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1

What is ARDS?

Acute resp distress syndrome

Non cardiac pulmonary edema and disruption of alveolar capillary membranes as a result of injury to the pulmonary vasculature and alveoli

2

What are the 2 types of ARDS?

1) Direct injury ARDS (direct injury to pulmonary system causes inflammation which activates mediators)

2) Indirect injury ARDS (Insult occurs somewhere else and mediators transported via blood to lungs)

3

What are causes of direct injury ARDS?

Aspiration, near drowning, toxic inhalation, pneumonia, O2 toxicity

4

What are causes of indirect injury ARDS?

Sepsis, shock, cardiopulmonary bypass, trauma, burns, pancreatitis, pulmonary embolus

5

What are the phases of ARDS?

1) Exudative
2) Fibro-proliferative
3) Recovery

6

What happens in the exudative phase of ARDS?

48-72 hrs after initial injury, mediators cause injury to pulmonary capillary membrane

Fluid moves into lungs with mediator activation results in:
1) Non cardiogenic pulmonary edema
2) Damage to alveolar capillary membrane
3) Compression of small airways increases air resistance
4) Inflammatory mediators cause bronchoconstriction
5) Protein + cellular debris form hyaline membrane over damaged alveoli cells

7

What are the systemic consequences of the exudative phase of ARDS?

Intrapulmonary shunting (blood shunts from R to L heart without participating in gas exchange at lungs d/t decreased ventilation)

Hypoxemia

Pulmonary HTN (from leakage of fluid into interstitium forming micro-emboli in capillary membranes) increase alveolar deadspace, possible silent units

Increase RV afterload decreases overall CO

8

What are the causes for pulmonary HTN in ARDS?

Micro-emboli in capillary membranes

Pulmonary vasoconstriction due to hypoxemia

9

What causes RV failure in ARDS?

Increase in RV afterload as a consequence of pulmonary HTN

10

What happens in the fibro-proliferative phase of ARDS?

New cells replace damaged cells in alveoli and capillaries, but are laid down in a disordered manner causing:

Fibrotic alveoli
Scarred capillaries

Pulmonary edema and inflammation begin to subside but cells still damaged

11

What are the systemic consequences of the fibro-proliferative phase?

Further pulmonary HTN resulting:

-Stiffening of lungs
-Decreased lung compliance
-Continued hypoxemia

12

What happens in the recovery phase of ARDS?

Over several weeks, alveolar-capillary membrane re-establishes itself

Type I and II cells recover, III cells remove hyaline membrane and clear out debris

13

How is ARDS diagnosed?

Occurs within 1 week of known insult

CXR showing bilateral infiltrates

Non cardiogenic pulmonary edema

P/F ratio classification

14

What are the P/F ratio classifications for ARDS?

P/F 201-300 mmHg --> MILD ARDS

P/F 101-200 mmHg --> MODERATE ARDS

P/F < 100 mmHg --> SEVERE AARDS

15

How are ABGs affected by ARDS?

Low PaO2 despite increased FiO2 (refractory hypoxemia)
Initially low PaCO2, then high as pt fatigues and retains. Later metabolic and mixed acidosis

16

What is refractory hypoxemia?

Low PaO2 despite increased FiO2

17

What is the clinical presentation for phase 1 ARDS?

Exudative phase

Resp distress
decreased breath sounds, crackles, wheezes
pallor, diaphoresis, anxiety, confusion
marked decrease in pH with hypercarbia and hypoxia
increase peak inspiratory pressure (from pulmonary congestion)
CXR showing bilateral infiltrates, pulm edema

18

What is the clinical presentation for phase 2 ARDS?

Fibro-proliferative phase

Decreased compliance, increased deadspace
Increased FiO2, PEEP requirements
Signs of RV failure
CXR showing pulmonary fibrosis

19

What is the clinical presentation of phase 3 ARDS?

Recovery phase

Gradual improvement in PO2, PCO2, hemodynamics
May have long term functional impairments

20

What are the principles of ventilation management for ARDS?

Focus on lung protection, prevent over-distention (volutrauma) and end-exp collapse (barotrauma)

1) Low tidal volumes (4-8ml /kg instead of 6-8mls/kg) maintain plateau pressure < 30cm H20 checked by RT

2) Permissive hypercarbia --> Vt must be lowered to achieve safe plateau pressure, therefore hypoventilation occurs unless contraindicated

3) PEEP used d/t refractory hypoxemia, high PEEP accepted but must monitor hemodynamics

4) Inverse ratio ventilation (IRV) --> Inspiratory phase prolonged with expiratory time shortened to keep alveoli open longer

21

How low should tidal volumes be for ARDS pts?

4-8 mls/kg

22

How much pH is accepted for ARDS pts?

pH > 7.25 acceptable with elevated pCO2

23

What are contraindications for permissive hypercarbia?

Increased ICP, severe metabolic acidosis, pulmonary hypertension, RV failure, ACS, seizures

24

How much PEEP will ARDS pts often require and what will their O2 settings be?

May require PEEP 10-15 cm H2O or higher

Maintain PaO2 55-88mmHg and SpO2 > 88

25

What must you monitor with higher PEEP?

Hemodynamics

26

What are cons if inverse ratio ventilation?

Decreased exp time allows for air entrapment resulting in "auto-peep". Possible hemodynamic instability and pt must be fully sedated and paralyzed

27

What are non-ventilation managements for ARDS?

Hemodynamic support, fluid management, ECMO, sedation/NMBAs, proning

28

Why is proning done for ARDS?

Dependent alveoli in lower lobes project posteriorly and collapse with secretions when pts lying supine. Proning:

-Helps mobilize secretions from dependent alveoli into the anterior chest
-Recruit posterior alveoli and open them
-Move heart away from compressing left lung
-Relieves abdominal pressure on lungs
-Improve airway clearance with postural drainage

29

When is proning best used for ARDS?

In early ARDS before fibrosis occurs

30

How long can pts be proned or in severe ARDS?

16 hrs a day