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Tuti Herawati, MN: Fakultas Ilmu Keperawatan Universitas Indonesia 2008
Tuti Herawati, MN: Fakultas Ilmu Keperawatan Universitas Indonesia 2008
KEPERAWATAN KLIEN
DENGAN ARDS
TUTI HERAWATI, MN
Pergerakan diafragma
Perubahan dalam tekanan transpulmonal
‘Compliance’ paru
Tahanan jalan nafas
Acute Respiratory Failure
Gagal Nafas Akut
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
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
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%
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%
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