Acute RespiRAtoRy DistRess synDRome

Presented by Omar AL-Rawajfah, RN, PhD

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Lecture Outlines • Etiology and Pathophysiology

– Definition – Systemic inflammatory response syndrome – Precipitating causes of ARDS – Mediator of sepsis, ARDS – Stages

• Assessment – Neurologic – Respiratory – Cardiovascular

• Nursing diagnoses • Collaborative management

– Airway management – Mechanical ventilation – Pharmacotherapy – Fluid and nutritional therapy

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Etiology and Pathophysiology

• Acute Lung Injury (ALI): a syndrome characterized by non-cardiogenic pulmonary edema, decreased lung compliance, refractory hypoxemia

• ARDS: is the most sever form of ALI • ARDS: a syndrome of inflammation and increased

permeability associated with a constellation of clinical, radiologic, and physiologic abnormalities unexplained by elevations in left atrial or pulmonary capillary pressure

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Etiology and Pathophysiology • Clinically ARDS is defined by:

– PaO2/FIO2 < 200 mmHG (normally > 300mm Hg) – Bilateral infiltration of lungs – Pulmonary Artery Occlusive Pressure (PAOP) < 18 mmHg (normally

5-15mm Hg) – Alveolar damage

• ARDS is characterized by the following criteria:[ – lung injury of acute onset, within 1 week of an apparent clinical insult

and with progression of respiratory symptoms – bilateral opacities on chest imaging not explained by other pulmonary

pathology (e.g. pleural effusion, pneumothorax, or nodules) – respiratory failure not explained by heart failure or volume overload – decreased arterial PaO2/FiO2 ratio:

• mild ARDS: ratio is 201 - 300 mmHg • moderate ARDS: 101 - 200 mmHg • severe ARDS: ≤ 100 mmHg

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Systemic Inflammatory Response Syndrome

• SIRS: is an overly aggressive host defense response to insult or tissue damage in the body

• The local injury response becomes total-body response • Most SIRS patients have bacterial infection • SIRS may be associated with trauma, hypoxia,

pneumonitis, burns, tissue necrosis, & sever peripheral vascular disease – Fever more than 38C or hypothermia less than 36 – HR > 90, RR > 20 PaCO2 < 32, WBC > 12,000

• Inflammatory cytokines produce in response to injury have negative effect in lung healing

• The hallmark of ARDS is accumulation of protein-rich fluid in the alveoli and interstitial spaces

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Precipitating causes of ARDS

• Direct pulmonary insults – Aspiration of GI contents – Inhalation of toxic substance – Diffuse pneumonia – Pulmonary contusion – Pulmonary embolism – End stage COPD – O2 toxicity

• Indirect pulmonary insults – Sepsis – Multiple trauma – Burn – Anaphylaxis – Tissue necrosis – Disseminated intravascular coagulation (DIC) – Cardiopulmonary bypass

Causes of ARDS

NEJM 2000;342,18:1334-1349

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Pathophysiology • The damage to the endothelial lining of the

alveolar-capillary membrane increases its permeability

• Shifting of the fluids and proteins into the alveoli inactivates surfactant result in alveolar collapse

• V/Q mismatch is occurred because of the blood passing through the lungs without gas exchange

• This condition is manifested by deterioration of oxygenation in spite of increased O2 supply

• In the process of lung healing, fibrosis and scarring further dispute gas exchange

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Mediators of Sepsis, ALI & ARDS

• Components of the host defense response: • Inflammation

– Vasodilatation, increased capillary permeability – Clotting within the interstitial space – Migration of granulocytes and monocytes to the tissue – Release of bradykinin, histamine, prostaglandines

• Modulation of Immune Response – Tumor Necrosis Factor (TNF) and Interleukin-1 are

stimulated by bacterial endotoxin and cause fever – Neutrophils attack the damaged pulmonary capillaries

endothelial lining result in organ damage in other organ system

– Arachidonic acid, thromboxane, & prostacyclcin believed to cause pulmonary hypertension, and smooth muscle construction

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Components of the host defense response • Coagulation

– Microthrombi and fibrin disposition – Intravascular coagulation decrease the size of available

pulmonary vascular beds – Tissue repair – Regeneration of native parenchymal cells and filling the gaps

with fibroblastic tissue creates persistent problem with gas exchange

– Fibroblastic tissue decrease the lung compliance – It is believed that progression of fibroproliferation to

pulmonary fibrosis is the responsible for 15-40% of death with ADRS

• Activation of hypothalamic-pituitary-adrenal axis – Stress responses → release of catecholamines – Increased vascular tone

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Stages of ARDS

• Phase I: Early exudative phase – Alveolar edema with fibrin & leukocytes debrise – Damage of type I pneumocytes and endothelial

cells

• Phase II: proliferative phase – Presistent capillary endothelial damage – Type II cell proliferation

• Phase III: fibroproliferative phase – Also called chronic ARDS – Thickening of the interstitium – Increased number of type II cells and fibrosis

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Lung injury score

• Chest radiograph score (0 – 4) • Hypoxemia score (0 – 4) • Positive End-Expiratory Pressure (0 – 4) • Compliance Score (0 – 4) • Total Score

– 0: no lung injury – 0.1 – 2.5 : mild to moderate lung injury – More than 2.5 sever lung injury – See important table 18-3

