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Vol. 32. Issue 7.
Pages 341-347 (August - September 1996)
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Vol. 32. Issue 7.
Pages 341-347 (August - September 1996)
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Estimulación hipercápnica y respuesta ventilatoria en el síndrome de apnea obstructiva del sueño. Comparación de reinhalación y estado-estable
Hypercapnic stimulation and ventilatory response in obstructive sleep apnea syndrome. Comparison of rebreathing and stable techniques
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J.G. Soto Campos*, S. Cano Gómez, J. Fernández Guerra, M.A. Sánchez Armengol, F. Capote Gil, J. Castillo Gómez
Servicio de Neumología. Hospital Universitario Virgen del Rocío. Sevilla
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El objetivo de este estudio fue valorar la respuesta ventilatoria a la estimulación con carbónico en pacientes con síndrome de apneas obstructivas durante el sueño (SAOS) sin enfermedad pulmonar obstructiva crónica (EPOC), examinando las diferencias entre enfermos hiper y normocápnicos y comparando los resultados obtenidos con las dos técnicas usualmente empleadas en la estimulación hipercápnica (rebreathing y estado-estable). Para ello, hemos estudiado a 15 pacientes obesos, todos ellos con índice de apnea-hipopnea (IAH) superior a 10 en el registro polisomnográfico practicado durante una noche completa, a los que realizamos las siguientes pruebas funcionales respiratorias: espirometría, determinación de resistencias de vías aéreas y volúmenes estáticos pulmonares mediante pletismografía y gasometría arterial. Posteriormente analizamos la respuesta ventilatoria mediante el método de estado-estable, con concentraciones de CO2 progresivamente crecientes (1-9%) y la técnica de rebreathing. En el grupo total de enfermos obtuvimos resultados similares mediante ambos métodos, en el análisis de: ΔVE/ΔPCO2, (0,64±0,35 frente a 0,67±0,48 1/min/mmHg; p=0,59), ΔVt/ΔPCO2 (28,33±16,23 frente a 26,42±16,94 ml/mmHg; p=0,9), ΔVt/Ti/ΔPCO2 (28,82±20,9 frente a 29,41±23,78 ml/s/mmHg; p=0,89) y ΔP0, l/ΔPCO2 (0,11±0,07 frente a 0,117±0,05 cmH2O/mmHg; p=0,58). Comparamos los resultados obtenidos por ambas técnicas dividiendo a nuestra población en 2 grupos de 7 y 8 pacientes respectivamente, según el nivel de PaCO2 en vigilia fuese superior o inferior a 45 mmHg. Los enfermos hipercápnicos (grupo I) tenían una mayor edad (61±3,5 frente a 50±9 años; p=0,04) sin presentar diferencias en el índice de masa corporal con respecto a los pacientes normocápnicos (grupo II) (37,59±6,4 frente a 34,56±4,75 kg/m2; p=0,33). Los resultados de ambas técnicas de estimulación hipercápnica fueron similares en los miembros de un mismo grupo existiendo una disminución estadísticamente significativa (p < 0,03), en los sujetos con hipercapnia diurna en ΔVE/ΔPCO2 ΔVt/ΔPCO2, ΔVt/Ti/ΔPCO2 y ΔP0,1/ΔPCO2. Concluimos que no existen diferencias en los resultados obtenidos en el estudio del control de la ventilación con las técnicas de rebreathing y estado-estable. Así mismo, la respuesta ventilatoria a la estimulación con CO2 en individuos con SAOS e hipoventilación diurna se encuentra disminuida en comparación con enfermos normocápnicos.

