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RS > Session 11: Pulmonary Embolism > Flashcards

Session 11: Pulmonary Embolism Flashcards

1
Q

Definition of embolism

A

Obstruction of a blood vessel by a foreign substance or blood clot that travels through the bloodstream from a distant site, lodging in a blood vessels and plugging that vessel.

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2
Q

What is a pulmonary embolism?

A

An embolus of material that has passed through the heart on the right side and lodged in a pulmonary artery.

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3
Q

What can an embolus be?

A

Thrombus

Tumour

Air

Fat

Gas

Amniotic fluid

Bullet

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4
Q

What is this sign called?

What type of embolism is it?

A

Donut sign

Peribronchial cuffing

Fat emoblism after long bone fracture

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5
Q

Clinicals signs of fat embolism.

A

Petechial rash

Tachycardia

Fever

Hypoxaemia

CNS effects

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6
Q

Why might there be CNS effects in fat embolism?

A

Because the fat droplets can squeeze by the pulmonary vessels and end up in the brain instead.

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7
Q

What is fat embolism syndrome?

A

A triad of lung, brain and skin symptoms.

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8
Q

What is an air embolus usually caused by and where does it commonly end up?

A

Usually iatrogenic due to central venous cannulae, pulmonary artery catheters or haemodialysis catheters.

They commonly end up in the brain as cerebral air embolisms.

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9
Q

What are pulmonary embolism most commonly caused by?

A

90% of them arise from DVTs in the legs and particularly popliteal vein.

Also more proximal veins such as pelvic vein

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10
Q

Some epidemiology of PEs.

A

Third commonest cause of vascular death after MIs and stroke.

Most common cause of preventable death in hospital patients.

One of the commonest cause of unexpected death.

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11
Q

A risk factor of thromboembolism is virchow’s triad.

Explain

A

Endothelial injury

Stasis of blood

Hypercoagulability

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12
Q

Risk factors for thromboembolism.

A

Pregnancy

Prolonged immobilisation

Previous VTE

Contraceptive pill

Long haul travel

Cancer

Heart failure

Obesity

Surgery

HRT

Thrombophilia

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13
Q

Give examples of hypercoagulable conditions.

A

Antithrombin III deficiency

Protein C or Protein S deficiency or resistance

Factor V Leiden

Lupus anticoagulant

Homocystinuria

Occult neoplasm

Connective tissue disorder

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14
Q

Pathophysiology of clinical outcomes in PE.

A

Acute right ventricular overload

Respiratory failure

Pulmonary infarction

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15
Q

Explain pathophysiology of acute right ventricular overload in PE.

A

Pulmonary hypertension leading to acute right ventricular dilatation and strain.

Inotropes are released to maintain systemic BP, they cause pulmonary vasoconstriction as well further exacerbating the problem.

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16
Q

What is the main cuase of death in PE?

A

RIght sided heart failure leading to cardiogenic shock with circulatory failure and/or cardiac arrest secondary to arrythmias.

IN about one third of patients there will be a right to left shunting through a patent foramen ovale that can lead to severe hypoxaemia and an increased risk of paradoxical embolisation and stroke.

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17
Q

Pathophysiology of respiratory failure in PE.

A

Ventilation perfusion mismatch leading to low right ventricle output and a shunt with patent foramen ovale.

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18
Q

Explain the pathophysiology of pulmonary infarction in PE.

A

Small distal emboli may create areas of alveolar haemorrhage that result in haemoptysis, pleuritis, and small pleural effusion.

This is however relatively uncommon

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19
Q

Symptoms of PE.

A

Dyspnoea

Pleuritic chest pain

Cough

Substernal chest pain

Haemoptysis

Syncope

Unilateral leg pain

Fever of less than 39 degrees

Chest wall tenderns upon palpation

20
Q

Physical signs of PE

A

Tachypnoea

Rales or decreased breath sounds

Accentuated S2

Tachycardia

Fever

Diaphoresis

CLinical signs and symptoms suggesting thrombophlebitis

Lower extremity oedema

Cardiac murmur

Cyanosis

21
Q

Main dx of PE.

A

Pneumothorax

Pneumonia

Myocardial infarction

Pericarditis

Pleurisy

MSK pain

22
Q

Investigations of PE

A

Blood gases

CXR

ECG

D-dimer

Imaging

23
Q

Why are ABGs done in PE?

A

Can show hypoxaemia and hypocapnia (respiratory alkalosis) due to hyperventilation.

In a small proportion of patients arterial PaO2 may be normal.

24
Q

Why is a CXR done in PE?

A

By far the most common finding in PE is a normal CXR.

It can however be used to exclude other pathologies.

It is not a useful tool for primary diagnosis.

25
Q

Why is an ECG done in PE?

A

May show signs of right ventricular strain.

T wave inversion in the right precordial leads like V1-V4 and the inferior leads II, III and aVF.

People who have had a PE are also acutely prone to supraventricular tachyarrhythmias.

It is not useful as a primary diagnostic tool.

26
Q

Why is D-dimer assessed in PE?

A

D-dimer is a fibrin degradation product, a small protein fragment released into the blood when a thrombus is degraded by fibrinolysis.

