Pulm HTN and PE + B&B Flashcards

1
Q

how is pulmonary HTN defined and what are 2 mechanisms by which it can occur?

A

pulm HTN: >25mmHg pressure at rest

due to either decrease in cross-sectional area of pulmonary vascular bed (most common) or increased pulmonary vascular blood flow

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2
Q

how does chronic obstructive or interstitial lung disease cause pulmonary HTN?

A

damaged alveolar capillaries —> increased resistance to blood flow —> increased pulmonary blood pressure

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3
Q

how can recurrent thromboemboli lead to the development of pulmonary HTN?

A

recurrent pulmonary emboli reduce the functional cross-sectional area of the pulmonary vascular bed —> increased pulmonary vascular resistance and HTN

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4
Q

what gene mutation is implicated in idiopathic/primary pulmonary arterial HTN?

A

germline mutations in BMPR2 (bone morphogenetic protein receptor 2) - leads to endothelial dysfunction and proliferation of vascular smooth muscle cells

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5
Q

which pulmonary vessels are most affected by pulmonary HTN?

A

arterioles and small arteries - most affected by medial hypertrophy and intimal fibrosis

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6
Q

describe the histological changes that occur in pulmonary vessels in pulmonary HTN

A

medial hypertrophy of pulmonary muscular and elastic arteries

also pulmonary arterial sclerosis and right ventricular hypertrophy

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7
Q

in which patients is idiopathic/primary pulmonary HTN most common?

A

women 20-40 years old

present with dyspnea/fatigue, sometimes anginal chest pain

over time (2-5 years) - respiratory distress, cyanosis, RV hypertrophy, cor pulmonale + thromboembolism + pneumonia

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8
Q

what is the origin of most pulmonary embolisms?

A

result of thrombus originating in lower extremity - begins where blood flow is turbulent (such as venous bifurcation or behind venous valve)

piece (emboli) breaks off and migrates via venous systems to the lungs

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9
Q

what kind of patients are at risk of pulmonary embolism originating from an emboli in the pelvic veins?

A

pregnant women, males with prostate disease, individuals with pelvic infection, etc

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10
Q

what kind of patients are at risk of pulmonary embolism originating from an upper extremity venous thrombosis?

A

patients with central venous catheter

(thrombus originate in sites with turbulent blood flow)

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11
Q

what is the typical clinical picture of a patient with a fat embolism that causes pulmonary embolism?

A

patient with long bone or pelvis trauma (such as closed fracture) - fat from bone marrow becomes embolus

patient will decompensate and develop ARDS

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12
Q

how does an amniotic fluid embolism develop into pulmonary embolism?

A

during delivery, premature rupture of amniotic sac causes amniotic fluid to enter mother’s blood through placenta

allergic reaction to amniotic fluid causes it to become embolus which travels via veins to lung

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13
Q

what is Virchow’s triad of peripheral clotting?

A

hypercoagulability
venous stasis
endothelial damage

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14
Q

explain why hypercapnia and acidosis are unusual findings in pulmonary embolism, unless shock is present?

A

PE increases dead space ventilation (wasted air, because alveoli is not being perfused) —> stimulates respiratory drive (tachypnea), resulting in HYPOcapnia and alkalosis

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15
Q

what is the most key finding of pulmonary embolism?

A

tachypnea!! very high respiratory rate is a major concerning finding!!

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16
Q

what is the scoring system used to evaluate a patient’s probability of having a pulmonary embolism?

A

Wells score: clinical pre-test probability scoring system, helps establish diagnosis of DVT or PE, used to estimate probability before imaging is ordered

17
Q

high levels of what biomarker is important in diagnosing pulmonary embolism?

A

D-dimer: high levels when there is clotting or inflammation occurring in the body

negative D-dimer can help rule out PE in some clinical situations (such as outpatients, patients who are clinically stable, patients with low probability on Wells score)

18
Q

why does pulmonary embolism cause hemodynamic collapse?

A

essentially a cause of acute right ventricular failure (pressure sharply rises, and RV cannot hold up)

19
Q

what are the 5 types of pulmonary HTN?

A
  1. Pulmonary arterial HTN (idiopathic/primary - normal PCWP)
  2. PH with left heart disease [2 ventricles in heart]
  3. PH associated with lung disease/ hypoxemia [rotate 3, it looks like the lungs]
  4. chronic thrombotic embolic hypertension [4 words]
  5. miscellaneous (HIV, hepatic diseases, sarcoidosis, IV drug use, etc) [miscellaneous = 5 syllables]
20
Q

how can chronic hypoxemia (from sleep apnea, for example) cause pulmonary HTN?

A

hypoxic vasoconstriction in lungs (meant to divert blood away from less ventilated regions)

21
Q

what is the most common cause/ type of pulmonary HTN?

A

type 2 - PH with left heart disease

right heart catheterization will show elevated pulmonary capillary wedge pressure (PCWP)

22
Q

What is the classic blood gas finding of pulmonary embolism?

A

low PaO2, low PCO2

increased dead space - ventilation without perfusion

23
Q

how can deep vein thrombosis be diagnosed?

A

lower extremity ultrasound

Often asymptomatic until PE

calf pain, palpable cord (thrombosed vein), Homan’s sign (calf pain with dorsiflexion of foot)

24
Q

What is the characteristic ECG finding of patients with pulmonary embolism?

A

S1Q3T3

deep S wave in lead I,
prolonged Q wave in lead III,
elevated T wave in lead III

*note this is not a specific finding

25
Q

Blood levels of what molecule can be important in ruling out pulmonary embolism when levels are normal?

A

D-dimer: degradation product of fibrin, sensitive but not specific

Useful when normal in setting of low to moderate Wells score

26
Q

what 2 diagnostic tools can be used in pulmonary embolism and which one is preferred?

A
  1. CT angiogram - preferred
  2. VQ (ventilation/perfusion) scan
27
Q

What setting is fat embolism most classically seen and how does a present?

A

long bone fracture (fat leaks from bone marrow)

—> ARDS (lung), confusion (neuro), petechiae (skin)

28
Q

What are the key features of amniotic fluid embolism?

A

during/shortly after labor – amniotic fluid enters maternal circulation and causes inflammatory/allergic reaction – often fatal

phase I: Respiratory distress, low oxygen, hypotension
phase II (hemorrhagic): bleeding, seizures