Pulmonary Embolism (PE) Flashcards

1
Q

what is a pulmonary embolism (PE)?

A

the luminal obstruction of one or more pulmonary arteries by an embolised venous thrombus, but can also be due to an embolised solid, liquid, or gas

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2
Q

what is the difference between a thrombus and an embolism?

A
  • a thrombus refers to a blood clot that is formed within a blood vessel and remains in its place of origin
  • embolism describes the process where the bloodstream carries a detached intravascular solid, liquid, or gaseous mass from its origin to a distant site
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3
Q

what is the aetiology of a PE?

A
  • DVT (e.g. calf)
  • fat embolism
  • air embolism
  • amniotic fluid embolism
  • septic emboli
  • de novo thrombosis
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4
Q

what are the pathological consequences of a PE?

A
  • ventilation/perfusion mismatch → impaired gaseous exchange → hypoxaemia (type 1 respiratory failure) and tachypnoea
  • pulmonary arterial hypertension (e.g. due to increased pulmonary vasculature resistance) → right ventricular overload +/- dysfunction
  • pleural and lung inflammation and infarction → pleuritic chest pain +/- haemoptysis
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5
Q

what is the virchow’s triad for VTE?

A
  • venous stasis: prolonged immobilisation (e.g. bed rest >5 days, major surgery within the last 2 months, recent trauma or fracture, paralysis of the lower limb, long-haul flights), venous insufficiency of the lower limb
  • hypercoagulable state: active malignancy, pregnancy and postnatal period, thrombophilia (e.g. antiphospholipid syndrome), use of combined hormonal contraception and oral hormone replacement therapy
  • endothelial injury: trauma, surgery, venous harvest, cigarette smoking, obesity
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6
Q

what are the symptoms of a PE?

A
  • dyspnoea
  • tachypnoea
  • pleuritic chest pain
  • features of concurrent DVT (e.g. unilateral red, painful swollen leg)
  • haemoptysis
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7
Q

what are the findings on examination of a PE?

A
  • tachycardia
  • tachypnoea
  • hypoxia
  • low-grade fever
  • pleural rub
  • gallop rhythm (e.g. a wide split-second heart sound and tricuspid regurgitant murmur)
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8
Q

what are the features of a massive PE?

A
  • haemodynamic instability (e.g. hypotension, cardiogenic shock)
  • presyncope/syncope
  • elevated JVP
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9
Q

what are the investigations for a PE?

A
  • respiratory examination
  • cardiovascular examination
  • 12-lead ECG
  • D-dimer
  • FBC
  • U&Es
  • LFTs
  • cardiac biomarkers (e.g. troponin, BNP)
  • coagulation
  • CXR
  • CTPA
  • ? V/Q planar scan/SPECT
  • ? echocardiogram
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10
Q

what may an ECG show in a PE?

A
  • sinus tachycardia
  • right ventricular strain pattern (e.g. T wave inversion in anterior leads (V1-V4) +/- inferior leads (II, III, aVF))
  • RBBB
  • RAD
  • the classic ‘S1Q3T3’ ECG change is only seen in <20% patients (e.g. large S wave in lead I, large Q wave in lead III, and inverted T wave in lead III)
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11
Q

D-dimer test has a high sensitivity but low specificity for VTE. which conditions can result in an elevated D-dimer in the absence of VTE?

A
  • pregnancy
  • malignancy
  • liver disease
  • severe infection/inflammatory disease
  • DIC
  • recent trauma/surgery/hospitalised patients
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12
Q

what are the possible findings of a CXR in a PE?

A
  • most patients with PE have a normal CXR
  • wedge-shaped pulmonary infarction
  • atelectasis
  • pleural effusion
  • raised hemidiaphragm
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13
Q

what is the alternative to CTPA in the diagnosis of PE?

A

ventilation-perfusion (V/Q) planar scan or SPECT

  • severe renal impairment (eGFR < 30 mL/min/1.73m2)
  • allergic to contrast media
  • at high risk from irradiation (e.g. pregnancy)
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14
Q

which investigation is recommended to aid the diagnosis of a PE in hemodynamically unstable patients?

A

echocardiography may show signs of right ventricular dysfunction that is suggestive of PE, including:

  • abnormal right ventricular ejection pattern (e.g. 60/60 sign)
  • mcconnel sign (e.g. reduced right ventricular free wall contractility compared with the apex)
  • right ventricular dilation and hypokinesis
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15
Q

what is the management of a PE (e.g. wells ≤4)?

A
  • D-dimer
  • if the D-dimer test result cannot be obtained within 4 hours, start interim therapeutic anticoagulation
  • if the D-dimer test is positive: offer immediate CTPA and give interim therapeutic anticoagulation if there is a delay
  • if the D-dimer test is negative: stop any interim therapeutic anticoagulation
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16
Q

what is the management of a confirmed PE with haemodynamic instability?

A

offer continuous UFH infusion, and consider thrombolytic therapy:

  • IV tissue plasminogen activator (tPA) (e.g. alteplase)
  • catheter-directed thrombolysis
  • open pulmonary embolectomy
17
Q

when can outpatient treatment be considered for low-risk PE according to NICE?

A
  • outpatient treatment for low-risk PE can be considered if a validated risk stratification tool determines suitability (e.g. PESI)
  • haemodynamic stability is a requirement
18
Q

what is the management of a confirmed PE without haemodynamic instability?

A
  • 1st-line: apixaban/rivaroxaban
  • 2nd-line: LMWH + dabigatran/edoxaban OR LMWH + warfarin
19
Q

how does the choice of anticoagulants vary in specific patient populations?

A
  • pregnant: LMWH only
  • active cancer: DOAC preferred over LMWH
  • severe renal impairment (eGFR < 15 mL/min/1.73m2): UFH or dose-adjusted LMWH
  • APS: initial LMWH and warfarin followed by warfarin monotherapy
  • all forms of anticoagulation contraindicated: inferior vena cava (IVC) filter
20
Q

what are NICE recommendations for anticoagulation duration in VTE patients?

A
  • minimum of 3 months of anticoagulation for all patients
  • further anticoagulation depends on the risk of: VTE recurrence + bleeding (e.g. ORBIT score)
21
Q

what is the rule of thumb for anticoagulation duration based on VTE type?

A
  • provoked: 3 months
  • unprovoked: 6 months
  • active cancer: 3-6 months
22
Q

what is the difference between a provoked and unprovoked PE?

A
  • provoked: associated with a recent (e.g. within 3 months) transient major risk factor
  • unprovoked: no recent (e.g. within 3 months) transient major risk factor + not using hormonal therapy
23
Q

what are the short-term complications of a PE?

A
  • sudden cardiac arrest/death (e.g. due to ventricular collapse due to massive embolism and occlusion of the pulmonary vasculature)
  • pulmonary infarction
  • right ventricular infarction (e.g. due to pulmonary hypertension and haemodynamic overload)
  • atelectasis
  • exudative pleural effusion
24
Q

what are the long-term complications of a PE?

A
  • increased risk of recurrence
  • chronic thromboembolic pulmonary hypertension (CTEPH)
25
Q

what is chronic thromboembolic pulmonary hypertension (CTEPH)?

A

occurs where fibrotic tissue replaces residual emboli causing chronic obstruction of the pulmonary vasculature, and hence pulmonary hypertension