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PHRM 844 > Pulmonary arterial hypertension > Flashcards

Pulmonary arterial hypertension Flashcards

(59 cards)

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1
Q

what is pulmonary arterial hypertension

A
  • progressive disease involving endothelial dysfunction -> elevated pulmonary arterial pressure and pulmonary vascular resistance
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2
Q

what is the mean pulmonary artery pressure (mPAP) in PAH

A

> 20 mmHg

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3
Q

what is pulmonary artery wedge pressure (PAWP) in PAH

A

<= 15 mmHg

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4
Q

what is the pulmonary vascular resistance (PVR) in PAH

A

> 2 Wood units

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5
Q

what is normal pulmonary arterial wedge pressure

A

4-12 mmHg

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6
Q

what is the gold standard way to diagnose PAH

A

right heart catheterization

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7
Q

what is another way other than right heart catheterization to evaluate PAH

A

echocardiogram

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8
Q

risk factors and associated conditions for PAH

A
  • collagen vascular disease
  • congenital heart disease
  • portal htn
  • HIV infection
  • drugs and toxins
  • pregnancy
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9
Q

main genetic factor for PAH

A

abnormal BMPR2 gene

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10
Q

what does PAH endothelial dysfunction cause

A
  • decreased NO2 synthase, prostacyclin production
  • increased thromboxane production, endothelin 1 production
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11
Q

what is PAH class 1

A

symptom free when physically active or resting

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12
Q

what is PAH class 2

A
  • slight limitation of physical activity - ordinary activity may cause Sx
  • comfortable at rest
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13
Q

what is PAH class 3

A
  • marked limitation in physical activity - less than ordinary activity causes Sx
  • comfortable at rest
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14
Q

what is PAH class 4

A
  • significant Sx w/ activity
  • Sx at rest
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15
Q

at what PAH class do we consider starting tx

A

class 2

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16
Q

PAH goals of therapy

A
  • alleviate Sx
  • improve QOL
  • prevent or delay disease progression
  • reduce hospitalization
  • improve survival
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17
Q

what is the result of a positive acute vasoreactivity test (AVT)

A

drop in mPAP >10 mmHg w/ PAP less than 40 mmHg w/ stable-improved cardiac output

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18
Q

when should CCBs be considered for PAH

A
  • positive responders to CCBs w/o right-sided failure or other CI to CCB
  • do not use w/o positive AVT
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19
Q

why should verapamil not be used for PAH

A

due to negative inotropic effects

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20
Q

what to do if patient does not improve to functional class I or II after CCB initation

A

start additional or alternative PAH therapy

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21
Q

recommended PAH first line CCBs if patient is a positive responder

A
  • long acting nifedipine 120-240 mg daily
  • long acting diltiazem 240-720 mg daily
  • amlodipine 20 mg daily
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22
Q

PDE-5i inhibition effects

A
  • decreases conversion of cGMP to GMP
  • increased levels of cGMP -> pulmonary vasodilation
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23
Q

PDE-5i meds for PAH

A
  • sildenafil
  • tadalfil
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24
Q

what do PDE-5i meds do that improves PAH

Study These Flashcards
A
  • improved 6MWD
  • functional capacity
25
when are PDE-5i meds first line for PAH
functional class II and III w/o rapid progression
26
sildenafil (revatio) half life
5 hours
27
tadalafil (adcirca) half life
15-35 hours
28
sildenafil dose adjustments
none
29
tadalafil dose adjustments
renal
30
PDE-5i meds major drug interactions
- avoid use with riociguat or nitrates (hypotension) - CYP3A4 substrates
31
PDE-5i drugs AEs
flushing, headache, dyspepsia, visual disturbances, priapism, tinnitus/hearing loss, sudden vision loss, hypotension
32
endothelin receptor antagonists moa
- ET receptors on vascular smooth muscle mediate vasoconstriction - overexpression of ET-1 in PH patients, correlates with remodeling - blocking ET -> vasodilation
33
when should endothelin receptor antagonists be used
an option in functional class II-IV
34
what is combo first line for class II and III without rapid progression
tadalafil + ambrisentan
35
what do endothelin receptor antagonists do
improve 6MWD, pro-BNP, delay time to clinical worsening, optimize hemodynamics
36
how soon are improvements expected with endothelin receptor antagonists
8-10 weeks
37
where are ETa receptors located
pulmonary smooth muscle walls
38
ETa receptors effects
promotes vasoconstriction, proliferation, inflammation
39
ETb receptors on endothelium effects
promote vasodilation, stimulate NO and prostacyclin production
40
ETb receptors on muscle cells of vascular walls effects
cause vasoconstriction and cell proliferation
41
what is going on with ET receptors in PAH
expression of ETb receptors are upregulated in the media of blood vessels (vasoconstriction)
42
soluble guanylate cyclase stimulator med
riociguat (adempas)
43
when could riociguat be used
may be used as an alternative to PDE-5i
44
why can't riociguat be used with PDE-5i
risk of hypotension
45
prostacyclins moa
stimulates cAMP pathway to increase pulmonary vasodilation
46
what is standard tx for severe PH w/ RV failure
parenteral prostacyclins -> subQ treprostinil
47
when are prostacyclins used in PAH
reserved for class III and IV patients
48
what other drug classes may prostacyclins be used with
combination w/ ERA + PDE-5i or riociguat
49
treprostinil half life
4 hours
50
what should not be done w/ IV treprostinil
IV infusion requires stable access, do not co-infuse with anything else
51
when is IV used over subQ
for patients who cannot tolerate subQ
52
why is subQ treprostinil better than IV
- subQ avoids risk of central lines - utilizes undiluted drug
53
common prostacyclin medication errors
- flushing of line - calc or conc error - programming error - pump turned off - inappropriate change in weight
54
when should lung transplantation be considered
for functional class III and IV patients w/ inadequate response to maximal pharmacotherapy
55
when are adjunct therapy considered
treat underlying/contributing conditions like htn/sleep apnea
56
when is anticoag adjunct therapy considered
- consider depending on cardiac function - warfarin: INR goal 1.5-2.5 - aspirin 81 mg daily
57
when is diuretic adjunct therapy considered
to maintain euvolemia
58
other supportive therapies
- immunizations (influenza, pneumococcal, COVID, RSV) - supplemental oxygen (pulmonary vasodilation) - iron supplementation if deficient - avoid air travel/high altitudes (may need supplemental O2 to keep saturations >91%)
59
why should pregnancy be avoided during PAH therapy
- estrogen containing contraceptives may increase VTE risk - Bosentan can cause birth defects - ERAs and riociguat are category X

PHRM 844 (13 decks)

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