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Assessment • ARDS usually developed 24 – 72 hrs of the insult • The assessment should be directed to know the patients at risk

for ARDS • Neurologic system

– Level of consciousness – Restlessness and anxiety – Lethargic and quite behaviors may indicate decompensate quickly

• Respiratory System – Dyspnea & tachypnea – Cough with think foamy sputum or hemoptysis – Close monitoring of SaO2 – Chest X-ray may be normal within the first 24 hrs then white out or

ground glass picture – As the hypoxemia worse cyanosis, pallor, diaphoresis occur – More widespread crackles and wheezes and absent breathing

sound over the collapse areas – Early ABG may be alkalotic changed to acidosis after while

because of combined respiratory & metabolic acidosis

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Early stage ARDS

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Late stage ARDS

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Assessment

• Cardiovascular System – Tachycardia and dysrhythmias – Cardiac failure is very possible specially for those

who had previous cardiac events – Cardiac arrest is possible too – Elevated pulmonary pressure without an increase

in vascular volume • Nursing Diagnosis

– Ineffective airway clearness – Impaired gas exchange – Ineffective breathing pattern – Decrease CO – Alter tissue perfusion….

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Collaborative Management

• Airway management – Endotracheal Intubation – Positive pressure ventilation – Consider tracheostomy for intubation more than 7

days

• Mechanical Ventilation – The goals of MV in ARDS are:

• Improve gas change and reduce hypoxemia • Reliving respiratory distress by reduce the work of

breathing • Prevent atelectasis • Permitting lung and airway healing • Avoid complications

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Collaborative Management

• Ventilator-Induced Lung Injury – Occurs in ARDS who treated with high pressure

and large TV – Because of alveolar collapse and protein leakage

small portion of the lung continue to work – In most of case only about one-third of the lung

participate in the gas exchange “small lung theory” or baby lung theory”

– When this small portion receive full TV and high pressure overdistention and injury occurs in these normal or nearly normal tissue

– The goal of the ventilation therapy is to recruit alveoli with PEEP and minimize the ventilator-induced injury

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Collaborative Management • Problem associated with conventional MV

– O2 toxicity • When O2 percentage more than 50% for longer than 12-

24hr • O2 toxicity can cause increased pulmonary

micropulmonary permeability, ↓surfactant producation, impedance of tracheal cilia

– Hypotension • Positive pressure ventilation in all forms increase the

intrapulmonary and interathoracic lead to decreased preload and thus decreased CO

– Barotrauma • Associated with different conditions such as

pneumothorax subcutaneous emphysema – Volutrauma

• Large shearing force: caused by repeated opening and closing of alveoli with each respiratory cycle

• May caused by high peak inspiratory pressure, high PEEP, large TV, high RR

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Barotrauma

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Management of ARDS • High-frequency Jet Ventilation

– Creates a constant airway pressure throughout the respiratory cycle that lower peak airway pressure and allows use of small TV

– It need sedation and paralysis – Need special type of ventilators – Need trained nurses

• Pressure-controlled inverse-ratio – It reveres the normal inspiratory and expiratory

time ratio (normally I:E = 1:2 or 1:3) reversed to be 2:1, 3:1, or 4:1

– It allows consistent gas delivery – Allows reduction of FIO2 and PEEP – Need trained nurse with special ventilator settings

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Management of ARDS • Super PEEP

– Greater than 15 mmHg – Maintain PaO2 greater than 60mm Hg – Associated with good survivor rate – Barotrauma and hypotension are common side effects – It is well accepted that pressure below 35-50 cm H2O is

safe and will not cause lung injury

• Pressure-controlled without inverse-ratio – Each breath is delivered to reach a preset pressure – Well tolerated by patient – TV is set 5-10 mL/Kg – TV is not constant – In case of bronchspasm, secretion the preset pressure

level reaches the peak quickly→ patient may be underventilated

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Additional lung protective techniques • Low TV ventilation

– Prevents overdistention of normal lung tissue • Permissive hypercarpia

– Using low TV and limited pressure normally increase the CO2 level

– Adult can tolerate higher level of CO2 with few side effects – Mild to moderate acidosis is well tolerated by adult – The metabolic system usually compensate within 1 or 2

days – Moderate acidosis have some positive effect such as

increasing the responsiveness to catecholamines • Intravascular oxygenation

– Direct oxygenation of the blood or direct removal of the CO2 from the blood

– Assists the injured lung and reduce the burden on healthy areas

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Additional lung protective techniques

• Pharmacologic support – Antioxidants (e.g. Ketoconazole)

• It is thromoxane A2 synthetase inhibitor • Associated with hepatic toxicity, renal toxicity

– Steroids

• Fluid therapy – Negative fluid balance has been beneficial in reducing the

associated pulmonary edema and improve the gas exchange

– Negative balance can be reached with diuretics – ARDS patient are maintained on the lower end of central

venous pressure (i.e 3-5 cm H2O) – Dopamine can be used to compensate the reduction in the

CO

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Additional lung protective techniques

• Nutrition • Body position • Use prone position

– Contraindication of prone position include: • Hemodynamic instability • Weight over 90kg • Abdominal girth more than 50 inches

• Preventing of infections – Strict aseptic techniques – Prevent aspiration

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Questions and answers