Non cardiogenic pulmunary edema Flashcards

BC 3.4.24

1
Q

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

A

seizures
traumatic brain injury

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2
Q

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

A
  • severe sympathetic drive from exercise and excitement
  • excessive barking leading to postobstructive type pulmonary edema
  • Physical exertion with resultant hypoglycemic effects on the brain
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3
Q

explain the proposed pathophysiological mechanism of NPE

A

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

  • 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
  • sympathetic stimulation directly causes increased capillary permeability –> edema independent of pulmonary capillary pressure changes
  • Production of reactive oxygen species may also play a role
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4
Q

How does NPE present of rads?

A

NPE most commonly showed a bilateral, symmetric, multifocal, mixed alveolar to interstitial lung pattern, focused in the caudal lung lobes or distributed throughout all lung fields.

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5
Q

What side of the lung is most commonly affected in case of unilateral distribution?

A

For the few animals with unilateral distribution, the changes were found
on the right side of the lung.

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6
Q

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

A

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

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7
Q

What is the prognosis for NPE in general?

A

Good. Resolve within a few days with minimal support.

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8
Q

T/F: in NPE caused by electrocution, most of the patients develop resp sign even if face of clear rads

A

F: respiratory signs after electrocution were only observed in about 30% of cases in 1 report, even in the face of radiographic changes.

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9
Q

What is the pathophys of NPE caused by electrocution?

A

same pathophysiologic mechanism as
NPE. Nervous tissue has a high tendency to conduct electricity, predisposing the CNS to damage by electrical current, which then is believed to cause a sympathetic discharge similar to other types of
NPE.

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10
Q

What do you expect to see in rads performed on dogs after after electrical injury?

A

Diffuse alveolar or mixed interstitial and alveolar pattern with a concentration
in the caudodorsal fields.

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11
Q

Name at least 6 causes of post obstructive
pulmonary edema.

A
  • tracheal collapse
  • strangulation including
    excessive pulling on a leash
  • brachycephalic airway syndrome
  • pharyngeal obstruction by a foreign body
  • laryngeal edema
  • laryngeal paralysis
  • laryngeal polyp
  • pharyngeal fibrosarcoma
  • excitement while being manually restrained.
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12
Q

Explain the pathophysiology of postobstructive pulmonary edema

A

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

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

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13
Q

What are the two types of postobstructive pulmonary edema?

A

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

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

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14
Q

How does post-obstructive pulm edema appear on CXR?

A

symmetric, alveolar–interstitial focal to
multifocal pulmonary pattern with a bilateral distribution usually in
the caudodorsal lung fields. In animals with a unilateral distribution
(39%), the pulmonary edema was found almost exclusively on the right
side.

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15
Q

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

A
  • correction of a traumatic diaphragmatic hernia
  • cats more common than dogs
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16
Q

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

A

within 24 hours after atalectasis - but can occur as instantly as within 1 minute

17
Q

Explain the pathophysiology of re-expansion pulmonary edema

A

No completely understood. Theories include:
* re-expansion causes significant negative interstitial pressure –> favor fluid shift from capillaries into interstitium
* pressure changes may cause capillary endothelial damage
* inflammatory mediators and ROS from ischemia-reperfusion injury

18
Q

T/F: to avoid re-expansion pulmunary edema in a pt with pleural effusion, the rate of fluid removal is more important than the quantity removed

A

T

19
Q

What drugs have been reported as cause of pulmunary edema in dogs and cats?

A

Dogs: cytarabine, ingested tetrahydrocannabinol, treatment with IV
lipid emulsion
Cat: vincristine overdose

20
Q

Explain the phatophys of lung injury due to drowning.

A
  • aspiration of liquid –> alterations/wash away surfactant –> alveolar collapse, ventilation–perfusion mismatch, and pulmonary hypertension.
  • aspiration of liquid –> damaging the alveolocapillary barrier and pneumocytes –> can later on lead to ARDS
  • Severe sympathetic surge as a response to stress and hypoxia may lead to a neurogenic-type edema
  • breathing against a vagally mediated laryngospasm –> similar to postobstructive pulmoanry edema
21
Q

Describe your ideal setting for HFNO (including cannulae size)

A
  • choose a cannula size that does not occludemore
    than 50% of the nostril diameter in order to avoid excessive pressure
    build-up and re-breathing of CO2
  • starting flow rate of 0.4–2 L/kg/min; alternatively, the
    flow rate can be based on the patient’s minute ventilation (TV of 10ml/kg x RR)
  • FiO2 should initially be set to 100% with the goal of decreasing it to the lowest concentration that will maintain an SpO2
    of 95% or higher.
  • T 37–38◦C (98.6–100.4◦F)
22
Q

What is lung protective ventilation?

A

ventilation with lower TV and higher PEEP in order to avoid lung overdistension and cyclic
collapse and re-opening of alveoli, both of which can exacerbate inflammation
in the lung

23
Q

What are the only 2 drugs recommended in people with ARDS?

A

neuromuscular blocking agents and glucocorticoids
+ negative fluid balance

24
Q

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

A

direct pulmonart vasodilatory properties