– He set any condition is clinically characterized by acute respiratory distress, radiologically by bilateral alveolar opacities and severe hypoxemia refractory to oxygen enrichment of inspired gases in the absence of abortion.
– This syndrome is characterized by severe disorder avéolocapillaire membrane permeability, resulting in pulmonary edema lesions, head of hypoxia and reduced lung volumes observed.
– Causes: Infectious and traumatic causes are most frequent (2/3 cases). In most cases it is the clinical expression of a systemic disease, inflammatory or septic in nature.
* Lung Infections
* Inhalation (gastric fluid, drowning, toxic gas, fire, smoke)
* Trauma: pulmonary contusion, respiratory burns
* Severe infection (peritonitis, sepsis)
* Trauma (multiple trauma, fat embolism, severe extensive burns)
* State of prolonged severe shock
* Massive transfusion, DIC, CEC.
* Acute Pancreatitis
* Pulmonary embolism (fat, amniotic, gas, cruoric)
* Other: acute vasculitis, toxic and drug causes
– Pulmonary involvement in ARDS is manifested histologically by an interstitial and alveolar pulmonary edema and hyaline membrane formation. diffuse alveolar damage (destruction of type I pneumocytes) later replaced by cuboid cells derived from type II pneumocytes. The evolution is towards healing or to pulmonary fibrosis.
– The hypoxemia in ARDS resulting different mechanisms. The main mechanism is an intra-pulmonary shunt (pulmonary territories perfused but not ventilated => VA / Q = 0). The enrichment of inspired oxygen gas does not correct the hypoxemia (-> refractory). The dissemination of disorders do not participate in hypoxemia in the acute phase of ARDS. The alveolar hypoventilation is mainly seen before intubation (exhaustion) with normal or hypercapnia.
– ARDS associated restrictive lung disease and decreased lung compliance. All lung volumes are reduced (CPT, CV, CRF).
– Inactivation of the surfactant causes the closure of the small airways leading to the formation atelectasis.
– There are often PAH; linked to several factors: obstruction of the pulmonary vascular bed by the inflammatory process, DIC, hypoxic pulmonary vasoconstriction and inflammatory; This PAH is usually moderate (pulmonary artery occlusion pressure is <18mmHg). This PAH is precapillary kind.
– Cardiac output is increased; systemic vascular resistance is low.