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Pulmonology > Lecture 19: Pulmonary Hypertension > Flashcards

Lecture 19: Pulmonary Hypertension Flashcards

1
Q

Ppa equation

A

(CO x PVR) + Pla (Pla = pressure of LA)

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2
Q

Psa equation

A

(CO x SVR) + Pra (Pra = pressure of RA)

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3
Q

What is the definition of pulmonary hypertension

A

Ppa great than 25 mm Hg

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4
Q

Three causes of pulmonary hypertension

A

Increased CO, increased Pla, increased PVR

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5
Q

Three reasons for increased PVR

A

Destruction of pulmonary vascular bed (ILD, emphysema, PE), hypoxic vasoconstriction (COPD, high altitude), small pulmonary artery/arteriole vasculopathy (PAH)

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6
Q

What is PAH? Describe/define

A

Pulmonary arteriole hypertension –> fibrotic/proliferative lesions in muscular arteries

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7
Q

Progression of PAH histologically (4)

A

Medial hypertrophy –> intimal thickening –> in situ thrombosis and plexiform lesion

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8
Q

Pathogenesis of PAH (3 pathways)

A

Upregulated endothelin pathway; downregulated NO pathway, decreased prostacyclin pathway

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9
Q

Four causes of PAH

A
  1. Idiopathic (~50%); 2. Heritable (BMPR2 mutation w/ 20% penetrance); 3. Drug and toxin induced; 4. Associated PAH (~50%)
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10
Q

Five Associated PAH diseases

A

Connective tissue disorders (~50%), congenital heart disease (high pressure/flow –> endothelial dysfunction), portal hypertension, HIV, schisotomiasis

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11
Q

Is PAH common?

A

Nope! 5-15 cases per 1 million

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12
Q

Median survival of untreated PAH

A

2.8 years

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13
Q

What happens to the RV if you “clamp” the pulmonary artery? What does this mean?

A

It fails quickly (decrease in SV) –> cannot handle increases in pressure

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14
Q

Does the RV have isovolmic contraction/relaxation? How can we create this?

A

No (more efficient: ejects blood while contraction and fills while relaxing); pulmonic stenosis makes RV behave like LV

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15
Q

Three consequences of increased RV afterload and their consequences. Ultimate consequence?

A

Increased RV wall stress (–> RV ischema); decreased RV output (–> decrased LV output); increased RV dilation (increased leftward septal shift and regurge); cardiogenic shock

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16
Q

Symptoms of PAH (2 main classes)

A

Low perfusion: dyspnea, fatigue, chest pain, palpitations, lightheadedness, syncope; Congestion: abdominal pain and fullness, peripheral edema

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17
Q

Physical exam of PAH (5), including heart findings (6)

A

Hypoxemia, tachycardia, hypotension, JVD, symptoms of RV failure; Heart findings: RV heave, split S2, systolic TR murmur, diastolic PR murmur, RV S3, RV S4

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18
Q

What is a RV heave a sign of?

A

RV dilatation

19
Q

A split S2 will have a loud A2 or P2 in PAH

A

P2

20
Q

Is PAH associated with pulmonary edema? Why?

A

NO: no significant rales because resistance is PRIOR to capillaries in pulmonary vasculature, so capillary pressures are low

21
Q

ECG in PAH (3)

A

RV hypertrophy/strain, incomplete/complete right bundle branch block, right atrial enlargement

22
Q

What procedure can confirm the presence of pulmonary hypertension?

A

Right heart catheterization

23
Q

If you wedge pressure is high (greater than 15 mm Hg), what is this consistent with?

A

Left sided disease

24
Q

If you wedge pressure is low (less than 15 mm Hg), what is this consistent with?

A

Precapillary disease

25
Q

Natural history of pulmonary hypertension

A

Over time with elevated pulmonary pressure, CO begins to drop because of RV heart failure; PVR will continue to rise and CO continues to fall (low perfusion sx); overtime, Pap will fall but Rap will rise (congestion sx)

26
Q

Tx for PAH (5 meds/classes)

A

Ca2+ channel blockers; prostanoids; endothelial receptor antagonists; PDE-5 inhibitors; riociguat

27
Q

When are Ca2+ channel blockers helpful for PAH? % patients?

A

If positive vasoreactivity test = able to vasodilate w/ administered vasodilator because this suggests a MUSCULAR problem; 13%

28
Q

Prostanoids: mechanism and drugs

A

Stimulates adenylate cyclase –> increased cAMP –> vasodilation, antiproliferation, platelet aggregation inhibition; epoprostenol (IV), treprostinil (SC, IV, PO inhalation), iloprost (inhalation)

29
Q

What is the only PAH medication with a proven survival benefit? What’s an important note about this medication?

A

Epoprostenol; require continuous IV administration

30
Q

Effects of prostanoids

A

Improve hemodynamics, functional capacity and survival

31
Q

Which has the longer half life, epoprostenol or trepostinil?

A

Trepostinil

32
Q

Endothelin receptor antagonists: mechanism

A

Activation of ETA and ETB receptors –> sustained vasoconstriction and proliferation of vascular smooth muscle cells; ETB receptors also mediate pulmonary ET clearance and induce endothelial cell production of local mediators of vascular tone (NO, prostacyclin); SO you want to block A not B

33
Q

Endothelin receptor antagonists: medicatons

A

Bosentan (PO), ambrisentan (PO), macitentan (PO)

34
Q

Phosphodiesterase-5 inhibitors: mechanism

A

Inhibition of cGMP-specific phosphodiesterase;

vasodilation, antiproliferation, platelet aggregation inhibition –> improve hemodynamics and functional capacity

35
Q

PDE-5: medications (2)

A

Sildenafil (PO, IV), tadalafil (PO)

36
Q

Riociguat: mechanism

A

Stimulates soluble guanylate cyclase (sGC) –> sGC converts GTP to cGMP; vasodilation, antiproliferation, platelet aggregation inhibition –> improves hemodynamics and functional capacity

37
Q

Cautions for use of pulmonary vasodilators

A

Decrease SVR –> system hypotension; abrupt medication withdrawal –> rebound pulmonary hypertension; worsen V/Q matching –> hypoxemia; increase pulmonary capillary pressure –> pulmonary edema

38
Q

Why do you get worse V/Q matching with pulmonary vasodilators? Who is this important for? What is a fix?

A

Pulmonary vasodilator will dilate areas of the lung that might be poorly ventilated; those with lung disease; give medication via inhalation

39
Q

Who do you avoid pulmonary vasodilators with? Why?

A

Those with elevated left atrial pressures; at risk for pulmonary edema because if you decrease the pre-capillary constriction, you increase the pressure in the avleoli which cannot be tolerated by the high pressure LA

40
Q

SEs of pulmonary vasodilators

A

Vasodilation: headache, dizziness, flushing, nasal congestion; ERAs: teratogenic, peripheral edema, anemia; bosentan: liver toxicity; prostanoids: jaw pain, delivery system problems (subcutaneous and intravenous)

41
Q

PAH: general treatment measures (4)

A

Supplemental O2, anticoagulation, digoxin (improved contractility), cardiopulmonary rehab (improve fxnl capacity)

42
Q

PAH: surgical therapies (3)

A

Atrial septostomy (unloads RV, but hypoexmia results); pulmonary thromboendarectomy (patients with CTEPH); lung transplant

43
Q

Pulmonary HTN: WHO Classificiations

A

1: PAH; 2: Left heart; 3: Lung disease; 4: Chronic thromboembolic pulmonary HTN; 5: Misc

Pulmonology (21 decks)

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