Noncardiogenic Pulmonary Edema - Unger. JVECC 2023

Question 1

Name the Starling’s equation for volume of flow from capillaries

Answer 1

fluid flux = filtration coefficient [(capillary hydrostatic pressure - interstitial hydrostatic pressure) - osmotic reflection coefficient (capillary oncotic pressure - interstitial oncotic pressure)]

Question 2

What determines the filtration coefficient of the Starling’s equation?

Answer 2

• size and number of pores
• surface area of capillaries
• thickness of capillary wall
• viscosity of the filtered fluid

represents the permeability of water

Question 3

What determines the osmotic reflection coefficient of the Starling’s equation?

Answer 3

capillary permeabiltiy to protein

Question 4

What does a osmotic reflection coefficient of 0 or 1 mean?

Answer 4

1 - capillary wall is impermeable to plasma proteins
0 - plasma proteins can freely cross the capillary membrane

reflection coefficient represents endothelial integrity

Question 5

Explain how the glycocalyx is proposed to affect microvascular fluid flux

Answer 5

glycocalyx with high cc albumin - subglycocalyx space virtually protein free

high colloid osmotic pressure gradient between glycocalyx and subglycocalyx space

the gradient is believed to opposed the transcapillary hydrostatic pressure - rather than the colloid gradient between plasma and interstitium

Question 5

Why does interstitial pulmonary edema resolved fater than alveolar edema? How are each of them resolved/removed?

Answer 5

interstitial edema can be resolved via lymphatic drainage
alveolar edema takes longer to resovled and this relies on Na-K-ATPase pumps on the basolateral membrane of type 1 and 2 pneumocytes

Question 5

What is the osmotic reflection coefficient for the transcapillary flux in lungs and how does it compare to other tissues?

Answer 5

0.7-0.95

lower than in other tissues –> i.e., the capillary endothelium is more permeable to plasma proteins&raquo_space; i.e., the osmotic pressue will be less of a determinant of flux

the higher osmotic reflection coefficient the less permeable to proteins

Question 6

What are the main determinants of pulmonary edema in the lungs?

Answer 6

• capillary hydrostatic pressure
• capillary permeability

Question 7

how does the cause of noncardiogenic pulmonary edema differ from cardiogenic pulmonary edema

Answer 7

noncardiogenic pulmonary edema does not result from cardiogenic causes OR fluid overload

due to:
* increased vascular permeability
* increased pulmonary transcapillary pressure without increased left atrial pressure
* combination af the two

Question 8

What is the definition of ARDS?

Answer 8

inflammatory disease of the lung, characterizied by a deranged immune Response to an insult

the insult can origninate from pulmonary or nonpulmonary disease

Question 9

In recent literature, what was the most common cause for ARDS in dogs and in cats?

Answer 9

dogs: aspiration pneumonia
cats: SIRS/sepsis

nonpulmonary disease as cause more common in cats compared to dogs

Question 10

What are the phases of ARDS? Describe the pathophysiology in brief for each phase

Answer 10

1. Exudative phase
   * pulmonary vascular leakage, hemorrhage, thrombosis, and inflammatory cell infiltration
   * first macrophages&raquo_space; then followed by neutrohpil infiltration
   * damage to both the vascular endothelium and alveolar epithelium (type 1 pneumocytes)
   * leading to protein-rich edema in the alveoli
   * hyaline membrane formation
   * alveolar edema dilutes surfactant&raquo_space; alveolar collapse
   * type II pneumocyte proliferation
2. Proliferative phase
   * type II pneumocytes continue to proliferate
   * fibrosis of the interstitium and alveoli
   * hyaline membranes still present
3. Fibrotic phase
   * collagen deposited in the alveoli, interstitium, and the vasculature

phase 2 and 3 often combined as fibroproliferative phase

Question 11

List the criteria for diagosing ARDS in people

Answer 11

• onset within 1 week
• bilateral opacities on CT or radiographs
• respiratory failure not fully explained by cardiac failure or fluid overload
• P/F 201-300 + PEEP min 5 cm H2O or CPAP (mild)
• P/F 101-200 + PEEP min 5 cm H2O (moderate)
• P/F 100 or lower + PEEP min 5 cm H2O (severe)

Question 12

List the criteria for diagnosis VetALI or VetARDS

Answer 12

1. onset within 72 hours (i.e., tachypnea or labored breathing)
2. known risk factor
3. evidence of pulmonary edema without increaesed pulmonary capillary pressure (i.e., no clinical or diagnostic evidence supporting left-sided failure, e.g., echo)
   * bilateral diffuse infiltrates in more than 1 lung lobe on radiographs
   * bilateral dependent density gradient on CT
   * proteinaceous fluid within the conducting airways
   * increased extravacular lung water
4. evidence of inefficient gas exchange
   * hypoxemia (P/F < 300 for VetALI, < 200 for VetARDS; increased A-a gradient, noncardiac shunt)
   * increased deadspace ventilation
5. evidence of diffuse pulmonary inflammation
   * Transtracheal wash/BAL neutrophilie or markers of inflammation
   * molecular imaging

Question 13

List examples for known risk factors of VetALI or VetARDS

Answer 13

• sepsis/SIRS
• severe trauma
• multiple transfusions
• smoke inhalation
• drowning
• aspiration of stomach contents
• drugs
• toxins

Question 14

What may be used as a surrogatefor PF ratio and how well does it correlate?

