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CPAP and sleep disorders - Braido - World Allergy Organization

WorkshopCPAP and sleep disordersFulvio BraidoAllergy and Respiratory Diseases DepartmentUniversity of Genoa


To explain better the pathophysiologyof obstructive sleep apnea and its consequencesTo emphasize the magnitude of the clinical problemTo make familiar the practical aspects of the treatmenttechniquesTo identify unmet needs


Hystory of Sleep Breathing DisordesBickelmann AG, Burwell CS, Robin ED, Whaley RD.Extreme obesity associated with alveolarhypoventilation. A pickwickian syndrome.Am J Med 1956; 21: 811-8.


OSA Mile Stones1956 – Bickelmann AG, Burwell CS, Robin ED, Whaley RD. Extreme obesityassociated with alveolar hypoventilation. A pickwickian syndrome. Am J Med 21: 811-8.1965 - Gastaut H, Tassinari CA, Duron B. Etude polygraphique des manifestationsepisodiques (hypniques et respiratoires) du syndrome de Pickwick. Rev Neural 112:568-79.1965 - Jung R, Kuhlo W. Neurophysiological studies of abnormal night sleep and thepickwickian syndrome. Prog Brain Res 18: 140-59.1970 - Lugaresi E, Coccagna G, Mantovani M, Brignani F. Effets de la trachéotomiedans les hypersomnies avec respiration périodique. Rev Neurol 123: 267-8.1972 - Lugaresi E. Organizer Symposium: Hypersomnia with Periodic Breathing.Rimini, Italy, May 25-27. Bull Physiopath Resp 8:967.1981 - Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleepapnoea by continuous positive airway pressure applied through the nares. Lancet i:862-5.


OSAIt is caracterized by repetitive collapseof the upper airways during sleep


Hpopnea: reduction in the airflow > 30%SO2 decrease > 3%at least 10 second


Apnoea: reduction in the airflow > 90% for at least 90% of the eventat least 10 second


No inspiratory effort


Obstructive Sleep Apnea (OSA)• Snoring• Recurrent episodes of upper airway obstructionduring sleep (apneas, hypopneas)• Arousals• Excessive and disabling daytime sleepiness• OSA Syndrome – features of OSA on sleep study+symptoms of daytime sleepiness


OSA OSAS


OSASIt is characterised by repetitive collapseof the upper airways during sleep


Pathophysiology ofObstructive Sleep Apnea (continued)Physiologic• Decreased function of upper airway dilatormuscles (more than 20 skeletal musclesnormally involved)• Decreased pharyngeal dilator reflex response• Decreased chemoreceptor drive/central drive(mixed with central sleep apnea)


Impact of sleep on ventilationFall in phrenic and hypoglossal activityReduce response to hypercapnia and hypoxiaReduction in upper ariways protective reflexesMinute ventlation fall (16%)PaCO 2 increase 4-6 mmHgPaO 2 decrease (So2 decrease 2%)Irregular breathing during light and fragmented sleepUpper airways caliber reduction


SLEEPCorticalimputsChemoreceptorsensitivityRespiratorymotorneuronesRespiratorymusclecontractionLung mechanics:Airflow resistanceFRCV/Q relationshipsHypoventilationHypoxemiaHypercapnia


Pathophysiology ofObstructive Sleep ApneaMechanical• Short, thick neck• Neck flexion, supine position• Nasal obstruction, congestion, polyps


Pathophysiology ofObstructive Sleep Apnea (continued)Anatomic• Enlarged tonsils and adenoids (esp. ages 3-5), enlargeduvula• Macroglossia• Retrognathia, craniofacial abnormalities• Compliant (floppy) pharynx, especially soft palate• Fat deposition in lateral walls of pharynx, pharyngealdilator muscles (obesity)• Submucosal edema in lateral walls of pharynx


OSA pathophysiologyUpper airway volumePharyngeal collapsibilityUA muscle activityLoss of UA protectivereflex?Instability of the controlof breathing ?Alteration ofchemosensitivity?


