Pulmonary Embolism Flashcards

1
Q

What is pulmonary embolism?

A

Pulmonary embolism is characterized by embolization, usually of thrombi (90-95% of PE is due to clots), but there are also emboli which are due to fat (PE due to fat occurs typically in case of orthopaedic surgery), or air. The thrombus is usually located in the peripheral veins (e.g. femoral veins, popliteal vein, etc.) and this is the source of emboli, which arrive to the pulmonary artery and can occlude pulmonary arteries peripherally or centrally. The more it’s central the more severe are the hemodynamic consequences. Peripheral pulmonary emboli can sometimes be asymptomatic or with few symptoms or subclinical.

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2
Q

What are the hemodynamic consequences of PE?

A

The thrombus obstruction causes an increase in pressure in the pulmonary artery causing an increases in RV afterload, the pressure which the RV needs to work against. This causes RV dilation, tricuspid valve regurgitation, RV ischemia, decreased contractility.
The severity of the hemodynamic response depends on the severity of the PE.

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3
Q

Risk factors for PE?

A

Hereditary factors : genetic predisposition like antithrombin deficiency, protein C deficiency, protein S deficiency.

Acquired factors : reduced mobility, advanced age, cancer, trauma, oral contraceptives.

It is important to note that 20% of patients with PE have no known risk factors, therefore lack of risk factors doesn’t exclude PE.

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4
Q

Signs and symptoms of PE? How is it diagnosed?

A

Symptoms of PE are completely aspecific : dyspnea, chest pain, cough, hemoptysis and syncope.
Signs include tachypnea, tachycardia, fever, cyanosis, signs of DVT.

Diagnosis is based on clinical signs, symptoms, ECG, lab tests and imaging.

Wells score and Geneva score take into consideration parameters and variables which must be looked into to diagnose PE.

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5
Q

ECG of pulmonary embolism?

A

Most common ECG change is tachycardia. The most specific ECG change is the S1 Q3 T3 pattern characterized by deep S wave in D1, prominent Q wave in D3 and T wave inversion in D3.

As PE causes RV dilatation the ECG could show signs of RBBB.

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6
Q

Pulmonary embolism on imaging?

A

Imaging is very important to confirm diagnosis of PE.
CXR :
Fleischner sign (20%)—> enlarged pulmonary arteries.
Westermark sign—> collapse of distal vasculature creating the appearance of a sharp cut off.
Hamptons hump—> wedge shaped infarct.

Echocardiography shows dilated RV, tricuspid regurgitation, pulmonary artery dilatation.

CT angiography shows direct visualization of the emboli and allows for RV dimension evaluation.

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7
Q

Initial stratification of risk for PE?

A

If we suspect PE in a patient we must asses if there are signs of shock or hypotension (systolic BP <90) if yes than it is classified as a high risk patient if no than not high risk patient.

In patient without shock or hypotension we evaluate clinical probability of PE, if high probability evaluate with CT angiography if low probability test D dimer using different cutoffs.

In patient with shock or hypotension we should immediately perform CT angiography, if not readily available perform echocardiography. If the patient is still unstable but there are no signs of RV overload look for other causes. If CT or echo is positive than we should start reperfusion therapy.

The evidence of indirect signs of RV overload alone is NOT ENOUGH to start reperfusion therapy as if the patient has an acute aortic syndrome reperfusion therapy will die.

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8
Q

What is D dimer? How is it used?

A

D-dimer, which is a fibrin degradation product that your body makes when a blood clot dissolves in your body. D-dimer is normally undetectable or only detectable at a very low level unless your body is forming and breaking down significant blood clots, it can also be increased in cases of cancer, sepsis and inflammation.

If a patient has a low probability score and negative D dimer test we can rule out PE with 99,5% certainty.
If a patient has a high probability score and a negative D dimer test we still cannot completely exclude PE as it was shown than around 10% of patients had VTE.

Cutoff for D dimer test should be adjusted according to age. If patient 50 or younger cutoff is 500 ng/ml, over that age if becomes patient age times 10. Ex. 78 yr old patient cutoff is 780 ng/ml.

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9
Q

What is McConnells sign?

A

It is the only specific echocardiographic sign in case of pulmonary embolism. It represents a specific pattern of regional right ventricular dysfunction characterized by akinesia of mid free wall and preservation of RV wall motion in basal and apical regions.

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10
Q

What is the PESI score?

A

PESI score is the pulmonary embolism severity index which classifies patients according to risk stratification parameter to allow physicians to choose the best therapeutic approach.

PESI class I or II—> patient with stable hemodynamic conditions and are usually discharged with anticoagulation therapy and home treatment.
PESI class III or IV—> patients with intermediate risk, patients need to be further stratified to decide suitable therapy whether it be anticoagulation therapy and/or rescue reperfusion.

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11
Q

What are some markers that are directly correlated with a worse prognosis in PE patients?

A

Troponins—> Troponin levels correlate with in-hospital mortality and clinical course in pulmonary embolism.

Brain natriuretic peptide—> BNP is useful to classify patients mid term mortality risk.

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12
Q

What are the two types of oral anticoagulation therapies used for PE patients?

A

VKA—> Vitamin K Antagonists, they are the only effective agents in patients with mechanical (valvular) prosthesis and are still used in patients with severe renal failure (GFR < 30). VKA target the synthesis
of coagulation factors II, VII, IX, X and are specific and effective.

NOAC—> New Oral AntiCoagulation agents have different targets of action :
- Factor Xa inhibitors like Apixaban, Edoxoban.
- Direct thrombin inhibitors acting on factor IIa like Dabigatran, hirudin.

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13
Q

How is chronic thromboembolic pulmonary hypertension diagnosed?

A

In a patients who has suffered from previous PE and undergone the correct therapeutic strategies withou achieving the complete resolution of the pulmonary emboli. In this case CTEPH is diagnosed bases on echocardiography.

In a patient with the same symptoms, echocardiography showing pulmonary hypertension, with no history of prior PE. A ventilation perfusion exam will be used to confirm or exclude the presence of CTEPH.

If it is rule in the only effective therapy consists in surgical removal of the thrombi, surgical thormboembolectomy.

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