BY. J. Dis. Chest (1976) 70, 138
Short Communication SLEEPING VENTILATORY PATTERNS IN PATIENTS WITH SEVERE CHRONIC AIRFLOW OBSTRUCTION CAUSING RESPIRATORY FAILURE R. RODRIGUEZ-ROISIN,* Lung Function
B. P. HICKEYt Unit, Brompton
AND T. J. H. CLARK
Hospital,
London
Summary During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their COz responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood Pco2, and was not seen in hypoxaemic patients with a normal Pco2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing during waking hours, and is linked to the arterial blood PCOZ.
INTRODUCTION
In normal subjects sleep produces an increase in alveolar carbon dioxide tension and a fall in breathing frequency. After a chance clinical observation that some patients with chronic obstructive bronchitis developed tachypnoea at night a group of such patients was studied to compare their sleeping and waking breathing patterns. Patients and Methods Fifteen patients with chronic airways obstruction and respiratory failure were studied. They were subdivided into two groups, nine having both hypoxaemia and hypercapnia (Group A) and six having hypoxaemia with a normal Paces (Group B). All had suffered from airflow obstruction for at least ten years. All gave a history of cigarette smoking. Diagnoses of chronic bronchitis, asthma and emphysema were based on a combination of clinical, radiological and physiological features. All were receiving controlled oxygen therapy via a Ventimask and none were receiving sedation or respiratory stimulants. No patient was febrile at the time of study. Ventilator-y patterns were assessed with a strain gauge pneumograph around the chest. Nocturnal recordings of at least one hour’s duration were made and these were compared with similar tracings obtained earlier in the day with the patient awake. All recordings were made by the same operator (R.R.R.) with the patient in his usual hospital bed and with the pneumograph left in place after recording the waking pattern. Nocturnal readings started about two hours after sleep started; * Present address: Servicio de Respiratorio, Clinica Medica C, Hospital Clinic0 y Provicial, Casanovas 143, Barcelona 11, Spain. t Present address : Pulmonary Laboratory, Eastern North Carolina Speciality Hospital, Wilson, North Carolina 27893, USA.
139
Sleeping Ventilatovy Patterns
usually between 23.00 and 0.200 hours. The recordings were analysed as follows: the mean respiratory frequency was obtained from fifty consecutive breaths at 15, 30, 45 and 55 min. The presence of sleep was confirmed by failure of the patient to respond to shining a torch in his eyes. If the patient awoke during the test or exhibited the features of rapid eye movement (REM) sleep, the procedure was discontinued and recommenced when the patient was asleep once more. Spirometry and lung volumes were measured as soon as the patient’s clinical condition was stable after admission and blood gas tensions were analysed within 12 hours of recording the breathing patterns. COz responsiveness was assessed by a rebreathing technique. An Eysenck personality inventory was also obtained, being scored in such a way that a high E score represents extroversion and high N score indicates neurotic traits.
RESULTS The details of each patient’s age, sex, height, clinical diagnosis, lung function studies and arterial blood gases are available upon request. No significant differences between A and B were found in terms of lung function, CO2 responsiveness, personality or waking ventilatory rates. There was, however, a statistically significant difference between their sleeping ventilatory rates (mean for group A 26.0, and for group B 18.1 breaths per minute; P 0.01) and their increase in respiratory rate during sleep also differs from normals (Fig. 1). DISCUSSION This study has shown that, unlike healthy subjects, some patients with chronic airways obstruction developed tachypnoea during sleep. This abnormal response was related to COs retention and unrelated to other clinical or physiological characteristics.
-
0 ’ Group Normal
1
Group Subjects
2
Group
A
Group’
B
Patients
Fig. 3. Comparisons of ventilatory rates when awake (A) and asleep (S) between normal subjects and patients with respiratory failure. Group 1 from Khatri and Freis (1967). Group 2 fromBiilow (1963). Groups A and B see text.
140
Sleeping Ventilatory
Patterns
Without simultaneous EEG recordings one cannot exclude REM sleep disturbances nor be certain that sleep has been achieved. Measurements were, however, made early in the night when REM sleep is less common and traces were obtained during disturbed sleep were discarded. Moreover, changes in respiratory frequency during REM sleep in normal subjects are slight. It is perhaps surprising that patients with COs retention should develop nocturnal tachypnoea and one may speculate that in them sleep removes a cortical inhibiting mechanism which slows their breathing frequency during the waking hours. Unfortunately we were unable to measure tidal volume and sleeping blood gas tensions and therefore cannot report changes in alveolar and total ventilation. The stimulus to the tachypnoea, whatever it is, must be powerful to provoke this sustained and probably inefficient change in the pattern of breathing. Our observations are of sufficient interest to warrant more detailed study both for confirmation and explanation. ACKNOWLEDGEMENT
We wish to thank the physicians of the Brompton Hospital for permission to study the patients under their care. R. R.-R. was supported by ‘Fundacion Pedro y Pons’, Facultad de Medicina, University of Barcelona, and B. P. Hickey by a fellowship of the Association of Commonwealth Universities. Requests for reprints should be addressed to Dr T. J. H. Clark, Brompton Hospital, Fulham Road, London SW3 6HP. REFERENCES BELOW, KHATRI,
K. B. (1963) Respiration and wakefulness I. M. & FREIS, E. D. (1967) Haemodynamic
in man. Acta physiol. stand. 59, suppl. 209, 1. changes during s1eep.J. czppl. Physiol. 22,867.
