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Management of Patients with
ACUTE RESPIRATORYDISTRESS SYNDROME
(ARDS)
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ARDSDefinitions
Severe form of respiratory failure with
mortality rate around 50%.
Complex clinical syndrome
Characterized by progressive hypoxemia.
ARDS
PaO2/FIO2 < 150 200 mmHg
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ARDSEpidemiology
Incidence: 5 71 per 100,000
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Caused by direct or indirect pulmonary injury.
a. Direct injury - aspiration, pulmonary
infection, near drowning, thoracic trauma or
toxic inhalation.
b. Indirect injury shock, sepsis,
hypothermia, DIC, multiple transfusioneclampsia, pancreatitis, burns
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ARDSPathophysiology
Profound inflammatory response:
Acute lung injury resulting from an unregulated
systemic inflammatory response, which damage the
alveolar capillary membrane.Injury to lung causing initiation of inflammatory
responses that release mediators (histamine),
serotenin.
Systemic inflammatory response syndrome thatactivate neutrophil, macrophages).
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Continue..
Increase in capillary membrane permeability, which
lead to: diffuse blood out of artery to interstitial
space.pulmonary edema,
Hypoxemia decrease lung compliance.Increase interstitial pressure & damage to alveolar
membrane allow fluid to inter alveoli which dilute &
deactivate surfactant. (damage epithelial type I) that
lead to hypoxemia.
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Pathophysiology continue.
Damage of epithelial type II leads to atelectasis
occurs, lungs become less compliant & gas exchange
impaired (Alveolar collapse due to V/Q mismatching,
hypoventilation, intrapulmonary shunting).Hyaline membrane forms & lungs become fibrotic.
Hypoxemia becomes refractory & resistant to
improvement even with supplemental O2.
Metabolic acidosis occurs leading to multiple organssystem dysfunction.
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Diffuse alveolar damage acute exudative phase (1-7days)
proliferative phase (3-10 days)
chronic/fibrotic phase (> 1-2 weeks)
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ARDSAcute 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
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Phase I
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ARDSAcute Exudative Phase
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ARDSProliferative Phase
Type II pneumocyte proliferate
differentiate into Type I cells
reline alveolar walls
Fibroblast proliferation
interstitial/alveolar fibrosis
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ARDSFibrotic Phase
Characterized by: local fibrosis
vascular obliteration
Repair process:
resolution vs fibrosis
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Phase II
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Phase III
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Phase IV
S
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ARDSPathophysiology
Interstitial/alveolar edema
Severe hypoxemia
due to intra-pulmonary shunt (V/Q = 0) shunt ~ 25% - 50%
Increased airway resistance
ARDS
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ARDSPathophysiology
High ventilatory demands high metabolic state
increased VD/VT
decreased lung compliance
Pulmonary HTN
neurohumoral factors, hypoxia, edema
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ARDS (Etiology)
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ARDS
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ARDSEtiology
Hospital-acquired infection/sepsis
massive blood transfusions
gastric aspiration
Community-acquired
trauma
pneumonia
drugs/aspiration/inhalations
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Clinical Manifestations
ARDS develops about 24-72 hrs post initialinsult.
Manifestations:
Stage I (first 12hrs): Dyspnea, Tachypnea, restlessness, normal CXR
Respiratory alkalosis.
Use of accessory respiratory muscles. Elevated PAP, normal PAWP.
S ( )
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Stage II (24hrs):
Client increases respiratory rate & usesaccessory muscles.
Client becomes cyanotic, dyspnic (severe) anddevelops crackles.
Increase agitation & restlessness.
X-ray show alveolar infiltration.Decrease SaO2 despite O2 therapy.
Metabolic acidosis.
Elevated PAP & Normal PAWP.
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Stage III (2-3 days)
Continued resp failure results (worsening hypoxemia),hemodynamic instability & mental confusion.
Systemic Inflammatory Syndrome presentation.
Increase interstitial & alveolar inflammatory exudates.
X-ray shows diffused alveolar infiltration & decreased lungvolume.
Decrease GI motility.
Generalized edema.
Poor skin integrity.
Increased WBC, decrease Hb & Platelets.
Abnormal clotting factors.
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Stage IV (>10 days).
Multiple organ failure or single respiratory system involvement w
gradual improvement over time.
Decrease UO, GI motility, impaired coagulation.
