Pulmonary embolism

Question 1

Kinds of venous thromboembolic (VTE) diseases

Answer 1

• DVT: stable hemodynamics, Rx is anticoagulation
• Non-massive PE: stable hemodynamics, Rx is anticoagulation
• Massive PE: unstable hemodynamics, Rx is thrombolysis
• Thrombi that are below the knees or in superficial veins almost never embolize, but if they extend above the knees there is a 50% chance it will embolize
• Acute mortality is due to massive PE causing R HF
• Chronic morbidity is pulmonary HTN

Question 2

Risk factors for PE

Answer 2

• Virchow’s triad: stasis, endothelial injury, hypercoagulability
• Includes surgery, pregnancy, prolonged immobility

Question 3

Pathophysiology of PE

Answer 3

• Since there is occlusion of pulmonary arteries, there is an increased in dead space
• There is also decreased surfactant production as perfusion decreases, thus causing alveoli to collapse
• Atelectasis and increased dead space lead to V/Q MM and hypoxemia
• There is a widened A-a gradient
• Hyperventilation occurs due to mechanical stimulation of large vessels (main cause) and also b/c of hypercapnia

Question 4

Hemodynamics of PE

Answer 4

• Acute PE can cause acute severe pulm HTN and acute RV failure
• RV dilation compresses the LV and leads to decreased CO and hypotension
• PE w/ hemodynamic compromise is a massive PE
• PE seldom cause infarcts because there is collateral circulation

Question 5

Clinical presentation of PE

Answer 5

• Sx: acute dyspnea, pleuritic chest pain, hemoptysis, others: anxiety, cough
• Signs: tachypnea, tachycardia, DVT signs
• ECG and CXR show non specific findings (often normal)
• Possible CXR findings: prominent PAs/IVC, decreased perfusion (westermark sign) and wedge-shaped infarct (hampton’s hump) are classic but rarely seen
• CT pulmonary angiography (CTPA): number one way to Dx PE
• CTPA shows vessel cut-off or filling defect (CTPA has replaced V/Q scan)
• Tn may be elevated- not ruled in if positive (low specificity) but is ruled out if negative (high sensitivity)
• D-dimer indicates if there is active anticoagulation, only helpful if negative b/c then it can be ruled out (high sensitivity)

Question 6

Assessing the likelihood of PE

Answer 6

• Ask 2 questions: 1) is another Dx unlikely?, 2) is there a major risk factor?
• Low: neither
• Intermediate: either
• High: both

Question 7

Rx of PE

Answer 7

• Anticoagulation is used not to cure the current PE/DVT, but to prevent propagation, embolization, and to help initiate resolution
• Anticoagulation is a prophylaxis, to prevent recurrent PE
• Use LMW heparin if the pt is hemodynamically stable
• Want the PTT to be >2x normal w/in 24hrs
• For massive PE, the goal of therapy is not only to prevent recurrent PE but to bust the current PE
• Thus want to give a thrombolytic (t-PA) to reverse PE, along w/ IV heparin (HMW) to prevent recurrence
• On top of this: support hemodynamics

Question 8

Chronic PE and pulm HTN

Answer 8

• PHTN when mPAP >25mmHg
• Characteristic finding in PHTN is remodeling of the pulmonary vasculature
• This is a plexogenic lesion (causes idiopathic PHTN)
• Plexogenic lesions consists of intimal proliferation and eccentric occlusion of the pulmonary vasculature
• Idiopathic or secondary, w/ chronic PE beings a cause of secondary PHTN

Question 9

Fat embolism syndrome

Answer 9

• Due to trauma (long bone fractures)
• The fat embolizations are not visualized on CTPA/CXR/VQ scan (any chest images)
• Production of toxic intermediaries (FFA) causes Sx
• Clinical triad: hypoxemia (dyspnea), neuro abnormalities (confusion) and petechial rash on anterior chest