Short Communication SLEEPING VENTILATORY PATTERNS IN PATIENTS WITH SEVERE CHRONIC AIRFLOW OBSTRUCTION CAUSING RESPIRATORY FAILURE R. RODRIGUEZ-ROISIN,* Lung Function
B. P. HICKEYt Unit, Brompton
AND T. J. H. CLARK
Hospital,
London
Summary During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their COz responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood Pco2, and was not seen in hypoxaemic patients with a normal Pco2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing during waking hours, and is linked to the arterial blood PCOZ.
INTRODUCTION
In normal subjects sleep produces an increase in alveolar carbon dioxide tension and a fall in breathing frequency. After a chance clinical observation that some patients with chronic obstructive bronchitis developed tachypnoea at night a group of such patients was studied to compare their sleeping and waking breathing patterns. Patients and Methods Fifteen patients with chronic airways obstruction and respiratory failure were studied. They were subdivided into two groups, nine having both hypoxaemia and hypercapnia (Group A) and six having hypoxaemia with a normal Paces (Group B). All had suffered from airflow obstruction for at least ten years. All gave a history of cigarette smoking. Diagnoses of chronic bronchitis, asthma and emphysema were based on a combination of clinical, radiological and physiological features. All were receiving controlled oxygen therapy via a Ventimask and none were receiving sedation or respiratory stimulants. No patient was febrile at the time of study. Ventilator-y patterns were assessed with a strain gauge pneumograph around the chest. Nocturnal recordings of at least one hour’s duration were made and these were compared with similar tracings obtained earlier in the day with the patient awake. All recordings were made by the same operator (R.R.R.) with the patient in his usual hospital bed and with the pneumograph left in place after recording the waking pattern. Nocturnal readings started about two hours after sleep started; * Present address: Servicio de Respiratorio, Clinica Medica C, Hospital Clinic0 y Provicial, Casanovas 143, Barcelona 11, Spain. t Present address : Pulmonary Laboratory, Eastern North Carolina Speciality Hospital, Wilson, North Carolina 27893, USA.
139
Sleeping Ventilatovy Patterns
usually between 23.00 and 0.200 hours. The recordings were analysed as follows: the mean respiratory frequency was obtained from fifty consecutive breaths at 15, 30, 45 and 55 min. The presence of sleep was confirmed by failure of the patient to respond to shining a torch in his eyes. If the patient awoke during the test or exhibited the features of rapid eye movement (REM) sleep, the procedure was discontinued and recommenced when the patient was asleep once more. Spirometry and lung volumes were measured as soon as the patient’s clinical condition was stable after admission and blood gas tensions were analysed within 12 hours of recording the breathing patterns. COz responsiveness was assessed by a rebreathing technique. An Eysenck personality inventory was also obtained, being scored in such a way that a high E score represents extroversion and high N score indicates neurotic traits.
RESULTS The details of each patient’s age, sex, height, clinical diagnosis, lung function studies and arterial blood gases are available upon request. No significant differences between A and B were found in terms of lung function, CO2 responsiveness, personality or waking ventilatory rates. There was, however, a statistically significant difference between their sleeping ventilatory rates (mean for group A 26.0, and for group B 18.1 breaths per minute; P 0.01) and their increase in respiratory rate during sleep also differs from normals (Fig. 1). DISCUSSION This study has shown that, unlike healthy subjects, some patients with chronic airways obstruction developed tachypnoea during sleep. This abnormal response was related to COs retention and unrelated to other clinical or physiological characteristics.
-
0 ’ Group Normal
1
Group Subjects
2
Group
A
Group’
B
Patients
Fig. 3. Comparisons of ventilatory rates when awake (A) and asleep (S) between normal subjects and patients with respiratory failure. Group 1 from Khatri and Freis (1967). Group 2 fromBiilow (1963). Groups A and B see text.
140
Sleeping Ventilatory
Patterns
Without simultaneous EEG recordings one cannot exclude REM sleep disturbances nor be certain that sleep has been achieved. Measurements were, however, made early in the night when REM sleep is less common and traces were obtained during disturbed sleep were discarded. Moreover, changes in respiratory frequency during REM sleep in normal subjects are slight. It is perhaps surprising that patients with COs retention should develop nocturnal tachypnoea and one may speculate that in them sleep removes a cortical inhibiting mechanism which slows their breathing frequency during the waking hours. Unfortunately we were unable to measure tidal volume and sleeping blood gas tensions and therefore cannot report changes in alveolar and total ventilation. The stimulus to the tachypnoea, whatever it is, must be powerful to provoke this sustained and probably inefficient change in the pattern of breathing. Our observations are of sufficient interest to warrant more detailed study both for confirmation and explanation. ACKNOWLEDGEMENT
We wish to thank the physicians of the Brompton Hospital for permission to study the patients under their care. R. R.-R. was supported by ‘Fundacion Pedro y Pons’, Facultad de Medicina, University of Barcelona, and B. P. Hickey by a fellowship of the Association of Commonwealth Universities. Requests for reprints should be addressed to Dr T. J. H. Clark, Brompton Hospital, Fulham Road, London SW3 6HP. REFERENCES BELOW, KHATRI,
K. B. (1963) Respiration and wakefulness I. M. & FREIS, E. D. (1967) Haemodynamic
in man. Acta physiol. stand. 59, suppl. 209, 1. changes during s1eep.J. czppl. Physiol. 22,867.
