John Cheyne and William Stokes: Periodic respiration

John Cheyne and William Stokes: Periodic respiration

The Journal of Emergency Medune, Vol 3, pp 233-236. Printed In the USA 1985 Copyright 0 1985 Pergamon f’ress Ltd ?? JOHN CHEYNE AND WILLIAM STOK...

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The Journal of Emergency Medune,

Vol 3, pp 233-236.

Printed In the USA

1985

Copyright 0 1985 Pergamon f’ress Ltd

??

JOHN CHEYNE AND WILLIAM STOKES: PERIODIC RESPIRATION George L. Sternbach, Department

of Emergency

MD, FACEP

Serwces, Stanford University MedIcal Center, Stanford CA 9430:5

0 Abstract-Modern descriptions of the phenomenon that has come to be known as CheyneStokes respiration (CSR) were initially reported by John Cheyne in 1818 and William Stokes in 1854. Seen in conjunction with a variety of conditions and illnesses, CSR is most widely recognized in association with neurologic and cardiovascular disease. The pathogenesis is uncertain and has been the subject of considerable disagreement. A number of clinical manifestations may accompany periodic respiration, including variations in level of consciousness, neurologic signs, systemic blood pressure, and cardiac rhythm. Although specific treatment for the respiratory pattern per se is seldom warranted, CSR may be abolished by the administration of oxygen, carbon dioxide, or aminophylline. Cl Keywords - periodic respiration; Cheyne-Stokes respiration

History like that of a person recollecting himself, wasrare, and large. -Hippocrates’ The respiration throughout,

In 1818 John Cheyne reported the case history of a patient who had suffered from a stroke and heart failure.2

A.B., sixty years of age, of a sanguine temperament, circular chest, and full habit of body, for years had lived a very sedentary life, while he indulged habitually in the luxuries of the table. . . In the latter end of January 1816, he consulted me . . . but he neglected my directions with regard to diet; nay, his appetite being remarkably keen, he ate more than usual, and took at least a pint of port wine or Madiera daily, as was his habit. Patients of similar disposition are not unknown even today. However, A. B. was not entirely well. He had long been subject to oedema of the ankles in the evening; for two or three years . . . he had remarked an occasional intermission in the pulse of his heart.

The patient suddenly developed palpitations and displayed signs of severe congestive heart failure. After an illness, lasting 3 months, he was “found in bed flushed, speechless, and hemiplegiac . . . all attempts to relieve him were unavailing.” Cheyne appeared most interested in the autopsy findings, which revealed a left cortical cerebrovascular accident and marked cardiomegaly accompanied by exl:ensive myocardial fatty infiltration. He concluded the clinical portion of his presentation with a remarkable observation.

Medical Classics is an ongoing feature of JEM, focusing on “classic” contributions emergency medicine. The section is routinely authored by George Sternbach, Stanford University Medical Center.

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234

The only particularity in the last period of his illness, which lasted eight or nine days, was in the state of the respiration. For several days his breathing was irregular; it would entirely cease for a quarter of a minute, then it would become perceptible, though very low, then by degrees it became heaving and quick, and then it would gradually cease again. This revolution in the state of his breathing occupied about a minute,

during which there were about thirty acts of respiration. Cheyne, a respected clinician, was the founder of the Dublin school, whose ranks were to include Robert Graves, Abraham Colles, William Stokes, and Robert Adams. These men were so prominent that some have been the subject of the “Medical Classics” series. In 1854 Stokes authored a book that contained a description of the respiratory phenomenon under consideration. which is unparalleled to this day.3 It consists in the occurrence of a series of inspirations, increasing to a maximum, and then declining in force and length, until a state of apparent apnoea is established. In this condition the patient may remain for such a length of time as to make his attendants believe that he is dead, when a low inspiration, followed by one more decided, marks the commencement of a new ascending and then descending series of inspirations. . . . I do not know any more remarkable or characteristic phenomena than those presented in this condition, whether we view the longcontinued cessation of breathing, yet without any suffering on the part of the patient, or the maximum point of the series of inspirations, when the head is thrown back, the shoulders raised, and every muscle of inspiration thrown into the most violent action; yet all this without rale or any sign of mechanical obstruction. The decline in length and force of the respirations is as regular and remarkable as their progressive increase. The inspirations become each one less deep than the preceding, until they are all but imperceptible, and then the state of apparent apnoea occurs. This is at last broken by the faintest possible inspiration; the next effort is a little stronger, until, so to speak, the paroxysm of breathing is at its height, again to subside by a descending scale.

