Bod: Respiratory: Pulmonary Edema

Front 1

What is the Starling equation?

Back 1

EVLW = K[(Pmv - Ppmv) - σ(πmv - πpmv)] - lymph flow

Front 2

c/c pleural effusion and pulmonary edema on CXR.

Back 2

Pleural effusion: radiodense white areas at the bottom of each lung.

Pulmonary edema: patchy white areas throughout the lung (can't tell cause)

Front 3

What are the two components of the lung interstitium?

c/c these two

Back 3

- Perimicrovascular (alveolar wall interstitium)

- Peribronchovascular (loose connective tissue spaces around bronchi and vessels)

The perimicrovascular space (alveolar wall) does not contain lymph vessels, but the peribronchovascular interstitum does contain lymph vessels. So normally any extra fluid in the perimicrovascular space move into the peribronchovascular space and is drained by the lymph vessels there.

Front 4

What are the physiological explanations for "Kerley B lines" and "bronchial cuffing?"

Back 4

These are examples of how drainage to the peribronchovascular interstitium (from the perimicrovascular interstitium) exceeds the lymphatics' ability to drain the fluid. A large amount of fluid can back up here without causing issues for the patient.

Front 5

What happens once the amount of fluid entering the peribronchovascular interstitium overwhelms the rate of fluid leaving via the lymphatics?

Back 5

The fluid starts to fill the alveoli.

Front 6

Rapid re-expansion of the lung can cause what?

Back 6

This can cause the pressure in the interstitium to become very negative, making fluid flow into the interstitial space --> pulmonary edema.

Front 7

What are two processes that cause the vast majority of pulmonary edema?

Back 7

1. Increased hydrostatic pressure gradients. i.e. LESS DRAINAGE of fluid.

2. Increased vascular endothelial permeabilities i.e. MORE FORMATION of fluid.

Front 8

What two etiologies of pulmonary edema are there?

Back 8

1. Cardiogenic (LVF, elevated pulmonary capillary wedge pressure)
2. Non-cardiogenic

Front 9

ARDS can be thought of as what type of pulmonary edema?

Back 9

Non-cardiogenic permeability pulmonary edema.

Front 10

What is the pathophysiologic picture of ARDS?

Back 10

There is diffuse alveolar damage --> proteinaceous edema fluid in alveoli --> hypoxemia --> but there is a loss of regulatory control (hypoventilated vessels DON'T constrict properly) --> Right to Left shunt --> Patients need high amounts of O2 --> continued administration of high levels of O2 can cause additional alveolar damage.

Front 11

What type of ventilatory defect does pulmonary edema cause?

What ramifications does this have for treatment?

Back 11

It causes a "stiffening" of the lungs and a restrictive pattern would be seen on PFTs.

This is important because it means that patients need high airway pressures (PEEP) if they are put on a ventilator --> this can lead to barotrauma.

Front 12

What is the mortality rate of ARDS?

Back 12

Still is about 40%. But most people don't die of respiratory failure, they die of sepsis, DVT.

Front 13

What is really the only "shunt" syndrome that we will see?

Back 13

ARDS

Front 14

What is the list of etiologies of ARDS?

Back 14

Infections:
- sepsis
- pneumonia

Hemodynamic:
- shock

Trauma:
- fat emboli
- lung contusion
- massive blood transfusions

Drugs:
- heroin
- cocaine

Inhaled toxins:
- smoke inhalation
- oxygen toxicity

Miscellaneous:
- aspiration
- pancreatitis
- ventilator-induced lung injury

Front 15

If you give 100% O2, what ratio do you use to determine the nature of the ventilation - perfusion status?

Back 15

PaO2/FiO2

If it is ≤ 200 then there is a right to left shunt

If it is between 200 and 300, then there is a V/Q mismatch.

If it is ≥ 300, then the lungs are normal.

Front 16

What are the clinical definition of ARDS?

Back 16

- Acute hypoxemic respiratory failure (with a large right-to-left shunt and with PaO2/FiO2 ≤ 200)
- Diffuse patchy infiltrates on CXR.
- Decreased lung compliance.
- Low or normal pulmonary capillary wedge pressure.