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Acute Lung Injury Acknowledgement is made to the following expert who contributed to the development of this module: Lorraine Iuliano, RN CCRN Glens Falls Hospital Revisions by: Karen Coppin MSN, RN, CCRN Deidre Dunn RN-BC, MSN Copyright 2005 Revised 2012 Linda Maguire MS RN CCRN 1 Susan Sparacino RN MSN

Objectives: 

Identify the major etiologies of Acute Lung Injury (ALI)



Discuss the pathophysiology of ALI



Describe the clinical management of patients with ALI

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Acute Lung Injury (ALI) 

Newer terminology for a syndrome that has been recognized in critical care for many years



Most commonly referred to as ALI but also known as  Stiff Lung  Wet Lung  Septic Lung  White Lung  Da Nang Lung  Adult hyaline membrane disease  Noncardiogenic pulmonary edema 3

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Acute Lung Injury (ALI) 

Defined as non - cardiac pulmonary edema and disruption of the alveolar –capillary membrane as a result of pulmonary vascular injury



Pulmonary manifestation of Multiple Organ Dysfunction Syndrome (MODS)



ARDS (Acute Respiratory Distress Syndrome)  Most severe form of ALI  Mortality rate is 30 – 50%

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Etiologies of ALI 

Direct lung injury  Pneumonia



Indirect lung injury  Sepsis

 Aspiration of

gastric

contents  Pulmonary contusion  Fat emboli  Near drowning  Reperfusion edema (post transplant)  Inhalational injury

 Severe

trauma

 Cardiopulmonary

bypass overdose  Acute pancreatitis  Multiple blood product transfusions  Drug

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ALI 

Characterized by:  Refractory 

hypoxemia

Poorly responsive to oxygen

 Diminished 

pulmonary compliance

Decreased compliance = increased stiffness

 Chest

X-ray compatible with pulmonary edema  Normal pulmonary artery wedge pressure 

Indicates that this pulmonary edema is noncardiac 6

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Pathophysiology of ALI 

Healthy lung  Intact

alveolar-capillary membrane of dry alveoli

 Maintenance



Acute Lung Injury  Endothelial

injury & increased vascular permeability  Alveolar epithelial injury  Ultimate influx of protein-rich edema fluid 7

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Pathophysiology of ALI 

Inflammatory-immune system initiates a systemic response



Neutrophils are attracted to lung interstitium



Neutrophils release a variety of biochemical mediators which injure capillary endothelium 9

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Pathophysiology of ALI 

These biochemical mediators contain and control infection and promote healing



Prolonged critical illness is associated with an amplified response of these mediators



So the original intent to defend and heal begins to destroy the body instead



The effect of the amplified mediator response is increased capillary and alveolar membrane permeability within the lungs 10

What is the Common Denominator? 

The common denominator is a serious insult to the body that directly or indirectly targets the lungs



When not the result of direct lung injury, the mechanisms that provoke lung damage appear to be systemic and immunologic



Blood-borne inflammatory and vasoactive mediators secondarily affect lung tissue

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Capillary Injury

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Capillary Injury 

Increased or altered capillary membrane permeability



Proteins leak into the interstitial space



Protein exerts osmotic pressure changes



Fluid now follows the protein and fills the interstitial space as well 13

Capillary Injury 

The hydrostatic pressure within the interstitial space increases



Fluid moves into the alveolar space since the alveolar membrane has altered permeability



Proteins also begin to infiltrate the alveolar space as well 14

Capillary Injury 

The fluid and protein destroy the Type ll cells, resulting in impaired surfactant production