Palabras clave:
Respuesta ventilatoria hipercápnica
Síndrome de apneas durante el sueño
Control de respiración
Método de reinspiraciones repetidas

The objetive of this study was to assess ventilatory response to stimulation with CO2 in patients suffering obstructive sleep apnea syndrome (OSAS) but without chronic obstructive pulmonary disease (COPD), by examining differences between hyper and normocapnic patients and comparing the results obtained with the usual techniques used to stimulate hypercapnia (rebreathing and stable-state). To this end, we studied 15 obese patients, all with an apnea-hypopnea index greater than 10 from a polysomnograph lasting a full night. The following lung function tests were performed: spirometry, air way resistance measures and static lung volumes by plethysmograph and arterial gasometry. We later analized ventilatory response by the stable-state method, with increasing CO2 concentrations (from 1 to 9%) and by the rebreathing method. Results from the two methods were similar for all patients: ΔVE/ΔPCO2 (0,64±0,35 vs 0,67±0,48 1/min/mmHg; p=0,59), ΔVt/ΔPCO2, (28,33±16,23 vs 26,42±16,94 ml/mmHg; p=0,9), ΔVt/Ti/ΔPCO2, (28,82±20,9 vs 29,41±23,78 ml/s/mmHg; p=0,89) y ΔP0, l/ΔPCO2 (0,11±0,07 vs 0,117±0,05 cmH2O/mmHg; p=038). We compared the results obtained by the two techniques by dividing the sample into two groups of 7 and 8 patients, respectively, depending on whether PaCO2 level before stimulation was higher or lower than 45mmHg. The hypercapnic patients (group I) were older (61±3,5 vs 50±9 years; p=0,04) but were not different with respect to body mass freom the normocapnic patients (group II) (37,59±6,4 vs 34,56±4,75 kg/m2; p=0,33). The results from the two techniques for stimulating hypercapnia were similar within each group, with a statistically significant decrease (p < 0,03) in patients with daytime hypercapnia in ΔVE/ΔPCO2 ΔVt/ΔPCO2, ΔVt/Ti/ΔPCO2 and ΔP0,1/ΔPCO2. We conclude that there are no differences in the results obtained with the rebreathing and stable state techniques. Likewise, ventilatory response to stimulation with CO2 in individuals with OSAS and daytime hypoventilation is less than of normocapnic patients.

Key words:
Ventilatory responses to CO2
Sleep apnea syndrome
Control of breathing
Rebreathing
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Bibliografía
[1.]
C. Guilleminault, A. Tilkian, W.C. Dement.
The sleep apnea syndromes.
Annu Rev Med, 27 (1976), pp. 465-484
[2.]
D.M. Rapoport, S.M. Garay, H. Epstein, R.M. Goldring.
Hypercapnia in the obstructive sleep apnea syndrome: a reevaluation of the “Pickwickian Syndrome”.
Chest, 89 (1986), pp. 627-635
[3.]
C.S. Burwell, E.D. Robin, R.D. Whaley, A.G. Bickelmann.
Extreme obesity associated with alveolar hypoventilation. A pickwickian syndrome.
Am J Med, 21 (1956), pp. 811-818
[4.]
A. Naimark, R.M. Cherniack.
Compliance of respiratory system and its components in health and obesity.
J Appl Physiol, 15 (1960), pp. 377-382
[5.]
H.C. Cullen, P.F. Formel.
The respiratory defects in extreme obesity.
Am J Med, 32 (1963), pp. 525-531
[6.]
H.S. Holley, J. Milic Emili, M.R. Becklade, D.V. Bates.
Regional distribution of pulmonar ventilation and perfusion in obesity.
J Clin Invest, 46: (1967), pp. 475-481
[7.]
T.D. Bradley, R. Rutherford, F. Lue, H. Moldofsky, R.F. Grossman, N. Zamel, et al.
Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea.
Am Rev Respir Dis, 134 (1986), pp. 920-924
[8.]
J.A. Leech, E. Önal, P. Baer, M. Lopata.
Determinants of hypercapnia in occlusive sleep apnea syndrome.
Chest, 92 (1987), pp. 807-813
[9.]
C.S. Chan, R.R. Grunstein, P.T.P. Bye, A.J. Woolcock, C.E. Sullivan.
Obstructive sleep apnea with severe chronic airflow limitation. Comparison of hypercapnic and eucapnic patients.
Am Rev Respir Dis, 140 (1989), pp. 1.274-1.278
[10.]
J. Krieger, E. Sforza, M. Apprill, E. Lampert, E. Weizenblum, J. Ratomaharo.
Pulmonary hypertension, hypoxemia and hypercapnia in obstructive sleep apnea patients.
Chest, 96 (1989), pp. 729-737
[11.]
S.M. Garay, D. Rapoport, B. Sorkin, H. Epstein, I. Freinberg, R. Goldring.
Regulation of ventilation in the obstructive sleep apnea syndrome.
Am Rev Respir Dis, 124 (1981), pp. 451-457
[12.]
F. Kunitomo, H. Kimura, K. Tatsumi, S. Okita, H. Tojima, T. Kuriyama, et al.
Abnormal breathing during sleep and chemical control of breathing during wakefulness in patients with sleep apnea syndrome.
