Acute Respiratory Distress Syndrome (ARDS)

Acute Respiratory Distress Syndrome (ARDS)

• ARDS involves severe lung inflammation and fluid buildup in the alveoli, leading to poor gas exchange and respiratory failure.
• Also known as "adult respiratory distress syndrome", "stiff lungs", "shock lung" and "acute respiratory dysfunction syndrome"

Key Terms

• Refractory hypoxemia: Severe low oxygen levels that do not improve with oxygen therapy.
• Infiltrate: Accumulation of substance like fluid, cells, or infection in lung tissue, visible on imaging.
• Acute Lung Injury (ALI): Lung inflammation and damage, impairs oxygen exchange, but is less severe than ARDS.
• Cytokines: Proteins that regulate immune and inflammatory responses.
• Cytokine Storm: Excessive release of cytokines, leading to widespread inflammation and tissue damage.
• Alveolar Capillary Membrane: Thin barrier between alveoli and capillaries where gas exchange happens.
• Permeable: Allowing fluids, gases, or substances to pass through.
• Type II Pneumocytes: Lung cells that produce surfactant and help repair alveolar damage.
• Surfactant: Substance that reduces surface tension in the alveoli, preventing collapse; deficient in ARDS.
• Transfusion-Related Acute Lung Injury (TRALI): Severe lung inflammation and fluid buildup caused by a blood transfusion.
• Transfusion-Associated Circulatory Overload (TACO): Fluid overload from a transfusion, leading to respiratory distress and heart strain.
• Transfusion-Related Immunomodulation (TRIM): Immune system changes caused by a blood transfusion, which may increase infection risk.
• Atelectasis: Collapse of lung tissue due to blocked airways or loss of surfactant.
• Tracheal Aspiration: Suctioning fluid or mucus from the trachea for analysis or to clear the airway.
• Exudative Phase: Early stage of lung injury with inflammation, fluid leakage, and impaired oxygen exchange.
• Fibrosing Alveolitis: Chronic lung condition with inflammation and scarring of the alveoli, leading to stiffness and impaired breathing.
• Resolution Phase: Final stage of lung healing after injury, where inflammation resolves and function improves.
• Neuropsychologic Deficits: Cognitive, emotional, or behavioral impairments caused by brain dysfunction.
• Tidal Volume: Amount of air moved in and out of the lungs with each normal breath.
• Fibrosis: Excessive tissue scarring that reduces lung elasticity and function.
• Airway Pressure Release Ventilation (APRV): Ventilator mode that allows spontaneous breathing while maintaining lung pressure to improve oxygenation.
• High-Frequency Oscillatory Ventilation (HFOV): Ventilator mode that delivers very small, rapid breaths to improve oxygenation while minimizing lung injury.
• Extracorporeal Membrane Oxygenation (ECMO): Life-support technique, oxygenates blood outside the body and removes carbon dioxide when the lungs or heart fail.

Pathophysiology

• ARDS is categorized as acute respiratory failure with:
  • Refractory hypoxemia, which persists even when 100% oxygen is given.
  • Decreased pulmonary compliance.
  • Dyspnea.
  • Non-cardiac related bilateral pulmonary edema.
  • Dense pulmonary infiltrates on X-ray with a ground glass appearance.
• ARDS occurs after acute lung injury (ALI) in individuals without pre-existing pulmonary diseases, stemming from conditions like sepsis, burns, pancreatitis, trauma, and transfusions.
• ALI triggers a systemic inflammatory response that activates pro-inflammatory cytokines, sustaining inflammation in the alveoli and pulmonary vasculature, known as "cytokine storm".
• Prolonged cytokine storm results in thick, swollen tissues that hinder gas exchange and promote scar tissue.
• The alveolar capillary membrane is the primary site of injury, being normally permeable only to small molecules but becoming more permeable to larger molecule when injured.
• This results in debris, protein, and fluid accumulating in the alveoli and lungs.
• COVID-19 related ARDS is characterized by thick exudate that inhibits gas exchange.
• Normal Type II pneumocytes produce surfactant, increasing lung compliance and preventing alveolar collapse.
• In ARDS, surfactant activity is reduced, leading to alveolar collapse.
• Edema forms around terminal airways, causing them to compress and close.
• As fluid continues to leak, it along with protein and blood cells collect in alveoli and spaces, compressing lymph channels and causing more fluid to collect.
• Poorly inflated alveoli receive blood but cannot oxygenate it, resulting in hypoxemia and V/Q mismatch.
• Transfusion reactions include:
  • TRALI: Severe lung inflammation and fluid buildup due to a blood transfusion.
  • TACO: Fluid overload from a transfusion, causing respiratory distress and heart strain.
  • TRIM: Immune system changes caused by a blood transfusion, potentially increasing infection risk.

Complications

• Complications arise from direct lung injury and include:
  • Atelectasis: Lung tissue collapse due to blocked airways or surfactant loss.
  • Shunting: Blood bypasses ventilated alveoli without oxygenation.
  • Decreased Lung Compliance: Stiffening of the lungs, making them harder to expand.

Signs & Symptoms

• Increased work of breathing
• Dyspnea
• Tachypnea
• Hyperpnea: Increased breathing depth and rate to meet body's oxygen demand
• Noisy respirations
  • Abnormal lung sounds often not heard due to edema occurring first
• Cyanosis
• Pallor
• Retraction intercostally: Between ribs
• Retraction substernally: Breastbone
• Sweating
• Hypotension
• Tachycardia
• Dysrhythmias
• Increased need for supplemental oxygen with little to no improvement in PaO2/SPO2

Labs / Diagnostics

• ABG shows low PaO2
• P/F ratio is less than 200 (PaO2 / FiO2)
• Sputum cultures for lung infection
• Chest X-ray: ground glass appearance
• ECG to rule out cardiac problems

Phases

• Exudative phase: Alveoli fill with fluid causing dyspnea and tachypnea
• Fibrosis alveolitis phase: Pulmonary hypertension, fibrosis, MODS may develop
• Resolution phase: Occurs 14 days after, damage may be permanent with neurological deficits due to chronic hypoxemia

Nursing Interventions

• Early recognition is a priority
• Infection control: Handwashing, catheters, wound care, contact protections
• Prone positioning and Q2 turns
• Intubation with mechanical ventilation
• Treat underlying cause (antibiotics, antivirals, diuretics)
• Conservative fluid management (limited IV fluids + diuretics to reduce pulmonary edema)
• Tube feedings or TPN for nutritional support

Monitoring

• Patients with tube feedings (keeps gastric sphincter open, allowing aspiration of gastric contents: this is the greatest risk)
• Monitor for swallowing problems & poor gag reflex, suction as needed
• Vital signs: hypotension, tachycardia, dysrhythmias
• Lung sounds hourly

Documentation

• Sweating
• Respiratory effort
• Change in mental status