Impaired surfactant production leads to alveolar collapse



Collapse of alveoli results in:  Intrapulmonary

right to left shunting

 Decreased functional residual capacity  Decreased lung

(FRC)

compliance 15

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Shunting 

Collapsed alveoli –> NO VENTILATION



Adequate pulmonary capillary flow



No Diffusion



Therefore O2 therapy not effective 16

Dead Space 

Microemboli lead to obstructed capillaries



Dead space refers to air NOT participating in gas exchange

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Silent Unit 

Collapsed alveoli



Collapsed capillary from microemboli



No ventilation and no perfusion

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Pathophysiology of ALI 

The mediators also cause  

Bronchospasm Destruction of elastin and collagen fibers of lung parenchyma



Microemboli form



Pulmonary arteries vasoconstrict

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The end results are… 

Pulmonary hypertension



Pulmonary edema



Atelectasis



Increased work of breathing



Hypoxemia “refractory to oxygen therapy”

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Clinical Presentation of ALI 

Tachypnea



Dyspnea, hyperventilation, respiratory distress



Labored breathing with retractions



Cyanosis



Initially normal breath sounds  crackles, wheezes



Tachycardia, hypertension



Restlessness and anxiety 21

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Diagnosis of ALI 

History  Presence of



precipitating event

Arterial Blood Gases  Hypoxemia  Due to shunt and silent units 

PaO2 less than 55 mmHg

 Hypocapnia  Tachypnea causing CO2 loss  

pCO2 20-30 mmHg (norm 35-45 mmHg) Respiratory alkalosis: pH more than 7.35-7.45 22

Diagnosis of ALI 

Chest X-Ray  Classic

“white out” pattern infiltrates & atelectasis

 Diffuse bilateral

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Diagnosis of ALI 

Quick shunt assessment  Multiply

the percentage of oxygen the patient is receiving by 5 to obtain estimated PaO2



Example  FIO2

50% x 5 = Expected PaO2 250

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Case Study 

S: 41 yr old female presents to the ED after 4 days of SOB, fever, chills and productive cough of green sputum



PMH: Asthma, Type 2 IDDM, HTN, current smoker



A: In ED: Temp-101.5, HR-128, RR-32, BP-143/101 ABG’s on 4L NC: pH 7.45, pC02 36, p02 57, HCO3 25, 02sat 88% CXR: Bilateral pulmonary infiltrates, left >right



R: Admit to telemetry  

Dx: Community Acquired Pneumonia Plan: Supplemental O2, Ceftriaxone, Azithromycin, Bronchodilators, IV Steroids 25

Case Study 

During Evening…..

more hypoxic…placed on 50% Venti mask  Repeat ABG’s: pH 7.43, pCO2 34, pO2 62, HCO323, O2sat 90%  RR 40 & shallow, c/o anterior pleutic chest pain  Expiratory wheezes and bilateral crackles  Transferred to ICU for closer monitoring, antibiotics broadened  Becoming

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Case Study 

During Night……  O2 sat decreased to 85% on 50% Venti  Placed on 100% NRB…  RR 35-40  O2 sats continued to decrease  Placed on Bipap 10/5 at 65%  BiPap titrated up to 100% to maintain

mask

sp02>92%

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Case Study 

Next Morning…..  BiPap 12/6 at 90%  RR mid 40’s  Repeat CXR: Suggestive

of ARDS and

worsened pneumonia  Decision to intubate

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Case Study 

What was the cause of ARDS?



What signs/symptoms did the patient demonstrate?



What about her ABG’s? 29

Management of ALI & ARDS 

Early identification & treatment of underlying cause



Appropriate respiratory/ventilatory support



Prevention of potential complications:  GI bleeding  Thromboembolism  Nosocomial infections



Early nutritional support 30

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Management of Ventilatory Support 

Support lung function until the alveolar capillary membrane heals



Maintain patent airway  May



require intubation

Maintain paO2 within an acceptable range  Use

the LOWEST FIO2 to produce acceptable paO2

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Oxygen Toxicity 

Atmospheric air contains nitrogen



Nitrogen expands the alveoli to help keep the alveoli open



100% oxygen washes out nitrogen and damages Type ll cells that produce surfactant



