Flashcards in Pulmonary Edema - Mechanisms Deck (28):
Two broad types of pulmonary edema?
What's special about the thickness of the alveolar capillary walls?
They're thin on the side facing the alveoli for gas exchange.
They're thick on the the other side for fluid exchange.
How do alveolar epithelial cells help keep fluid out of the alveoli?
Tight junctions keep out solutes bigger than urea...
Active Na+ transport across Type II epithelial cells drives out the small amount of fluid that does get into airspaces.
90% of fluid in the alveoli gets pumped out. What happens to the rest?
It's reabsorbed via lymphatics.
Mild edema vs. severe edema?
Mild edema is confined to the interstitial space.
Severe edema is in the airspaces.
What are the 2 parts of the Earnest Starling equation that describes the driving force for fluid movement across a membrane?
2 situations in which the microvascular oncotic pressure is reduced, leading to edema?
What's the Sieving Effect, and how is it a protective factor against edema when hydrostatic pressure is elevated?
When hydrostatic pressure is high, solutes will build up in the capillaries - mitigating movement of fluid into alveoli.
What are 3 "anatomic sinks" where edema fluid can go initially?
(this keeps the fluid away from the gas exchange areas)
What Na+ transporters are involved in the Type II alveolar epithelial cells?
ENaC, apical (which, recall, is amelioride sensitive)
Na+/K+ ATPase, basolateral.
(Pulmonary edema is a very rare side effect of amelioride...)
Do the Na+ pumps on Type II epithelial cells like being bathed in gastric acid?
Nope, not at all.
This makes the pulmonary edema caused by ARDS/aspiration worse.
What's a drug that conveniently seems to upregulate ENaC?
As a general rule, is edema worse in ARDS or in CHF?
It's usually worse in ARDS.
In CHF, the safety mechanisms against edema are upregulated.
In ARDS, those safety mechanisms are impaired.
5 edema safety factors?
1. Decreased interstitial oncotic P, increased capillary oncotic P.
2. Increased interstitial hydrostatic P, decreased cap hydrostat P.
3. Anatomic sinks.
4. Increase in transepithelial Na+ transport.
5. Reserve capacity of lymphatic drainage.
2 things that cause hydrostatic pulmonary edema other than CHF?
Fluid overload (esp. in IV resuscitation, for eg. sepsis).
Acute or chronic kidney injury.
What causes the edema in ARDS?
Increase in capillary permeability, due to widespread endothelial injury.
Why doesn't the Sieving Effect help in ARDS?
Endothelial injury allows free flow of solutes, so there's no increased oncotic pressure of capillaries.
How can edema from CHF vs. ARDS be determined?
CHF will probably have a gradual onset history, have other symptoms like leg swelling.
Also CHF will have high BNP, echo findings.
How long does recovery take from hydrostatic pulmonary edema vs. CHF?
Hydrostatic pulmonary edema can be rapidly reversed pharmacologically.
ARDS doesn't remit until the endothelium/epithelium heals, which can take days to weeks.
What precipitates ARDS? (there are lots of things - 2 main categories)
Direct lung injury - pneumonia, aspiration, others.
Indirect - sepsis, severe trauma and shock.
4 phases of ARDS?
Exudative (permeability pulmonary edema).
What's the broad term for what's seen in histology of ARDS?
Diffuse alveolar damage.
What's a pathognomonic histologic finding in early ARDS?
What kind of pattern of inflammation is seen in histology of ARDS?
Chronic inflammatory cells.
(then granulation tissue, collagen deposition, then reepithelialization)
Can ARDS and hydrostatic pulmonary edema exist at the same time?
How might you increase the capillary oncotic pressure in hydrostatic pulmonary edema?
(this provides transient benefit in setting of hypoalbuminemia)
Does albuterol help in ARDS?
Nope. The Type II epithelial cells are too injured.
It causes tachycardia without benefit.