Flashcards in Pathophysiology of the Acute Respiratory Distress Syndrome Deck (17):
1. Define acute respiratory distress syndrome.
a complex set of inflammatory events that are responsible for diffuse alveolar damage and increased permeability pulmonary edema due to a wide variety of pulmonary and systemic diseases.
2. Describe the causes of acute respiratory distress syndrome.
due to direct lung parenchymal injury or systemic stimulation of an inflammatory response (SIRS)
majority are caused by pneumonia with extra pulmonary sepsis and trauma following behind: others include aspiration of gastric contents, acute pancreatitis and near drowning
between 30-40% of patients that develop ARDs die, although most die from complications of their underlying risk factors rather than from unsupportable hyperemic respiratory failure, most survivors do not have significant long-term pulmonary dysfunction
3. Analyze the pathogenesis of lung injury at ARDS. Contrast pathogenesis at different sites of injury (alveoli, interstitial, etc.).
for increased lung permeability, there must be injury to capillary endothelium as well as the alveolar epithelium
4. Describe how neutrophils contribute to the pathophysiology of ARDS.
neutrophils: migration to air spaces and activation in early ARDS and can contribute directly or indirectly to lung injury; they produce and release potent toxins, including proteases, arachidonic acid metabolites and oxygen radicals
5. Describe the pathophysiology (including gas exchange, fluid shifts, etc.) and clinical correlates of the acute phase of ARDS.
inflammation and endothelial cell damage of early phase ARDs cause acute permeability of pulmonary microvascular endothelium. if lymphatics are overwhelmed, the alveolar edema of high protein content forms with rapid evolvement from interstitial to alveolar edema
flooded alveoli are coated with hyaline membranes from protienaous infiltrate accompanied by necrosis of type IIpneumocytes and endothelial cells
grossly this results in decreased static lung compliance, intrapulmonary shunting (hypoxemia), increased dead space and pulmonary (hypercapnia) hypertension
6. Describe the pathophysiology of the subacute and chronic phases of ARDS.
chronic or "fibroproliferative" phase begins within a couple days, an intense proliferative reaction including endothelial cells, type II epithelial cells and fibroblasts, as well as mesenchymal cells
with some reparative value, significant remodeling of the lung can occur but can also result in severely fibrotic lung
nosocomial infection, ventilator induced lung injury and oxygen toxicity may exacerbate initial lung injury response
remodeling can occur that can cause normalization of pulmonary funciton
7. Contrast mechanisms that increase permeability pulmonary edema (neurogenic, fat embolism syndrome, etc.).
neurogenic pulmonary edema: transient but profound increase in sympathetic tone associated with increased intracranial pressure causes pulmonary HTN edema and endothelial damage
high altitude pulmonary edema: associated with exercise over 9,000 feet caused by a combination of high pressure and shearing impact of damage
neither of the above is associated with ARDS
fat embolism syndrome: associated with long bone fracture due to fat emboli that are released from marrow, accompanied by a pathopneumonic petechial rash of head, chest, axilla and sub conjunctiva, sometimes associated with focal neurological signs
8. Identify pathologic feature of ARDS (ie. diffuse alveolar damage).
acute: lungs are heavy, firm, red, and boggy exhibiting congestion, interstitial and intra-alveolar edema, inflammation, fibrin deposition and diffuse alveolar damage characterized by fibrin rich edema fluid with cytoplasmic elements that form a hyaline membrane to replace dying type I cells
type II cells proliferate during the organizing stage and granulation tissue forms that usually resolves leaving minimal functional impairment
fibrotic phase can result in fibrotic thickening of alveolar septa, caused by proliferation of interstitial cells and deposition of collagen
1. Describe how severity of ARDS is determined.
severity is defined by the severity of the hypoxemia with concurrent hypoxemia interventions
mild: P/F >200 but 100 but <100mmHG
Describe the diagnostic criteria for ARDS via the Berlin Definition.
1. sx w/in 1 wk of insult
2. bilateral opacities that cannot be explained by pleural effusions, lobar collapse, lung collapse or pulmonary nodules.
3. sx. and imaging are not fully explained by cardiac failure or fluid overload (clinical judgement)
4. Moderate to severe hypoxemia, defined by the ratio of arterial oxygen tension to the fraction of of inspired oxygen as a fraction of 1
2. Describe the epidemiology and causes of acute respiratory distress syndrome.
new clinical syndrome, encompassing distinct disorders that share common clinical and pathyphysiologic features
190,000 case in US/year associated with 74,000 deaths (more than AMI) (occupying 9% of ICU beds)
Explain the most important advance in the management of patients with ARDS.
use of lower tidal volumes when ventilating patients: (6mL/kg) of predicted body weight is associated with a relative risk reduction of 22%
4. Describe how macrophages contribute to the pathophysiology of ARDS.
macrophages: stimulated and activated, are a source of eytokines that amplify ARDS by activating neutrophils, increasing their adhesion to the endothelium, directly injuring endothelium and induing production of secondary response cytokines
3, 4. Describe how endothelium contribute to the pathophysiology of ARDS.
endothelium: promotion of neutrophil adhesion and migration by changes in permeability characteristics; through release and metabolism of inflammatory vasoactive and procoagulatnt substances
3. How do cytokines/arachadonic acid metabolites contribute to the pathophysiology of ARDS.
cytokines amplify the inflammatory response, those most firmly associated with ARDS include TNF-a, IL-1B and IL-8
Describe the distribution of lesions found in ARDS.
typically distributed heterogeneously, with more edema collecting in the dependent portions of the lung, some lung is filled with fluid and ceases to be involved in ventilation, other areas are subject to various degrees of interstitial and alveolar edema (less compliant)