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Y3 Medicine: Respiratory > Pulmonary Embolism > Flashcards

Pulmonary Embolism Flashcards

1
Q

What is a pulmonary embolism?

A

A consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities. Approximately 51% of deep venous thrombi will embolise to the pulmonary vasculature, resulting in a PE.

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2
Q

What is Virchow’s triad?

A

Triad of factors that predispose to thrombus formation in the venous system:

  1. Venous stasis
  2. Trauma
  3. Hypercoagulability
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3
Q

What are the risk factors for pulmonary embolism?

A
  • Increasing age
  • Diagnosis of deep vein thrombosis
  • Surgery within the last 2 months
  • Bed rest > 5 days
  • Previous thromboembolic event
  • Active malignancy
  • Pregnancy
  • Combined oral contraception (COCP)
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4
Q

What are the symptoms of PE?

A
  • Dyspnoea
  • Tachypnoea
  • Chest pain
  • Cough and haemoptysis
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5
Q

What are the signs of PE?

A
  • Tachycardia
  • Hypotension
  • Hypoxaemia
  • Signs of DVT (e.g. typically pain and swelling in one leg)
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6
Q

Describe the chest pain experienced in a pulmonary embolism

A

Acute pleuritic chest pain worse on inspiration. The pain is normally localised to one side of the chest.

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7
Q

What investigations should be ordered for a PE?

A
  • Computed tomographic pulmonary angiography (CTPA)
  • Echocardiography
  • D-dimer
  • FBC
  • ECG
  • Urea and electrolytes
  • Coagulation studies
  • LFTs
  • VQ scan
  • ABG
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8
Q

What is the definitive investigation used to diagnose a PE?

A

Computed tomographic pulmonary angiography (CTPA)

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9
Q

Why investigate computed tomographic pulmonary angiography (CTPA)? And what may this show?

A
  • Preferred investigation for definitive confirmation of PE.
  • PE is confirmed by direct visualisation of thrombus in a pulmonary artery; appears as a partial or complete intraluminal filling defect.
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10
Q

Why investigate echocardiography? And what may this show?

A
  • Use echocardiography for haemodynamically unstable patients who cannot have CTPA.
  • The presence of any signs of right ventricular (RV) dysfunction is sufficiently suggestive of PE to confirm the diagnosis and justify urgent reperfusion treatment (usually thrombolysis).
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11
Q

Why investigate D-dimer? And what may this show?

A
  • Use a clinical probability score to determine whether a patient needs D-dimer testing.
    Request D-dimer testing in any haemodynamically stable patient whose Wells (or Geneva) score categorises them as ‘PE unlikely’.
  • Elevated (typically >500 ng/mL).
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12
Q

Why investigate FBC? And what may this show?

A
  • May indicate thrombocytopenia or anaemia. These patients are at an increased risk of complications from bleeding when taking an anticoagulant.
  • Baseline values.
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13
Q

Why investigate ECG? And what may this show?

A
  • An ECG is not diagnostic of PE but can be useful to support the diagnosis of PE or rule out other causes.
  • Various presentations:
    • Normal sinus rhythm
    • Sinus tachycardia
    • New right bundle branch block (complete or incomplete)
    • QR pattern in V1
    • S1Q3T3 pattern
    • T wave inversion in V1-V4
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14
Q

Why investigate urea and electrolytes? And what may this show?

A
  • Check baseline renal function. Doses of some anticoagulants (e.g., low molecular weight heparin, fondaparinux, apixaban, rivaroxaban, dabigatran, edoxaban) may need to be adjusted in patients with renal impairment.
  • Baseline values.
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15
Q

Why investigate coagulation studies? What may this show?

A
  • Order international normalised ratio (INR), prothrombin time (PT), and activated partial thromboplastin time (aPTT). These are needed to establish baseline values before starting anticoagulation.
  • Baseline values.
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16
Q

Why investigate LFTs? And what may this show?

A
  • Abnormal LFTs can influence the choice of anticoagulation.
  • Baseline values.
17
Q

Briefly describe the use of a ventilation-perfusion (VQ) scan

A

Ventilation-perfusion (VQ) scan involves using radioactive isotopes and a gamma camera to compare the ventilation with the perfusion of the lungs. They are used in patients with renal impairment, contrast allergy or at risk from radiation where a CTPA is unsuitable.

First, the isotopes are inhaled to fill the lungs and a picture is taken to demonstrate ventilation. Next a contrast containing isotopes is injected and a picture is taken to demonstrate perfusion. The two pictures are then compared. With a pulmonary embolism there will be a deficit in perfusion as the thrombus blocks blood flow to the lung tissue. This area of lung tissue will be ventilated but not perfused.

18
Q

How does PE affect an ABG? And why?

A

Patients with a pulmonary embolism often have a respiratory alkalosis when an ABG is performed. This is because the high respiratory rate causes them to “blow off” extra CO2. As a result of the low CO2, the blood becomes alkalotic.

It is one of the few causes of a respiratory alkalosis, the other main cause being hyperventilation syndrome. Patients with a PE will have a low pO2 whereas patients with hyperventilation syndrome will have a high pO2.

19
Q

What scoring system is used to identify PE?

