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Pulm > Lec 19 Pulmonary Vascular Disease > Flashcards

Lec 19 Pulmonary Vascular Disease Flashcards

1
Q

What is ohms version of equation of Pulm artery pressure?

KNOW THIS!!

A

Ppa = (CO * PVR) + Pla

Pla = left atrial pressure
b/c change in P = CO * R

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2
Q

What is ohm’s version of equation of pulm artery pressure?

A

Psa = (CO*PVR) + Pra

Pra = right atrial pressure b/c changes in P = CO*R

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3
Q

How do pulm vessels differ from systemic vessels?

A

less muscle and elastin

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4
Q

What is definition of pulmonary hypertension?

A

mean Pa > 25

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5
Q

What are 3 mechs of what will cause increased pulm artery pressure?

A
  • increased CO
  • increase left atrial P
  • increased PVR
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6
Q

What are some things that cause increased CO and thus lead to high pulm artery pressure?

A
  • congenital heart defects w/ L to R shunt
  • cirrhosis
  • anemia
  • A-V malformations
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7
Q

What are some things that cause increased left atrial P and thus lead to high pulm artery pressure?

A
  • systolic/diastolic LV failure
  • mitral valve disease
  • restrictive cardiomyopathy
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8
Q

What are some things that cause incraesed PVR and thus lead to high pulm artery pressure?

A
  • destruction pulm vascular bed in ILD, emphysema, PE
  • hypoxic vasoconstriction in COPD, high altitude
  • small pulm artery vasculopathy [PAH]
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9
Q

What is group 1 pulmonary hypertension?

A

pulmonary arterial hypertension

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10
Q

What is group 2 pulm HTN?

A

due to left heart disease

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11
Q

What is group 3 pulm HTN?

A

due to lung disease, hypoxia

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12
Q

What is group 4 pulm HTN?

A

due to thromboembolic disease

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13
Q

What is group 5 pulm HTN?

A

miscellaneous “other”

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14
Q

What are some pathological signs seen in pulmonary arterial hypertension?

A
  • medial hypertrophy
  • intimal thickening
  • in situ thrombosis
  • plexiform lesions
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15
Q

What is pathogenesis of pulmonary hypertension?

A
  • increased endothelin pathway –> vasoconstriction and proliferation of smooth muscle
  • decrease NO path –> less vasodilation/antiproliferation
  • decrease prostacycline path –> less vasodilation and antiproliferation
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16
Q

What are 4 possible etiological categories of PAH?

A
  • idiopathic
  • genetic
  • drug/toxin induced
  • associated w/ other disease
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17
Q

What is genetic cause of pulmonary arterial hypertension?

A
  • mutation in BMPR2
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18
Q

What drugs/toxins can cause pulmonary arterial htn?

A
  • anorexigens [fen phen]
  • grapeseed oil
  • illicits
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19
Q

What are some diseases associated with PAH?

A
  • connective tissue [SLE, scleroderma]
  • congenital heart disease –> increased pulm pressure/flow
  • portal htn
  • HIV
  • schistosomiasis
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20
Q

WHat is prevalence of PAH?

A

5-15 / 1 million adults

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21
Q

How prevalent is PAH in pts with CHD?

A

30% of pts who do not have CHD repaired will develop PAH

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22
Q

What is survival of untreated idiopathic PAH?

A
  • median survial 2.8 years

34% survival at 5 years

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23
Q

What is difference RV and LV?

A
  • LV concentric shape; thick free wall

- RV crescent shape; thin free wall; lacks circumferential constrictor fibers; more compliant

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24
Q

What is definition preload?

A

wall stress at end of diastole

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25
Q

What is definition afterload?

A

wall stress during ventricular ejection

26
Q

What is contractility?

A

intrinsic ability of myocardium to contract independent of load

27
Q

What happens to LV if dildate RV?

A

compress LV

28
Q

Why do you get such rapid decompensation in PAH?

A

high pulm pressure means increased RV afterload

RV afterload –> increased RV wall stress –> ischemia and decreased output leading to decreased CO

RV afterload –> decreased RV output –> also decreases CO

RV afterload –> increase RV dilatation –> leftward septal shift and tricuspid regurg –> also decrease RV output and LV preload leading to more decreased CO

significant decrease LV —> leading to cardiogenic shock

29
Q

What are symptoms of PAH?

A

from low perfusion

  • dyspnea
  • fatigue
  • chest pain
  • palpitation

from congestion –> ab pain and fulness, peripheral edema

30
Q

What do you seen on physical exam in PAH?

A
  • hypoxemia, tachycardia, hypotension
  • JVP distension
  • RV head, split S2, loud P2, systolic tricuspid murmur
  • RV S3/S4
  • hepatomegaly, pulsatile liver, ascites
  • lower extremity edema
31
Q

Do you see rales in pure PAH?

A

nope! no pulmonary edema in pure PAH

32
Q

WHat do you see on chest xray in PAH?