Craniofacial size and Obesity can infuenceupper airway caliber.Watanabe et al, AJRCCM 165:260, 2002


Axial Upper Airway MR ImagesNormal SubjectApneic PatientSubjects with OSA have smaller upper airway in wakefulness


OSA Patients Have Elevated Activity of Their Genioglossus MuscleDuring Wakefulness (Lost during sleep)Mezzanotte et al, JCI 89:1571, 1992


Altered Upper Airway DilatorMuscle in English BulldogChronic load and altered pattern of usage inducemyopathic changes and following impaired abilityto maintain pharyngeal patencyPetrof et al, J Appl Physiol 76:1746, 1994


Eupneic Inspiration(Revised from Fig. 2-1 in Levitzky’s Pulmonary Physiology)Atmospheric Pressure : 0 cm H 2ONo flowAtmospheric Pressure : 0 cm H 2OFlow inInspiratoryforceAlveolarpressure:0 cm H 2 OOutward recoilof chest wallInward recoilof alveoliAlveolarpressure:-1 cm H 2OEND EXPIRATIONIntrapleural pressure:-5 cmH 2OTransmural pressure=0 cmH 2O - (-5cmH 2O)= +5 cmH 2OIntrapleural pressure:-8 cmH 2OTransmural pressure=-1 cmH 2O - (-8cmH 2O)= +7 cmH 2ODURING INSPIRATION


Atmospheric Pressure : 0 cm H 2ONo flowForced InspirationAtmospheric Pressure : 0 cm H 2OFlow inInspiratoryforceAlveolarpressure:0 cm H 2 OOutward recoilof chest wallInward recoilof alveoliAlveolarpressure:-23 cm H 2OIntrapleural pressure:-5 cmH 2OIntrapleural pressure:-30 cmH 2OTransmural pressure=0 cmH 2O - (-5cmH 2O)= +5 cmH 2OEND EXPIRATIONTransmural pressure=-23 cmH 2O - (-30 cmH 2O)= +7 cmH 2ODURING INSPIRATION


Evidence for risk factorsRisk factors: strong evidence• obesity• snoring• male sex• middle age and older• craniofacial abnormalitiesRisk factors: some evidence• Menopause• Family member with OSAS• Smoking• Nasal congestion at night


Demographic pattern of occuranceSnoring and sleepiness are the strongest predictor of OSA60% of men and 40% women between ages 41-65 yearsabitually snore.Thus is diagnostic utility is limited.InspirationExpiration


Demographic pattern of occuranceObesity is a very strong risk factor for OSAall measure of obesity - neck and waist girths, weight, skin folds -predict OSAAn increase of 1 Kg/m 2 in BMI yelds an estimated 30% increasedin the odds of developing OSAAn increase (decrease) of 1 kg/m 2 in BMI yields and estimated 9%increase (decrease) in AHImale: female ratio for OSA prevalence is 2:1


Obstructive Sleep ApneaUpper airway anatomySites of obstruction duringsleep apneaHard PalateTongueTongueHyoid boneLarynxSoft PalateNasopharynxEpiglottisOropharynxLaryngopharynx


Fat Is Deposited in Tongue inObese SubjectsNashi et al, Laryngoscope 117:1467, 2007


A Obese Mouse sleeping upright to protect his upperairwayThe standing sleeping mouse


Brennick et al, AJRCCM 179:158, 2009)


OSA prevalence by age:Sleep Heart Health StudyYoung T et al, Arch Intern Med 2002


By age 50 ys, incidence rates among men and women are similarCleveland FamilyStudy: interaction ofage with gender andBMIThe effect of BMI deacreases with age and may be irrilevant in elderlyTishler et al, JAMA 2003


Frequency ans severity of OSA inpre post menopausal women


Clinical Features•Loud snoring•Excessive daytime somnolence•Intellectual deterioration•Personality changing•Erectile disfunction•Nocturnal enuresis•Morning headachesGuilleminault, et al 1978Sleep Apnea Syndrome


