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Pulmonology Exam > Vascular Lung Diseases > Flashcards

Vascular Lung Diseases Flashcards

1
Q

pulmonary edema as a result of increased capillary hydrostatic pressure

A

(pulmonary edema: a condition caused by excess fluid in the lungs; this fluid collects in the numerous air sacs in the lungs, making it difficult to breathe
*precipitating events include: MI, mitral stenosis, fluid overload, pulmonary venoocclusive disease
*interstitial edema can progress to alveolar edema (excess fluid)
*results in decreases in O2 saturation

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2
Q

3 mechanisms that can increase pulmonary artery pressure

A
  1. increased pulmonary vascular resistance (pulmonary arterial abnormalities)
  2. increased left atrial pressure (left heart abnormalities or global volume overload)
  3. increased pulmonary blood flow (congenital heart disease, often with left to right shunting)
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3
Q

classification of pulmonary hypertension

A

*mean pulmonary artery (PA) pressure is > 20 mmHg

*pre-capillary pulmonary HTN if: left atrium/wedge pressure </= 15 mmHg
*post-capillary pulmonary HTN if: left atrium/wedge pressure > 15 mmHG

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4
Q

recall: formula for calculating pulmonary vascular resistance

A

pulmonary vascular resistance = (mean pulmonary artery pressure - pulmonary capillary wedge pressure) / cardiac output

= (MPAP - PWCP)/CO

note - normal PVR (pulmonary vascular resistance) is 1.9 to 3.1 Wood units

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5
Q

pulmonary hypertension: defined

A

*pulmonary hypertension (PH) is defined as mPAP > 20 mmHg
*precapillary PH is likely present at pulmonary vascular resistance > 3 Wood units (or PCWP < 15)
*postcapillary PH is likely present at PCWP > 15 mmHg

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6
Q

how to determine the cause of pulmonary hypertension

A

*EKG
*transthoracic echocardiogram
*CXR
*ventilation/perfusion scanning
*polysomnography
*additional tests for infectious, hematologic, autoimmune, endocrine, and metabolic disorders

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7
Q

pulmonary arterial hypertension - pathology

A

*common sequence of changes in blood vessel, from early to late:
1. intimal hyperplasia
2. medial hypertrophy
3. vessel occlusion
4. plexiform lesion
5. fibrinoid necrosis

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8
Q

plexiform lesions in pulmonary arterial hypertension

A
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9
Q

classes of treatments of pulmonary arterial hypertension

A
  1. endothelin-receptor antagonist (ERA)
  2. phosphodiesterase type 5 inhibitor (PDE5i)
  3. prostacyclin derivative (PG)
  4. guanylate cyclase stimulator (sGC)
  5. calcium channel blocker (CCB)
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10
Q

3 pathways of pulmonary arterial hypertension

A
  1. endothelin-1 pathway (promotes cell growth)
    -treated using endothelin-receptor antagonists
  2. prostacyclin (PGI2) pathway (increases vasodilation)
    -treated using prostacyclin derivatives
  3. nitric oxide pathway (increases vasodilation)
    -treated using phosphodiesterase type 5 inhibitors and guanylate cyclase stimulators
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11
Q

treatment of pulmonary hypertension in all of the WHO groups

A

*LOOP DIURETICS
*supplemental oxygen (if SpO2 < 90%)

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12
Q

treatment of pulmonary hypertension group 1 (pulmonary arterial hypertension)

A

*loop diuretics & supplemental oxygen, plus pulmonary vasodilators

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13
Q

treatment of pulmonary hypertension group 2 (PH due to left heart disease)

A

*loop diuretics & supplemental oxygen, plus afterload reduction, ionotropic agents

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14
Q

treatment of pulmonary hypertension group 3 (PH due to lung disease)

A

*loop diuretics & supplemental oxygen, plus bronchodilators

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15
Q

treatment of pulmonary hypertension group 4 (PH due to arterial obstructions)

A

*loop diuretics & supplemental oxygen, plus pulmonary thromboendarterectomy, sGCis

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16
Q

treatment of pulmonary hypertension group 5 (PH due to multifactorial mechanisms)

A

*loop diuretics & supplemental oxygen, plus treatment of underlying cause

17
Q

pulmonary arteriovenous malformations (AVMs) - overview

A

*abnormal connection between pulmonary arteries and veins
*bypass the alveolar capillary system, creating a “shunt”; results in lower systemic PaO2 and hypoxemia
*suspect in a patient with hypoxemia or cyanosis who has mucosal or facial telangiectasia (ex. Hereditary Hemorrhagic Telangiectasia)

