Perfusion/Oxygenation: Acute Respiratory Distress Syndrome (ARDS) - Coggle…
Perfusion/Oxygenation: Acute Respiratory Distress Syndrome (ARDS)
Etiology: pneumonia causing direct lung damage
Pulmonary tissue damage initiates inflammatory response and rapid accumulation of neutrophils within the endothelial and alveolar spaces
Neutrophils release immune mediators (proteases, cytokines), causing vascular vasodilation and increased capillary permeability.
Accumulation of interstitial fluid narrows the airway and increases airway resistance. Lack of ventilation impairs lung compliance and contributes to hypoxemia.
Fluid leaks into alveoli, interfering surfactant release and alveolar expansion. Hypoventilation causes alveoli collapse and creates dead space where oxygen exchange can't occur. Body compensates for V.Q. mismatch by breathing faster, works harder, and increases O2 demand.
Lack of surface area for gas exchange leads shunting of blood flow through impaired lung tissue. Blood is unable to be adequately oxygenated and extremities may fail to perfuse. Hypoxemia develops as CO2 accumulates. Respiratory acidosis may occur.
Structural injury to pulmonary tissues causes vasoconstriction and subsequent pulmonary hypertension. Collagen and fibrosis deposits in response to trauma further impairs gas exchange.
Pulmonary & systemic sepsis
Trauma or injury to lung tissue
ABGs showing respiratory acidosis, pH <7.35, PaCO2 >45, & PaO2 <55.
Sputum culture to assess for pneumonia
BNP and echocardiogram to rule out CHF as contributing factor
Chest xray to determine lung tissue infiltrates
Dyspnea, tachypnea, crackles
Pleuritic chest pain
Productive cough, sputum production
JVD & edema from pulmonary congestion into venous system
Oxygen sat <92%
Deep vein thrombosis & Pulmonary embolism
Mechanical ventilation, increasing mortality and risk of hospital-acquired infection.
Psychiatric illness including depression, anxiety, and PTSD
Mechanical ventilation to promote hemodynamic stability while addressing underlying issue
Maintain at low tidal volume rather than traditional
Utilize positive end-expiratory pressure value (12-18 cm H2O)
Low-volume fluid therapy
Sedation may be required
Perform appropriate care to prevent infection
Heparin to prevent venous thromboembolism
Pharmacological prophylaxis against stress ulcers