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24 Cards in this Set

  • Front
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definition of pulmonary hypertension

-pulmonar artery systolic pressures greather than ____ at rest or ___ with exercise
pulmonary arter systolic pressures of greater tahn 25mmHg at rest or 30 mmHg with exercise
symptoms of pulmonary hypertension
-asymptomatic
-lower body edema
-RUQ pain or fullness
-shortness of breath on exertion
-weakness, fatigue
-chest pain and exertional syncope
-sudden death
Direct signs of pulmonary hypertension

heart sounds
increased or palpable P2 (the pulmonary component of S2)

-may have a systolic ejection murmur or a narrowed splitting of S2

-thus, direct signs of pulmonary hypertension are subtle, not always present and frequently underappreciated
Name the indirect signs of pulmonary hypertension:
Signs of Right ventricular hypertrophy: para-sternal heave (lift); right sided S4 sound
increased atrial "a" wave"

Signs of right Ventricular Fialure:

-tricuspid regurg: Holosystolic murmur, "V" wave in jugular veins, pulsatile liver
-volume overload: elevated jugular venous pressure right sided S3, peripheral edema
what do you see?

what would you see on an EKG?
signs of pulmonary hypertension

-CXR: large pulmonary arteries

-"pruning" of pulmonary vasculature

EKG: "P" Pulmonale; right bundle block; rightward axis deviation
Diagnosis of pulmonary hypertension

-direct vs. indirect?
direct measurement of pressure: Swan-Ganz catheterization; advanced: Accuracy, can follow response to therapy; disadvantage: invasive, complications

-Indirect estimation of pulmonary artery pressure: Doppler echocardiography
Adv: non-invasive, suggests alternative diagnosis. Disadv: accuracy, depends on TR jet, no cardiac output measurement
-etiologies of pulmonary hypertension
increase in flow through pulmonary circulation

-increase in pulmonary vascular resistance

-increase in pulmonary venous pressure

PA=CO x PVR
Etiology of Pulmonary Hypertension (Clinical types)
Hypoxic vasoconstriction (COPD, OSA, Neuromuscular disease, kyphoscoliosis, altitude)

-decreased pulmonary vasculature bed (emboli, emphysema, primary pulmonary HTN, HIV, collagen vascular disease, fibrotic lung disease, drugs)

-Volume or pressure overload (congenital heart disease, left sided heart failure, mitral stenosis, pulmonary veno-occlusive disease)
clinical classifcation of pulmonary hypertension
-pulmonary arterial hypertension
-pulmonary veno-occlusive disease (PVOD)
-PH owing to left heart disease
-PH with lung diseases/hypoxemia
4) chrnoic thromboembolic pulmonary hypertension

-PH with unclear multifactorial mecahnisms
drugs for pulmonary hypertension
endothelin receptor antagonists (bosentan, selective ET-A inhibitiors (oral)

-PDE-5 inhibitors: sildenafil and Tadalafil

-combination therapy

-atrial septostomy

-transplant

-nitric oxide

-Phosphodiesterase type 5 inhibitor (leads to vasodilation, prevents breakdown of cAMP)

-prostacyclin derivatives (prostacyclin, Iloprost, Treprostinil)
symptoms/clinical manifestations of pulmonary thromboembolism?
asymptomatic
leg swelling, redness, pain,

SOB (73%) (on exertion)
-pleuritic chest pain (66%), cough (37%), hemoptysis (13%), syncope, sudden death (8%)
risk factors for PE (in general)
Virchow's triad?
1) Stasis
2) Hypercoagulability
3) endothelial damamge
Risk factors for PE

acquired vs. congenital

name the congental risk factors

name the acquired factors
Congenital: Thrombophilia (Factor V Leiden, Thrombin gene mutations, protein C and S deficiency, Antithrombin III deficiency)

Acquired: immobility of Lower Extremities, Surgery (esp. orthopedic of LE), trauma, stroke, heart failure, medical illness, critical illness, pregnancy, exogenous estrogens, malignancy, inflammatory disorders, nephrotic syndrome, APLA, smoking, age)
clinical signs of PE

in terms of lung and heart and extremities
increased RR
-hypoxemia, crackles, pleural friction rub

cardiac: tachycardia, hypotension, right sided S4, elevated jugular venous pressure, increased P2

extremities: leg swelling, redness
Adjunctive tests in PE:

-EKG?

-CXR?


-ABG?
EKG: sinus tachycardia, T wave inversion, rightward axis, RBBB, S1Q3T3

-CXR: Normal, Atelectasis, Pleural effusion, Hampton's hump, Westermark's sign

-ABG: hypocapnia and hypoxemia. A-a gradient not very useful
describe the investigational approach to diagnosing a patient wih suspected PE
Well's critieria; if over 6 points 78% chance of PE

Diagnositc testing: D-Dimer and dead-space measurement

-assessment of lower extremities for DVT

-ventilation/perfusion scanning

-CT angiography of pulmonary arteries

-MRI thorax for PE

-pulmonary angiography
what is D-dimer?
quantitative measure of degraded, crosslinked fibrin

-levels lower than 200-500ng/ml are associated with a low chance of having a pulmonary embolism

-levels can be elevated by about any inflammatory, malignant, infectious condition as well as pregnancy and recent surgery

-performs best in patients with a low clinical supspicion and no risk factors
when investigating for a PE how do you assess the lower extremities for DVT?
compression

doppler ultrasonography or venography

-very useful in symptomatic patient

-over half patients with PE may have negative compression ultrasound of LE

-serial examinations may be useful to identify patients at low risk for subsequent PE
Ventilation-perfusion scanning

-in theory areas with PE should have ____ventilation and _____perfusion
normal ventilation

absent perfusion

V/Q scan- advantages- longtime use, safety and availability

disadvantages- frequent non-diagnostic results, radiation exposure
describe CT angiogram of pulmonary arteries; useful for?
PE

-involves a rapid bolus of IV contrast and then rapid, high resolution CT scanning through the pulmonary arteries

-in a positive study filling defects are seen within the pulmonary arteries
gold standard test for diagnosis of pulmonary emboli

-invasive and potentially dangerous; measurable mortality, around 0.5%

-negative test virtually excludes PE
pulmonary angiography
treatment of pulmonary emboli
-anticoagulation with heparin or low molecular weight Heparin or Fondaparinux then coumadin

-removal of aggravating cause when possible

-thrombolysis for hemodynamically unstable patients

-IVC filters in cases of LE DVT in patients who cannot be anti-coagulated
_____ ____ is a disease of insidious onset with protean physical findings
pulmonary hypertension
-the three major mechanisms of pulmonary hypertension are:
hypoxic vasoconstriction, loss of the pulmonary vascular bed and volume or pressure overload