ASUHAN

KEPERAWATAN KLIEN
DENGAN ARDS

TUTI HERAWATI, MN

FAKULTAS ILMU KEPERAWATAN

UNIVERSITAS INDONESIA
2008
 OBJECTIVES
 Memahami tentang gagal nafas dan ARDS
 Menjelaskan patofisiologi terjadinya gagal nafas dan ARDS
 Mengenali tanda dan gejala
 Memahami jenis pemeriksaan fisik dan diagnostik
 Merumuskan diagnosa keperawatan
 Merencanakan tindakan keperawatan
 FISIOLOGI PERNAFASAN
 Ventilation
Pertukaran udara antara alveoli dan atmosphere
 Diffusion
Pertukaran CO2 & O2 antara alveoli dan kapiler
 Transport/perfusi
 Pertukaran O2 dari alveoli ke sel-sel
 pertukaranCO2 dari sel-sel ke alveoli
 Proses Ventilasi

 Pergerakan diafragma
 Perubahan dalam tekanan transpulmonal
 ‘Compliance’ paru
 Tahanan jalan nafas
 Acute Respiratory Failure
Gagal Nafas Akut

 Gangguan pertukaran gas yang tiba-tiba dan

mengancam kehidupan.
 Secara klinis didefinisikan jika Pa O2<60mmHg
atau PaCO2 >50mmHg
 Type I – Acute hypoxemic respiratory failure
 Type II - Acute hypercapnic respiratory failure
 Type III – Combined hypoxemic and hypercapnic failure
 RESPIRATORY FAILURE & ITS COMPONENTS

 Lung failure/ gas exchange/ type I

V/Q mismatch
Impaired diffusion
shunt
 Pump failure/ventilation failure/ type II
nervous system
thorax cage
muscle of respiration
 EXAMPLES OF DISEASE THAT
CAUSES RESPIRATORY FAILURE
Lung failure:
COPD, Pulmonary emboli, ARDS, pneumonia, CHF
Pump failure:
brain: Drug overdose, CVA, head trauma,
spinal cord, neuromuscular: myasthenia gravis, polio,
trauma/tumor
chest wall: flail chest, burn eschar
 Balance of Ventilation to Perfusion

 Alveolar dead space

 Collapsed alveoli from pneumonia or atelectasis
 Shunting
 Anatomical
 Blood moves from the right side to left side of the heart
without being oxygenated
 Physiological
 Blood moved by alveoli without picking up oxygen
 VQ Mismatch

 Physiological shunt
 Low ventilation–perfusion ratio
 Alveolar dead space
 High ventilation–perfusion ratio
 Silent unit
 Both ventilation and perfusion are decreased
Acute respiratory Distress Syndrome
 Adult Respiratory distress Syndrome
 White Lung
 Definisi ARDS
 In 1967 Ashbaugh, Bigelow, Petty & Levine:
dyspnea, tachypnea, ↓ lung compliance, diffuse
alveolar infiltrate.
 In 1988 Murray et al. expanded the definition.
 In 1994 the American European consensus
conference, ARDS: PaO2/FiO2 ≤ 200 mmHg,
bilateral infiltrates, PAWP ≤ 18 mmHg or no
evidence of left atrial hypertension.
 Definisi lanjut...
Sindrom klinis (nonkardiogenik pulmonary edema)
yang menyebabkan hipoksemia dan penurunan
‘compliance’ paru yang dapat menyebabkan
gangguan oksigenasi dan ventilasi.
 ARDS
Etiology

Direct injury - aspirasi, infeksi paru,

tenggelam, trauma dada or toxic inhalation
Indirect injury – shock, sepsis,
hypothermia, DIC, multiple transfusion
eclampsia, pancreatitis, burns
 ARDS
Pathophysiology

 Profound inflammatory response

 Diffuse alveolar damage

 acute exudative phase (1-7days)
 proliferative phase (3-10 days)

 chronic/fibrotic phase (> 1-2 weeks)

 ARDS
Acute Exudative Phase

 Basement membrane disruption

 Type I pneumocytes destroyed
 Type II pneumocytes preserved

 Surfactant deficiency
 inhibited by fibrin
 decreased type II production

 Microatelectasis/alveolar collapse
 ARDS
Pathophysiology
 ARDS
Pathophysiology
 ARDS
Pathophysiology
 ARDS
Proliferative Phase
 Type II pneumocyte
 proliferate
 differentiate into Type I cells

 reline alveolar walls

 Fibroblast proliferation
 interstitial/alveolar fibrosis
 ARDS
Proliferative Phase
 ARDS
Fibrotic Phase
 Characterized by:
 local fibrosis
 vascular obliteration