Answer 14

SF ratio - use SpO2 as alternative for PaO2

recent publications showed moderate correlation if SpO2 was between 80-97%
- correlation was shown to be stronger in mechanically ventilated dogs

Question 15

What is the cut off of the pulmonary edema fluid protein to plasma protein ratio to differentiate pulmonary edema from high-permeability versus hydrostatic pressure increases?

Answer 15

0.65 or higher indicates high-permeability edea

using only the protein cc in pulmonary edema fluid showed poorer diagnostic discrimination

Question 16

How commonly is TRALI diagnosed in cats and dogs?

Answer 16

Has never been definitively diagnosed in companion animals

Question 17

What are the two recognized pathophysiologic mechanisms of TRALI?

Explain each pathophysiology and what type of blood products they are associated with

Answer 17

1. Immune TRALI
   * caused by granulocyte antibodies in donor blood&raquo_space; react with neutrophils in the recipient’s blood&raquo_space; neutrophils become activated&raquo_space; sequester in the lung&raquo_space; initiate finlammation
   * associated with plasma-containing products (e.g., FFP, platelet transfusions)
2. Non-immune TRALI
   * storage of blood products&raquo_space; accumulation of bioactive mediators (e.g., lipids)
   * recipients must already be in an activated state due to another underlying disease
   * associated with stored pRBCs, platelets
   * not associated with fresh blood products or plasma

Question 18

List the criteria for diagnosing TRALI in people

Answer 18

• onset during or within 6 hours of a transfusion
• if non-immune TRALI: risk factor present or mild ARDS present, but respiratory status deteriorated based on stable respiratory status for 12 hour prior to transfusion
• bilateral pulmonary edema on imaging
• no left atrial hypertension or if present not judged to be the cause
• P/F <300 or SpO2 <90% on room air

Question 19

What are the two reported primary neurologic causes of neurogenic pulmonary edema in dogs?

Answer 19

• seizures
• traumatic brain injury

Question 20

What are the proposed causes of neurogenic pulmonary edema in hunting dogs?

Answer 20

• severe sympathetic drive from exercise and excitement
• excessive barking leading to postobstructive type pulmonary edema

Question 21

Explain the two theories for the development of neurogenic pulmonary edema

Answer 21

Both theories are on the basis of brain injury causing fulmonant sympathetic stimulation

1. vasoconstriction –> increaed arterial and venous pressures –> increased left ventricular afterload –> overwhelmed LV –> left sided congestion + vasoconstriction –> shunting of blood to the central organs –> increased pulmonary capillary hydrostatic pressure –> endothelial damage –> exudation of protein-rich fluid
2. sympathetic stimulation directly causes increased capillary permeability –> edema independent of pulmoanry capillary pressure changes

Question 22

If neurogenic pulmonary edema causes unilateral changes on radiographs, what side is more common?

Answer 22

right side

Question 23

what is the proposed pathophysiology of electrocution induced neurogenic pulmonary edema?

Answer 23

suspected to the same as from TBI or seizures –> nervous tissue has a high tendency to conduct electricity –> CNS damage –> sympathetic surgery

Question 24

Explain the pathophysiology of postobstructive pulmonary edema

Answer 24

forcible inspiration against a closed epiglottis&raquo_space; drastically decreased intrathoracic pressure
-» decreases the pulmonary interstitial hydrostatic pressure
-» increases venous return to the RA/RV and lungs
-» combination causes an increased transcapillary pressure gradient&raquo_space; pulmonary edema
-» negative intrathoracic pressure increases LV afterload –> further increases pulmonary capillary pressure

additional sympathetic surge from dyspnea (similar to neurogenic pulmonary edema mechanism)

Question 25

What are the two types of postobstructive pulmonary edema?

Answer 25

Type 1: acute onset during obstruction from marked sudden negative intrathoracic pressure

Type 2: chronic airway obstruction –> exhalation against obstruction causes intrinsic PEEP
* when the obstruction is relieved –> the PEEP abades –> sudden drop in pressure –> mechanism similar to Type 1

Question 26

What is the most common reported cause of re-expansion pulmonary edema in dogs and cats? Which species is more commonly affected?

Answer 26

• correction of a traumatic diaphragmatic hernia
• cats more common than dogs

Question 27

How soon after re-expansion does pulmonary edema typically happen?

Answer 27

within 24 hours after atelectasis is resolved - but can occur as instantly as within 1 minute

Question 28

Explain the pathophysiology of re-expansion pulmonary edema

Answer 28

Not completely understood. Theories include:
* re-expansion causes significant negative interstitial pressure –> favors fluid shift from capillaries into interstitium
* pressure changes may cause capillary endothelial damage
* inflammatory mediators and ROS from ischemia-reperfusion injury

Question 29

Explain components leading to lung damage from drowning

Answer 29

• aspiration of liquid –> alterations in surfactant –> alveolar collapse
• aspiration of liquid –> damaging the alveolocapillary barrier and pneumocytes –> can later on lead to ARDS
• breathing against a vagally mediated laryngospasm –> similar to postobstructive pulmoanry edema

Question 30

how much of the nostril diameter are HFNO cannulas supposed to cover

Answer 30

no more than 50%
to prevent excessive pressure build-up and re-breathing of carbon dioxide

Question 31

What is the proposed mechanism by which furosemide helps in noncardiogenic pulmonary edema?

Answer 31

direct pulmonary vasodilatory properties