ARDS

Question 1

What is ARDS

Answer 1

Acute Respiratory Distress Syndrome/Adult Respiratory Distress Syndrome

Question 2

Defining features ARDS

Answer 2

1. Noncardiogenic pulmonary edema
2. Severe Hypoxemia
3. Characteristic x-ray changes (diffuse patchy infiltrates)
4. Decreased Lung Compliance

Question 3

Direct Causes of ARDS

Answer 3

Pneumonia
Aspiration
Pulmonary Contusion

Question 4

Indirect Causes of ARDS

Answer 4

Sepsis
Shock States (pulmonary hypoperfusion)

Question 5

What is ALI

Answer 5

Acute Lung Injury

Can refer to a spectrum of pulmonary injury and hypoxic respiratory failure.

Question 6

Berlin definition of ARDS

Answer 6

Timing : With in 1 week of clinical insult

Imaging: Bilateral Opacities (not effusions, nodules)

Origin Of Edema: Respiratory failure not fully explained by cardiac failure or fluid overload.

Oxygentaion: PaO2/FiO2 with CPAP/PEEP > 5cmH20
Mild: 200 -300 mmHg
Moderate: 100 - 200 mmHg
Severe: < 100 mmHg

Question 7

Pathophysiology Exudative phase of ARDS

Answer 7

(approx 24h)
Chemical Mediators (histamine, leukotrines) induced interstitial and alveolar edema.
Endothelial and epithelial walls permeable to proteins
Destruction of Type 1 cells (structure cells)

Question 8

Pathophysiology Proliferative phase of ARDS

Answer 8

(approx 2-10 days)
Destruction of Type 2 cells (decreased surfactant production and decreased compliance)
Microemboli Formation
Inflammatory cascade
Early deposition of collages
impaired gas exchange and refractory hypoxemia

Question 9

Pathophysiology Fibrotic phase of ARDS

Answer 9

(>10 days)
Thickening of interstitial wall with fibrosis, macrophages
Protein-based layer in areas inside alveoli (poor gas exchange)

Question 10

Pathophysiology Resolution phase of ARDS

Answer 10

(over several weeks)
structural and vascular remodeling to reestablish a-c membrane.
clearing of the protein membrane and transport of fluid out of the alveoli
Proliferation of Type 2 cells and production of surfactant, differentiation into Type 1 cells.

Question 11

Clinical Manifestations Exudative of phase of ARDS

Answer 11

Restlessness, Dyspnea, Tachypnea
Course Crackles 
Increasing Hypoxia 
\+/- assisted ventilation
CXR: patchy infiltrates primarily in dependent lung areas. Normal heart size

Question 12

Clinical Manifestations Proliferative of phase of ARDS

Answer 12

SIRS fully manifested with hemodynamic instability
Increased WOB /worsening hypoxia
Mechanically ventilated
CXR: diffuse alveolar infiltrates, decreased lung volume. normal heart size.

Question 13

Clinical Manifestations Fibrotic of phase of ARDS

Answer 13

Multi organ involvement
Difficult to oxygenate, dropping FiO2, rising PaCO2
Progressive Lung fibrosis and increasing airway pressures. High pneumo risk
CXR: persistent infiltrates, recurrent pneumothoraces

Question 14

Clinical Manifestations Resolution of phase of ARDS

Answer 14

Improving clinical presentation
Improving ABG’s
Improving CXR

Question 15

PA catheter findings supportive of ARDS

Answer 15

PADP and PCWP difference greater than (1-4 mmHg)

Indication of lung pathology.

Question 16

Two pronged approach to ARDS management

Answer 16

Treat the underlying cause

Support the patients physiological functions (cellular oxygenation) until the effects of ARDS resolve.

Question 17

Protective Lung Strategies

Answer 17

Plateau pressure < 30 cmH20
Tidal Volumes < 6cc/Kg
Permissive Hypercapnia

Question 18

Peak Inspiratory Pressure (PIP)

Answer 18

Product of flow, airway diameter and compliance
“Dynamic Compliance”
Represent airway resistance to airflow

Question 19

Plateau Pressure (Pplat)

Answer 19

No flow state at end of inspiration
“Static compliance”
direct representation of lung tissue compliance

Question 20

Regional Over Distention (in relation to ventilation)

Answer 20

The tendency of airflow to go towards more compliant areas of the lung resulting in over distention, injury and release of inflammatory mediators (to those areas)

if Vt <6 mm/kg and Pplat < 30cmH20 the incidence of regional over distention is reduced.

Question 21

Permissive Hypercapnia

Answer 21

Sacrificing tidal volume and accepting increasing PaCO2 values in order to maintain Pplat <30 mmHg and Vt < 6cc/kg.

pH > 7.20
PaCO2 55- 100 mmHg

Question 22

Refractory Hypoxemia

Answer 22

Hypoxemia that doesn’t improve with increasing Fi02

Question 23

Why use PEEP in ARDS

Answer 23

preventing alveoli collapse
reduction in work of breathing
distention and thinning of the alveolar capilallry membrane to support diffusion (Flick’s law)
keeps the FiO2 low preventing toxic effects of high O2 over a period of time.

Question 24

“Biphasic” fluid management strategy for ARDS

Answer 24

Early and adequate fluid resuscitation during SIRS and hemodynamic instability .
Restrictive fluid strategy afterwards to goal of maintaining adequate preload and CO

Question 25

Why use Kinetic beds in ARDS

Answer 25

Optimization of gas exchange

• change in dependent areas, redistribution of pulmonary blood flow.
• gradual changes in position better (heodynamicly) tolerated than manual patient re-positioning.

Question 26

Prone Positioning

Answer 26

Used in cases of severe ARDS and refractory hypoxemia.
Can be done early in ARDS diagnosis or late as a “rescue” therapy.

8h at a time in 24h period
Goal is to use gravity to alter pulmonary blood flow from posterior dependent/ consolidated areas to anterior and better ventilated ones.