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21 Cards in this Set
- Front
- Back
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Unlike the systemic circulation, the pulmonary circulation is a __ pressure, ___ resistance system @ normal.
Does it have high compliance? Can it accommodate increased CO easily w/o increasing resistance/pressure? |
low, low
Yes Yes. Yes. |
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What are the two mechanisms the lung vasculature uses to avoid increases in pulmonary vascular resistance?
What is the simple definition of Pulmonary hyperT? |
Recruitment & distension
mean PAP >/= 25mmH at rest |
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PAH is a intrinsic/extrinsic type of P-HTN?
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intrinsic to the lung/pulmonary circulation.
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What are some 'passive' mechs of p-HTN?
Hyperkinetic? Occlusive? Obliterative? Vasoconstrictive? |
^LAP (mitral stenosis, regurg, LV dysfunction)
high flow states (VSD, ASD) Chronic PE emphysema, interstitial lung dz, vasculitis, sarcoidosis hypoxia, scleroderma |
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What is the most common cause of PAH worldwide?
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schistosomiasis
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What is Chronic thromboembolic pulmonary hypertension? (CTEPH)
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pt has a PE that was never resolved --> persistent occlusion of pulmonary vessels.
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What are some things seen on clinical evaluation of a pt with p-HTN?
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JVD, accentuated S2, RV heave, right sided gallops, peripheral edema
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What test can let you distinguish between extrinsic causes of PH and intrinsic causes?
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Rt ht catherization:
measures pulmonary pressures, PCWP, and CO. |
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Criterion for PAH dx?
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Mean PAP >/= 25 mm Hg at rest or 35 mmHg with exercise
PCWP </= 15 mm Hg PVR >/= 3 Wood Units (240 dynes.sec.cm-5) |
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What is the basis for the WHO functional classifications?
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I: no limitations
II: ordinary phy. actv causes undue dyspnea or fatigue, chest pain, or near syncope III: Less than ordinatry activity -> sx IV: inability to perform phys actv.; Rt ht failure, Syncope. Dyspnea and fatigue may be present @ rest. |
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What is Endothelin's relationship to PAH?
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Potent endogenous vasoconstrictor & smooth muscle mitogen
May contribute to increase in vascular tone & vascular hypertrophy Patients with IPAH have high concentrations of endothelin 1 in plasma |
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Is there evidence for inhaled NO as an effective tx for PH?
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no.
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What is the tx for PH?
Can it actually reverse remodeling changes? Does it improve clerance of endothelin? |
Acute vasodilatory response --> CCB
No: Endothelin pathW (-sentan) NO pathW - sildenafil Protaglandin/Prostacyclin - epoprostenol - treprostinil - iloprost Yes. Yes. |
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What adjunct tx doubles 3 year survival?
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AntiCoag
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Death beyond the first few hours post-embolism is generally due to what?
What is the pathophysiological consequences of a PE? |
recurrence, thus it is preventable.
^alveolar dead space Pneumoconstriction Hypoxemia - shunt, VQ mismatch Hyperventilation Depletion of surfactant (takes 24 hrs) Pulmonary infarction |
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With a PE, if we see a decrease in cross-sectional area of the vascular bed of ___ magnitude(%), we see sig. PH, Rt HF, and systemic Hypotension.
What humoral reflex mechanisms (2) are seen? |
50-60%
hypoxic vasoconstriction, mediator release |
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How do you Dx PE?
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VQ scan or a contrast assisted CT.
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What are Sx of acute PE?
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Tachycardia, Increased P2
S3, S4 Lower extremity edema hypotension cyanosis SOB Apprehension (feeling of doom) Hemoptysis |
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Sx of which dz closely resemble that of PAH?
How do you scan for it? |
CTEPH
VQ scan |
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Name the dz:
Pulmonary-renal syndrome ANCA+ Associated with upper airway/oral lesions. Anti-GBM antibodies Pulmonary-renal sx Vasculitis w/ DAH PH w/o evidence of vasculitis Pain, thromboembolic dz, effusions, etc... |
Wegeners
Goodpasture's SLE... it presents in very varied ways. |
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Is CTEPH correctable?
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yes, surgically; thus it must not be missed on Dx.
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