Acute Pulmonary Embolism

When a vessel in the body in constricted by any substance, a part of this substance
called embolus, migrates in a pulmonary artery. This creates a blockage that limits
any exchange between the blood and lung. This condition is called an embolism.

CAUSES OF ACUTE PULMONARY EMBOLISM

DEEP VEIN THROMBOSIS (DVT)

MOST COMMON CAUSE OF PE

A part of thrombus (blood clot) present in the deep veins, most commonly lower
limbs, breaks off and travels to a pulmonary artery.

Risk factors for DVT: Virchow’s triad

Stasis of blood flow
Muscular activity helps with blood flow,
thus, muscular inactivity is a risk factor for stasis
➔ muscular inactivity:
Post-surgery, fracture, post-CVR paralysis, long travel (>= 8h plane, car)
➔ venous valves:
Varicose veins (incompetent, leaky valves). Blood backflow -> stasis
➔ compression of vein
o Pregnancy (uterus compresses iliac vein)
o May-Turner syndrome (right iliac artery compresses left iliac artery)
o Obesity (fatty tissue compresses veins)

Vessel wall (endothelial injury)

o physical injury: trauma, surgery, vascular catheter
o chemical injury: Exposure to toxins or medication (eg. smoking)
o inflammation: eg. vasculitis
o infection: some infections damage the endothelium
o radiation: during medical treatments
o atherosclerosis: hypertension and obesity are risk factors
Hypercoagulability:
1Genetic causes
a.increase in procoagulant enzymes
-Factor V Leiden
-Prothrombin gene mutation (precursor of thrombin)
b.decrease in anticoagulant enzymes
-Protein C/S deficiency
-Antithrombin III deficiency
- Heparin induced thrombocytopenia (HIT) antibodies interacts with platelet factor IV
in response to heparin, forming blood clot.

2.Acquired causes
a.increase in procoagulant enzymes
-Estrogen increased (from pregnancy or OCP medication)
-Lung cancers/pancreatic cancers are associated increase of procoagulant activity

b.decrease in anticoagulant enzymes

-Nephrotic syndrome (causes excretion of antithrombin III)
-Antiphospholipid syndrome (antibodies attack protein C/S and phospholipid)
Age is also a risk factor for PE

OTHER CAUSES OF ACUTE PULMONARY EMBOLISM

-gas embolism: bubble forming in pulmonary artery, common in scuba diving due to
the sudden change of pressure of the water
-fat embolism: in long bones fracture, fat globules within the medullary cavity of the
bone can enter the circulation and create a pulmonary embolism
-amniotic embolism: leak of amniotic fluid in pregnant women, some of the proteins
acts as embolus
-sceptic embolism: common in IV dugs abuser, tricuspid valve site of vegetation
Pathophysiology
Embolus comes from deep vein of lower limb, passes through inferior or superior
veina cava, it arrives at right atrium and passes to the right ventricle. From the
right ventricle it goes to the pulmonary trunk.

Then it blocks one of these:

➔ right pulmonary artery
➔ left pulmonary artery
➔ pulmonary trunk (saddle embolism -> sudden death)
➔ smaller arteries
All the circulation following the blockage are affected
Increase of pressure
➔ Increased pulmonary vascular resistance
➔ increase pulmonary artery pressure (back flow to right side of the heart)
➔ increase right ventricular pressure
➔ pulmonary heart disease (col pulmonale)
decrease Stroke Volume -> decrease Cardiac Output -> decrease Blood Pressure

Ventilation/perfusion
In alveoli, ventilation is normal but perfusion is low.
O2 level is decreased leading to hypoxemia
➔ Hypoxemia -> Dyspnea
➔ tachypnea
➔ decrease CO2 level -> V/q mismatch
➔ PH increase
➔ respiratory alkalosis
clinical features
-tachypnea/dyspnea
-tachycardia
-chest pain
-hypotension
-signs of DVT:
-asymmetric swollen and redness (eg. edema)
-pain in leg
-hard/sore veins
Diagnosis
Well’s score

If PE unlikely
Do D-Dimer assay
➔ positive -> do CT
➔ negative -> no PE

if PE likely
do CT
➔ positive -> PE confirmed
➔ negative -> no PE
➔ unsure -> DO FURTHER TESTS

D-dimer assay : D-Dimer is a small protein present in blood after blood clot is
degraded. The test is used for PE diagnosis

Arterial blood gas

➔ O2 is decreased -> hypoxemia
➔ CO2 is decreased = pH increased = Pulmonary Embolism
Tests
CT pulmonary angiography
➔ definitive test
➔ shows decrease in blood supply

Chest x-ray
➔ usually normal
➔ common findings
o enlarged pulmonary artery
o wedge opacity
o elevated diaphragm
o pleural effusion
EKG
➔ used to exclude MI and pericarditis
➔ usually normal
➔ common findings include
o Sinus tachycardia
o Right ventricular strain om V1-V4 (inversion of T-wave)
o S1Q3T3 on lead 1 and lead 3 (lead 1 deep 5 wave, lead 3 deep Q and
T wave)
Treatment
If patient has submassive PE (hemodynamically stable)
➔ Anticoagulant
If contraindicated.
▪ do Inferior vena cava filter

If patient has a massive PE (hemodynamically unstable)

➔ Thrombolytics
If contraindicated.
▪ do Embolectomy

Medications
Anticoagulants (prevent blood clot formation)
➔ Heparin
o Unfractionated heparin
▪ IV
▪ APTT monitored
▪ Hospitalized

o Low weight molecular heparin

▪ Subcutaneous
▪ Often serves as a bridge

➔ Warfarin
o Warfarin K antagonist
o Taken orally
o Needs 5 days to begin
o INR monitored

➔ Thrombolytics
o Breaks down blood clots
o Has a risk of second hemorrhage
o Used on massive PE patients

Surgery and interventions

➔ Inferior vena cava filter (catheter used to clear through inferior vena cava)
➔ Embolectomy (surgery to remove embolus from pulmonary artery)