Difficulty maintaining adequate oxygenation.
Worsening hypoxemia & hypercapnia.
Sepsis, pneumonia, & multi-system involvement.
X-ray shows persistent infiltrates & new pneumonic infiltrates &
Pneumothorax.
Thickening of interstitial wall with fibrosis, macrophages, &
remodling of arterioles.
ARDS
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ARDSClinical Features
Acute dyspnea/tachypnea rales/rhonchi/wheezing
Resistant hypoxemia
PaO2/FIO2 < 150 200 mmHg
CXR diffuse, bilateral infiltrates
No evidence of LV failure (PAWP < 18 mmHg)
ARDS
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ARDSClinical Features: CXR
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Diagnosis of ARDS
Physicians diagnose ARDS when:
A person suffering from severe infection or injury develops
breathing problems. A chest x-ray shows fluid in the air sacs of both lungs.
Arterial blood gases show a low level of oxygen in the blood
Other conditions that could cause breathing problems have
been ruled out.
ARDS can be confused with other illnesses that have similarsymptoms. The most important is congestive heart
failure. In congestive heart failure, fluid backs up into the lungs
because the heart is weak and cannot pump
well. However, there is no injury to the lungs in congestive
heart failure. Since a chest x-ray is abnormal forboth ARDS and congestive heart failure, it can be difficult to
tell them apart.
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Diagnostic procedureABGs
Hypoxemia PaO2 < 60mmHg.Respiratory acidosis.
CXR
After 24 hrs of onset shows white out period.PFTsDecrease lung compliance & reduced vital capacity.
PAP
Differentiates ARDS from pulmonary edema.
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managing
Monitoring:Respiratory
Hemodynamic
Metabolic
Infections
Fluids/electrolytes
Managements
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Managements
History to identify contributing factors for ARDS (behavioral,social, medications).
Treat cause if possible, for example give antibiotics.
Intubation & mechanical ventilation with O2 set to maintain PO2>60mmHg, & O2Sat is 90% or more.
Low tidal volume.
High PEEP.
Inverse ration of ventilation 2:1or 3:1.Monitor fluid balance (I &O), ABGs level & VS.
Nutrition enteral or TPN:
35-45 kcal/day.
Risk for aspiration.
Prevent complications (DVT, Nosocomial infection, skinbreakdown).
Positioning (frequent changed, prone),
Sedation to promote comfort & reduce respiratory efforts.
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Pharmacological Managements
Antibiotics.
Bronchodilators & mucolytics.
Exogenous surfactant replacement therapy.
Nitric oxide (inhaled to cause selective pulmonaryvasodilation & reduce pulmonary hypertension) inthe first 24hrs of ARDS.
Antioxidant, antilipids, antibodies, anticytokineagent did not show positive effects on the outcome
of ARDS treatment.
ARDS
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ARDSTreatment: Standard
Rx underlying cause
Adequate oxygenation/ventilation
PaO2 > 60 mmHg; SaO2 > 90%
PEEP usually needed to meet O2 goals
Prevents/corrects alveolar collapse
converts: (V/Q = 0) to V/Q mismatch
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PEEP Effects
Increases transpulmonary distendingpressure
Displaces edema fluid into interstitium
Decreases atelectasis Decrease in right to left shunt
Improved compliance
Improved oxygenation
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Prone Positioning
Positioning the patient in the proneposition has been shown to improve
oxygenation and reduce ventilator
induced lung injury.
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How does the lung heal?
Resorption of alveolar fluid
Removal of alveolar protein
Type II cell proliferation
Resolution of inflammation
C li ti f ARDS
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Complications of ARDS
Anyone who stays in the hospital for a long period oftime is at greater risk for complications. Common
complications in ARDS patients are infections withhospital-acquired infections and pneumothorax.
Infections
The lungs or other parts of the body may become
infected. Infections are treated aggressively to preventsepsis
from developing. Cultures help determine theappropriate antibiotic therapy.
PneumothoraxSubcutaneous Emphysem.
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Conclusion
ARDS is breathing failure that can occur in
critically ill persons with underlying illnesses. It isa life-threatening
condition that occurs when there is severe fluid
build-up in both lungs. Knowledge about its
causes, treatments,
and complications will help the nurse or other
healthcare provider to more effectively manage
patient care andprovide support to family members.
Th k Y
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Thank You