Pulmonary embolus (PE)

Question 1

Why do PE’s occur?

Answer 1

· Consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities.

· Thrombus formation in the venous system is a result of Virchow’s triad:

1. Venous stasis.
2. Trauma / vessel wall damage.
3. Hypercoagulability.

Question 2

What is the prophylaxis of VTE?

Answer 2

· LMWH, unfractionated heparin, DOAC’s, fondaparinux.

· Compression stockings, intermittent pneumatic compression (Flotron’s).

Question 3

Which score is used to measure the clinical probability of PE?

Answer 3

Wells’ score.

Question 4

What is the epidemiology of a PE?

Answer 4

· Slightly higher incidence in black people.
· Possibly more common in men.
· More common with older age.

Question 5

What is the pathophysiology of a PE?

Answer 5

· Clots usually develop in the deep venous system and embolise.
· DVT’s are composed of fibrin and entrapped RBCs.
· Platelet aggregation is seen, not this isn’t present at the site of thrombus attachment.
· PE develops when a thrombus dislodges and becomes trapped in the pulmonary vasculature.
· This obstruction increases pulmonary vascular resistance, increasing the work of the right ventricle.
· The right ventricle compensates by increasing the heart rate using the Frank-Starling preload reserve via dilation.
· Further increases in PVR overcome the right ventricle’s compensatory mechanisms, leading to over-distension of the right ventricle.
· This increases RV end-diastolic pressure and decreases RV cardiac output.
· Decreased RV cardiac output leads to decreased LV preload.
· The LV filling and cardiac output decreases, lowering MAP and leading to hypotension and shock.

Question 6

Mortality is often due to which conditions?

Answer 6

Cardiogenic shock secondary to right-ventricular collapse.

Question 7

What is the aetiology of a PE?

Answer 7

Virchow’s triad : vessel wall damage, venous stasis, hypercoagulability.

Question 8

How does vessel wall damage lead to a PE?

Answer 8

· Endothelial damage promotes thrombus formation at the venous valves.
· Damage can result from trauma, previous DVT, surgery, venous harvest and CVC insertion.

Question 9

How does venous stasis lead to a PE?

Answer 9

· Poor blood flow and stasis promotes thrombus formation.
· Stasis and congestion result in valvular damage, further promoting thrombus formation.
· Associated with age >40 years, immobility, GA, paralysis, spinal cord injury, MI, stroke, varicose veins, CHF and COPD.

Question 10

How does hypercoagulability lead to a PE?

Answer 10

· Other inherited and acquired conditions.
· Cancer.
· High-oestrogen states - OCP, HRT, obesity, pregnancy.
· IBD.
· Nephrotic syndrome.
· Sepsis.
· Blood transfusion.
· Inherited thrombophilia - Factor V Leiden, prothrombin gene mutation, protein C and S deficiency, antithrombin deficiency and antiphospholipid antibody syndrome.

Question 11

List the common risk factors.

Answer 11

· Increasing age. 
· Diagnosis of DVT. 
· Surgery within the last 2 months. 
· Bed rest >5 days. 
· Previous VTE. 
· FHx of VTE. 
· Active malignancy. 
· Recent trauma or fracture. 
· Pregnancy/Post-natal period. 
· Lower extremity paralysis.
· Inherited thrombophilia.

Question 12

List the weak risk factors.

Answer 12

· Obesity. 
· Smoking.
· COPD.
· CHF. 
· CVC.
· Recent air travel. 
· Recent MI.

Question 13

List the common signs and symptoms related to a PE.

Answer 13

· Chest pain - pleuritic. 
· Dyspnoea. 
· Tachypnoea.
· Presyncope or syncope - larger clot and poorer prognosis. 
· Hypotension. 
· Feeling of apprehension. 
· Cough.
· Tachycardia.
· Fever. 
· Unilateral swelling/tenderness of calf. 
· Haemoptysis. 
· Elevated JVP.

Question 14

What investigations would you request if you suspected a patient had a PE?

Answer 14

· Wells' / geneva score.
· CTPA. 
· Ventilation/Perfusion (V/Q) scan.
· Coagulation studies. 
· U&Es. 
· FBC. 
· D-dimer - elevated. 
· BNP. 
· CXR. 
· ECG. 
· ABG.

Question 15

Differentials?

Answer 15

· Unstable angina. 
· STEMI/NSTEMI. 
· CAP.
· Acute bronchitis. 
· Acute CHF/asthma/COPD exacerbation. 
· Pericarditis.
· Cardiac tamponade - Beck's triad - hypotension, muffled heart sounds, elevated JVP. 
· Pneumothorax. 
· Costochondritis. 
· Panic attack.

Question 16

What are the treatment options for a PE?

Answer 16

· Respiratory support.
· IV fluids.
· Anti-coagulation - heparin and warfarin, rivaroxaban, apixaban, dabigatran, enoxaparin and warfarin.
· Vasoactive agents - if low BP - noradrenaline, dobutamine.
· Thrombolysis (alteplase) / Embolectomy.
· IVC filter.

Question 17

Complications?

Answer 17

· Acute bleeding during treatment. 
· Recurrent VTE. 
· Pulmonary infarction.
· Cardiac arrest/death. 
· Chronic thromboembolic pulmonary HTN. 
· Heparin-associated thrombocytopenia.