Atelectasis, Pulmonary Edema, ALI and ARDS

Question 1

What does atelectasis refer to?

Answer 1

Either incomplete expansion of the lungs or a collapse of the lungs after being inflated.

Question 2

What are the three types of atelectasis and explain each one?

Answer 2

1. Resorption: complete obstruction of an airway leading to reduced lung expansion.
2. Compression: Fluid, tumor, or air accumulate within the pleural cavity and compress the lungs.
3. Contraction: fibrosis over the lung stops it from being able to expand.

Question 3

What is a major difference between resorption and compression atelectasis?

Answer 3

In resorption, mediastinum shifts towards the collapsed lung and in compression the mediastinum shifts away from the collapsed lung.

Question 4

How do we define pulmonary edema on histo?

Answer 4

Pink material in alveolar spaces

Question 5

What are the two big picture causes of PE?

Answer 5

Hemodynamic problems or direct injury to the capillaries leading to increased permeability

Question 6

When we say hemodynamic problems causing PE, what are we talking about?

Answer 6

We are talking about increasing hydrostatic pressure or decreasing oncotic pressure.

Question 7

3 common causes of increasing hydrostatic pressure?

Answer 7

Left sided heart failure (most common), volume overload and pulmonary vein obstruction

Question 8

What are 3 common causes of decreasing oncotic pressure?

Answer 8

Low albumin, nephrotic syndrome, and liver disease

Question 9

Histologically, what are the cells we see with Pulmonary Edema?

Answer 9

Hemosiderin laden macrophages or heart failure cells. These are macrophages that have taken up RBCs.

Question 10

What are 4 causes of injury to the alveolar wall that will lead to pulmonary edema?

Answer 10

Bacterial infection, sepsis, smoking, and aspiration

Question 11

How do we define acute lung injury? What are we essentially saying this is?

Answer 11

we are essentially saying this is pulmonary edema not caused by cardiac failure. So a good definition is sudden hypoxemia and bilateral lung infiltrates in the absence of cardiac failure.

Question 12

So then what is ARDS essentially then?

Answer 12

A very severe manifestation of ALI.

Question 13

What is the classic histo manifestation of both ALI and ARDS?

Answer 13

Diffused alveolar damage

Question 14

More than half of ARDS cases are associated with what 4 conditions?

Answer 14

Sepsis, pulmonary infections, gastric aspiration, and mechanical trauma (including head injuries).

Question 15

What PaO2/FIO2 is required for ALI and ARDS?

Answer 15

Less than 300 and less than 200

Question 16

What are the 4 stages of the pathogenesis of ARDS?

Answer 16

1. Endothelial activation due to injury releasing a whole bunch of nonsense
2. Adhesion of neutrophils to the damaged endothelium and then they exit to the alveoli
3. Accumulation of interstitial and intraalveolar fluid
4. Resolution of the injury by TGFB and PDGF causing alveoli to become fibrotic

Question 17

What is basically at the heart of the patho of ARDS?

Answer 17

Cycle of inflammation and endothelial damage.

Question 18

What is a characteristic feature of ARDS/ALI and what exactly is it?

Answer 18

Formation of a hyaline membrane within the alveoli. It is the combo of protein rich edema with necrotic pneumocytes.

Question 19

What 3 things does she want us to know that equal hyaline membranes?

Answer 19

Edema + proteins (like fibrin) + cell debris

Question 20

What are two other complications because of the patho of ARDS besides the diffuse alveolar damage?

Answer 20

Because the type 2 cells are getting their butts kicked, you have stiff lungs and collapsed alveoli because of a drop in surfactant. Also, you are not exchanging gas as well so the ventilation/perfusion ratio is jacked. You are still sending blood, but not adding oxygen.

Question 21

How do they like to break up ARDS into stages? What is happening in each one?

Answer 21

1. Exudative: edema, hyaline membranes and neutrophils
2. Proliferation: tons of fibroblasts and early fibrosis
3. Fibrotic: extensive fibrosis and loss of alveolar cells

Question 22

Talk about an important note about the two options after the second stage?

Answer 22

It can either resolve completely and the lung will have normal tissue and cells or there will be complete fibrosis to the area and the damage will be irreversible.

Question 23

What are the two clinical symptoms of ALI?

Answer 23

Dyspnea and tachypnea

Question 24

When it crosses over into ARDS, what symptoms are we seeing now?

Answer 24

Cyanosis, hypoxemia, respiratory failure and the appearance of bilateral infiltrates on X ray that they call “white out”

Question 25

How do we define Acute Interstitial Pneumonia?

Answer 25

It is essentially widespread ALI without a known cause or etiology