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GAGAL NAPAS AKUT dan PENGELOLAANNYA

aryono hendrasto

Pendahuluan

ARDS (ATS & ESICM) Gagal nafas akut, sering fatal Kerusakan parenkhim paru Compliance paru , permeabilitas kapiler Edema interstitial Tanpa tekanan hidrostatik

Nama lain:

Gangguan pertukaran gas tingkat alveoler

Wet Lung, Shock Lung Post Traumatic Pulmonary Insufficiency Adult Hyaline Membrane Disease Ventilator Lung/ Pump Lung Aspiration Pneumonia Congestif Atelectasis Smoke Inhalation Insidens : 150.000/tahun (AS) Mortalitas: 40% - 70%

Etiologi
Fluid overload Left heart failure Trauma : fractured ribs, flail chest, pneumohemothorax, contusion of lung and heart Sepsis Shock Atelectasis Inadequate tracheobronchial toilet Thromboembolism Fat embolism Aspiration pneumonia Bacterial pneumonia Viral pneumonia Abdominal distention Multiple blood transfusionparticulate matter Oxygen toxicity Humoral substances - Pancreatitis - Endotoxin - Vasoactive drugs - Kinins - Histamine - Prostaglandins Transfusion reactions Head injuries Burns Drug abuse-heroin pulmonary edema Anaphylaxis Metabolic, eg. hypophosphatemia Preexisting lung disease

PATOFISIOLOGI
Respiratory failure
INJURY Capillary endothelium Type I cell damage Pulmonary capilliary leak Type II cells Surfactant Inactivation Interstitial and Alveolar Oedema Shunt, Low compliance Low FRC Hypoxaemia Atelectasis Differentiation Into type I cells

Pulmonary fibrosis
Microvascular obliteration Sepsis Multi-organ failure

repair of capillary membrane

DEATH

GAMBARAN KLINIS
12-48 jam Takhipnoe Dispnoe Sianosis Hipotensi Edema perifer

Krepitasi paru
Stadium terminal : - TV - pCO2 - asidosis metabolik - syok - kesadaran

DIAGNOSIS
Tabel kriteria diagnosis ARDS : A. Clinical Setting 1. Catastrophic event

a. Pulmonary
b. Nonpulmonary, eg. Shock 2. Exclusions c. Chronic pulmonary disease d. Left heart abnormalities 3. Respiratory distress (judged clinically) e.Tachypnea >20, usually greater

f. Laboured breathing
B. X-ray : Diffuse Pulmonary Infiltrates 1. Interstitial (initially) 2. Alveolar (later)

C.

Physiologic
1. PaO2 < 50 with FiO2 >0,6 2. Overall compliance < 50 ml/cm -usually 20-30 ml/cm 3. Increased shunt fraction Qs/Qt and deadspace ventilation Vd/Vt

D.

Pathologic 1. Heavy lungs, usually >1000 g 2. Congestive atelectasis 3. Hyaline membranes 4. Fibrosis

PENATALAKSANAAN
Target utama : Kembangkan alveoli Oksigenasi jaringan/sirkulasi adekuat

Keseimbangan cairan, elektrolit, asam basa

Integritas membran kapiler alveoli utuh kembali Atasi faktor pencetus Terapi penunjang

a.

Ventilasi mekanik :

- PaO2 < 50 mmHg


- FiO2 60% : oksigenasi tidak adekuat PEEP b. Terapi cairan : - CVP/PCWP - Koloid - NaCl 3% + Furosemid c. Cardiac Support :

- Preload optimal
- Inotropik - Vasodilator

d. Nutrisi, mencegah :
- kelemahan otot - imunitas - hipoalbumin

e. Fisioterapi :
- keluarkan sekret paru f. Obat-obat lain : - kortikosteroid - antibiotik - heparin - antioksidan

- ECMO

g. Ultrafiltrasi h. Obat lain yang telah dicoba : - prostasiklin - prostaglandin - ketanserin - danazol

KOMPLIKASI
Infeksi paru Emboli /infark paru Barotrauma akibat PEEP Gastrointestinal

Kardiovaskular
MOF

PROGNOSA
Kurang baik

RINGKASAN
ARDS : - gagal nafas akut - edema paru non kardiogenik - 4 tahap gambaran klinik Penyebab pada bayi berbeda Gejala klinis timbul 12-48 jam Penatalaksanaan : - ventilasi mekanik - optimalisasi perfusi jaringan - keseimbangan cairan, elektrolit, asam basa, faktor pencetus. - nutrisi, fisioterapi, ultrafiltrasi, obat-obatan. Komplikasi : - sistem respirasi

- sistem gastrointestinal
- sistem kardiovaskular - MOF Prognosa : ad malam