 Repair process:
 resolution vs fibrosis
 ARDS
Pathophysiology
 Interstitial/alveolar edema

 Severe hypoxemia
 due to intra-pulmonary shunt (V/Q = 0)
 shunt ~ 25% - 50%

 Increased airway resistance

 ARDS
Pathophysiology
 High ventilatory demands
 high metabolic state
 increased VD/VT

 decreased lung compliance

 Pulmonary Hypertension
 neurohumoral factors, hypoxia
 ARDS
Clinical Features

 Acute dyspnea/tachypnea
 rhonchi/wheezing

 Resistant hypoxemia
 PaO2/FIO2 < 150 – 200 mmHg

 CXR
 diffuse, bilateral infiltrates

 No evidence of LV failure
 (PAWP < 18 mmHg)
 ARDS
Clinical Features: CXR
 ARDS
Diagnosis

 Resistant hypoxemia
 PaO2/FIO2 < 150 – 200 mmHg

 CXR
 diffuse, bilateral infiltrates

 No evidence of LV failure
 (PAWP < 18 mmHg)
 Nursing Assessment
 Riwayat penyakit dan faktor pencetus
 Monitor tanda distress pernafasan, penggunaan otot
bantu nafas, perubahan SaO2,perubahan suara nafas,
hypoxia, crackles, pink frothy sputum
 Monitor AGD: acidosis/alkalosis
 Pengkajian Neurologi (20% of CO is required for
normal brain function)
 Monitor status hemodynamic (TD, PAWP, CO, SvO2)
 ARDS
Treatment: Standard
 Terapi sesuai dengan penyebab

 Adequate oxygenation/ventilation
 PaO2 > 60 mmHg; SaO2 > 90%

 PEEP tuk memenuhi kecukupan O2

 Prevents/corrects alveolar collapse
 converts: (V/Q = 0) to V/Q mismatch
 ARDS
Optimal PEEP
 ARDS Network protocol

FIO2 - 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0

PEEP - 5 5-8 8-10 10 10-14 14 14-18 18-22

www.ardsnet.org ARDS Network, N Engl J Med 2000; 342:1301

 ARDS
Nursing diagnosis
 Gangguan pertukaran gas b.d kerusakan membran
alveoli-kapiler, perubahan compliance paru
 Bersihan jalan nafas tidak efektif b.d peningkatan sekresi
trakeobronkial
 Pola nafas tidak efektif b.d hiperventilasi, kelelahan otot
pernafasan, disfungsi neuromuskular, gangguan
muskuloskeletal
 Altered nutrition (<) related to increased metabolic
demands
 Nursing Intervention for improving gas exchange
 Administer antibiotic, cardiac medications and diuretics as ordered for
underlying disorder
 Administer O2 to maintain PaO2 0f 60 mmHg or Sa O2 >90
 Lower VT 6 ml/KgBw
 Permissive hypercapnia
 FiO2 maintain lowest to maintain PaO2
 acidosis: sodium bicarbonate & ↑ RR ventilator
 PEEP: improve arterial oxygenation & ventilating collapse alveoli
 Monitor fluid balance by intake & output measurement, daily weight,
measurement PAWP
 Provide measures to prevent atelectasis & promote chest expansion &
secretion clearance, as ordered (incentive spirometer, nebulization, turn
frequently, head of bed elevated 30 degrees.
 Monitor adequacy of alveolar ventilation (measuring RR, VC, inspiratory
force & ABG levels.
 Nursing Intervention for maintainning
airway clearance
 Administer medications to increase alveolar ventilation
such as bronchodilators, corticosteroids
 Perform chest physiotherapy
 Administer IV Fluids and mucolytics
 Suction patient as needed
 ARDS
Treatment: Mechanical Ventilation (MV)
 Pressure controlled ventilation
 Controlled airway pressures
 Controlled inspiratory times

 Patient comfort

 Effectiveness:
 PCV = VCV
 ARDS
Treatment: Other Modalities
 Antiinflammatory agents
 Steroids may have a role
 Antioxidants
 Surfactant replacement
 Increased alveolar fluid removal
 Effect sodium channels
 Activate Na+-K+-ATPase pump
 ARDS
Prognosis
 Mortality
 30% - 50%
 Death from respiratory failure = 15% - 18%
 Most common cause of death - sepsis/infection

 Outcomes
 Majority have near-normal lung function
 Small % develop pulmonary fibrosis
 Neuropsychiatric sequelae – may be high
The
End