ACUTE RESPIRATORY

DISTRESS SYNDROME

— Tri Mustikowati
— Medical Surgical Nursing Departement
— https://youtu.be/KXw8LXKcmrw  
ACUTE RESPIRATORY
DISTRESS SYNDROME
• Definition
Is a sudden and progressive form of acute
respiratory failure in which the alveolar capillary
membrane becomes damages and more permeable
to intravascular fluid.

(Suatu bentuk gagal nafas akut yang terjadi

mendadak dan progresif, di mana membran kapiler
-alveoli menjadi rusak dan lebih permeabel
terhadap cairan intravaskuler)
ETIOLOGY
Ø Direct lung injury
§ Aspiration of gastric contents or other
substances (aspirasi isi lambung atau substansi
lain)
§ Near drowning (tenggelam)
§ Inhalation of toxics substances (menghirup
substansi beracun)
§ Viral/bacterial pneumonia
§ Chest trauma
§ Embolism
§ Oxygen toxicity
§ Radiation pneumonitis
Ø Indirect lung injury
§ Sepsis
§ Severe pancreatitis
§ Multiple blood transfusion
§ Multiple trauma
§ Severe head injury
§ Shock states
§ Nonpulmonary systemic disease
§ Cardiopulmonary by pass
§ Anaphylaxis
§ Narcotic drug abuse
PATHOPHYSIOLOGY
• Due to stimulation of the inflamatory and
immune system.
——> cause an atraction of neutrophils to
the pulmonary interstitium
——> The neutrophils cause a release of
biochemical, humoral and cellular mediator
——> produce changes in the lung :
v increase pulmonary capillary membrane
permeability
v destruction of elastin and collagen
v Formation of pulmonary microemboli
v Pulmonary artery vasocontriction
PATHOPHYSIOLOGY  
— Terjadi  karena  stimulasi  sistem  imun  dan  inflamasi  
—  menyebabkan  reaksi  neutrofil  ke  interstitium  paru  
——>  Neutrofil  menyebabkan  pelepasan  mediator  
biokimia,  humoral  dan  seluler    
     —>  menghasilkan  perubahan  di  paru-­‐paru:        
Ø    meningkatkan  permeabilitas  membran  kapiler  paru,  
Ø  penghancuran  elastin  dan  kolagen    
Ø Pembentukan  mikroemboli  paru  
Ø Vasokonstriksi  arteri  pulmonal  
 
 
THREE PHASE
— INJURY or EXUDATIVE PHASE
§ occurs approximately 1 to 7 days (usually 24 to
48 hours)
§ Interstitial and alveolar edema and atelectasis
§ Severe V/Q mismatch and shunting of pulmonary
capillary blood
§ Diffusion limitation
§ Less compliant because of decrease surfactan,
pulmonary edema and atelectasis
— Hypoxemia  and  the  stimulation  of  juxtacapillary  
receptors  in  the  stiff  lung  parenchyma  (J  reflex)  
initially  cause  an  increase  in  RR  and  decrease  in  tidal  
volume.  
— This  breathing  pattern  increase  CO2  removal  
• This  breathing  pattern  increase  CO2  removal  
(respiratory  alkalosis)  
— CO  increases  in  response  to  hypoxemia,  a  
compensatory  effect  to  increase  pulmonary  blood  
flow.  
— However,  as  atelectasis,  pulmonary  edema,  and  
pulmonary  shunt  increase,  compensation  fails,  and  
hypoventilation,  decrease  CO2,  and  decreased  tissue  
O2  perfusion.  
• REPARATIVE or PROLIFERATIVE PHASE
§ Begins 1 to 2 weeks after the initial lung injury.
§ An influx of granulocytes, monocytes and
lymphocytes and fibroblast proliferation as part
of the inflamatory response.
§ Increased pulmonary vascular resistance and
pulmonary hypertension because the presence of
fibroblasts and inflammatory cells obliterate
the pulmonary vasculature.
— Mulai  1  hingga  2  minggu  setelah  cedera  paru-­‐paru  
awal.    
— Masuknya  granulosit,  monosit  dan  limfosit  dan  
proliferasi  fibroblast  sebagai  bagian  dari  respon  
inflamatori.    
— Peningkatan  resistensi  pembuluh  darah  paru  dan  
hipertensi  pulmonal  karena  kehadiran  fibroblas  dan  
sel-­‐sel  inflamasi  melenyapkan  vaskulatur  pulmonal.  
§ Lung compliance continues to decrease
§ hypoxemia
— Fibrotic phase
§ 2 to 3 weeks after the initial lung injury
§ Also called the chronic or late phase of ARDS
§ Completely remodeled by sparsely collagen and
fibrous tissues
§ There is diffuse scarring and fibrosis
§ Hypoxia continues
CLINICAL MANIFESTATION
— For several hours to 1 to 2 days the patient may
not experience respiratory symptoms or may
exhibit only dyspnea, tachypnea, cough, and
restlessness.
— ABGs usually indicate mild hypoxemia and
respiratory alkalosis
As ARDS progreses
— Respiratory discomfort ——> the work of
breathing is increases
— Tachypnea and intercostal and suprasternal
retraction
— Tachycardia, diaphoresis, changes in sensorium
with decreased mentation, cyanosis and pallor
— Crackles and rhonchi
— Chest x-ray demonstrates diffuse and
extensive bilateral interstitial and alveolar
infiltrates.
— Pleural effusions may also be present
COMPLICATIONS
— Nosocomial Pneumonia
— Barotrauma
— Stress ulcers
— Renal failure
MANAGEMENT  
• ABC  ?  
• Focus  pada  pengendalian  masalah  primer  
(misalnya  syok,  sepsis)  
• Pertahankan  hidrasi  adequate  
• Bantu  nafas  dengan  ventilator:  
– Lakukan  pemberian  distensi  optial  pada  alveoli  
(meninggikan  tidak  volume,  PEEP)  
– Volume  cycle  
– TV  10-­‐15  cc/kg  bb  
– RR  12-­‐14/mnt  
– Beri  O2  optimal  >60mmHg  
– Tambahkan  ‘dead  space’  jika  PCO2  <  30  mmHg  
– Humidifikasi  optimal  
— Posisi  prone  karena  dapat  meningkatkan  PaO2  
dari  70  ke  90  mmHg.  Secara  periodik  namun  tetap  
diubah-­‐ubah  agar  alveoli  yang  masih  baik  diberi  
kesempatan  ‘bernafas’  
— Supportive  therapy  seperti  dopamine,  dobutamine  
— Diuretic    
— Pemasangan  IV  line    
NURSING ASSESSMENT
• Subjective data :
o Important health information
- past health history
- medications
- surgery or other treatments