A

dilated pulmonary arteries

restro-sternal space disappears in lateral view

33
Q

What do you see on EKG in PAH?

A
  • RV hypertrophy/strain
  • RBBB
  • right atrial enlargement
34
Q

What is use of right heart cath? What does it tell you?

A
  • confirms diagnosis of pulmonary hypertension

- tells you hemodynamic profile –> RAP, PAP, PCWP, CI, PVR

35
Q

What does PCWP tell you about etiology of pulmonary hypertension?

A
  • if PCWP > 15 suggests PH type 2 [due to left heart disease]
  • if PCWP < 15 consistent w/ pulm HTN that occurs before capillaries = type I [PAH]; III [lung disease; or IV [thromboembolic]
36
Q

What is natural history of pulmonary hypertension?

A

in asymptomatic/compensated: CO still pretty high and RAP low; PAP/PVR rising

in symptomatic/decompensated: CO declining; PAP/PVR really high

in overt R HF: high PVR but PAP starts to decrease as CO drops and RAP increase = signs of low perfusion and congestion

37
Q

What are the names of the 4 Ca channel blockers?

A

amlodipine/nifedipine

diltiazem/verapamil

38
Q

What is use of Ca channel blockers in pulm htn?

A
  • result in pulmonary arterial vasodilation

- beneficial if positive vasoreactivity test [vasoresponder]

39
Q

What is test to see if patient is vasoresponder?

A
  • give short-acting vasodilator like epoprostenol/adenosine/inhaled NO
  • a vasoresponder will have decreased PAP by > 10 to absolute < 40 without concurrent drop in CO

only makes up 13% of population of pts with idiopathic PAH

40
Q

What is mech of prostanoids?

A
  • stimulate adenylate cyclase –> incrase cAMP

- cause vasodilation, antiproliferation, platelet aggregation inhibition

41
Q

What is effect of prostanoids?

A
  • improve hymodynamics; functional capacity
42
Q

What is the one prostanoid that increases survival?

A

epoprostenol

43
Q

What are the 3 types of prostanoids and their mech of administratiON?

A 
epoprostenol = IV
treprostinil = SC, IV, PO, inhale
iloprost = inhaled
44
Q

How is eoprostenol administered? half life?

A

1/2 life = 3-5 min

continuous IV admin

45
Q

Which prostanoid is just synthetic prostacyclin?

A

epoprostenol

46
Q

How is treprostinil administered?

A

IV and subcutanous = bioequivalent

1/2 life is 2-4 hrs

47
Q

Where are the two types of endothelin receptor antagonists located? action?

A
  • ETA/ETB on smooth muscle cells and cardiac myocytes
  • ETB also on endothelial cells

both cause vasoconstriction/ proliferation smooth muscle

ETB also mediates pulmonary clearance and induces production of local mediators

48
Q

What are the 3 endothelin receptor antagonists?

A
  • bosentan
  • ambrisentan
  • macitentan
49
Q

What is order of highest affinity for ETA/ETB among the 3 endothilin receptor antagonists?

A

ambrisentan > macitentan > bosentan

affinity ETA: ETB

50
Q

WHat is effect of endothelin receptor antagonists?

A

improve hemodynamics and functional capacity

51
Q

WHat is mech/effect of phosphodiesterase 5 inhibitors?

A
  • inhibits cGMP specific phosphoidesterase

cause vasodilation/ antiproliferation/ platelet aggregation inhibition

improve hemodynamics and functional capacity

52
Q

What are the 2 phosphodiesterase 5 inhibitors?

A

sildenafil [PO/IV]

tadalafil [PO

53
Q

What is mech of action of riociguat?

A

stimulates solumble guanylate cyclase [sGC] –> converts GTP to cGMP

54
Q

What is effect of riociguat?

A

vasodilation, antiproliferation, platelet aggregation inhibition

improves hemodynamics and functional capacity

55
Q

What are some things you need to consider when you are giving vasodilators?

A
  • vasodilation will decrease SVR not just PVR –> caution in hypotensive patients
  • abrupt medication withdrawal causes rebound pulmonary HTN –> need to wean gradually
  • can worsen V/Q match leading to hypoxemia –> caution in intrinsic lung disease
56
Q

What are side effects common of pulmonary vasodilators?

A

vasodilation –> headache, dizziness, flushing, nasal congestion

57
Q

What is a side effect of bosentan?

A

liver tox

58
Q

What are side effects common to endothelin receptor antagonists?

A
  • teratogenic, peripheral edema, anemia
59
Q

What are side effects of prostanoids?

A

jaw pain

60
Q

What are general treatment measures of pulm HTN?

A
  • give supplemental O2 to maintain saturation > 90%
  • anticoagulation
  • digoxin to improve contractility
  • cardiopulmonary rehab to improve functional capacity
61
Q

What surgical treatments available for pulm HTN?

A
  • atrial septostomy –> unloads RV at cost of hypoxemia
  • pulm thromboendarectomy in case of chronic thromboembolic pulm htn
  • lung transplant

Pulm (24 decks)

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