Results in alveolar collapse



High percentages of O2 for extended periods may promote ALI 

However, 100% O2 may be required to manage ARDS patients 32

Management of Ventilatory Support 

Low Tidal Volume  6ml/kg  Limits 

the effect of barotrauma

Excessive pressure in the alveoli

 Maintain

lowest Peak Inspiratory Pressure possible  Respiratory rate 20 – 30 

Allow for adequate CO2 elimination

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Management of Ventilatory Support 

Permissive Hypercapnia  Uses

low tidal volume with normal respiratory rate to limit the effects of barotrauma  PaCO2 should not exceed 80 – 100mmhg  Arterial pH maintained at 7.20 or greater 

To maintain pH sodium bicarbonate is given or respiratory rate and/or tidal volume is increased

 Contraindications 

Increased ICP, pulmonary HTN, seizures, cardiac failure 34

Management of Ventilatory Support 

Pressure Control Ventilation (PCV)  Each

breath delivered with a preset amount of inspiratory pressure 

Volume will vary

 Benefit 

Limits high Peak Inspiratory Pressure to prevent barotrauma

 Concern 

As lungs become less compliant (stiffer) difficult to maintain adequate tidal volume and PaCO2 35

Management of Ventilatory Support 

Inverse Ratio Ventilation (IRV)  Can

be volume or pressure controlled shortens expiratory time

 Prolongs inspiratory time and  Reverse of the normal I:E ratio  Decreases Peak

Inspiratory Pressure

 Goal  Helps keep the alveoli open  Disadvantages  Auto- PEEP 



Shortened expiratory phase leads to air trapped in lower airways causing unintentional PEEP

Not well tolerated 

Requires sedation and neuromuscular blockade 36

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Management of Ventilatory Support 

Positive End Expiratory Pressure (PEEP)  Goal  Improve oxygenation while reducing FiO2 to less toxic levels  Usual range 10 -15 cm  May need higher levels

H 2O

 Benefits  Opens collapsed alveoli  Decreases intrapulmonary shunting  Increases compliance  Disadvantages  Decreased cardiac output  Potential for barotrauma & pneumothorax 37

Management of Ventilatory Support 

High-Frequency Oscillatory Ventilation  Used

for patients who are refractory to previously described treatments  Requires a special vent  Delivers very low tidal volume at very high rates 

Rate 300 – 3000/min

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Management of Ventilatory Support 

Extracorporeal and Intracorporeal Gas Exchange  Last

resort the lungs to rest by proving oxygenation through an artificial device

 Allow

ECMO ECCO2R  IVOX  

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Cardiovascular Support 

Goal is to maximize cardiac output and oxygen delivery to the tissues  Fluid 

management

Maintain optimal circulating volume

 Inotropic/vasoactive 

support

Maintain blood pressure

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Pharmacological Support 

Goal is to reduce O2 demand 

Narcotics Sedation  Antibiotics  Anti-pyretics  Neuromuscular Blocking Agents 

 

Paralyze muscles Must use sedation with these agents

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What Happened to Case Study Patient? 

Intubated and mechanically ventilated



Difficult to maintain O2 sats after being off PEEP to intubate



Suctioned for thin, pink secretions suggestive of non cardiac pulmonary edema



Sedated and paralyzed



Vent settings: TV 450, RR 24, PEEP 20 cm, FIO2 100% 42

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Nutritional Support 

Nutrition consult



Increased caloric needs



Early nutrition support  Enteral

feedings preferred

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Positioning 

HOB elevated at least 30◦



Turn and position at least every two hours  Good

lung (side) down



Continuous lateral rotation



Prone positioning 44

Activity 

Assess patient tolerance to activity  Patient

can desaturate rapidly & have prolonged recovery from activity



Ensure recovery of oxygen saturation between nursing interventions

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Emotional Support 

Extremely critically ill



May not recover



Prolonged recovery period (months)



Coordination of care and patient advocacy  



Ensure consistent plan of care of multidisciplinary team Ensure consistent message to family

End of life decision making 46

Questions

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