1. ARDS Background
    -major form of hyopxemic respiratory failure; pathological response to alveolar injury -- NOT a disease

    AKA: non-cardiogenic pulmonary edema

    • Central Features:
    • -severe arterial hypoxemia (PaO2 on FiO2 <200)
    • -diffuse bilateral pulmonary infiltrates
    • -Non-cardiogenic (LVDEP < 18mmHg)
    • -poor compliance (stiff lungs)
    • -PEEP sensitive physiology
  2. ARDS Epidemiology
    Incidence: 75/100,000

    Traditional mortality = 40-60% (majority due to multisystem organ failure)

    Mortality decreases with low volume ventilation (to 30%)

    Survivors tend to have normal function within a year
  3. Physiology of fluid movement in alveolar interstitium
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    • Movement into the interstitium is determined by the Starling Equation (balance of hydrostatic and osmotic pressures)

    Normally net movement of fluid is into the interstitial space

    Lymphatics are effective in absorbing the leaked protein and fluid
  4. Two Mechanisms of Fluid Accumulation
    • 1. Cardiogenic
    • -due to increased hydrostatic pressure in capillaries (↑ LVEDP
    • -permeability barrier intact (leak of protein-poor fluid)

    • 2. Non-cardiogenic Pulmonary Edema (aka ARDS)
    • -compromised permeability of capillary endothelial (insult to type 1 pneumocytes) and alveolar epithelial barriers
    • -fluid tends to have a high protein content

    May have a combination of Non-cardiogenic with super imposed with increased capillary hydrostatic pressure... bad news bears ☹

    -Don't want to volume overload pts with non-cardiogenic edema; keep euvolemic (or dry)
  5. ARDS Etiology
    -ARDS results from any number of factors that all cause diffuse injury to the pulmonary parenchyma

    • Inhaled Injurious Agents
    • -Aspiration (gastric, drowning, etc.)
    • -Toxic irritants (smoke, nitrogen dioxide, 100% FiO2 in predisposed individuals)
    • -Bilateral Pneumonia

    • Circulating Insults
    • -Sepsis
    • -Shock (accompanied by other etiologic factors)
    • -Trauma
    • -DIC
    • -Embolism (amniotic fluid, fat)
    • -Multiple Transfusion
    • -Pancreatitis
    • -Neurogenic
    • -Mechanical Ventilation
  6. ARDS net
    Trial showed dramatic reduction in mortality in ventilated patients:

    • -Low lung volume ventilation
    • -Permit hypercarbia to achieve low tidal volume
    • -keep patients euvolemic (aggressively) to ensure LVEDP < 18mmHg at all times
  7. Inhaled Injurious Agents
    • 1. Aspiration
    • -gastric contents (chemical burn)
    • -salt water (fills alveoli, hypertonic --> leakage from pulmonary vessels)
    • -fresh water (cellular edema, inactivates surfactant)

    • 2. Toxic Gas Inhalation
    • -NO2
    • -Smoke
    • -Ammonia
    • -High O2 for long periods of time
  8. Pneumonia
    -most common underlying clinical problem associated with development of ARDS

    • -pneumocystis jiroveci
    • -viral
  9. Sepsis
    -one of the most common precipitants of ARDS

    -can be due to microorganisms and/or their products (endotoxin)
  10. Embolism
    • -fat
    • -amniotic fluid
    • -drugs
    • -narcotics
    • -sedatives
    • -ASA (rare)
    • -thiazides (rare)
  11. Pancreatitis
    -enzymes released into circulation from damaged pancreas lead to direct and/or indirect injury of pulmonary cells
  12. Neurogenic
    • -trauma
    • -intracranial hemorrhage
    • -seizures

    may be due to intense sympathetic activation --> high pulmonary capillary pressures and mechanical damage to endothelium
  13. ARDS Pathogenesis
    Injury of pulmonary capillary endothelial cells, alveolar epithelial cells (mostly type I cells) or both

    • 1. Inflammation of pulmonary parenchyma (usually NPs)
    • 2. Activation of vascular endothelium (expression of leukocyte adhesion molecules)
    • 3. Release of cytokines, proteases and oxidants
    • 4. Release of procoagulants, activation of coagulation system
  14. ARDS theories
    • -Oxygen toxicity (only limited number of cases)
    • -Surfactant (primary problem in newborns, secondary role in adults)
    • -Ventilator associated lung injury (damage through overdistension)
  15. ARDS Pathology
    -Damage to type I alveolar cells

    • -Interstitial and alveolar fluid
    • -Areas of alveolar collapse/scattered bleeding
    • -inflammatory cell infiltrate
    • -presence of hyaline membranes (protein-rich edema fluid that has filled the alveoli)
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    • -hyperplasia of type II alveloar cells
    • -accumulation of fibroblasts (fibrosis)
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  16. Pathophysiology
    • 1. Shunting
    • -alveolar flooding preventing ventilation

    • 2. V/Q mismatch
    • -changes in blood flow do not necessarily follow the same pattern as changes in ventilation

    • 3. Secondary alterations in function of surfactant
    • -decreased production due to damage to type II alveolar cells
    • -inactivation

    • 4. Increased pulmonary vascular resistance
    • -hypoxic vasoconstriction
    • -increased interstitial pressure (fluid) decreases size of pulmonary vessels
    • -blockages by microthrombi/proliferative changes

    • 5. Decreased pulmonary compliance
    • -fewer functional alveoli --> less volume entering lung for any given inflation pressure)

    • 6. Decreased FRC
    • -group of alveoli containing little or no gas

    • -Patients also get increased pulmonary vascular resistance secondary to:
    • --Pulmonary arterial hypoxemic vasoconstriction
    • --Increased LVEDP
  17. Clinical Features
    General lag of 1+ days before sx (first is usually dyspnea)

    • 1. Dyspnea
    • 2. Tachypnea
    • 3. Rales
    • 4. Decreased PO2, normal/decreased PCO2, increased AaDO2 (alveolar-arterial difference in partial pressure of O2)
    • 5. CXR: interstitial and alveolar edema
  18. Diagnostic Approach
    • 1. CXR
    • -edema
    • -diffuse, symmetrical

    • 2. ABG
    • -hypoxemia
    • -hypocapnia (?????)
    • -PaO2/FiO2 < 200 = ARDS

    • 3. PCWP
    • -determine if cardiogenic or non-cardiogenic
    • -ARDS: should be normal
    • -can determine if hydrostatic P in capillaries is contributing
  19. Treatment
    • 1. Tx underlying cause
    • 2. Interrupt pathogenic sequence of events in capillary leak
    • 3. Support gas exchange until pulmonary processes improve

    • Mechanical Ventilation:
    • -Avoid overdistention (volutrauma)
    • -Tolerate permissive hypercapnia if necessary

    • PEEP:
    • -avoid recruitment-derecruitment
    • -increase oxygenation (recruits lung)

    • Corticosteroids
    • -may be effective in fibroproliferative phase (last ditch effort)

    • Nitric Oxide
    • -better perfusion of well ventilated areas
    • -better V/Q matching
  20. PEEP
    • Optimal PEEP
    • -keep on steep side of curve
    • -maximal alveolar recruitment w/o injury to alveoli due to opening and closing

    • Image Upload 4
    • -Wean off slowly!!! (start to wean FiO2 first, avoid transport)
    • -Go right back up if the patients Desat
Card Set
Pulmonary II