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Cardio Exam 2 > Lec 33 Pulmonary Hypertension > Flashcards

Lec 33 Pulmonary Hypertension Flashcards

1
Q

What types of vessels in pulm vasculatrue have most resistance?

A

small vasculature = arterioles and venules

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2
Q

What is flow/resistance of pulm circulation?

A

high flow

low resistance

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3
Q

What is capacitance of pulm circulation?

A

high capacitance to accommodate increased CO

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4
Q

What are the major causes of pulmonary hypertension?

A
  • left heart disease
  • chronic thrombotic or embolic disease
  • parenchymal lung disease or chronic hypoxemia
  • miscellaneous –> sarcoidosis
  • pulmonary arterial hypertension
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5
Q

What is the most common cause of pulmonary hypertension?

A

left heart disease

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6
Q

What are the major causes of pulmonary arterial hypertension?

A
  • idiopathic = primary pulmonary hypertension
  • heritable
  • drug/toxin induced
  • associated w/ other disease
  • persistant plum HTN of newborn
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7
Q

What is general definition of pulmonary hypertension?

A

resting mean pulm arterial pressure > 25 mmHg

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8
Q

What is general definition of pulmonary arterial HTN?

A

resting mean PAP > 25 AND

  • PCWP/LAP/LVEDP < 15 mmHg
  • pulmonary arteriolar resistance > 3 woods units
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9
Q

What 3 vascular changes happen in PAH?

A
  • vasoconstriction
  • smooth muscle and endothelial cell proliferation
  • thrombosis in situ
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10
Q

What is effect of vascular remodeling in PAH?

A

decrease flow

increase resistance

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11
Q

What are plexiform lesions?

A

hallmark of advanced pulmonary HTN

proliferation of cells that compromise lumen of small pulmonary artery

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12
Q

What are the mechanisms leading to PAH?

A
  • homeostatic imbalance of vascular effectors [vasoconstors, prothrombotic, mitogenic factors]
  • environmental

genetic

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13
Q

What is role of prostacyclin and thromboxane A2 in PAH?

A

prostacyclin = vasodilator, inhibits platelet activation

TXA2 = vasoconstrictor, platelet agonist

in PAH levels of TXA2 > > prostacyclin

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14
Q

What is role of serotonin in PAH?

A
  • vasoconstrictor
  • promotes smooth muscle cell hypertrophy
  • elevated in PAH
  • impaired serotonin reuptake in PAH patients
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15
Q

What is role of Endothelin 1 in PAH?

A
  • potent vasoconstrictor, stimulates smooth muscle cell proliferation

increased in PAH

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16
Q

What is role of NO in PAH?

A
  • vasodilator, inhibits smooth cell proliferation

- endothelial isoform of NO synthase decreased in pts with PAH

17
Q

What is role of hypoxia in PAH?

A
  • in systemic circulation –> hypoxia induces vasodilation
  • in pulm beds –> induces vasoconstriction [to improve V/Q mismatch]

chronic hypoxia –> structural remodeling, SMC proliferation

18
Q

What is role of anorexigens in PAH?

A
  • linked to higher risk for PAH

- fen-phen

19
Q

What is role of CNS stimulants in PAH?

A

cocaine/methamphetamines cause medial hypertrophy of pulm arteries

20
Q

What is role of TFG-B in PAH?

A
  • bone morphogenetic protein receptor type 2 [BMPR2]

modulates growth of vascular cells
mutant –> lose control, extra growth

incomplete penetrance –> may be necessary but insufficient to cause disease

21
Q

What genetic pathways predispose to PAH?

A
  • TFG-B mutation

- serotonergic path mutation

22
Q

What is role of serotonergic path in PAH development?

A

variant gene expression of serotonin receptor –> increase serotonin dependent vascular remodeling

23
Q

WHat is theory of cause of PAH?

A

causes multiple hits to get the disease

risk factors + genetic predispostion + cell dysfunction + inflammation

24
Q

What happens in presymptomatic/compensated PAH?

A

higher PAP pressure but able to compensate

CO ok

25
Q

What happens in symptomatic/decompensating PAH?

A

RV facing consequences of years of pressure –> weakens –> CO starts to drop and RAP rises

manifests as fatigue, lower extremity edema, elevated neck veins

26
Q

What happens in declining/decompensated PAH?

A

CO way down
RAP way up
pulm artery pressure reaches inflection point and starts to go down = sign of how poor your RV is function you can’t even get fluid into pulm vasculature

eventually get RV failure

27
Q

What is prognosis of PAH?

A

3 year survival 60%

28
Q

What are symptoms of PAH?

A
  • dyspnea
  • fatigue
  • SOB
  • chest pain
  • syncope
  • palpitations
  • edma
29
Q

What are physical findings in PAH?

A
  • elevated jugular venous distension
  • tricuspid regurg due to increase pulm artery P
  • accentuated S2
  • S3 gallop
  • peripheral edema
  • hepatomegaly, pulsatile liver, ascites
30
Q

What doe you see on EKG with PAH?

A
  • not sensitive enough to be a screening tool

see

  • RV hypertrophy = big V1 QRS; big S in V5/6
  • R axis deviation = I down; aVF up
  • R atrium enlarged = big P wave in II, III, aVF
31
Q

What do you see on CT with PAH?

A
  • enlarged central pulm arteries

- reduced caliber of peripheral vessels

32
Q

What diagnostic workup for PAH?

A
  • do clinical exam
  • look for sings of RV or RA enlargement or increased pressure

primary screening = do echo

rule out other common causes of pulm HTN

if you see high pressure on pulm arteries –> confirm with invasive cath lab measurement of pressures

33
Q

What should you screen for if you think PAH?

A
  • screen for thromboembolic disease
  • work up for infectious disease or connective tissue disorder
  • screen for chronic lung disease
34
Q

What is treatment for PAH?

A
  • give ox –> maintain saO2 > 90%
  • routine vaccinations
  • give diuretics carefully for volume overload symptoms
  • maybe digitalis
  • warfarin b/c of prothrombotic state of PAH

can give vasoactive agents

35
Q

What should you avoid in PAH

A
  • avoid vasoconstrictors –> nicotine, sympathomimetics
  • avoid deep valsalva
  • avoid pregnancy
36
Q

How does phosphodiesterase 5 inhibitor help in pAH?

A

prevents breakdown of cGMP –> get vasodilitory effects of NO

Cardio Exam 2 (19 decks)

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