Pulmonary Hypertension Flashcards

1
Q

In people PH is defined as a PAP of or above XXXX

A

> 25 mm Hg

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2
Q

Postcapillary PH is defined as increased PAP + a PWP of above XXXX.

A

15 mm Hg

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3
Q

How does LHD lead to PH?

A

LHD causes volume overload of the LA –> will increase pulmonary venous pressure

initially should be without increase in pulmonary vascular resistance, but increased pressure can cause remodelling and constriction –> postcapillary can cause secondary precapillary PH

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4
Q

What are the 3 cardiovascular changes that can lead to PH?

A
  • increased pulmonary blood flow (e.g., congenital shunt)
  • increased pulmonary vascular resistance (e.g., PTE, pulmonary fibrosis, heart worm, etc.)
  • increased pulmonary venous pressure (LHD)
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5
Q

Explain how you can extrapolate an approximate systolic PAP from an echocardiogram

A

with the modified Bernoullie equation

measure tricuspid valve regurgitation velocity (TRV)

Pressur gradient = 4 x TRV ^2
TRV in m/s

ideally for systolic PAP estimate need RA pressure, but no validated method to measure this on echo in SA, so this is ignored

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6
Q

What are factors besides PH that can influences and alter TRV?

A

pulmonary or tricuspid stenosis
RV function, pericardial restain

poor patient cooperation
labored brathing

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7
Q

What echocardiographic measurement can be used to estimate mean or diastolic PAP?

A

Pulmonary regurgitation jet velocity –> Mean PAP

add RA pressure –> diastolic PAP

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8
Q

List 4 changes to the ventricles that are indicative of PH

A

RV hypertrophy (dilation/eccentric or wall hypertrophy/concentratic)
ventricular septal flattening
LV underfilling/decreased size (not in LHD-induced PH)
RV systolic dysfunction

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9
Q

Name 4 changes to the PA on echo, indicative of PH

A
  • PA enlargement PA:Ao > 1
  • Peak early diastolic PR velocity > 2.5 m/s
  • Right pulmonary artery distensibility < 30%
  • lower RV outflow time, systolic notching of the doppler RV outflow
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10
Q

Name 2 changes to the RA and CVC on echo indicative of PH

A

RA enlargement
CVC enlargement

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11
Q

In addition to PH echo changes, what must be present on echo to identify LHD-PH?

A
  • unequivocal LA enlargement
  • signs of LHD (LV dysfunction or MV or AV disease)
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12
Q

List the 6 categories of PH classifications

A

Pulmonary hypertension
Vascular Occlusive disease
Left-heart disease
Respiratory disease
PTE
Parasites
Mxed

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13
Q

Fill in the blanks

A
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14
Q

What triscuspid regurgitation pressure gradient cutoff indicates at least moderate PH

A

> 46 mm Hg

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15
Q

What 2 breeds are predisposed to PH from interstitial lung disease?

A

West Highland White Terrier
Pekingese

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16
Q

What cardiac auscultation abnormalities may be heard with PH?

A
  • right systolic murmur (TR)
  • diastolic murmur if severe PH
  • split second heart sound - takes longer to eject
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17
Q

Fill in the gaps

A
18
Q

List 5 changes to thoracic radiographs indicative of PH

A
  • tortuous/blunted/dilated pulmonary arteries
  • Pulmonary trunk bulging
  • assymmetric radiolycent lung fields on VD/DV
  • patchy diffuse alveolar infiltrates
  • R-sided cardiac enlargement
19
Q

List 7 clinical changes indicative of HW disease

A
  • hyperbilirubinemia
  • Resp distress
  • Coughing
  • Exercise intolerance
  • Ascites
  • anemia
  • collapse
20
Q

Name 3 clinical changes indicative of Angiostrongylus disease

A

CNS signs
respiratory signs
bleeding diathesis

21
Q

Name 8 risk factors (i.e. diseases) for PTE development

A
  • IMHA
  • PLN
  • PLE
  • heartworm disease
  • hyperadrenocorticism
  • sepsis
  • neoplasia
  • DIC
22
Q

What are the 3 pathways leading to pulmonary arterial vasoconstriction?

A
  • nitric oxide
  • endothelin
  • prostacycline
23
Q

Name an alternative PDE5-i to sildenafil that has a longer half-life. Which medication is superior in clinical efficacy and outcome?

A

tadalafil
no difference in superiority of outcome

24
Q

Explain the recommendations for PDE5-i administration in PH class 1d1

A

1d1 - congenital shunt

if left-to-right shunt –> occlusion is recommended and PDE5-i is not expected to make as much of a difference

if right-to-left –> initial PDE5-i therapy is thought to stabilize patient, may even reverse some shunt and may reduce risk of shunt occlusion

25
Q

Explain how PDE5-i inhibitors may cause pulmonary edema in classes 1d1, 1’ and 2

A

pulmonary vasodilation can increased pulmonary blood flow –> will increase volume in LA and increase risk of pulmonary edema

26
Q

What are situations when PDE5-i should be administered to PH class 2 patients

A

when there is concurrent precapillary PH, i.e., PVR is increased as well

27
Q

What is the MOA of pimobendan and how does it presumably help with PH?

A

Increases efficacy of Ca+ binding to troponin C
PDE3-i

can help with RV systolic dysfunction
lowering LA pressure

28
Q

What is the MOA of milrinone and how can it help with PH?

A

PDE3-i

pulmonary vasodilation
positive inotrope

29
Q

What is the MOA of toceranib and imatinib?

A

tyrosine kinase inhibitor

30
Q

How can arginine supplementation help with PH?

A

precursor for NO –> vasodilation

31
Q

What is likely the most common cause of PH in dogs?

A

LHD

32
Q

What is the Eisenmenger sign?

A

right-to-left shunt –> venous blood reaches circulation

causes polycytemia and cyanosis

33
Q

What are the cutoffs for mild, moderate and severe PH by the PAP?

A

< 50
51-75
>75

34
Q

How is NO produced and how does it induce vasodilation?

A

endothelial cells
L-arginine –> nitric oxide synthase –> NO

activates guanylyl cyclase –> GTP becomes cGMP
cGMP activates Protein kinase G –> reduces Ca++ in cytosol via SERCA upregulation –> vasodilation

35
Q

How do phosphodiesterase inhibitors cause vasodilation?

A

phosphodiesterases inactivate cGMP –> inhibiting phosphodiesterases increases cGMP levels

36
Q

What are 2 other functions of NO besides vasodilation?

A

inhibits platelet activation
reduces smooth muscle hypertrophy

37
Q

Where is prostaglandin I2 produced and how does it cause vasodilation

A

produced in the vascular endothelial cells

actis with the cAMP pathway

38
Q

What receptor does endothelin-1 bind to. What are its effects?

A

ETA - endothelin-1 A receptor
vasoconstriction

+ stimulates growth factors

39
Q

Where is thromboxane produced, stored, and what are its effects?

A

produced in the platelets and stored there

vasoconstriction and platelet activation

40
Q

How is serotonin produced, stored and what are its effects?

A

produced from tryptophan in GI tract –> stored in platelets

released after vascular endothelial damage –> vasoconstriction, vascular remodeling

41
Q

What echo views can be used to measure TRV?

A

R parasternal basilar short axis
L parasternal long axis

42
Q

What are clinical signs strongly suggestive or possible suggestive of PH?

A

strongly:
* syncope
* resp distress
* activity/exercise leads to resp distres
* R-sided HF (ascites)

possibly:
* tachypnea at rest
* increaed resp effort at rest
* prolonged post-exercise tachypnea
* cyanosis, pale gums