What is ARDs
acute form of respiratory failure
- Associated with hypoxemia
- increasing permeability of capillary-alveolar membrane
What happens with increased permeability of capillary-alveolar membrane?
- Proteins and fluid leak into the alveoli
- Leads to extensive edema
- Atelectasis
- Poor gas exchange
Damaged Type 2 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
2. Indirect systemic cascade effect initiated by lysosomal substances
Who’s at risk for 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 for 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 of ARDs
□ 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
3 Stages of ARDs
- Injury or Exudative Phase
- Reparative or Proliferative Phase
- Fibrotic or Chronic Phase
Stage 1 of ARDs
Injury or Exudative Phase
- occurs 1-7 days (usually 24 to 48 hours) after the direct lung injury
- Characterized by interstitial and alveolar (non-cardiogenic pulmonary edema) and atelectasis
- Type 2 Cells are unable to produce surfactant
- Severe VQ mismatching and shunting occurs leading to hypoxemia not responsive to increasing O2 concentrations
Stage 2 of ARDs
Reparative or Proliferative Phase
-begins 1-2 weeks after the initial injury
□ Neutrophils, monocytes, lymphocytes & fibroblasts multiply as part of an ongoing inflammatory response
□ Increased PVR & Pulmonary HTN
□ Hypoxemia worsens due to diffuse limitations & intrapulmonary shunting
Stage 3 of ARDs
Fibrotic or Chronic Phase
-occurs approx. 2-3 weeks after the initial injury
□ 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
-Hypoxemia and juxtacapillary receptors cause:
□ Increase in RR
□ Decrease on tidal volume □ Respiratory alkalosis
□ Increase in CO
S/S of Early compensation
□ Hyperventilation
□ CO2 levels fall
□ Development of hypocapnea
□Continuing hypoxemia
Patient Presentation Late Stages
□ Dyspnea is obvious □ Grunting respirations □ Intercostal & suprasternal retractions □ Cyanosis □ VQ imbalance □ Rhonchi and crackles □ Tachycardia □ Arrhythmias □ Diaphoresis □ Confusion □ X-ray with widespread consolidation
Latent Stages
- hypoxia persists even with O2 therapy
- ABG’s: PaO2 and PCO2 continue to decline, Resp. Alkalosis, Met. Acidosis
Terminal Stages
no longer compensate with hyperventilation
-great elevation of CO2/Resp. acidosis
If patient survives ARDs,
some type of pulmonary disability forever
Goals of Treatment
□ Increase O2 to the tissues
□ Increase PCO2
□ Decrease O2 consumption
Increase O2 to Tissues
- maximize pt existing ventilation
- provide O2 therapy
- provide early ventilatory assistance (intubation, mechanical ventilation with PEEP, decrease VT)
Increase PCO2
- Enhance CO2 retention
- Prevent hyperventilation
Enhance CO2 retention
- rebreather masks
- increase mechanical dead space
Prevent hyperventilation
- use a controlled mode of ventilation
- decrease the RR
- chemical paralysis
Decrease O2 consumption
- Prevent tachycardia
- Ensure bedrest
- Treat fever
- Prevent pain
Other Goals of Treatment
- Treat fluid and electrolyte imbalances
- support stress response
