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Pulmonology > 16: Pulmonary Hypertension > Flashcards

16: Pulmonary Hypertension Flashcards

1
Q

Pulmonary vasculature characteristics

A
  • High flow, low resistance: PVR ~1/15 of SVR due to large cross-sectional area
  • High capacitance: can accomodate ↑CO
  • Arterioles offer very little resistance
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2
Q

Physiologic causes of PHTN

A
  • PHTN: mean PPA ≥ 25 mmHg (normal = 14)
  • PPA = (CO x PVR) + PLA
    • ​↑CO: congenital heart defects w/ L-R shunt, cirrhosis, anemia, AV malformations
    • ↑PLA: LVF, mitral valve dz, restrictive cardiomyopathy
    • ↑PVR: destruction/obliteration of pulmonary vascular bed (ILD, PE), hypoxic vasoconstriction (COPD, high altitude), small pulmonary artery/areteriole vasculopathy (PAH)
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3
Q

Pulmonary Arterial Hypertension (PAH)

A
  • Mean PAP ≥ 25mmHg + PCWP/LVEDP ≤ 15mmHg
    • Indicates normal pressure in L heart
  • Triggering lesion is intrinsic arteriopathy
    • Idiopathic PAH
    • Heritable
    • Drug/toxin-induced
    • Persistent PH of newborn
    • Associated w/ CTD, HIV, portal HTN, CHD, schistosomiasis, chronic hemolytic anemia
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4
Q

Classifications of PH

A
  1. Pulmonary arterial hypertension
  2. PH due to L heart dz
  3. PH due to lung dz and/or hypoxia
  4. Chronic thromboembolic PH
  5. PH w/ unclear multifactorial mechanisms
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5
Q

PAH vascular pathology

A
  • Fibrotic and proliferative lesions in muscular arteries of less than 500 um diameter
  • Medial hypertrophy
  • Intimal thickening/fibrosis
  • In situ thrombosis
  • Plexiform lesion: focal intimal thickening followed by exuberatn endothelial cell proliferation
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6
Q

Homeostatic imbalances in PAH

A
  • ↑Endothelin-1
  • ↓Prostacyclin
  • ↓Nitric oxide

Leads to vasoconstriction, prothrombosis, cell proliferation

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7
Q

Therapeutic targets for PAH

A
  1. Endothelin-receptor antagonists
  2. Exogenous NO
  3. Phosphodiesterase type 5 inhibitor
  4. Prostacyclin derivatives
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8
Q

Top 5 associated causes of PAH

A
  1. Connective tissue/collagen vascular dz (scleroderma)
  2. Congenital heart dz
  3. Portopulmonary dz (portal HTN)
  4. Drugs/toxins
  5. HIV
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9
Q

Right ventricle in PAH

A
  • Embryologically different from LV: arise from different embryological origins
  • Structurally different from LV: LV concentric, RV crescent; RV LV free wall ~8-11mm, RV ~2-3mm; RV lacks circumferential constrictor fibers
  • Functionally different from LV: RV more compliant, myocardial energy expenditure ~1/5th that of LV
  • RV dilatation –> IV septum bulging into LV –> impaired LV filling/stroke volume
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10
Q

PAH clinical presentation

A
  • Dyspnea
  • Fatigue
  • Syncope/near syncope
  • Chest pain
  • Palpitations
  • Leg edema
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11
Q

PAH risk factors

A
  • FHx
  • Prematurity
  • Connective tissue dz
  • Congenital heart dz
  • Portal HTN
  • Environmental/drug factors
  • HIV
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12
Q

PAH PEX findings

A
  • Accentuated pulmonary component of S2
  • Early systolic click
  • Midsystolic ejection murmur
  • Left parasternal lift
  • RV S4
  • Increased jugular a wave
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13
Q

PAH CXR findings

A
  • Peripheral hypovascularity (pruning)
  • RV enlargement into retrosternal clear space
  • Prominent proximal pulmonary arteries
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14
Q

Chronic thromboembolic pulmonary hypertension (CTEPH)

A
  • Curable form of PH
  • Group IV PH
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15
Q

Cardiac catheterization

A
  • Gold standard of PH
  • Exclude CHD
  • Measure wedge pressure or LVEDP
  • Establish severity and prognosis
  • Test vasodilator therapy
  • Hemodynamics:
    • Pulmonary venous HTN: ↑PCWP, normal PVR
    • PAH, PH w/ respiratory dz, CTEPH: normal PCWP, ↑PVR
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16
Q

Optimal treatment strategy

A

Anticoagulants + diuretics + oxygen + digoxin

17
Q

Acute vasoreactivity testing

A
  • Administer short-acting vasodilator (epoprostenol, adenosine, NO)
  • Acute robust responder: ↓mPAP by > 10 mmHg to absolute value of < 40 mmHg, without concurrent drop in CO
    • More likely to have sustained beneficial response to high dose calcium channel blockers (CCB)
18
Q

Calcium channel blockers

A
  • Diltiazem & **Verapamil **
  • Give to acute robust responders
19
Q

Prostanoids

A
  • **epoprostenol **(IV)
  • stimulate adenylate cyclase –> ↑cAMP –> vasodilation, antiproliferation, platelet aggregation inhibition
  • improved hemodynamics, functional capacity and survival
  • SFx: jaw pain, delivery system problems
20
Q

Phosphodiesterase-5 inhibitors

A
  • **Sildenafil **(PO, IV)
  • Inhibition of cGMP-specific phosphodiesterase –> vasodilation and antiproliferation
  • improve hemodynamics and functional capacity
21
Q

Endothelin receptor antagonists

A
  • **Bosentan **(PO)
  • ETA, ETB receptors expressed on SMCs and cardiac myocytes; activation –> vasoconstriction and proliferation of vascular SMCs
  • improve hemodynamics and functional capacity
  • SFX: liver toxicity, teratogenic, peripheral edema, anema
22
Q

Pulmonary vasodilator considerations

A
  • Decrease SVR –> systemic HoTN
  • Worsen V/Q mismatch –> hypoxemia
  • Abrupt med withdrawal –> rebound PH
  • ↑pulmonary capillary pressure –> edema
  • SFx: HA, dizziness, flushing, nasal congestion
23
Q

General treatment measures for PH

A
  • Optimize preload: diuretics, salt restriction
  • Supplemental O2
  • Anticoagulation
  • Digoxin
  • Cardiopulmonary rehab: ↑functional capacity
24
Q

Surgical therapies for PH

A
  • Atrial septostomy: unload RV at cost of hypoxemia
  • Pulmonary thromboendarectomy: for CTEPH
  • Lung transplant

Pulmonology (16 decks)

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