GAGAL NAPAS AKUT dan GAGAL NAPAS AKUT dan PENGELOLAANNYA PENGELOLAANNYA Muhammad Husni Thamrin Muhammad Husni Thamrin Smf Anestesi dan Smf Anestesi dan Terapi Intensif RS Dr. Terapi Intensif RS Dr. Moewardi Moewardi
GAGAL NAPAS AKUT dan PENGELOLAANNYAMuhammad Husni ThamrinSmf Anestesi dan Terapi Intensif RS Dr. Moewardi
PendahuluanARDS (ATS & ESICM)Gagal nafas akut, sering fatalKerusakan parenkhim paruCompliance paru , permeabilitas kapiler Edema interstitialTanpa tekanan hidrostatik Gangguan pertukaran gas tingkat alveoler
Nama lain:Wet Lung, Shock LungPost Traumatic Pulmonary InsufficiencyAdult Hyaline Membrane DiseaseVentilator Lung/ Pump LungAspiration PneumoniaCongestif AtelectasisSmoke InhalationInsidens : 150.000/tahun (AS)Mortalitas: 40% - 70%
EtiologiFluid overloadLeft heart failureTrauma : fractured ribs, flail chest, pneumohemothorax, contusion of lung and heartSepsisShockAtelectasisInadequate tracheobronchial toiletThromboembolismFat embolismAspiration pneumoniaBacterial pneumoniaViral pneumoniaAbdominal distentionMultiple blood transfusion-particulate matterOxygen toxicityHumoral substances- Pancreatitis- Endotoxin- Vasoactive drugs- Kinins- Histamine- ProstaglandinsTransfusion reactionsHead injuriesBurnsDrug abuse-heroin pulmonary edemaAnaphylaxisMetabolic, eg. hypophosphatemiaPreexisting lung disease
PATOFISIOLOGIRespiratory failureINJURYCapillary endotheliumType I cell damageType II cells Pulmonary capilliary leakSurfactantInactivation
Interstitial and Atelectasis DifferentiationAlveolar OedemaInto type I cells
Shunt, Low FRCLow compliance Hypoxaemia
Pulmonary fibrosisrepair of capillary membraneMicrovascular obliteration Sepsis Multi-organ failure DEATH
12-48 jamTakhipnoeDispnoeSianosisHipotensiEdema periferKrepitasi paruStadium terminal :- TV - pCO2 - asidosis metabolik- syok- kesadaran GAMBARAN KLINIS
DIAGNOSISTabel kriteria diagnosis ARDS :Clinical Setting1. Catastrophic event a. Pulmonary b. Nonpulmonary, eg. Shock2. Exclusions c. Chronic pulmonary disease d. Left heart abnormalities3. Respiratory distress (judged clinically) e.Tachypnea >20, usually greater f. Laboured breathingX-ray : Diffuse Pulmonary Infiltrates1. Interstitial (initially)2. Alveolar (later)
C.Physiologic1. PaO2 < 50 with FiO2 >0,62. Overall compliance < 50 ml/cm -usually 20-30 ml/cm3. Increased shunt fraction Qs/Qt and deadspace ventilation Vd/VtPathologic1. Heavy lungs, usually >1000 g2. Congestive atelectasis3. Hyaline membranes4. Fibrosis
PENATALAKSANAANTarget utama :Kembangkan alveoliOksigenasi jaringan/sirkulasi adekuatKeseimbangan cairan, elektrolit, asam basa
Integritas membran kapiler alveoli utuh kembaliAtasi faktor pencetusTerapi penunjang
Ventilasi mekanik :- PaO2 < 50 mmHg- FiO2 60% : oksigenasi tidak adekuat PEEPTerapi cairan :- CVP/PCWP- Koloid- NaCl 3% + FurosemidCardiac Support :- Preload optimal- Inotropik- Vasodilator
d. Nutrisi, mencegah :- kelemahan otot- imunitas- hipoalbumine. Fisioterapi :- keluarkan sekret paruf. Obat-obat lain :- kortikosteroid- antibiotik- heparin- antioksidan- ECMO
g. Ultrafiltrasih. Obat lain yang telah dicoba :- prostasiklin- prostaglandin- ketanserin- danazolKOMPLIKASIInfeksi paruEmboli /infark paruBarotrauma akibat PEEPGastrointestinalKardiovaskularMOFPROGNOSA Kurang baik
RINGKASANARDS : - gagal nafas akut- edema paru non kardiogenik- 4 tahap gambaran klinikPenyebab pada bayi berbedaGejala klinis timbul 12-48 jamPenatalaksanaan : - ventilasi mekanik - optimalisasi perfusi jaringan - keseimbangan cairan, elektrolit, asam basa, faktor pencetus. - nutrisi, fisioterapi, ultrafiltrasi, obat-obatan. Komplikasi : - sistem respirasi - sistem gastrointestinal - sistem kardiovaskular - MOFPrognosa : ad malam