ARDS Flashcards
Three characteristics of pulmonary edema:
- Heavy, wet lungs: basal initiation (dependent edema)
- Hemodynamic: Cardiogenic
- Permeability: increased capillary permeability
Pulmonary edema: hemodynamic characteristics
- Increased hydrostatic pressure: left sided CHF
- Engorged alveolar capillaries
- Intra-alveolar granular pink precipitate
- Alveolar microhemorrhages
- Hemosiderin-laden mac’s (heart cells)
What are the consequences of long-standing pulmonary edema?
- Mitral stenosis
- Increased heart cells
- Fibrosis and thickening of alveolar walls
- Soggy lungs become brown and indurated (firm or hard due to fibrous elements)
What are the characteristics of microvascular injury in pulmonary edema?
- Injury to capillaries of the alveolar septa
- Primary injury to the vascular endothelium or alveolar epithelial cells: no increase of hydrostatic pressure.
- Fluid and proteins into interstitial space and potentially alveoli
- Pneumonia=localized edema
Diffuse alveolar damage (DAD) morphology: acute
- Congestion, interstitial, and intra-alveolar edema, inflammation and fibrin deposition.
- Fibrin rich edematous fluid with cytoplasmic and lipid remnants, necrotic epithelial cells.
DAD morphology: organizing type
- Type II pneumocytes (**) undergo proliferation
- Results in organizing fibrin exudate and intra-alveolar fibrosis
- Leads to more pneumocyte proliferation and collagen deposition.
ARDS onset:
Rapid Respiratory insufficiency Cyanosis Arterial hypoxemia (refractory oxygen therapy) Multi-organ failure
Chest radiographs of ARDS reveal what?
Diffuse alveolar infiltrates
ARDS causes: infectious
Sepsis Viral Mycoplasma Pneumocystis Miliary TB Gastric aspiration
ARDS causes: physical
Mechanical trauma/head injuries
Burns and radiation
ARDS causes: inhaled irritants
Smoke
Gases
Chemicals
ARDS causes: chemical
Heroin
Aspirin (ASA)
Barbituates
ARDS causes: hematologic
TACO
DIC
Other causes of ARDS:
Pancreatitis
Uremia
Bypass Sgx
What happens in ARDS?
- Capillary endothelial or alveolar epithelial injury.
- Increased vascular permeability and flooding.
- Decreased diffusion capacity.
- Surfactant abnormalities (damaged Type II pneumos)
ARDS in the long run, what happens?
Exudate and destruction are poorly resolved.
Leads to organization and scarring-chronic disease
Immune responses due to ARDS:
- Elevated pro-inflammatory mediators.
- Decreased anti-inflammatory molecules.
- Proinflammatory: NF-kB (required)
- Bacterial infection: toll-like receptors–> innate immune response–> NF-kB
* Effects transcriptional selectivity (increased IL-10)
Immediate immunologic reaction to ARDS: what is released?
IL-8:
- neutrophilic chemotactic and activating agent
- Pulmonary macrophages
Released IL-1 and TNF role in ARDS?
Further activation and sequestration of neutrophils.
Vascular spaces, intersititium, and alveoli
Other things released by ARDS?
Oxidants
Proteases
Platelet-activating factor
Leukotrienes
ARDS presentations clinically:
- Radriographs normal at first
- Non-homogenous spread.
- Decreased functional lung volume.
- VQ mismatch
- 60% mortality
Acute interstitial pneumonia
- Widespread acute lung injury
- Unknown cause
- 50 years of age without sex predilection.
- Presents like URTI
- Progresses similar to ARDS
- 50% mortality