Explanation for Hypersomnolenceor Excessive Daytime Sleepiness• Repeated arousals (may be hundreds per night) interferewith sleep architecture, especially rapid eye movementsleep• Abnormal sleep architecture leads to daytime somnolence,decreased attentiveness, blunted mentation, depression,personality changes


Description of Sleep Apnea Event• Upper airway Intermittent obstruction• Decreased alveolar ventilation• Decreased alveolar PO 2 ; increased alveolar PCO 2• Decreased arterial PO 2 ; increased arterial PCO 2• Stimulation of arterial and central chemoreceptors;• Arousal - Secondary hyperventilation


Effects of Breathhold on Arterial PO 2 and PCO 2Arterial Partial Pressure(mmHg)10080604020O 2CO 210 20 30Time (sec)All figures created by Betsy Giaimo


Effects of Hematocrit on Human Blood Viscosity8Relative Viscosity6420.2 0.4 0.6 0.8Hematocrit


Possible Explanation for Nocturia• Increased blood viscosity and arterial hypertension• Increased right ventricular afterload• Increased right ventricular end diastolic pressure andvolume• Increased right atrial volume• Increased secretion of atrial natriuretic peptide fromatrial myocytes,• Increases sodium excretion, and stretches receptorsthat suppress ADH secretion from the posteriorpituitary gland


Effects of Arterial PO 2 and PCO 2 on Cerebral Blood FlowArterial PCO 2(mm Hg)20 40 60 80 100100Cerebral Blood Flow(ml/100mg/min)75502520 40 60 80 100Arterial PO 2(mm Hg)


Explanation for Morning Headaches• Hypoxia and hypercapnia during obstruction causedilatation of cerebral blood vessels


CONDITIONS ASSOCIATED TOOSA


Signs of Obstructive Sleep Apnea• Systemic hypertension• Pulmonary hypertension (right axis deviationon ECG)• Polycythemia• Cor pulmonale• Bradycardia during apneic event• Tachycardia after airflow restored• Typically no respiratory abnormality whileawake


Risk FactorsOSASSexAgeObesitySmokingAlcoholCardiovascularPathologies


Mechanisms for CardiovascularConsequences of OSAArnardottir E et al, Sleep 32:447, 2009


Possible Explanation for SystemicHypertension• Repeated increases in sympathetic tone and systemicblood pressure during arousals may cause vascularremodeling and changes in endothelial function


OSAS & Arterial HypertensionArterial hypertension is especiallyfrequent in patients Suffering from OSASPartisen M et Al. Sleep Res 1983;12:273Kryger M et Al. WB Saunders 1989Pekkarinen T et Al. Clin Endocrinol 1987; 27 649-654.Cozzi Fet Al Pediatrics 1985; 75:836-843Bliwise D et Al Am J Public Haelth 1988:78:544-54725 - 38%


OSAS = Indipendent risk for theArterial Hypertension?Carlson J et Al Am J Respir Crit Care Med 1994;150:72-77Fischer J et Al Pneumollogie 1993; 47 (Supl.1):151-154Risk 2.1


Prospective Study of the Association betweenSleep-Disordered Breathing and HypertensionPaul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta,Ph.D., and James Skatrud, M.D.Volume 342:1378-1384 May 11, 2000 Number 19


NEJM Volume 342:1378-1384 May 11, 2000 N°19


Identifiable Causes of Hypertension1°Sleep apneaDrug-induced or drug-relatedChronic kidney diseasePrimary aldosteronismRenovascular diseaseChronic steroid therapy and Cushing syndromePheochromocytomaCoarctation of the aortaThyroid or parathyroid diseaseChobanian AV, Bakris GL, Black HR, et al.The Seventh Report of the Joint National Committee on Prevention,Detection, Evaluation, and Treatment of High Blood Pressure:the JNC 7 rep.JAMA. 2003;289:2560-2572.