Am Rev Respir Dis, 139 (1989), pp. 164-169
[13.]
C.E. Sullivan, R.R. Grunstein, O. Marrone, M. Berthon-Jones.
Sleep apnea. Pathophysiology: upper airway and control of breathing.
obstructive sleep apnea syndrome: clinical research treatment, pp. 49-69
[14.]
A.S. Rebuck.
Mesurement of ventilatory response to CO, b rebreathing. Chest.
70, (1976), pp. 118-121
[15.]
J.A. Dempsey.
CO2 response: stimulus definition and limitations.
Chest, 70 (1976), pp. 114-118
[16.]
Sociedad Española de Patología Respiratoria (SEPAR).
Normativa para la espirometría forzada.
Ed. Doyma, (1985),
[17.]
A.B. Dubois.
A rapid plethysmographic method for measuring thoracic gas volumen. A comparison with a nitrogen washout method for measuring functional residual capacity in normal subjects.
J Clin Invest, 35 (1956), pp. 322-326
[18.]
N.K. Burki.
Measurements of ventilatory regulation.
Clin Chest Med, 10 (1989), pp. 215-226
[19.]
J.M. Bland, D.G. Altman.
Statistical methods for assessing agreement between two methods of clinical measurement.
Lancet, 1 (1986), pp. 307-310
[20.]
R.S. Kronennberg, C.W. Drage.
Attenuation of the ventilatory and heart rate responses to hypoxia and hypercapnia with aging in normal men.
J Clin Invest, 52 (1973), pp. 1.812-1.819
[21.]
R.L. Iones, J.M. Neary, G.R. Thomas.
Valores normales de la respuesta de la ventilación hipercápnica: efectos de la edad y capacidad ventilatoria.
Respiration (ed. esp.), 4 (1994), pp. 183-188
[22.]
N.S. Cherniack, D.H. Lederer, M.D. Althose, S.G. Kelsen.
Occlusion pressure as a technique in evaluating respiratory control.
Chest, 70 (1976), pp. 137-141
[23.]
M.D. Milic-Emili, M.M. Grunstein.
Drive and timing components of ventilation.
Chest, 70 (1976), pp. 131-133
[24.]
C. Guilleminault, J. Cumminskey.
Progressive improvement of apnea index and ventilatory response to CO2, after tracheostomy in obstructive sleep apnea syndrome.
Am Rev Respir Dis, 126 (1982), pp. 14-20
[25.]
H. Kimura, K. Tatsumi, F. Kunitomo, S. Okita, H. Tojima, S. Kouchiyama, et al.
Progesterone therapy for sleep apnea syndrome evaluated by occlusion pressure responses to exogenous loading.
Am Rev Respir Dis, 139 (1989), pp. 1.198-1.206
[26.]
C.E. Sullivan, M. Berthon Jones, F.G. Issa.
Remission of severe obesity-hypoventilation syndrome after short-term treatment during sleep with nasal continouus positive airway pressure.
Am Rev Respir Dis, 128 (1983), pp. 177-181
[27.]
K.R. Cooper, B.A. Phillips.
Effect of short sleep loss on breathing.
J Appl Physiol, 53 (1982), pp. 855-858
[28.]
J.V. Weil, E. Byrne-Quinn, J.E. Sodel, G.P. Pilley, R.P. Grover.
Acquired attenuation of chemorreceptor function in chronically hypoxic man at high altitude.
J Clin Invest, 50 (1971), pp. 186-195
[29.]
N.H. Edelman, S. Lahiri, L. Brando, N.S. Cherniack, A.P. Fishman.
The blunted ventilatory response to hipoxia in cyanotic congenital heart disease.
N Engl J Med, 282 (1970), pp. 405-411
[30.]
A.R. Gold, A.R. Schwartz, R.A. Wise, P.L. Smith.
Pulmonary function and respiratory chemosensitivity in moderately obese patients with sleep apnea.
Chest, 103 (1993), pp. 1.325-1.329
[31.]
M. Lopata, E. Önal.
Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation.
Am Rev Respir Dis, 126 (1982), pp. 640-645
[32.]
M. Kryger, L.F. Quesney, D. Holder, P. Gloor, P. MacLeod.
The sleep deprivation syndrome of the obese patient. A problem of periodic nocturnal upper airway obstruction.
Am J Med, 56 (1974), pp. 531-538
Copyright © 1996. Sociedad Española de Neumología y Cirugía Torácica
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