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pulmonology > Pulmonary vascular disorders > Flashcards

Pulmonary vascular disorders Flashcards

1
Q

What is pulmonary hypertension?

A
  • increase in pulmonaray arterial pressure from increased pulmonary vascular resistance
  • can be caused by number of factors, all which force the heart’s right side to work harder to pump blood to the lungs. The right chambers may enlarge as they struggle to function, and blood is often forced backward through the tricuspid valve
  • pulmonary artery systolic pressure is greater than 30 mm Hg or a pean PAP of more than 20 mm Hg
  • poor prognosis especially in setting of cor pulmonale
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2
Q

Classification of pulmonary hypertension?

A
  1. pulmonary arterial hypertension
  2. pulmonary hypertension secondary to left heart disease (most common)
  3. pulmonary htn secondary to lung disease/chronic hypoxia
  4. chronic pulmonary thromboembolic disease
  5. pulmonary HTN with unclear multifactorial mechanisms
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3
Q

What are sxs of pulmonary htn?

A
  • dyspnea on exertion (may be at rest in severe cases)
  • fatigue
  • chest pain (anginal)
  • syncope with exertion
  • nonproductive cough
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4
Q

what are the signs of pulmonary HTN?

A
  • narrow splitting of S2 with loud pulmonary component
  • R ventricular hypertrophy
  • R atrial enlargement
  • enlarged central pulmonary arteries on CXR
  • JVD
  • R sided heart failure sxs: hepatomegaly, and LE edema
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5
Q

What should a work up of pulmonary HTN include?

A
  • CXR
  • CT of chest
  • PFTs
  • echocardiography with Doppler flow
  • R sided cardiac catheterization with vasodilator challenge
  • V/Q scanning if suspect disease is from chronic thromboembolic disease
  • exclude HIV and collagen vascular disease
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6
Q

Tx of pulmonary HTN?

A
  • approach depends on underlying cause (tx first)
  • vasodilators:
    oral Ca channel blockers (1st line)
    oral phosphodiasterase inhibitors (sildenafil)
    oral endothelin receptor antagonists ( ambrisentan)
    continuous infusion of prostacyclin agents (epoprostenol)
  • supplemental O2 if hypoxemia present
  • may require chronic anticoag.
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7
Q

What is Cor Pulmonale?

A
  • RV systolic and diastolic failure secondary to pulmonary disease or from pulmonary vascular disease
  • poor prognosis
  • most commonly caused by: pulmonary HTN, COPD, or idiopathic pulmonary fibrosis
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8
Q

Why does the R side of the heart hypertrophy in Cor Pulmonale?

A
  • due to high BP in the pulmonary blood vessels, usually caused by chronic lung disease
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9
Q

Sxs of Cor Pulmonale?

A
  • chronic productive cough
  • exertional dyspnea
  • wheezing
  • easy fatigability
  • weakness
  • RUQ pain (Liver is distended)
  • dependent edema
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10
Q

Signs of Cor Pulmonale?

A
  • cyanosis
  • clubbing
  • distended neck veins
  • RV heave or gallop
  • prominent lower sternal or epigastric pulsations
  • hepatomegaly
  • dependent edema
  • ascites
  • severe lung disease
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11
Q

Dx studies for Cor Pulmonale?

A
  • Polycythemia secondary to chronic hypoxemia
  • SaO2 less than 85% (give O2 and % should increase)
  • EKG: may show RAD, peaked P waves, deep S waves in V6, may see Q waves in inferior leads because of vertically placed heart
  • PFTs: confirm underlying lung disease
  • echo: should show normal LV size and function, RV and RA dilation and RV systolic dysfunction (tricuspid regurg)
  • CT or VQ scanning to rule out chronic thromboembolic disease
  • serum BNP may be chronically elevated from RV dysfunction
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12
Q

Tx of Cor Pulmonale?

A
  • tx chronic respiratory failure
  • supp O2:
    may improve survival, helps to decrease RV after load by reducing pulmonary vascular resistance
  • manage RHF sxs with:
    fluid and salt restrictions, and diuretics (don’t use too much -cause hypotension)
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13
Q

Why is it so impt to dx PEs?

A
  • 3rd leading cause of death of hospitalized pts
  • many cases are missed
  • key is prevention and always considering this in DDx when applicable
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14
Q

What can cause a PE?