JAMA.October 8, 2003;290:1906-1914.


OSAS & Ischemic CardiopathyECG ST elevation concomitant to apnoea induced Oxygen desaturationAm. J. Respir. Crit. Care Med., Volume 164, Number 12, December 2001, 2147-2165Sleep Apnea and Cardiovascular DiseaseRichard S. T. et Al


OSAS & Ischemic cardiopathySnorers/Normal-- >Probability risk 2.3D’Alessandro et Al. Br Med J 1990;300:1557-58Apneics/NormalHeart failure risk in OSAS 23.3 times comparedto normal subjectsHung J et Al Lancet 1990;336:261-264


OSAS & Ischemic CardiopathyOSAS minimum prevalence amongCoronaropathic subjects is about 16%Andreas S et Al Coron Artery Dis 1996;7:541-545


62 patients with established CADDuring the follow-up period (post-myocardial infarction),cardiovascular death occurred in six of 16 OSA patients(37.5%) compared with 4 (9.3%) in the non-OSA group(p = 0.018)Peker Y, et AlAm J Respir Crit Care Med. 2000;162:81-86OSA is represents a risk factor for death in post-yocardial infarction


Systematic RevisionJAMA. 2003;290:1906-1914Obstructive Sleep Apnea Implications for Cardiac and Vascular DiseaseAbu S. M. Shamsuzzaman, et AlThe post-MI changes of cardiac functionmay predispose to the development ofOSA, or may affect OSA severity.


Effects of Obstruction on PulmonaryCirculation and Right Ventricle• Hypoxic and hypercapnic pulmonary vasoconstrictioncause pulmonary hypertension• Chronic nighttime hypoxia may cause erythropoiesisand polycythemia• Increased hematocrit increases blood viscosity• Hypoxic pulmonary vasoconstriction (HPV), increasedblood viscosity, pulmonary hypertension increase rightventricular afterload• Increased right ventricular afterload may lead to rightventricular hypertrophy and eventually cor pulmonale


Possible Explanations for Bradycardia DuringObstruction, Tachycardia after Airflow Restored• Stimulation of arterial chemoreceptors usually increasesheart rate because it increases tidal volume (lunginflation reflex)• Stimulation of arterial chemoreceptors withoutstretching the lungs causes bradycardia• After arousal leads to restoration of airflow, large tidalvolumes stretch lungs and cause tachycardia• May hyperventilate immediately after arousal, thenhypoventilate until CO 2 is restored


Artrial FibrillationVentricular ExtrasystoleCardiaco arrestSinus bradycardiaAtrioventricular blockBenefit of Atrial Pacing in Sleep Apnea SyndromeStephane Garrigue, M.D. et AlNEJM Volume 346:404-412 February 7, 2002 Number 6


Cardiac arrhythmias, snoring, and sleep apneaV Hoffstein and S MateikaDepartment of Medicine, St. Michael's Hospital, Toronto, Canada.458 patients. 82 % of patients with mean nocturnal oxygen saturation< 90 % had arrhythmias vs 40 % of patients with meannocturnal oxygen saturation > 90 %70 % of patients with AHI > 40 had arrhythmias vs 42%with AHI < or 40


Sleep-disordered breathing and cardiovasculardisease: cross-sectional results of theSleep Heart Health StudyShahar E, Whitney CW, Redline S, et al.Am J Respir Crit Care Med. 2001;163:19-25“modest to moderate effects of sleep-disorderedbreathing on CVD manifestations within a rangeof the AHI that is typically considered "normal"or only mildly elevated (1-10 respiratory eventsper hour of sleep)”


Sleep-disordered breathing and cardiovasculardisease: cross-sectional results of theSleep Heart Health StudyShahar E, Whitney CW, Redline S, et al.Am J Respir Crit Care Med. 2001;163:19-25modestly elevated risk coupled with a highprevalence of mild sleep-disordered breathingmight have considerable public health implications


OSAS & Cerebral vascular pathologySnorers/controls stroke risk= 1.7-3.4Partinen et Al Lancet 1985;8468:1325-1326Palomaki et Al Stroke 1991; 22:1021-1025Spriggs et Al Q J Med 1992;83: 555-562Smirne S Eur et Al Respir J 1993; 6:1357-1361Neau J et Al Acta Neurol Scand 1995;92: 63-68However, it remains unclear whether sleep apnea isan independent risk factor for cerebrovasculardisease.


