Therapeutics Pulmonary Ronald Flashcard

Etiologies for Acute Lung Injury/Acute Respiratory Distress Syndrome

Direct Lung Injury

  • Common causes: Bacterial pneumonia, Aspiration pneumonia
  • Less Common: Viral pneumonia, Fat emboli, Inhalation injury, Near drowning, Pulmonary contusion

Indirect Lung Injury

  • Common causes: Sepsis, Severe trauma or shock with multiple transfusions
  • Less common: Blood product transfusions, Acute pancreatitis, Burns, Disseminated intravascular coagulation, Drug overdose, Head injury, Trauma

Acute Lung Injury/Acute Respiratory Distress Syndrome: Risk Factors

  • Chronic alcoholism
  • Advancing age
  • Hypoproteinemia
  • Cigarette smoking
  • Chronic lung disease
  • Acidemia
  • Multiple predisposing conditions

Acute Lung Injury/Acute Respiratory Distress Syndrome: Two primary types of cells affected

  1. Type I alveolar cells — epithelial cells across which gas exchange occurs
  2. Type II alveolar cells — surfactant-producing cells

Acute Lung Injury/Acute Respiratory Distress Syndrome: Type of cell damage and physiologic outcome

  • Type I alveolar cells: damage leads to deposition of proteins, fibrin, and cellular debris –> hyaline membranes –> decrease lung compliance and decreased oxygenation capabilities
  • Type II alveolar cells: decreased surfactant production –> alveolar collapse

Three Phases of Acute Lung Injury/Acute Respiratory Distress Syndrome Pathophysiology

Exudative Stage

damage to alveolar and vascular endothelium (both type I and type II alveolar cells) –> leakage of fluid, protein, and inflammatory cells into interstitial space and alveoli

 

Proliferative Stage

type II cells proliferate with some epithelial cell regeneration, fibroblastic reaction, and remodeling –> increased fibrosis with decreasing compliance

 

Fibrotic Stage

some patients progress to this irreversible phase of collagen deposition in alveolar, vascular, and interstitial beds –> chronic fibrotic changes –> decreased pulmonary function upon recovery of acute issues

4 Criteria to Assess for Diagnosis Acute Lung Injury/Acute Respiratory Distress Syndrome

Oxygenation

  • ALI – PaO2/FiO2 < 300 mmHg
  • ARDS – PaO2/FiO2 < 200 mmHg

Onset

  • Acute — within 72 hrs of hypoxemia and chest x-ray changes

Chest Radiography

  • Bilateral infiltrates — consistent with pulmonary edema

Cardiac Assessment

  • No clinical evidence of left atrial hypertension or PCWP < 18 mmHg

 


Both Nonpharmacologic and Pharmacologic Treatment for Acute Lung Injury/Acute Respiratory Distress Syndrome

  • Fluid and Hemodynamic Management
  • Lung-Protective Ventilation
  • Nutrition
  • Corticosteroids
  • Beta-Adrenergic Agonists

Acute Lung Injury/Acute Respiratory Distress Syndrome: Rationale for Fluid and Hemodynamic Management

  • Main characteristics of ALI/ARDS = increase lung water
  • Normal fluid balance in lung — interaction of oncotic pressure and hydrostatic pressure
  • Oncotic pressure reduced in ARDS — edema can occur with relatively minimal changes in hydrostatic pressure
  • Minimizing fluid administration can help reduce changes in hydrostatic pressure within blood vessels –> decreasing fluid shifts to extravascular spaces

Acute Lung Injury/Acute Respiratory Distress Syndrome: Rationale for Lung-Protective Ventilation

  • Low-tidal volume ventilation (6-8 ml/kg) = standard of care
  • In ARDS — injured portion of the lung is non-compliant and inflates poorly while the still healthy portions of the lung are still compliant and can overinflate and stretch excessively
  • The overextension of the still healthy lung leads to spreading of lung damage and further progression of ARDS
  • Pplat — represents the pressure in the smaller airways and alveoli — keeping the Ppat < 30 cm H2O protects the still healthy portions of the lung from overdistension and further injury
  • Permissive Hypercapnea — allowance of higher pCO2 levels (> 45 mmHg) and lower pH (< 7.35) values to achieve lower tidal volume ventilation

 

Acute Lung Injury/Acute Respiratory Distress Syndrome: Rationale for Nutrition

  • N-3 polyunsaturated fatty acids (GLA and EPA) serve as precursors of eicosanoids which modulate the intensity and duration of the inflammatory response
  • N-3 polyunsaturated fatty acids have been shown to decrease neutrophil migration, decrease production of reactive oxygen species, and decrease formation of inflammatory cytokines

Acute Lung Injury/Acute Respiratory Distress Syndrome: Rationale for Corticosteroids

  • Currently not recommended for ALI/ARDS — but if they are used, they must be used early on (higher risk of death found if steroids started > 13 days after ARDS onset)
  • ARDS –> upregulation of inflammatory response (cytokines, macrophages, etc.)
  • Corticosteroids inhibit numerous factors in the inflammatory pathway as well as increase anti-inflammatory mediators (IL-1 antagonists, IL-10, etc.)
  • Thought to play a role in treating ongoing inflammation, cell proliferation, and abnormal collagen deposition found in persistent ALI/ARDS
  • No change in overall mortality, but has shown improvement in oxygenation, shock-free days, and ventilator-free days

Acute Lung Injury/Acute Respiratory Distress Syndrome: Rationale for Beta-Adrenergics

  • Unproven treatment
  • Stimulate resorption of pulmonary edema fluid by pumping fluid from the alveoli via Na+K+ ATPase pump –> decreased pulmonary fluid
  • Found to help reduce inflammation and decrease pulmonary endothelial permeability
  • Patients with ARDS can have increased airway resistance –> resistance can be decreased by the bronchodilating effects of beta-agonists either IV or inhaled

Variables Associated with Increased Mortality due to Acute Respiratory Distress Syndrome

  • Concurrent liver failure
  • Long duration of mechanical ventilation
  • Prolonged non-pulmonary organ failure
  • Advanced age
  • Low PaO2/FiO2
  • High plateau pressures — indicating lung compliances/stiffness
  • Hypoproteinemia
  • Length of hospitalization prior to ARDS

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