Asuhan keperawatan pada

klien dengan ARDS

Ns. Wantiyah, M.Kep.

Learning Outcomes
Mahasiswa mampu:
1. Menguraikan konsep dasar ARDS
2. Menganalisis asuhan keperawatan pada

klien dengan ARDS

ARDS ???
Acute respiratory distress syndrome (ARDS; previously

called adult respiratory distress syndrome) is a clinical

syndrome characterized by a sudden and progressive
pulmonary edema, increasing bilateral inltrates on
chest x-ray, hypoxemia refractory to oxygen
supplementation, and reduced lung compliance
penurunan progresif kandungan oksigen arteri yang
terjadi setelah penyakit atau cedera serius
ARDS atau Sindroma Distres Pernafasan Dewasa
(SDPD) adalah kondisi kedaruratan paru yang tiba-tiba
dan bentuk kegagalan nafas berat, biasanya terjadi
pada orang yang sebelumnya sehat yang telah
terpajan pada berbagai penyebab pulmonal atau nonpulmonal (Hudak & Gallo, 1997 ).

Adult Repiratory Distress

Syndrome (ARDS)
Denition: diffuse pulmonary alveolocapillary injury associated with

noncardiogenic pulmonary edema and resulting in severe respiratory

distress and hypoxemic respiratory failure.
very rapid form of respiratory FAILURE characterized by acute lung
inflamation and difues alveolocapillary injury
Injury to pulmonary capillary endothelium
inflammation and platelet activation
surfactant inactiviation
Atelectasis
Also called: Stiff lung, shock lung, wet lung
Pathologic hallmark: diffuse alveolar damage (DAD)
DAD resutls in loss of integritry of the alveolar-capillary barrier
transudation of protein-rich fluid across the barrier
pulmonary edema
hypoxemia from intrapulmonary shunting

Etiologi
Hudak & Gallo ( 1997 ), gangguan yang dapat
mencetuskan terjadinya ARDS adalah ;
Sistemik :
Syok karena beberapa penyebab
Sepsis gram negative
Hipotermia
Hipertermia
Takar lajak obat ( Narkotik, Salisilat, Trisiklik, Paraquat,
Metadone, Bleomisin )
Gangguan hematology ( DIC, Transfusi massif, Bypass
kardiopulmonal )
Eklampsia
Luka bakar

Pulmonal :

Pneumonia ( Viral, bakteri, jamur, penumosistik karinii )

Trauma ( emboli lemak, kontusio paru )
Aspirasi ( cairan gaster, tenggelam, cairan hidrokarbon )
Pneumositis
Non-Pulmonal :
Cedera kepala
Peningkatan TIK
Pascakardioversi
Pankreatitis
Uremia

Pathophysiology
Exact mechanism by which condition result is not known

fully, but most likely mediated in part by: Reactive

Oxygen radicals and Proteolytic enzymes from
neutrophils Cytokines, complement of endotoxin may
also be involved
Pathological effects
Alveolar capillary damage and mediator release
Increased endothelial, epithelial membrane permeability
Changes is small airway diameter
Injury to pulmonary vasculature
Disruptions in systemic O2 transport
Alveolar flooding of protein rich fluid

Kerusakan sistemik

Pe perfusi jaringan

Hipoksia seluler

Pelepasan faktor-faktor

biokimia

( enzim lisosom, vasoaktif, system

komplemen,
asam metabolic, kolagen, histamine )

Pe permeabilitas kapiler

paru

Pe aktivitas surfaktan

Edema interstisial alveolar paru

Kolaps alveolar yang progresif

Pe compliance paru

Pergerakan cairan paru

pada kasus ARDS :
- Terjadi peregangan /
deposisi dari mebran
hialin
- Intraalveolar Epithelial
junction melebar
-Terjadi edema
interstisial, cairan
intravascular keluar,
protein keluar masuk ke
dalam alveoli
-Endotel kapiler paru
pecah
- Eritrosit keluar dari
intavaskuler masuk ke
dalam paru
menyebabkan fenomena
frozzy sputum

THE STAGES OF ARDS:

