By Iraj Khan

 The pathophysiology of pulmonary embolism.

Although pulmonary embolism can arise from
anywhere in the body, most commonly it arises from
the calf veins. The venous thrombi predominately
originate in venous valve pockets (inset) and at other
sites of presumed venous stasis. To reach the lungs,
thromboemboli travel through the right side of the
heart.
 The temporal pattern of presentation (acute, subacute, or chronic) – Patients
with PE can present acutely, subacutely, or chronically:
 Acute – Patients with acute PE typically develop symptoms and signs immediately
after obstruction of pulmonary vessels.
 Subacute – Some patients with PE may also present subacutely within days or
weeks following the initial event.
 Chronic – Patients with chronic PE slowly develop symptoms of pulmonary
hypertension over many years (ie, chronic thromboembolic pulmonary
hypertension;
• Hemodynamically unstable PE is that which results in hypotension<90 mmHg or a
drop in systolic blood pressure of ≥40 mmHg from baseline for a period >15
minutes or hypotension that requires vasopressors or inotropic support
• Hemodynamically stable PE is defined as PE that does not meet the definition of
hemodynamically unstable PE. There is a spectrum of severity within this
population ranging from patients who present with small, mildly symptomatic or
asymptomatic PE (also known as "low-risk PE") to those who present with mild or
borderline hypotension that stabilizes in response to fluid therapy, or those who
present with right ventricle dysfunction (also known as "submassive" or
"intermediate-risk" PE
 The anatomic location (saddle, lobar, segmental, subsegmental) – Saddle PE
lodges at the bifurcation of the main pulmonary artery, often extending into the
right and left main pulmonary arteries. Approximately 3 to 6 percent of patients
with PE present with a saddle embolus
 Described chest radiographic signs include:
 Fleischner sign: enlarged pulmonary artery (20%)
 Hampton hump: peripheral wedge of airspace opacity and implies lung infarction
(20%)
 Westermark sign: regional oligaemia and highest positive predictive value (10%)
 pleural effusion (35%)
 knuckle sign
 Palla sign : enlarged right descending pulmonary artery
 Chang sign : dilated right descending pulmonary artery with sudden cut-off
 CT
 Acute pulmonary emboli
 CT pulmonary angiography
(CTPA) will show filling defects
within the pulmonary vasculature
with acute pulmonary emboli.
When the artery is viewed in its
axial plane the central filling
defect from the thrombus is
surrounded by a thin rim of
contrast, which has been called
the Polo Mint sign.
 IV

- bolus plus infusion

- target ptt 1.5-2.5x control apt
 Subcutaneous (apt not monitored)

 SubQ

- Enoxaparine BID or OD
- Dalteparin OD
 Fondaparinux –Subcutaneous
Contraindicated in patients with
severe renal failure
 Warfarin: After administration of
heparin; INR 2.0 to 3.0