Mortality and apnea index in obstructive sleepapnea.Experience in 385 male patients.He J, Kryger MH, Zorick FJ, Conway W, Roth T.Chest. 1988 Jul;94(1):9-14.385 male OSA patientsProbability of cumulative eight-year survival was96 +/- 0.02 (SE) for HAI = less than 20vs63 +/- 0.17 for AHI greater than 20


EFFECTS of OSAS TREATMENTON OSAS-RELATEDCARDIOCIRCULATORY DISEASES


Refractory hypertension and sleep apnoea:effect of CPAP on blood pressure andbaroreflex.Logan AG Et AlEur Respir Journal 2003 Feb;21(2):241-7.11.0 +/- 4.4 mmHg reduction in 24-h systolic BP7.8 +/- 3.0 mmHg reduction in nightime diastolic BP


Pepperell JC,, et al. Ambulatory blood pressure after therapeutic andsubtherapeutic nasal continuous positive airway pressure for obstructivesleep apnoea: a randomised parallel trial.Lancet. 2002;359:204-210Becker HF, Jerrentrup A, Ploch T, et al. Effect of nasal continuous positiveairway pressure treatment on blood pressure in patients with obstructivesleep apnea.Circulation. 2003;107:68-73“several months of CPAP therapy resulted in a smallbut significant reduction of daytime blood pressureof between 1.3 and 5.3 mm Hg”


Nocturnal ischemic events in patients with obstructive sleep apneasyndrome and ischemic heart disease: effects of continuouspositive air pressure treatment.Peled N, Abinader EG, Pillar G, Sharif D, LavieAm Coll Cardiol. 1999 Nov 15;34(6):1744-9Treatment with continuous positive airwaypressure significantly ameliorated the nocturnalST depression time from 78 min to 33 min (p


The Cardiomyopathy of Obstructive Sleep ApneaRobert Joseph Thomas, MDAnnals of Internal Medicine1 September 1996 | Volume 125 Issue 5 | Page 425Cardiovascular Effects of Continuous Positive Airway Pressurein Patients with Heart Failure and Obstructive Sleep ApneaKaneko et al. 348 (13): 1233 NEJM, March 27, 2003


DiseaseAsthmaPrevalence300 millionCOPDAllergicrhinitisSleepapnea210 million400 million>100 millionGlobal Alliance against Chronic Respiratory Diseaseswww.who.int/respiratory/gard


How common is OSA?• US study in 1993: 24% of men and 9% ofwomen had AHI>5 (age 30-60)• 4% of men and 2% of women reporteddaytime sleepiness also (OSAS)• UK study in 1991: 1% of men had OSAS• Prevalence likely to increase as obesitylevel rises


Ferini-Strambi L et al, 2004• Minimally symptomatic or asymptomatic OSAis estimated to occur in 1 of 5 adults• OSA with daytime impairment (OSAsyndrome) occur in 1 of 20 adults and is rarelyrecognized


Symptoms attributed to sleep apnea rankedin order of frequency selected


QuestionnariesEpworth Sleepiness ScaleLimited utily of ESS and other sleepines scales to predict the presence of OSAS


Clinical ImpressionsUpper airways abnormalitiesHigh-arched palateLarge tongheTonsillar hypertrophyRedundant soft palatal tissueRetrognathiaMicrognathiaAllergic Rhinitis FeaturesMorphometric measurementsMeasuring neck sizePerforming skin fold thickness measurements