A
  • air
  • amniotic fluid (during active labor)
  • fat (long bone fractures) like the femur
  • FBs (talc in IV drug users)
  • parasite lungs
  • septic emboli: due to IV drug use - vegetation embolizes
  • tumor cells: thrombosis in renal vein - travel to lungs
  • most common cause is a venous thrombus
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15
Q

Where do most of the PEs come from?

A
  • 50-70% of pts with PE have lower extremity DVT when evaluated
  • calf veins: if localized calf veins rarely travel to the lungs, 20% of thrombi here migrate proximally to popliteal and femoral veins
  • ***popliteal and ileofemoral: 50-60% of pts with thrombi here will develop PE (why prophylaxis is so impt)
  • emboli usually not single, will find multiple
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16
Q

What are the RFs for PEs and DVTs?

A
  • Virchow’s triad:
    venous stasis
    injury to vessel wall
    hypercoagulability
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17
Q

What factors promote venous stasis?

A
  • immobility
  • postop state
  • obesity
  • hyperviscosity: polycythemia
  • increased central venous pressure: low cardiac output, pregnancy (varicose veins because of compression of venous system)
18
Q

Where could vessel damage come from?

A
  • prior episodes of thrombosis (damage to valves and veins - increase varicosities and increase stasis)
  • ortho surgery
  • trauma
19
Q

What factors are associated with hyper coagulability?

A
  • surgery
  • meds: hormones (estrogen)
  • disease: malignancy: pancreas and lung
  • genetic: Factor V leiden (most common inherited), dysfunction of Protein C, protein S, antithrombin 3, prothrombin gene mutation, hyper-homocysteinemia, antiphospholipid antibodies (lupus anticoagulant, anticardiolipin AB)
20
Q

What physiologic changes occur with PE?

A
  • reflex bronchoconstriction and vasoconstriction from neurohormonal responses
  • R ventricular failure if massive thrombus
  • Pulmonary vascular obstruction: increased pulmonary vascular resistance. Causes physiologic deadspace: ventilation of the lung without perfusion - hypoxemia due to R to left shunting of blood
  • decreased cardiac output
  • surfactant depletion causing atelectasis
21
Q

Signs and sxs of PE?

A
  • dx may be difficult, findings depend on the size of the embolus and common signs and sxs are nonspecific
    -sxs:
    dyspnea, pleuritic chest pain, cough, leg pain, hemoptysis, palpitations, wheezing, anginal pain
  • signs: tachypnea, crackles, tachycardia, S4, S3, accentuated S2, low grade fever, homan’s sign, pleural friction rub, and cyanosis
22
Q

What dx studies are done for PEs?

A
  • EKG
  • ABG: low blood gas and give O2 and doesn’t move think PE
  • D-dimer
  • troponin I or T
  • BNP
  • CXR
  • CT angiography
  • V/Q scan
  • venous ultrasound of the extremities
  • pulmonary angiography
  • MRI
23
Q

What will you find on an EKG if pt positive for PE? Trademark sign?

A
  • S1Q3T3
    s waves in lead 1
    Q waves in lead 3
    inverted T waves in 3
24
Q

What does PQRSTT findings mean in an EKG?

A
  • P: PE EKG findings may include:
  • Q: waves in lead 3
  • R: bundle branch block
  • S: wave in lead 1
  • Tachycardia
  • inverted T waes in lead 3
25
Q

What will an arterial blood gas show?

A
  • not dx: isn’t sensitive or specific for PE
  • may show hyperventilation and or possible hypoxemia
  • hyperventilation would cause low CO2 so resp. alkalosis
26
Q

What is a D dimer and what does it tell us?

A
  • degradation product of cross linked fibrin
  • elevated in the presence of thrombus
  • in the setting of thromboembolism: sensitivity is high but specificity is low
  • so if negative - most likely no clot but if positive it could be any clotting not just PE (elevated in stroke, MI, DVT, CVD)
27
Q

What cardiac tests are done? are they helpful?

A
  • Troponin I, Troponin T and BNP
  • may all be elevated due to R ventricular strain and or acute RV failure
  • these tests aren’t helpful for dx PE and may often confuse the matter
28
Q

What radiologic studies are done if suspect a PE?

A
  • CXR
  • CT angiogram of the chest
  • V/Q scan
  • lower extremity venous ultrasound
  • pulmonary angiography: previous gold std but rarely used as there are safer less invasive options
  • MRI: used primarily in research
29
Q

What will we see on CXR that is positive for a PE?