George L. Sternbach

Whereas Cheyne had not sought to explain the phenomenon, Stokes believed it to be related to cardiac disease. There is a symptom which appears to belong to a weakened state of the heart, and which, therefore, may be looked for in many cases of the fatty degeneration. I have never seen it except in examples of that disease. The symptom in question was observed by Dr Cheyne, although he did not connect it with the special lesion of the heart. Stokes considered periodic respiration to be ominous as an indicator of prognosis. This symptom, as occurring in its highest degree, I have only seen during a few weeks previous to the death of the patient.

Commentary Periodic or Cheyne-Stokes respirations (CSR) are seen in conjunction with a variety of clinical conditions (Table 1). Perhaps best recognized is its association with neurologic disorders. CSR has been described in patients with stroke owing to hemorrhage, infarction, and embolism, as well as in patients with head injury, brain tumor, subarachnoid hemorrhage, meningitis, and encephalitis.4 Although no correlation with a particular neuroanatomic site has been consistently demonstrated, CSR is found more frequ‘ently in cerebrovascular accidents involving the hemispheres than the brainstem. Cardiac disease, especially that producing congestive failure, is known to be associated with CSR. As was the case with Cheyne’s patient, ,many individuals displaying CSR have both cardiac and neurologic disease. Since Stokes declared the necessity for cardiac involvement for the development of periodic respiration, controversy has existed regarding the role of the cardiac and neural systems in the production of CSR. Some have suggested that the disorder may be attributed entirely to cardiovascular disease,6

Cheyne

235

& Stokes

Table 1. Conditions Associated With Cheyne-Stokes Respirations Pathologic: Neurologic

Cardiovascular

Other

Cerebrovascular accident Head injury Subarachnoid hemorrhage Cerebral tumor Meningitis Encephalitis

Congestive hear-l failure Coronary artery disease Hypertensive cardiovascular

Morphine intoxication CO* narcosis Narcolepsy Uremia

disease

Nonpathologic: High altitude Sleep Prematurity Advanced age Sedation

whereas others have considered neurologic involvement essential.’ Other pathologic conditions in which CSR is seen include CNS respiratory depression due to morphine intoxication, narcolepsy and carbon dioxide (C02) narcosis due to pulmonary hypoventilation or the obesity cardiorespiratory syndrome (Pickwickian). CSR has also been described in uremia.4 A number of situations in which CSR has been demonstrated have been devoid of clear indication of disease. CSR has been observed during sleep in patients with cardiorespiratory illness,8,9 but also in normal subjects.‘o Such respiration also occurs frequently in apparently normal elderly individuals, among patients who are sedated, and in 30% to 75% of premature infants during the first month of life.4 CSR is a consistent finding among normal individuals at high altitude, being seen more commonly in those unacclimatized to such an environment. 1’ A variety of clinical manifestations may accompany periodic respiration. Fluctuation in the level of consciousness may occur and is probably produced by changes in cerebral blood flow. The sensorium is depressed during the apneic phase, and this may be accompanied by conjugate gaze deviation, hyporeflexia, and the appearance

of abnormal plantar reflexes.4 Nystagmus and pupillary constriction may also occur during apnea, whereas convulsive movements and spasmodic facial contractions have been described during hyperpnea.12 Systemic blood pressure also occasionally displays variation with the ventilatory cycles.4 In addition, substantial changes in heart rate and rhythm have been demonstrated in association with CSR. In one series, patients with normal sinus rhythm or sinus tachycardia during the apneic phase displayed premature ventricular contractions, sinus bradycardia, Wenckebach phenomenon, second-degree A-V block, and sinus arrest during hyperpnea. Most rhythm disturbances occurred in patients with cardiac disease and failure. Digitalis toxicity was present in some.13 The pathogenesis of such dysrhythmias is thought to relate to an interaction between respiratory periodicity and increased vagal tone. The bradydysrhythmias are usually responsive to administration of atropine.14 As indicated above, there is disagreement concerning the pathophysiology of CSR. Increased lung-to-brain circulation time is known to be present in m.any patients. This has led to consideratio-n of the importance of a circulatory-induced delay in information regarding the status of ventilation provided to the neural respiratory

