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Respiratory Insufficiency Sleep Apnoe-Hypopnoe Syndrome (SAHS). Attila Somfay. SZTE Tüdőgyógyászati Tanszék, Deszk. Classification of respiratory insufficiency. Progression in time – acute (pH!) - chronic Pathophysiolog y - type I (hypoxemia = PaO2 <60 Hgmm)
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Respiratory InsufficiencySleep Apnoe-Hypopnoe Syndrome (SAHS) Attila Somfay SZTE Tüdőgyógyászati Tanszék, Deszk
Classification of respiratory insufficiency • Progression in time – acute (pH!) • - chronic • Pathophysiology-type I (hypoxemia=PaO2<60 Hgmm) • -type II (hypoxemia + hypercapnia=PaCO2>50 Hgmm) • Pathomechanism - V/Q mismatch • - hypoventilation • - limited diffusion • - right-left shunt • Etiology - airway • - lung parenchyma • - lung vasculature • - chest wall and pleura • - neuromuscular
Alveolar gas equation: PA (mmHg)=(PB-47) x FIO2 – 1.2 x PaCO2 102 = 150 - 48
VCO2 PCO2= VA
Diminished diffusion • Transit (contact)time: 0.75 s • Equilibration: 0.25 s • Exercise+ diminished diffusion: PaO2<60 Hgmm • PaCO2 : no change or decreases • Causes: alveolitis fibrotisans, sarcoidosis, pneumoconiosis, connective tissue diseases, drugs, irradiation, alveolar cell cc, Goodpasture-sy, CHF
Mechanism of exercise induced hypoxaemia
Right-left shunt • Anatomic: lung (a-v malformation), heart (ASD, VSD, Eisenmenger-sy) • Functional: V/Q=0; ARDS, atelectasia, oedema, haemorrhagia • Hypercapnia: no or rarely • Hypoxemia: cannot be corrected by 100% O2
Ventilation-perfusion mismatch • “Functional shunt”, most frequent cause of hypoxemia • COPD, ILD, pulmonary embolism • Regional differences in airway resistance and lung compliance • Hypercapnia: only in severe cases (e.g.blue bloater COPD) • Hypoxemia: correctable with small incraese in FIO2
Oxigen supplementation in chronic resp. insuff. only way to prolong survival in case of chronic resp.insuff. NOTT: Ann Intern Med, 1980 BMC: Lancet, 1981 • Indication: (stable condition) • PaO2 < 55 mmHg or SAT < 88% • 55 mmHg < PaO2 < 60 mmHg with pulmonary hypertension, polyglobuliaor right heart failure • Aim: PaO2 ≈ 60 mmHg vagy SAT ≈ 90 % • CAVE: CO2 retention in COPD (max.1-2 L/min)! • Dosage: > 15 h/day
PaO2 < 55 Hgmm PaO2 > 55 Hgmm
Diagnosis of ARDS • Acuteonset (1-3 days) • One or more risk factors • Chest X-ray: new, bilateral, snow flake – like infiltrates • Exclusion: heart failure, fluid overdose, chronic lung disease • Hypoxemia not corrected with O2: - mild: PaO2/FIO2200-300 mmHg - moderate: 100-200 mmHg - severe: < 100 mmHg
Non-invasive ventilation (NIV) in global respiratory insufficiency - BiPAP
Sleep apnoe-hypopnoe syndrome (SAHS) • Dg: apnoe >5/h , >30/sleep period, SAT decrease:minimum 4% • Apnoe: > 10 s • Arousal (EEG) defraction of sleep • Apnoe index: Number of apnoe/h:<5 - mild: 5-15 - moderate: 15-30 - severe: >30
Types of SAHS • Central (kb. 5%) • Obstructive (site:pharyngeal level) • Mixed Risk factors: - obesity - alcohol - sedatives
Symptoms of SAS • Daytime sleepiness • Morning headache, tenebrosity • Change in personality • Strong hoarsness • Movements during sleep • Enuresis nocturna • Impotency • Hypertonia, arrhythmias • Right heart failure
Score: 0 – 24 Upper limit of normal: 9 Normal : 5.9 ± 2.2 SAS: 16 ± 4.4
Diagnosis of SAS (poliszomnográfia) • EEG • EOG • EMG • EKG • ABG, pulzoximetry • Detection of airflow • Detection of breathing movements, leg movements • Voice recording • Video
Therapy of SAS • Change in life style • nCPAP, BiPAP • Medroxiprogesteron (Provera) • Surgery • Acetazolamid (Diamox, Fonurit) • Almitrin • Protryptilin