Pulmonary Hypertension and PTE Flashcards

1
Q

How is pulmonary hypertension defined?

A

A pulmonary arterial systolic pressure > 24mm Hg or arterial pressure > 19mm Hg

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2
Q

What the basic mechanism for pulmonary hypertension?

A
  • blood flows from the right ventricle –> pulmonary artery –> capillary –> veins –> L atrium
  • if there is issues with vasoconstriction/ dilation, platelet activation, smooth muscle proliferation
  • ex. pulmonary artery vasoconstriction, increased pulmonary blood flow, or back up of blood in the veins
  • pulmonary vasoconstriction be initially be from hypoxia (shunting of blood) – chronic will be an issue
  • Endothelin-1 and serotonin can also vasoconstrict
  • arachidonic metabolites of the pulmonary artery: prostacyclin (inhibits platelet activation, vasodilates) and thromboxane A (platelet activation, vasoconstriction)
  • PDGF also increases in people with idiopathic pulmonary hypertension
  • NO (nitric oxide) = vasodilator
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3
Q

What are the 5 groups of pulmonary hypertension? which is most common in dogs?

A
  1. due to congenital or vascular disease. Ex. shunts, heartworm
  2. due to heart disease. This is the most common cause in dogs. Ex. MVD
  3. due to pulmonary issue, ex. pulmonary fibrosis. 30-74% of Westies
  4. due to PTE, ex. heartworm
  5. miscellaneous. ex. cancer, granuloma (compressive lesion)
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4
Q

What are the most common signs of pulmonary hypertension?

A
  • exercise intolerance
  • cough
  • dyspnea
  • syncope
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5
Q

How is pulmonary hypertension diagnosed?

A

Echo!
- gold standard is R ventricle catheterization in people
- look for: signs of pulmonic valve insufficiency, tricuspid valve regurgitation
- Peak tricuspid regurgitation > 2.8m/s or peak pulmonic insufficiency > 2.2m/s = strongly suggests pulmonic hypertension
- other signs: flattening of the septum, R atrial enlargement, main pulmonary artery enlargement, R ventricular eccentric/ concentric hypertrophy

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6
Q

What’s the utility of NT-proBNP and cardiac troponin 1 in diagnosing pulmonary hypertension?

A

NT-proBNT
- will be elevated in dog with both cardiac disease and those with concurrent pulmonary hypertension – ie. cannot differentiate between the 2
cTnI
- elevated in dogs with pulmonary disease but cannot tell if there is also concurrent pulmonary hypertension

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7
Q

How is pulmonary hypertension treated?

A
  • endothelin-1 antagonist and prostacyclin analogs = cost prohibitive in vet med, also not sure if it works
  • phosphodeisterase (PDE) 5 inhibitors = sildenafil, tadalafil (Cialis), and vardenafil –> leads to vasodilation by increase cGMP will increases NO level
  • PDE5 inhibitors can also reduce cardiac remodeling, fibrosis, apoptosis, ventricular hypertrophy and improve L heart function in people
  • tadalafil = long acting, Vardenafil = not much in vet med (also long acting)
  • pimobendan PDE3 inhibitors = Ca2+ sensitizer, good for group II with MVD –> can reduce NT-proBNT level
  • TKI, ex. imatinib –> inhibits activation of PDGF and PDGF receptors
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8
Q

What’s the outcome of dogs with pulmonary hypertension?

A

variable, pending underlying cause
- lack well defined prognostic factors
- with PDE5 inhibitors ~ 3m

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9
Q

What are the most common signs of PTE?

A

variable
- dyspnea
- tachypnea
- lethargy

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10
Q

How is PTE diagnosed?

A

antemortem diagnosis can be difficult to achieve
- CXR: nonspecific
- look for other concurrent issues that can predispose the patient to PTE
- ex. Cushing’s, DIC, pancreatitis, IMHA, PLN/ PLE, etc
- check TEG (look for hypercoagulable state), D-dimer (normal or low rules out acute PTE)

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11
Q

How is PTE treated?

A
  • antithrombotics (ex. streptokinase, urokinase, or tissue plasminogen inhibitor) = controversial
  • heparin
  • clopidegral
  • Aspirin = beneficial thromboprophylaxis, especially in IMHA and PLN
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