOKES RESPIRATION 43 Nominally negative feedback. Gain is greater than unity. Respiratory Nerves Ventilation Center Circulation Stabilizing factors: A, a short lung to artery (brain) circulation time, B, the buffering effects of the FRC and bicarbonate reserve, and C, the longitudinal mixing of blood during lung to artery passage. FIG. 1. A SCHEMA OF THE RESPIRATORY CONTROL SYSTEM. The time de- lay introduced by the feedback pathway via the circulation is considered to be much greater than the temporal delay at any other portion of the loop. addition to a re-examination of the nature of cyclic tained for analysis by the method of Van Slyke and Neill respiration it appeared desirable to study the spe- for Cao2 and Caco2. pH was determined by a Cambridge model R pH meter, cific effect of large cyclic variations in blood gases and PacO2 calculated from Singer and Hasting's nomo- on center and pH respiratory function. gram. Ventilatory activity was recorded in Patients 1-3 by means of a thermocouple near the external nares. METHODS In Patients 4-9 expired CO2 was continuously monitored Nine patients with typical Cheyne-Stokes respiration by an infrared CO2 meter 2 (Figures 2 and 3) In Pa- were studied over a 2-year period. Although all gave evi- tient 4, measurements were made during right-heart dence of heart disease with some degree of failure (Table catheterization. In this patient cardiac output was deter; I) none complained of orthopnea at the time of study. mined by the direct oxygen Fick method. Lung-to-artery All measurements were made with the patient supine. mean circulation time was estimated from indocyanine dye After infiltration with 1 per cent procaine, percutaneous curves by dye injection into a peripheral branch of one femoral arterial puncture was performed and arterial pulmonary artery and sampling from the femoral artery blood was sampled continuously (0.5 ml per second) (8). In Patients 5-9 cardiac output was measured by the through a Wood cuvet oximeter which in turn led to a dye method, using venous injection. Lung-to-artery cir- galvanometer system and allowed continuous graphic culation time was estimated by measuring arm-to-lung: recording of variations in arterial oxygen saturation 1 circulation time (ether) and subtracting this value from with an approximate 1-second delay due to sampling the arm-to-artery circulation time obtained by the dye dead space. Multiple arterial samples were also ob- method or by injection of Decholin. A,F Bywm -32 sooe PAC02 30- .24.--2O- 20 sc _ 25 20- PoC02 ABOVE: Continuous recording of A: arterial oxygen saturation and B: COz content of expired gas. BELOW: Arterial COz tension sampled at times indicated. FIG. 2. SIMULTANEOUS, CONTINUOUS RECORDING OF ARTERIAL OXYGEN SATURATION (OXIMETER) AT TOP AND EXPIRED Co2 (PACO2) IN THE CENTER. Paco, derived from multiple arterial samples is indicated by the dashed line. Pulmonary artery to systemic artery circulation time was 48 seconds. Period of respiratory cycle was approximately 100 seconds (Patient F.F.). 1 Waters Corp., Rochester, Minn. 2 Beckman model LB-1. 44 RAMON L. LANGE AND HANS H. HECHT FIG. 3. AT TIME OF RECORDING COMPLETE APNEA DID NOT OCCUR. Variations in depth and rate of respiration have a period of approximately 60 seconds. The lung-to-artery circulation time was estimated to be 28 seconds. The lower line represents continuous recording of Sao2 (oximeter). Blood gas values were obtained by (Van Slyke) chemical analysis (Patient D.D.). Seven patients expired within 2 to 24 months after spinal fluid showed xanthochromia and other find- study. In five, complete postmortem examination was ings consistent with a recent cerebrovascular ac- obtained. cident. S.G. also expired several months after RESULTS the study. No autopsy was performed but it was Table I shows the clinical characteristics and clear that she had suffered a left hemiplegia, ap- postmortem data of the patients studied. All but parently caused by a cerebral arterial thrombosis. one were males and all were older than 59 years. In F.F., D.D. or C.H. there was no clinical evi- Heart disease with left ventricular dilatation was dence for cerebrovascular disease. D.D. and F.F. present in all. Postmortem examination of H.D. died in heart failure and at autopsy neither had revealed multiple cerebral and midbrain infarc- any evidence of organic brain disease. G.Y. and tions. In W.M. friable mural thrombi were found R.S. suffered from hypertensive cardiovascular in the left ventricle. Postmortem examination was and renal disease with azotemia and renal acidosis. not obtained in C.B. but a few weeks prior to the No organic brain disease was seen in R.S. at physiological study he had manifested mental con- autopsy. G.Y. is living and shows no neurological fusion, and subsequent examination of cerebro- abnormalities. TABLE I Clinical, laboratory and postmortem findings in patients with Cheyne-Stokes respiration * X-ray Postmortem Patient, Age, Sex Clin. diag. Duration Sensorium Neurol. sign LVE PC ECG Heart Brain 1. C.B., 81 6 HCVD, MI 8 mos Clear Pastpointing, 4+ 2+ RBBB Died, no P.M. term. hemipl. 2. H.D., 77 ci ASHD, azot. 12 mos Confused Poor memory 1 + 1 + LVH Mult. Mult. small MI, LVE infarct. 3.
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