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