A
  • wedge shaped peripheral defect (Hampton’s hump) in setting of pulmonary infarct
  • atelectasis
  • parenchymal infiltrates
  • pleural effusion
  • prominent central pulmonary artery (westermark sign)
  • the above findings are nonspecific
  • *** a normal CXR is the most common finding: if normal in setting of acute hypoxemia without prior hx of lung disease is highly suggestive of PE
30
Q

What is CT pulmonary angiography?

A
  • IV contrast and ionizing radiation exposure
  • overall sensitivity and specificity 83/96%
  • if clot is proximal pulmonary arteries: most sensitive for detecting PE in larger pulmonary arteries
  • ***if clot is in distal pulmonary arteries: may miss as many as 75% of subsegmental defects compared with pulmonary angiography
  • bottom line is that a normal CT scan doesn’t exclude PE in high risk pts.
31
Q

What is the V/Q scan?

A
  • nuclear medicine test: admin of different inhaled and IV injection of radioisotopes
  • perfusion scan is compared to the ventilation scan
  • abnormal if there is ventilation without perfusion to segmental lung area
  • read as high, low or intermediate (indeterminate) probability of PE
  • helpful if they read as normal or high probability of PE
  • 75% of these scans in the PIOPED study were nondx
  • Highly suggestive of emboli if there is a mismatch
32
Q

When is a lower extremity venous ultrasound helpful?

A
  • helpful for ruling out or in DVT of the lower extremities
  • Quite accurate for the detection of proximal LE DVT (common femoral or popliteal veins)
  • less accurate when:
    distal or recurrent thrombi,
    asymptomatic patients (low positive predictive value)
33
Q

Use of pulmonary angiography?

A
  • gold std for dx
  • able to establish a definitive dx in 97% of pts with DVT in the PIOPED 1 study
  • role in dx of PE:
    if dx of PE is in doubt when there is a high clinical pretest probability of PE
  • or when dx of PE must be established with certainity
34
Q

What may a workup for a PE include?

A
  • D-dimer
  • EKG
  • CXR
  • doppler ultrasound for lower extremities
  • ** CT angiogram of chest with PE protocol or V/Q scan (pick one of 2)
35
Q

What is the systematic approach to the eval of the PE?

A
  • takes into consideration significant risk factors for PE
  • in nonpregnant pts can use:
    wells criteria or PERC rule
36
Q

What is included in the PERC rule for PE?

A
  • rules out PE if no criteria are present and pre test probability is less than 15%:
  • 50 or older
  • HR of 100 or more
  • O2 sat on room air: less than 95%
  • prior hx of venous thromboembolism
  • trauma or surgery within 4 weeks
  • hemoptysis
  • exongenous estrogen
  • leg swelling
37
Q

What is the Well’s criteria for DVT?

A
  • active cancer (tx or palliation in last 6 months)
  • bedridden recently longer than 3 days or major surgery within 12 weeks
  • calf swelling of more than 3 cm compared to other leg
  • collarteral superficial veins present
  • entire leg swollen
  • localized tenderness along deep venous system
  • pitting edema, confined to sx leg
  • paralysis, paresis, or recent plaster immobilization of lower extremity
  • previously documented DVT
  • *** used to calculate pretest probability of PE in non pregnant patients (unlikely if 4 or less), and likely if score is greater than 4)
38
Q

Wells criteria score?

A
  • 4 or greater:
    D-dimer greater than 500 ng/mL proceed to imaging study (CTA or VQ scan)
  • however if high probability score of greater than 6 can skip the D dimer and go directly to imaging
  • if less than 4: and D dimer less than 500 ng/mL no further testing needed
39
Q

Who is PERC for?

A
  • Pulmonary Embolism Rule out Criteria
  • only for patients with low probability of PE
  • apply this:
    pt with low likelihood of PE but need to rule out:
    if all 8 criteria are met, than no further testing needed
  • if not meeting all 8 criteria than further testing with D dimer or imaging is needed
40
Q

What is the tx for a PE?

A
  • hospitalization
  • supp oxygen
  • heparin (LMWH, UFH)
  • assess for fibrinolytics if significant hemodynamic compromise (shock or syncope)
  • outpt anticoag. for 3-6 months depending on the clinical situation
  • inferior vena cava filter if large clot burdern or unable to anticoagulate as an outpt (not used too often today)

pulmonology (20 decks)

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