ARDS Flashcards
What is ARDS?
□An acute form of respiratory failure
□Associated with hypoxemia
□Increasing permeability of capillary-alveolar membrane
□Proteins and fluid leak into the alveoli
□Leads to extensive edema
□Atelectasis
□Poor gas exchange
Damaged Type II Alveolar Cells
□Decreased surfactant production □Decreased alveolar compliance and recoil □Lend to atelectasis □Decreased overall lung compliance □Alveolar collapse □Altered gas exchange
What causes the leaking?
□Direct Injury
□Inhalation or aspiration of a lung-toxic substance
□Indirect systemic cascade effect initiated by lysosomal substances
Who’s At Risk? Pulmonary Related (Direct)
□Lung contusion □Embolism □Near-drowning □Pneumonia □Smoke inhalation □Aspiration □Inhalation of toxic gases or vapors □Radiation pneumonitis □Oxygen toxicity □Pulmonary edema
Who’s At Risk?
Non-pulmonary Related (Indirect)
□Linked to trauma of any kind! □Shock / Hemorrhage □Multiple blood transfusions □Infections □Sepsis/Septic shock □Drug abuse □MODS □Aspiration □Burns □Eclampsia □Cardiopulmonary bypass □Fluid overload □Fractures □Drug reaction
Patient Presentation
Early Stages
□Minor changes in orientation □Unusual interpersonal exchanges □Shifts in mood □Pulse and temperature may be elevated □Breath sounds may be normal □Cough with pink, frothy sputum
Patient Presentation
Early Stages
□Minor changes in orientation □Unusual interpersonal exchanges □Shifts in mood □Pulse and temperature may be elevated □Breath sounds may be normal □Cough with pink, frothy sputum
Three Stages of ARDS
□Injury or Exudative Phase
□Occurs 1-7 days (usually 24 to 48 hours) after the direct lung injury
□Reparative or Proliferative Phase
□Begins 1 -2 weeks after the initial injury
□Fibrotic or Chronic Phase
□Occurs approx. 2-3 weeks after the initial injury
Injury or Exudative Phase
□Characterized by interstitial and alveolar edema (non-cardiogenic pulmonary edema) and atelectasis
□Type II cells are unable to produce surfactant
□Severe VQ mismatching and shunting occurs leading to hypoxemia not responsive to increasing O2 concentrations
Injury or Exudative Phase
□Hypoxemia & juxtacapillary receptors cause:
□Increase in RR
□Decrease on tidal volume
□Respiratory alkalosis
□Increase in CO
Signs & Symptoms
Early compensation
□Hyperventilation
□CO2 levels fall
□Development of hypocapnea
□Continuing hypoxemia
Reparative / Proliferative
□Neutrophils, monocytes, lymphocytes & fibroblasts multiply as part of an ongoing inflammatory response
□Increased PVR & Pulmonary HTN
□Hypoxemia worsens due to diffuse limitations & intrapulmonary shunting
Patient Presentation
Later Stages
□Dyspnea is obvious □Grunting respirations □Intercostal & suprasternal retractions □Cyanosis □VQ imbalance □Rhonchi and crackles □Tachycardia □Arrhythmias □Diaphoresis □Confusion □X-ray with widespread consolidation
Fibrotic Phase
□Called the chronic or late phase
□Lung tissue becomes dense & fibrous
□Diffuse scarring completes
□Surface area for gas exchange is reduces because of the interstitium is fibrotic
□Hypoxemia continues and pulmonary HTN worsens
Latent Stages
□Hypoxia persists even with O2 therapy
□ABG’s
□PaO2 and PCO2 continue to decline
□Respiratory alkalosis
□Metabolic acidosis
□Terminal Stages
□No longer compensate with hyperventilation
□Great elevation of CO2/Respiratory acidosis
