Pulmonary embolism Flashcards

1
Q

What is pulmonary embolism?

A

Occlusion of pulmonary vessels, most commonly by a thrombus that has travelled from another site.

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2
Q

What is the aetiology of PE? (x7)

A

• Over 95% originate from DVT of lower limbs • Rarely from right atrium in AF • Other agents that can embolise include amniotic fluid embolus, air embolus, fat emboli, tumour emboli and mycotic emboli (fungal)

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3
Q

What are the risk factors for PE? (x8)

A

Surgical patients, immobility, obesity, OCP (oral contraceptive pill), heart failure, malignancy, pregnancy, and post partum.

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4
Q

What is the pathophysiology of pulmonary thromboembolism?

A

Thrombus formation from venous stasis, vessel wall damage, and hypercoagulability (Virchow’s triad).

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5
Q

What are the types of pulmonary embolism?

A

Massive (SBP less than 90), and submassive (not hypotensive, but usually evidence right heart dysfunction or myocardial injury signs such as elevated troponin)

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6
Q

What is saddle pulmonary embolism?

A

Embolism becomes lodged in bifurcation of artery.

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7
Q

What is the effect of PE on the heart?

A

Embolism increases pulmonary vascular resistance which leads to right ventricular distension and eventually decreased RV output. This leads to decreased LV preload leading to hypotension and shock.

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8
Q

What is the epidemiology of PE: Proportion of DVT population?

A

Occur in 10-20% of those with confirmed proximal DVT.

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9
Q

!!! What are the symptoms of PE: Small? Moderate? Large? Proximal? Multiple small recurrent?

A

• Depends on size and site • SMALL: may be asymptomatic • MODERATE: sudden onset dyspnoea, cough, haemoptysis, pleuritic chest pain • LARGE or PROXIMAL: all of the above plus central pleuritic chest pain, shock, collapse, right heart failure, or sudden death. • MULTIPLE SMALL RECURRENT: symptoms of pulmonary hypertension

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10
Q

!!! What are the signs of PE: Small? Moderate? Large? Proximal? Multiple small recurrent?

A
  • SMALL: earliest sign if tachycardia or tachypnoea
  • MODERATE: tachypnoea, TACHYCARDIA, pleural rub, low oxygen saturation despite oxygen saturation
  • LARGE or PROXIMAL: shock, cyanosis, signs of right heart strain such as raised JVP, left parasternal heave and accentuated S2 heart sound
  • MULTIPLE SMALL RECURRENT: signs of pulmonary hypertension and right heart failure
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11
Q

What clinical probability assessments can be used for PE? (x2)

A

Well’s score and Revised Geneva score

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12
Q

What is Well’s score? Interpretation?

A

Based on signs and risk factors. Higher than 4 indicates high probability of PE, while 4 or less indicates that PE is unlikely.

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13
Q

What is the Revised Geneva score?

A

Based on signs and risk factors. 11 or higher indicates high probability, 4-10 intermediate probability and 3 or lower low probability of PE.

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14
Q

What are the investigations for PE when low probability?

A

D-dimer blood test (fibrin degradation products). If negative, then PE can be ruled out.

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15
Q

!!! What are the investigations for PE when high probability? But first?

A

• Start anticoagulation, then… • Spiral CT pulmonary angiogram: sensitive to medium/large emboli

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16
Q

What other imaging methods are there for PE? (x4)

A
  • Ventilation-perfusion (VQ) scan: administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas. This identifies areas of ventilation and perfusion mismatch that would indicate infected lung
  • Pulmonary angiography: gold standard but invasive
  • Doppler USS of the lower limb: for venous thrombosis (should be performed when Well’s score predicts high risk)
  • Echocardiogram: may show right heart strain
17
Q

How do you investigate PE if CTPA is contraindicated?

A

For example, contraindicated in pregnant women because of radiation, or in someone allergic to the contrast.

Instead, you can do a V:Q - ventilation:perfusion lung imaging.

18
Q

What may ECG show in PE? (x4)

A

Tachycardia, right axis deviation or RBBB. Classical SI, QIII, TIII pattern is relatively uncommon but highly indicative of right heart strain in PE (large S wave in QRS complex in lead I, large Q wave in lead III and inverted T wave in lead III).

19
Q

How is PE managed if haemodynamically stable? (x3)

A
  • Oxygen
  • Anticoagulation with subcutaneous heparin or LMWH, and then warfarin loading (INR 2-3) for a minimum of 3 months
  • Analgesics for pain
20
Q

How is PE managed if haemodynamically unstable? (x5)

A

• Give oxygen • IV fluid resuscitation – treat hypotension and shock • Anticoagulation with subcutaneous heparin • Thrombolysis with tPA if cardiac arrest is imminent • Vasotive drug such as noradrenaline is anticoagulation and thrombolysis contraindicated

21
Q

What are surgical interventions for PE and their indications? (x2)

A
  • Embolectomy when thrombolysis contraindicated
  • IVC filters (aka Greenfield filter) for recurrent pulmonary emboli despite adequate anticoagulation or when anticoagulation is contraindicated
22
Q

What is primary prevention for PE? (x4)

A

Graduated pressure stockings (TEDs) and heparin prophylaxis in those at risk (e.g., undergoing surgery). Early mobilisation and adequate hydration post-surgery.

23
Q

What are the complications of PE? (x3)

A

Pulmonary infarction, pulmonary hypertension, right heart failure.

24
Q

What is the prognosis of PE?

A

30% untreated mortality, 8% with treatment due to recurrent emboli or underlying disease.

25
Q

How is DVT investigated?

A

Well’s score for DVT is calculated, and low probability (less than 2) means D-dimer, and high probability (more than or equal to 2) means proceed to Doppler scan.

26
Q

What is meant by warfarin loading in PE management, and how long are patients on warfarin? When is LMWH stopped?

A

Once the INR has stabilized, usually between a therapeutic range of 2–3, the low molecular weight heparin may be stopped and the patient is to continue on warfarin for a minimum of three months. If this is a first presentation of pulmonary embolism, treatment usually ranges from three to SIX months. If there is a recurrent history of pulmonary embolism, the patient will usually stay on warfarin for life. Patients who have pulmonary emboli secondary to a malignant process (e.g. ovarian carcinoma, bronchogenic carcinoma) will usually be on life-long treatment dose low molecular weight heparin as studies have shown improved anti-coagulation when compared to warfarin.