A normal D-dimer rules out PE in those at low likelihood of having a PE.

In those with a high likelihood the negative predictive value of D-dimer is too low to use.

27
Q

What kind of imaging is used for investigating PE?

A

Pulmonary angiography

CXR

Ventilation perfusion scintigraphy

28
Q

Treatment of PE (low risk patients)

A

Oxygen

Immediate heparin (IV or subcutaneous Low molecular weight heparin)

29
Q

Treatment of PE (high risk patients)

A

Oxygen

Haemodynamic support

Respiratory support

Exogenous fibrinolytics like streptokinase

Percutaneous catheter directed thromboectomy

Surgical pulmonary embolectomy

30
Q

Heparinisation reduces mortality.

How?

A

Stops thrombus propagation in the pulmonary arteries and allows the body’s fibrinolytic system to lyse the thrombus.

It also stop the thrombus propagation at the embolic source and reduces the frequency of further pulmonary embolisms.

Does not dissolve the clot itself.

31
Q

What to watch out for in heparinisation?

A

Heparin-induced thrombocytopenia

32
Q

Explain how heparin induced thrombocytopenia might occur.

A

HIT is the most important and most frequent drug-induced immune-mediated thrombocytopenia.

The body produces antibodies to a portion of heparin that also recognise heparin-platelet complexes. The binding of the antibody to the platelets activates them and platelet clumps are formed leading to thrombi.

This results in a low platelet count and at the same time it increases the risk of thromboses.

33
Q

How to treat HIT.

A

Cessation of all formulations of heparin.

Use non-heparin based anti-coagulants

34
Q

What are patients given after the intitial heparinisation?

A

Oral anticoagulants suchs as warfarin

This is done for 3 months and indefinitely if there is cancer or no identifiable risk factor.

35
Q

What is rivaroxaban?

A

A direct oral anticoagulant that is now increasingly prescribed as it lowers the risk of bleeding.

36
Q

What is done if no form of anti-coagulation can be used?

A

An inferior vena cava filter is being put in.

37
Q

Give examples of conditions where a patient can’t be safeuly put on anticoagulative agents.

A

Oesophageal varices

Previous haemorrhagic strokes

Severe thrombocytopenia

38
Q

Outpatient prevention of DVT/PE

A

Recognise and address risk factors such as obesity, smoking and sedentary lifestyle.

Advise people with thrombophilia or any other risk factors to not travel for 4 hours.

39
Q

Inpatient prevention of DVT/PE.

A

DVT prophylaxis after surgery

DVT prophylaxis for patients with malignancy

40
Q

Golden standard for investigation of pulmonary embolism.

A

CT Pulmonary angiography

41
Q

How does rivaroxaban work?

A

Factor 10a inhibitor

42
Q

How do we decide high likelihood vs low likelihood of PE?

A

Well’s criteria

43
Q

A 32-year-old woman is brought to the emergency department 4 hours after the onset of severe shortness of breath. She has no recent history of trauma, hospital admission, or operations. She had an episode of deep venous thrombosis 10 years ago that required treatment in the hospital. Her respirations are 34/min. Pulse oximetry on room air shows an oxygen saturation of 65%. A CT Pulmonary Angiography scan shows a large filling defect in the right pulmonary artery.

Which of the following hypercoagulability disorders is the most likely underlying cause of these findings?

A) Antiplatelet antibody syndrome

(B) Antithrombin III deficiency

(C) Factor V Leiden mutation

(D) Protein C deficiency

(E) Protein S deficiency

A

Factor V Leiden mutation is the most common

44
Q

A 37-year-old woman with right lower extremity edema is evaluated because of the sudden onset of shortness of breath and pleuritic chest pain. A diagnosis of pulmonary embolism is made. Which of the following signs, if present on physical examination, would be the most specific indicator of pulmonary arterial hypertension in this patient?

– (A) Increased jugular venous pressure

– (B) P2 louder than A2

– (C) Peripheral edema

– (D) Presence of an S3

– (E) Pulmonary crackles

A

B

45
Q

3) The most common clinical sign in patients with pulmonary embolism is which of the following?

– (A) Increased jugular venous pressure

– (B) Tachypnea

– (C)Tachycardia

– (D) Substernal chest tenderness

– (E) Unilateral lower extremity oedema

A

B

46
Q

4) A 63-year-old man is brought to the emergency department because of a 4-day history of increasingly severe left leg pain and swelling of his left calf and the sudden onset of left sided pleuritic chest pain and dyspnaea.. On examination, lower extremity pulses are palpable bilaterally. The remainder of the physical examination shows no abnormalities. A CT scan of the abdomen shows a 3-cm mass in the body of the pancreas; there are liver metastases and encasement of the superior mesenteric artery. Ultrasonography of the left lower extremity shows a femoropopliteal venous clot. Which of the following is the most likely cause of this patient’s symptoms?

– (A) Peripheral artery disease with claudication

– (B) Hypercoagulability from advanced malignancy

– (C) Pneumonia with pleural effusion

– (D) Splenic artery aneurysm and embolic disease of the left lower extremity

– (E) Superior mesenteric artery syndrome

A

B

RS (28 decks)

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