18
Q

pulmonary arteriovenous malformations (AVMs) - clinical presentation

A

*cyanosis
*telangiectasias
*rarely, stroke due to “paradoxical” embolism

19
Q

venous thromboembolic disease - overview

A

*includes deep vein thrombosis (DVT) and pulmonary embolism (PE)
*a major and common preventable cause of death
*risk factors: cancer, hospitalization, surgery, pregnancy, smoking, estrogen-containing hormone therapy, immobility (long plane or car rides)

20
Q

pathogenesis of venous thrombosis

A

*Virchow’s Triad: blood stasis, endothelial injury, and hypercoagulability
*often forms at the valve pockets of the veins, composed primarily of red cells and thrombin

21
Q

clinical presentation of DVT

A

*history: recent surgery, hospitalization, or long trip (car/plane); pt may report any or none of:
-swelling, pain, cramping/soreness, purple coloration of the skin
*exam: any or none of:
-swelling in an extremity
-palpable superficial “cord” in a vein, +/- warmth
-Homen’s sign: calf pain when you dorsiflex the foot
-rare presentation: extreme purplish discoloration of a limb (“phlegmasia cerulea dolens”)

22
Q

diagnosing DVT

A
  1. Wells Clinical Model helps assess probability of DVT using history & exam findings (very sensitive for DVT; low score helps rule out DVT)
  2. blood D-dimer levels (very sensitive; normal levels help rule out DVT)
  3. ultrasound of deep veins (very specific for presence of clot; positive findings rule in DVT)
23
Q

treatment options for DVT

A

*anticoagulants for 3+ months (heparins, oral direct thrombin inhibitors, factor Xa inhibitors)
*thrombolysis
*if the above are too high risk: inferior vena cava filter (to delay/prevent embolism)

24
Q

thromboembolism - defined

A

*pieces of a clot in a deep vein (most often from the femoral veins) break off and travel in the bloodstream until they are stopped by the pulmonary circulation

25
Q

clinical presentation of pulmonary embolism: history

A

*usually sudden onset of symptoms
*shortness of breath
*chest pain
*cough, can be hemoptysis
*presence of malignancy

26
Q

clinical presentation of pulmonary embolism: exam

A

*tachycardia
*S1Q3T3 on EKG
*ACUTE RESPIRATORY ALKALOSIS with hypoxemia
*cyanosis
*signs of DVT may or may not be present

27
Q

features of small pulmonary embolisms

A

*frequently unrecognized
*repeated emboli may result in pulmonary hypertension

28
Q

features of medium-sized pulmonary embolisms

A

*sometimes pleuritic pain, dyspnea, and slight fever
*cough may produce blood-stained sputum
*may produce pleural friction rub
*chest radiograph is often normal or nearly so

29
Q

features of massive (large) pulmonary embolisms

A

*hemodynamic collapse with shock, pallor, and cardiac arrest
*hypotension with rapid, weak pulse and neck vein engorgement
*sometimes fatal

30
Q

diagnosing pulmonary embolism

A

*Wells Score for PE, D-dimer, ultrasound of deep veins can be helpful but does not rule out PE
*CT scan is used to confirm diagnosis
*CT Pulmonary Angiogram of Chest (visualizes clot in the pulmonary circulation; requires IV contrast dye)
*Ventilation-Perfusion Scanning (V/Q scan) [detects radioactive gas (V) and IV labeled protein (Q); a mismatch with a perfusion defect can diagnose PE]

31
Q

treatment of pulmonary embolism

A

*IV thrombolysis for massive PE
*anticoagulants for 3+ months (heparin, etc)
*possible newer technologies (PA catheters with ultrasound; suctioning of clot using vacuum catheters)

32
Q

examples non-thrombotic pulmonary emboli

A
  1. air embolism
  2. FAT EMBOLISM
  3. AMNIOTIC FLUID EMBOLISM
  4. septic embolism
33
Q

non-thrombotic pulmonary emboli: fat embolism

A

*adipose tissue enters vasculature
*causes vascular occlusions, petechiae, altered mental status
*typical scenario: after fracture of a long bone such as femur (fatty marrow embolizes)

34
Q

non-thrombotic pulmonary emboli: amniotic fluid embolism

A

*amniotic fluid enters the vasculature
*causes DIC, cyanosis, hypotension
*typical scenario: after childbirth, mother has sudden cardiovascular collapse, respiratory failure, and signs of DIC

35
Q

non-thrombotic pulmonary emboli: air embolism

A

*entrance of atmospheric air into the vasculature
*causes sudden increase in PA pressure and occlusion of small vessels
*typical scenario: a large bore central venous catheter gets disconnected and left open to air

36
Q

non-thrombotic pulmonary emboli: septic embolism

A

*infected material enters the vasculature
*causes inflammatory nodules that can cavitate wherever they dislodge
*typical scenario: multiple randomly-distributed lung abscesses in a patient who uses illicit IV drugs

Pulmonology Exam (36 decks)

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