Effects ofacetazolamide inpatients withthesleep apnoeasyndrome

Thereisas yetno convincing evidence thatacetazolamide, a carbonic anhydrase inhibitor, iseffective inobstructive sleep apnoea.Astudy wastherefore designed toexamine theeffect ofacetazolamide (250mg/day) on sleep events andventilatory control during wakefulness innine patients withthesleep apnoeasyndrome. Ineight oftheninepatients theapnoeaindex andthetotal duration ofapnoeawerereduced byacetazolamide, andthemean(SEM)apnoeaindex ofall patients changed from25-0(67)to181(58)episodes anhour. Furthermore, thetotal timeofarterial oxygen desaturation (Sao2-more than4% depression inSao2 fromthebaseline sleeping level-divided by total sleep time wasalso significantly decreased andits mean(SEM)value improved from24-1(7 9) 13-6(4-8)% oftotal sleep time. Fiveofthesevenpatients withvarying degrees ofdaytime hypersomnolence hadtheir symptomsobviously improved. There wasnopatient whosepredominant typeofapnoeawasconverted fromtheobstructive tothecentral type, orvice versa.Inthestudies of wakefulness, metabolic acidosis, an increase ofarterial oxygentension (Pao2) anda decrease of arterial carbon dioxide tension (PaCo2) wereobserved. Theslopes oftheocclusion pressure response andtheventilatory responsetocarbon dioxide increased, andthecarbon dioxide ventilatory response line shifted totheleft. Itissuggested that acetazolamide cannot remove apnoeacompletely buthasa beneficial effect inmild casesofobstructive sleep apnoeathrough anaugmentation ofcentral (CO2, H+)drive andastabilising effect onventilatory control. Owingtoinsufficient knowledge aboutthepatho- genesis ofthesleep apnoea syndrome, effective treat- mentformostsuchpatients hasyettobeestablished. Current treatment isbasedmerely onthephysical findings ofthepatients, thetypeofapnoea, andthe severity ofthesyndrome. Drugs suchasprotriptyline'2 andmedroxyprogesterone acetate34 forobstructive andcentral sleep apnoea werereported tobeeffective inonly afewpatients. Acetazolamide induces metabolic acidosis by inhibiting carbonic anhydrase intherenal tubular structures andstimulates ventilation. Furthermore, it mayincrease cerebral carbon dioxide tension (Pco2) byimpeding carbon dioxide transport andmaysup- press formation ofcerebrospinal fluid bicarbonate at thesametime, resulting inasustained increase in alveolar ventilation.