Ards Yordan

7/29/2019 Ards Yordan

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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

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