Pulmonary Oedema Flashcards
Definition of pulmonary oedema
An increase in extravascular water in the interstitium and alveolar compartment of the lung
Factors that influence fluid exchange
- Diffusion (Fick’s law) 2. Filtration (balance between hydrostatic and osmotic forces) 3. Pinocytosis (vesicular transport)
Fick’s law
J = -PS(Co-Ci) J = diffusion per unit time P = permeability S = surface area Ci = [inside] Co = [outside]
What is the biggest determinant of osmotic forces?
Albumin
Describe teh factors that influence fluid accumulation in the lung
Any factors that influence fluid exchange have the ability to affect fluid accumulaiton in the lung:
- Diffusion
- Filtration; and
- Pinocytosis
Filtration is the biggest determinant of fluid exchange. Filtration is determined by Starling’s forces as well as capillary permeability.
There are also protective mechanisms.
- The interstitium can accomodate a 50% increase in volume (Pa <palv>
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Explain conditions that favour pulmonary oedema
F = k [(Pc + πi) - (Pi + πc)]
Increased capillary pressure (P__c)
- Increased pressure in pulmonary artery (PPA)
- Increased pressure in left atrium (PLA)
Decreased interstitial pressure (Pi)
Increased filtration coefficient (k)
- Increased vascular surface area
- Increased permeability
Decreased capillary oncotic pressure (πc)
- Decreased albumin concentration
Increased interstitial oncotic pressure (πi)
Discuss the effects of pulmonary oedema on respiratory function
- Causes decreased lung volume and therefore decreased compliance (stiff lungs) which increased WOB.
- Increased shunt (flooded regions have Q but no V)
- V/Q mismatch (extent varies).
- Decrease in SA available for gas exchange and (possible) hyaline membrane formation in ALI/ARDS.
Cardiogenic pulmonary oedema
Also known as hydrostatic pulmonary oedema.
Increased capillary pressure (Pc) → increased pressure in pulmonary artery (PPA) → increased pressure in left atrium (PLA)
Pc = PLA + 0.4(PPA - PLA)
Pc is sensitive to increase in PLA.
In cardiac failure there is an increase in PLA. This means that left cardiac failure favours oedema.
Right cardiac failure exacerbates the situation (increased venous pressure impedes lymph flow).
Therapeutic considerations in cardiogenic pulmonary oedema
If you treat the cause you usually resolve the problem.
Also often required support for respiratory insufficiency (non-invasive or invasive ventilation).
ARDS and ALI
Also known as *non-cardiogenic *or permeability oedema.
Insult (direct or secondary) causes an increase in permeability, therefore increasing the filtration coefficient (k).
This occurs independently of hydrostatic pressure and results in a protein rich fluid.
Example of direct insultrs in ARDS and ALI
- Aspiration pneumonia
- Pneumonia
- Inhalation injury
- Pulmonary contusions
- Fat embolism
- Near drowning
- Reperfusion injury
Examples of indirect insults in ARDS and ALI
- Sepsis
- Severe trauma
- Shock
- Pancreatitis
- Cardiopulmonary bypass
- Transfusion ALI
- Burns
- Head injury
- Drug overdose
Discuss the therapeutic considerations for non-cardiogenic pulmonary oedema
*There are currently no effective treatments for the underlying condition. *
Support respiratory insufficiency (non-invasive or invasive ventilation)
Design of appropriate ventilation strategies is a challenge
Comparison of cardiogenic and noncardiogenic pulmonary edema
Cardiogenic
- Increased hydrostatic pressure
- Increased fluid filtration
- Intact endothelial barrier
- Alveolar flooding by bulk flow
- Protein poor edema fluid
- Tight epithelial barrier.
_Non-cardiogenic _
- Normal hydrostatic pressure
- Increased permeability
- Disrupted endothelial barrier
- Alveolar flooding fue to increased epithelial permeability
- Protein right edema fluid
- Disrupted epithelial barrier
- Presence of neutrophils and macrophages