o Functional health patterns

- health perception-health management
- Nutritional-metabolic
- activity-exercises
- sleep-rest
- cognitive-perceptual
- coping-stress tolerance
— Objective Data :
o General
- restlessness, agitation
o Integumentary
- pale, cool, clammy skin or warm flushed
skin, peripheral and central cyanosis
o Respiratory
- shallow, increased respirations
progressing to decreased rate, use of
accessory muscles, stridor, friction rub
— Cardiovascular
- tachycardia progressing to bradycardia,
arrythmias, extra heart sounds
— Gastro intestinal
- abdominal distension with tympani
— Neurologic
- somnolence, confusion, slurred speech,
tremors, seizures, coma
NURSING DIAGNOSIS
— Ineffective  breathing  pattern  due  to  fluid  
accumulation  in  the  lung  
— Impaired  gas  exchange  due  to  fluid  in  alveoli  
— Activity  intolerance  due  to  limited  energy  reserves  
— Anxiety  due  to  dyspnea  
PLANNING

— The overal goal :

Ø PaO2 within limits of normal for age or baseline
values
Ø SaO2 greater than 90%
Ø Patent airway
Ø Clear lungs on auscultation
RESPIRATORY THERAPY
— Oxygen administration
Ø Primary goal : to correct hypoxemia
Ø O2 administered via mask with high flow system
— Mechanical ventilation
Ø Apply PEEP
INTERVENTION  
• Pertahankan  ABC  
• Tempatkan  pasien  bergantian,  highfowler,  supine  
dan  juga  prone  
• Bantu  pengeluaran  secret    
• Pasang  IV  line  minimal  satu  line    
• Catat  urine  output  
• Nutrisi  parenteral.    
• Timbang  berat  badan  setiap  hari  
— Monitor  Tanda  vital  ,suara  nafas,  kesadran,  
sirkuasi  dan  akral.  Siapkan  untuk  monitoring  
hemodinamik  infasive  
— Aktif  berkomunikasi  dengan  pasien  dan  keluarga  
untuk  mengurangi  kecemasan  
— Persiapkan  ICU:  lengkapi  dokumen  medik/
perawat,  X-­‐ray,  AGD,  dampingi  pasien  ke  ICU    
EVALUATION
— The expected outcomes for the patient with
ARDS are similar those for a patient with
respiratory failure in NCP.
— Normal RR & quality or respiration
— Normal mental status
— Normal breath sound
— Normal blood pressure & other vital signs
— ABG in normal range