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
Goals of Treatments
□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 tidal volume
□Decrease atelectasis
□PEEP or CPAP
□Schedule “sighs”
□Serial chest x-rays
□Give bronchodilators
□Nebulizer treatments
Increase PCO2
□Enhance CO2 retention
□Rebreather masks
□Increase mechanical dead space
□Prevent hyperventilation
□Use a controlled mode of ventilation
□Decrease the respiratory rate
□Chemical paralysis
Decrease O2 Consumption
□Prevent tachycardia
□Ensure bedrest
□Treat fever
□Prevent pain
Other Goals of Treatment
□Treat hypotension, if present
□Monitor hemodynamic readings
□Minimize the hypotensive effects of PEEP
□Administer adrenergics
□Administer volume expanders to increase serum osmotic pressure
□Treat fluid & electrolyte imbalances
□Possibly restrict fluids
□Administer diuretics
□Monitor albumin & phosphate levels
□Support stress response
□Administer glucocorticoids
□Decrease adverse responses
Direct Nursing Care
□Recognize those at risk □Hand washing imperative □Use of aseptic technique when suctioning □Assess early warning signs (↑O2 need) □Assess & treat infections early □Proper nutritional support □Aggressive pulmonary toilet
Direct Nursing Care
□Assess:
RR O2 need Lung sounds Color O2 sats ABG’s Chest x-rays CBC (esp. WBC’s) Electrolytes Cultures
Direct Nursing Care
□Meds:
□Surfactant via OETT □Corticosteroids □Diuretics □Pulmonary vasodilators □Beta 2 Adrenergics (Albuterol)
Direct Nursing Care
□Positioning
□EVB interventions include rotation of patient position or proning
□Mobilizes secretions and improves oxygenation
□Decrease incidence of nosocomial infections (pneumonia), skin breakdown, ICU LOS
Direct Nursing Care
□Support:
□Mechanical ventilation
□Use lowest FiO2 to maintain a PaO2 of 60 mmHg or greater
□PEEP increased in 3-5 CM. H2O until FiO2 < 60%
□High frequency jet ventilators
□Suctioning PRN
□ECMO (extracorporeal membrane oxygenation)
Direct Nursing Care
□Family Support:
□Death issues need to be addressed (50-80% mortality)
□DNR issues (potential ventilator dependence)
□Family anxiety (hopelessness)
□Unfamiliar environment
Complications
□Lung scarring (pulmonary fibrosis) □Collapsed lung (pneumothorax) □DVT (blood clots) □Infections (r/t ventilator) □Permanent lung dysfunction □Memory, cognitive & emotional problems
The Eight “P’s” for ARDS Treatment
□Prevention □PEEP □Pipes □Pumps □Paralysis □Positioning □Protein (nutrition) □Protocol/Bundle Driven Care