Three stages of ARDS:
1.Exudative stage (0-7 days) accumulation in
the alveoli of excessive fluid, protein and
inflammatory cells that have entered the air spaces
from the alveolar capillaries. The exudative phase
unfolds over the rst 2 to 4 days after onset of lung
injury.
.Capillary congestion
.Alveolar cell necrosis
.Edema and hemorrhage
.Neutrophils within capillaries
.Formation of hyaline membranes in alveoli spaces
and ducts

2.Fibroproliferative (or proliferative) stage: Connective

tissue and other structural elements in the lungs proliferate

in response to the initial injury. Under a microscope, lung
tissue appears densely cellular pneumonia sepsis and
rupture of the lungs causing leakage of air into surrounding
areas.
Proliferative
.Production of type 2 pheumocytes
.Ingestion fo hyaline membranes by macrophages
.Resolution of neutrophilic inflammation
Fibrotic
.Interstitial brosis
.Parenchymal restructuring
3. Resolution and Recovery the lung reorganizes and
recovers. Lung function may continue to improve for as long
as 6-12 months and sometimes longer, depending on the
precipitating condition and severity of the injury..

MANIFESTASI KLINIK
Gejala klinis utama pada kasus ARDS adalah :
Penurunan kesadaran mental
Takikardi, takipnea
Dispnea
Terdapat retraksi interkosta
Sianosis
Hipoksemia
Auskultasi paru : ronkhi basah, krekels,
stridor, wheezing
Auskultasi jantung : BJ normal tanpa murmur
atau gallop

Clinical Manifestations
Signs and symptoms (24 hrs to 7 days):
Progressive dyspnea, adventitious sounds,
hypoxemia
Rapid, shallow breathing --> Hyperventilation -->
respiratory alkalosis
Adventitious breath sound (ronchi, crackles, stridor)
Chest retractions, cyanosis, mottling
Decreased tissue perfutsion --> Organ dysfunction
--> metabolic acidosis
Decreased lung compliance
Unresponsive hypoxemia
Inflitrates in lung visible with X-ray
Decreased CO --> Hypotension --> Death

Kriteria Diagnostik
1. gagal napas akut
2. Gambaran inltrat paru
3. hipoksemia

PEMERIKSAAN PENUNJANG
1. Pemeriksaan hasil Analisa Gas Darah :
Hipoksemia ( pe PaO2 )
Hipokapnia ( pe PCO2 ) pada tahap awal karena
hiperventilasi
Hiperkapnia ( pe PCO2 ) menunjukkan gagal ventilasi
Alkalosis respiratori ( pH > 7,45 ) pada tahap dini
Asidosis respiratori / metabolik terjadi pada tahap lanjut
2. Pemeriksaan Rontgent Dada :
Tahap awal ; sedikit normal, inltrasi pada perihilir paru
Tahap lanjut ; Interstisial bilateral difus pada paru,
inltrate di alveoli
3. Tes Fungsi paru :
Pe komplain paru dan volume paru
Pirau kanan-kiri meningkat

Penatalaksanaan Medis
1. Mengidentikasi dan mengatasi
2.
3.
4.
5.

penyebab, cegah infeksi

Ventilasi adekuat terapi oksigen,
ventilator (PEEP dan CPAP)
Dukungan sirkulasi
Memastikan volume cairan adekuat
Nutrisi : 35-45 kkal/kgBB

Treatment
Mechanical ventilation and O2
Pulmonary arterial catheter (PAC) to measure

cardiac flow and pressure

Manage fluids
Manage and control Infections
Supportive: Prone position
Prevention of organ failure (kidney, liver)
Drug treatment investigative:
Anti-inflammatory, steriods
Nitrous oxide
Exogenous surfactant
Recumbinant Human Protein C

Nursing management...
Assessment:
Ns. Diagnosis:
1. Impaired gas exchange r/t ventilation-

perfusion imbalances (alveolar-capillary

membrane changes)
2. Risk of Decreased tissue perfussion
3. PK: Sepsis
. Intervention: critically ill care O2
therapy (VM), position, ventilation
monitoring, acid-base management,
infection prevention, psychology support