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George L. Sternbach

control centers. However, circulatory delay is not invariably present in patients with CSR. Increased respiratory center sensitivity to CO1, found in those displaying CSR, has caused some to postulate that this respiratory pattern results from inappropriate periods of hyperventilation followed by posthyperventilatory apnea.’ Other hypotheses incorporate the roles of both the circulatory and neurologic systems in the pathogenesis of periodic respiration.14 Although Stokes was extremely pessimistic regarding the prognostic significance of periodic respirations, subsequent study has not entirely borne out his fears. In one series of stroke patients, survival was greatest in those with a normal respiratory pattern, lowest in patients with hyperventilation or periodic breathing without apnea. Patients with classic CSR had an intermediate prognosis.5 However, in another study of a mixed group of neurosurgical patients, the presence of CSR was found to be of no significant prognostic importance.15 Management of the patient with CSR

should be chiefly directed at the underlying disorder. CSR itself generally requires no specific therapy. However, significant fluctuations in blood gas values have been demonstrated during the course of CSR. One series documented a range in pH of 0.20, Pcol of 14 torr; Paz of 20 torr, and oxyhemoglobin saturation of 18% .’ Obviously, fluctuations of this magnitude may attain significance in certain patients. The Pcoz is at its lowest at the onset of apnea and then increases until maximum hyperventilation is again reached. Oxyhemoglobin saturation varies in inverse fashion. CSR may be abolished by the administration of oxygen, carbon dioxide, or aminophylline.14 Any of these therapeutic options may be inappropriate for the patient with cardiorespiratory or neurologic disease. Intravenously administered aminophylline has been shown to terminate CSR, but may decrease cerebral blood flow, rendering it unsuitable for use in the patient with an acute neurologic event.

REFERENCES The Theory and Practice of Medicine. New York, Philosophical Library, 1964,

I. Hippocrites:

pp 111-112. 2. Cheyne J: A case of apoplexy in which the fleshy part of the heart was converted to fat. Dublin Hosp Rep 1818; 2:216-223. 3. Stokes W: The D&eases of the Heart and the Aorta. Dublin, Hodges & Smith, 1854, pp 323-324. 4. Dowel1 AR, Buckley CE III, Cohen R, et al: Cheyne-Stokes respiration. A review of clinical manifestations and critique of physiologic mechanisms. Arch Intern Med 1971; 127:712-726. 5. Rout MW, Lane DJ, Wagner L: Prognosis in acute cerebrovascular accidents in relation to respiratory pattern and blood gas tensions. Br Med J 1971; 3:1-9. 6. Guyton AC, Crowell JW, Moore JW: Basic oscillating mechanism of Cheyne-Stokes breathing. Am J Physiol 1956; 187:395-398.

7. Brown HW, Plum F: The neurologic Cheyne-Stokes respiration. Am JMed 849-860. 8. Tobin MJ, Chadha TS, Jenouri G, et al: patterns. 2. Diseased subjects. Chest

basis of 1961; 30:

Breathing 1983; 84:

286-294.

9. De Olazebal JR, Miller MJ, Cook WR, et al: Disordered breathing and hypoxia during sleep in coronary artery disease. Chest 1982; 82:548-551. 10. Tobin MJ, Cohn MA, Sackner MA: Breathing abnormalities during sleep. Arch Intern Med 1983; 143:1221-1228.

11. Waggener TB, Brusil PJ, Kronauer RE, et al: Strength and cycle time of high-altitude ventilatory patterns in unacclimatized humans. J Appl Physiol 1984; 56:576-581. 12. Harp HR, Sieker HO, Heyman A: Cerebral circulation and function in Cheyne-Stokes respiration. Am J Med 1961; 30:861-869. 13. Massumi RA, Nutter DO: Cardiac arrhythmias associated with Cheyne-Stokes respiration: A note on the possible mechanisms. Dis Chesf 1968; 54: 21-32. 14. Tobin MJ, Snyder JV: Cheyne-Stokes respiration revisited: Controversies and implications. Crit Care Med 1984; 12:882-887. 15. North JB, Jennett SJ: Abnormal Breathing patterns associated with acute brain damage. Arch Neural 1974; 31:338-344.