Assessment of the Upper AirwaysDirectvisualisationEndoscopyRhinometryRhinomanometryImaging


Clinical ImpressionsHistory + Physical examination: sensitivity 50%Hoffstein & Szalai Sleep 1993Bed partner report of apnea an snoring:Sensitivity 78%Specificity 64%Positive predictive value 64%Kapuniai et al Sleep 1988


Integration of Multiple FactorsWitnessed apneaSnoringNocturnal chokingExcessive daytime sleepinessMotor vehicle accidentsMale sexObesityHypertension80%


American Sleep Disorders Association, 1994Level I Level II Level III Level IVParameters> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 4, includingventilation (atleast twochannels ofrespiratoryactivity)Minimum ofoneBodyPositionPersonnelDocumentedorobjectivelymeasuredIn costantattendanceMay beobjectivelymeasuredNot inattendanceMay beobjectivelymeasuredNot inattendanceNotmeasuredNot inattendanceInterventions Possible Not possible Not possible Not possible


Ossimetria Holter


Flow evaluation


Flow evaluation


Flow evaluation


Level I Level II Level III Level IVParameters> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 4, includingventilation (atleast twochannels ofrespiratoryactivity)Minimum ofoneBodyPositionPersonnelDocumentedorobjectivelymeasuredIn costantattendanceMay beobjectivelymeasuredNot inattendanceMay beobjectivelymeasuredNot inattendanceNotmeasuredNot inattendanceInterventions Possible Not possible Not possible Not possible


MicrophoneFlow sensor(or PneumoFlow ® )Body positionsensor withintegratedthoracic sensorECG electrodesAbdominal sensorOxygen saturationsensorPressure sensorActivity sensor


VALIDATION STUDIES• Esnaola S et al, Eur Respir J 1996 (MesamIV)• Zucconi M et al, Eur Respir J 1996(MicroDigitrapper)• Ficker JH et al, Respiration 2001 (Somnocheck)⇒ The diagnostic accuracy of manualanalysis was found to be superior tothat of automatic analysis


Level I Level II Level III Level IVParameters> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 7, EEG,EOG, EMGchin, ECG,flow,respiratoryeffort, SaO2> 4, includingventilation (atleast twochannels ofrespiratoryactivity)Minimum ofoneBodyPositionPersonnelDocumentedorobjectivelymeasuredIn costantattendanceMay beobjectivelymeasuredNot inattendanceMay beobjectivelymeasuredNot inattendanceNotmeasuredNot inattendanceInterventions Possible Not possible Not possible Not possible


Management Options in OSASSubjective Indicators:• Sleepiness.• Quality of life• Mood• Symptoms• WorkObjective Indicators:• Comorbidity: (Cardiovascularand Respiratory diseases,Hypertension )• Neuropsychiatric andbehavioral complications• AHI, ODI, RDI


CPAP for OSAS• AHI >20 with or without symptoms• AHI 5-19 with sleepiness, behavioralcomplicationsModified ACCP Statement


TREATMENT• AHI > 25 and severe clinics• AHI < 25 and mild clinics• AHI < 25 and severe clinics• AHI > 25, mild clinics• Alterations of soft tissues orof the scheletonnCPAP + sleep hygieneSleep hygiene and dietSleep hygiene , diet andtemporary nCPAPSleep hygiene and dietSurgery, especially inyoung and/or non obesepatients


Lack of efficacy for acervicomandibular support collar inthe management of obstructive sleepapneaSkinner et al, CHEST 2004


AIM: To bring the mandibule ahead


Management Options in OSASNasal Continuous Positive Airway Pressure TherapyCPAP provides a splint


Upper airway dilator muscle activitySplinting of upper airwayHypoxemiasuction pressureDiaphragm efficiencyUpper airwaycollapseExcessivedaytimesleepnessNasal CPAPend expiratorylung volumePharyngeal crosssectionalareasnoringSplinting of upper airwayUpper airway mucosal Edema


