ARDS Flashcards

1
Q

What is ARDs

A

acute form of respiratory failure

  • Associated with hypoxemia
  • increasing permeability of capillary-alveolar membrane
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2
Q

What happens with increased permeability of capillary-alveolar membrane?

A
  • Proteins and fluid leak into the alveoli
  • Leads to extensive edema
  • Atelectasis
  • Poor gas exchange
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3
Q

Damaged Type 2 Alveolar Cells

A
  • decreased surfactant production
  • decreased alveolar compliance and recoil
  • lend to atelectasis
  • decreased overall lung compliance
  • alveolar collapse
  • altered gas exchange
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4
Q

What causes the leaking?

A
  1. Direct injury

2. Indirect systemic cascade effect initiated by lysosomal substances

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5
Q

Who’s at risk for pulmonary related (direct)?

A
  • Lung contusion
  • Embolism
  • Near-drowning
  • Pneumonia
  • Smoke inhalation
  • Aspiration
  • Inhalation of toxic gases or vapors
  • Radiation pneumonitis
  • Oxygen toxicity
  • Pulmonary edema
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6
Q

Who’s at risk for non-pulmonary related (indirect)?

A

-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

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7
Q

Patient Presentation Early Stages of ARDs

A
□ 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
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8
Q

3 Stages of ARDs

A
  1. Injury or Exudative Phase
  2. Reparative or Proliferative Phase
  3. Fibrotic or Chronic Phase
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9
Q

Stage 1 of ARDs

A

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
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10
Q

Stage 2 of ARDs

A

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

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11
Q

Stage 3 of ARDs

A

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

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12
Q

-Hypoxemia and juxtacapillary receptors cause:

A

□ Increase in RR
□ Decrease on tidal volume □ Respiratory alkalosis
□ Increase in CO

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13
Q

S/S of Early compensation

A

□ Hyperventilation
□ CO2 levels fall
□ Development of hypocapnea
□Continuing hypoxemia

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14
Q

Patient Presentation Late Stages

A
□ Dyspnea is obvious
□ Grunting
respirations
□ Intercostal & suprasternal retractions
□ Cyanosis
□ VQ imbalance
□ Rhonchi and crackles
□ Tachycardia
 □ Arrhythmias
 □ Diaphoresis
 □ Confusion
□ X-ray with widespread consolidation
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15
Q

Latent Stages

A
  • hypoxia persists even with O2 therapy

- ABG’s: PaO2 and PCO2 continue to decline, Resp. Alkalosis, Met. Acidosis

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16
Q

Terminal Stages

A

no longer compensate with hyperventilation

-great elevation of CO2/Resp. acidosis

17
Q

If patient survives ARDs,

A

some type of pulmonary disability forever

18
Q

Goals of Treatment

A

□ Increase O2 to the tissues

□ Increase PCO2

□ Decrease O2 consumption

19
Q

Increase O2 to Tissues

A
  • maximize pt existing ventilation
  • provide O2 therapy
  • provide early ventilatory assistance (intubation, mechanical ventilation with PEEP, decrease VT)
20
Q

Increase PCO2

A
  • Enhance CO2 retention

- Prevent hyperventilation

21
Q

Enhance CO2 retention

A
  • rebreather masks

- increase mechanical dead space

22
Q

Prevent hyperventilation

A
  • use a controlled mode of ventilation
  • decrease the RR
  • chemical paralysis
23
Q

Decrease O2 consumption

A
  • Prevent tachycardia
  • Ensure bedrest
  • Treat fever
  • Prevent pain
24
Q

Other Goals of Treatment

A
  • Treat fluid and electrolyte imbalances

- support stress response

25
Q

How to Treat fluid and electrolyte imbalances

A
  • possibly restrict fluids
  • admin diuretics
  • monitor albumin and phosphate levels
26
Q

How to support stress response

A
  • admin glucocorticoids

- decrease ADR

27
Q

Direct Nursing Care

A

□ 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

28
Q

dead space

A

whats left in the lungs at the end of respiration

29
Q

Nursing Assessment

A
  • RR
  • O2 need
  • Lung sounds
  • Color
  • O2 sats
  • ABGs
  • CXR
  • CBC (esp. WBCs)
  • Electrolytes
  • Cultures
30
Q

Meds

A
  • surfactant via OETT
  • Corticosteroids
  • diuretics
  • pulmonary vasodilators
  • Beta 2 adrenergics (Albuterol)
31
Q

Positioning

A
  • EVB interventions include rotation of patient position
  • Mobilizes secretions and improves oxygenation
  • Decrease incidence of nosocomial infections (pneumonia), skin breakdown, ICU LOS
32
Q

Direct Nursing Care: Mechanical Ventilation

A

□ Use lowest FiO2 to maintain a PaO2 of 60 mmHg or greater

□ PEEP increased in 3-5 CM.H2O untilFiO2

33
Q

Family Support

A

□ Death issues need to be addressed (50- 80% mortality)

□ DNR issues (potential ventilator dependence)

□ Family anxiety (hopelessness)

□ Unfamiliar environment

34
Q

Complications

A

□ Lung scarring (pulmonary fibrosis)

□ Collapsed lung (pneumothorax)

□ DVT (blood clots)

□ Infections (r/t ventilator)

□ Permanent lung dysfunction

□ Memory, cognitive & emotional problems