A

Wells Score

20
Q

Briefly describe the Wells Score

A

Assessing the clinical probability of a PE:

  • Clinical signs of DVT (3)
  • HR >100 BPM (1.5)
  • Surgery or immobilisation within 4 weeks (1.5)
  • Previous PE or DVT (1.5)
  • Haemoptysis (1)
  • Active cancer (1)
  • Alternative diagnosis less likely than PE (3)

Interpretation:

  • Score >4→ immediate CTPA or treat empirically
  • Score <4→ do D-dimer
21
Q

What scoring system is used to assess bleeding in PE?

A

HAS-BLED

22
Q

Briefly describe the treatment for PE

A
  • Anti-coagulation
  • Thrombolysis
23
Q

What anti-coagulants are used in an acute PE?

A

Start LMWH or unfractionated heparin (UFH) prior to thrombolysis. Continue anticoagulation with UFH for several hours after the end of thrombolysis before switching to apixaban or rivaroxaban.

24
Q

Briefly describe thrombolysis

When is it used?

A

Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous.

Where there is a massive PE with haemodynamic compromise there is a treatment option called thrombolysis. It is only used in patients with a massive PE where the benefits outweigh the risks.

25
Q

What drugs are used as thrombolytics in PE?

A
  • Alteplase
  • Streptokinase
  • Urokinase
26
Q

If thrombolysis is contra-indicated, what are the other treatment options for PE?

A

Surgical embolectomy or percutaneous catheter-directed therapy.

27
Q

Give exampls of low-molecular weight heparins (LMWH)

A

Enoxaparin and dalteparin

28
Q

Briefly describe the long-term management of PE

A

Continue anticoagulation for at least 3 months for all patients with PE. DOACs have emerged as an equally effective and safer option than heparin/warfarin.

29
Q

How long is anti-coagulation required for following a PE?

A

3 months if there is an obvious reversible cause (then review).

Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.

6 months in active cancer (then review).

30
Q

What are the 2 different ways in which thrombolysis can be performed?

A

There are two ways thrombolysis can be performed:

  1. Intravenously using a peripheral cannula
  2. Directly into the pulmonary arteries using a central catheter (this is called catheter-directed thrombolysis)
31
Q

Briefly describe catheter-directed thrombolysis

A

In catheter-directed thrombolysis a catheter is inserted into the venous system, through the right side of the heart and in to the pulmonary arteries. The operator can then administer the thrombolytic agent directly into the location of the thrombus. Special equipment can also be used to physically break down the thrombus and aspirate it. There is a risk of damaging the pulmonary arteries doing this.

32
Q

What are the complications of PE?

A
  • Acute bleeding during event
  • Pulmonary infarction
  • Cardiac arrest/ death
  • Recurrent venous thromboembolic event
33
Q

What differentials should be considered for PE?

A
  1. Unstable angina
  2. STEMI
  3. NSTEMI
  4. Pneumonia
34
Q

How does PE and unstable angina differ?

A

Differentiating signs and symptoms:

  • Typical cardiac chest pain is described as a retrosternal pressure or heaviness radiating to the jaw, arm, or neck
  • Pain may be intermittent or persistent
  • Differentiating risk factors include long-standing hypertension, diabetes, or hypercholesterolaemia
  • Can be difficult to differentiate from PE on the basis of signs and symptoms alone

Differentiating investigations:

  • ST segment depression in contiguous leads on ECG
  • Normal troponin I or T. These tests may be elevated in PE. Negative diagnostic imaging study for PE
  • Critical stenosis of a coronary artery on coronary angiography
35
Q

How does PE and NSTEMI differ?

A

Differentiaing signs and symptoms:

  • Presents with central chest pain that is classically heavy in nature, like a sensation of pressure or squeezing
  • Examination findings are variable and range from normal to a critically ill patient in cardiogenic shock
  • Often difficult to differentiate from PE in acute setting

Differentiating investigations:

  • ECG does not show ST-elevation but serum levels of cardiac biomarkers are raised
  • ECG may show non-specific ischaemic changes such as ST depression or T wave inversion
  • May see bilateral increased pulmonary vascular congestion on chest radiograph consistent with congestive heart failure (CHF)
  • Elevated troponin I or T (note: these may also be elevated in the setting of PE)
  • Regional wall motion abnormality of the left ventricle on echocardiography
36
Q

How does PE and STEMI differ?

A

Differentiating signs and symptoms:

  • Presents with central chest pain that is classically heavy in nature, like a sensation of pressure or squeezing
  • Examination findings are variable and range from normal to a critically ill patient in cardiogenic shock
  • Often difficult to differentiate from PE in acute setting

Differentiating investigations:

  • STEMI is diagnosed by persistent ST segment elevation in 2 or more anatomically contiguous ECG leads in a patient with a consistent clinical history
  • Elevated troponin I or T (note: can also be elevated in PE)
  • Regional wall motion abnormality of the left ventricle on echocardiography
  • Critical stenosis of a coronary artery on coronary angiography
37
Q

How does PE and pneumonia differ?

Note: community acquired

A

Differentiating signs and symptoms:

  • May be difficult to differentiate on the basis of signs and symptoms
  • Cough productive of purulent sputum
  • Fever above 39.0°C; generally higher than in PE

Differentiating investigations:

  • White blood cell (WBC) count normally >11 x 10⁹/L (>11,000/microlitre)
  • Chest x-ray (CXR) may show a focal opacity and other features of pneumonic consolidation (note: this can also be seen with PE)
  • Sputum culture grows an organism known to cause pneumonia
  • Negative diagnostic imaging study for PE

Y3 Medicine: Respiratory (15 decks)

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