6050RDIP


Epworth Scale2015**10BeforeAfter50PlaceboCPAPJenkinson et al., Lancet 1999


Comparison of SF-36 scores before and after CPAPtherapy in Patients (n = 45), and Irish Normative DataVariablesBeforeCPAPAfterCPAPp ValueNormativeValues,Physical functioning 75 80 0.006 95Role limitation (physical) 50 100 0.0004 100Role limitation (emotional) 66.7 100 0.01 100Social functioning 66.7 100 0.0004 100Mental health 76 80 0.02 80Energy/vitality 35 60 0.001 67Pain 77.8 88 0.33 84General health perception 67 67 0.05 77


50SF-36**6050**4030201040302010PrimaDopo0PlaceboCPAP0PlaceboCPAPMental ComponenentSummaryPhysical ComponentSummaryJenkinson et al. Lancet 1999


Impact of Nasal ContinuousPositive Airway PressureTherapy on the Quality of Lifeof Bed Partners of PatientsWith Obstructive SleepApnea SyndromeDoherty LS, Kiely JL,Lawless G, McNicholas WT.Chest, 2003


Comparison between Partners ESS scoresbefore and after CPAP therapy (n=45)VariablesBefore CPAPAfter CPAPp ValuePatientESS16 (11–20)8 (4–15)0.001Anxiety8 (5–9)6 (3–8)0.001Depression5 (3–8)4 (2–6)0.02PartnerESS4 (1–8.5)2 (1–5)0.007Anxiety7 (5–11)7 (4–8)0.02Depression4 (2–6)4 (1–5)0.1


70AHI6050403020100AHIBaseline after 1 month After onenight withoutCPAP CPAPKribbs et al. Am Rev Respir Dis 1993


14121086420Baseline 3 months 12 monthsDaytime SleepenessMunoz et al. Eur Respir J 2000


Nasal Continuous Positive Airway Pressure TherapyTitrationChoise of Device: CPAP, Auto-CPAPMask SelectionHome monitoring


Figura 15. Dispositivi per l’erogazione di CPAP


OSAS Treatment• Nasal CPAP is the treatment of choice• Results in successful treatment in 95%• Not as costly as surgery• Long term compliance rates of 60 -70%• Improved long term survival (vs. UPPP)• Can re-titrate the pressure if the patient’sclinical condition changes


POTENTIAL BARRIERS TO CPAPADHERENCE• Mechanical• Psychological• Educational• Physical


CPAP ADHERENCE:MECHANICAL BARRIERS:• Positive Airway Pressure System• Interface System• Humidification• Nasal congestion• Rhinorrhea• Epistaxis• Sinus discomfort• Oronasal dryness• Skin rash• Abrasion• Conjunctivitis• Chest discomfort• Difficulty exhaling• Aerophagia• Pneumothorax (rare)• Pneumoencephaly (rare)


CPAP ADHERENCE:PSYCHOLOGICAL BARRIERS• Claustrophobic• Embarrassment• Vanity• Personality Type Disorders• Support System


CPAP ADHERENCE:EDUCATIONAL BARRIERS• Comprehension• Patient’s knowledge of obstructive sleep apnea• Patient’s knowledge of interface system• Patient’s knowledge of delivery system


CPAP COMPLIANCE:PHYSICAL BARRIERS• Physical Handicaps• Extreme Obesity• Nasal Dryness• Stomach Distention• Retrognathic• Under Treated• Over Treated• Sinus Problems• Puffing• Ear Discomfort• Eye Irritation• Material Sensitivity


To explain better the pathophysiologyof obstructive sleep apnea and its consequencesTo emphasize the magnitude of the clinical problemTo make familiar the practical aspects of the treatmenttechniquesTo identify unmet needs


WorkshopCPAP and sleep disordersFulvio BraidoAllergy and Respiratory Diseases DepartmentUniversity of Genoafulvio.braido@unige.it

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