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Flashcards in Pulmonary Embolus Deck (17)
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Where does a pulmonary embolus originate from?

Thrombi rarely develop de novo in the pulmonary vasculature. Clots usually form in the deep venous system of the lower extremities and embolise.

The pathophysiology is therefore directly related to that of deep vein thrombosis (DVT). DVT in the upper extremities is associated with a lower incidence of PE.



How can a pulmonary embolus be life-threatening?

  • PE occurs when a thrombus dislodges and becomes trapped in the pulmonary vasculature
  • This obstruction increases pulmonary vascular resistance (PVR), increasing the work of the right ventricle
  • The right ventricle compensates by increasing heart rate using the Frank-Starling preload reserve via dilation
  • Further increases in PVR overcome the right ventricular (RV) compensatory mechanisms, leading to over-distension of the right ventricle, increased RV end-diastolic pressure, and decreased RV cardiac output (RV decompensates)
  • Decreased RV output leads to decreased left ventricular (LV) preload
  •  As left ventricle filling and cardiac output decrease, lowered mean arterial pressure progresses to hypotension and shock
  • In previously healthy individuals, this can occur when as little as 50% of the pulmonary vasculature is occluded


What are major risk factors for developing PE?

  • major surgery (abdominal, pelvic)
  • lower limb fracture
  • late pregnancy
  • malignancy
  • previous VTE
  • reduced mobility


What are the symptoms of PE?

  • acute dyspnoea
  • pleuritic, stabbing chest pain
  • haemoptysis
  • dizziness
  • syncope


What signs are looked for in clinical examination for PE?

  • pyrexia 
  • tachypnoea
  • tachycardia 
  • cyanosis
  • hypotension
  • raised JVP
  • pleural rub
  • pleural effusion


What is the pathophysiology of a massive PE?

  • due to massive embolus occluding proximal pulm artery or the pulmonary artery bifurcation ('saddle embolus')
  • -> blood cannot enter lungs
  • -> sudden inc in resistance to pulmonary BF
  • -> sudden pulmonary hypertension
  • right side of heart doesn't have time to compensate
  • -> onset of acute right heart failure (cor pulmonale)
  • also, blood cannot pass through lungs -> decreased filling of left side of heart + therefore decreased left ventricular output
  • presents as haemodynamic compromise in form of shock, collapse + sudden death


What are the signs and symptoms of a massive PE?

  • severe central chest pain
  • sudden onset of shock
  • pale + sweaty
  • marked tachypnoea + tachycardia
  • hypotensive
  • central cyanosis
  • right ventricular heave
  • raised JVP
  • accentuated S2 + a gallop rhythm
  • syncope


What is the Wells criteria?

  • calculated in pts w/ suspected PE
  • clinical probability score alone is not enough to diagnose or exclude PE - must be combined w/ other tests
  • if Wells' score suggests PE unlikely, then do a D-dimer


What are important investigations for PE?

  • ECG -> may show tachycardia, new right axis deviation, new right bundle branch block, S wave in lead I, Q wave with T-wave inversion in lead III
  • CXR -> band atelectasis, elevation of hemidiaphragm, prominent central pulmonary artery, oligaemia at site of embolism 
  • ABG -> hypoxia + hypocapnia (T1 RF)
  • Cardiac troponins + BNP -> elevated
  • Plasma D-Dimer -> elevated
  • V/Q scan 
  • CTPA (gold std) -> direct visualisation of thrombus in pulm artery; appears partial or complete intraluminal filling defect
  • USS -> clots in pelvic/ileofemoral veins
  • MRI -> if CTPA contraindicated
  • Echocardiography -> right ventricular dysfunction


What is the investigation of choice for a massive PE?

  • CTPA or echocardiography
  • imaging should be performed within 1 hour in massive PE


What is the use of a ventilation/perfusion scan in diagnosing PE?

  • good diagnostic investigation, widely available
  • pulmonary embolus is suggestive when:
    • pulmonary 99mTc scintigraphy demonstrates under-perfused areas
    • but not accompanied by a ventilation defect scintigram performed after inhalation of radioactive xenon gas
  • test reported as a probability (low, medium, high) of PE
  • interpreted in context of history, exam + other ix
  • normal V/Q scan has a negative predictive value of 97%


PE: CTPA or V/Q scan?

British thoracic society + NICE:

  • CTPA now recommended initial lung-imaging modality for non-massive PE
  • advantages compared to V/Q = speed, easier to perform out-of-hours, reduced need for futher imaging + possiblity of providing an alternative diagnosis if PE excluded
  • if CTPA negative, pts do not need further investigations or treatment for PE
  • V/Q scanning may be used initially if appropriate facilities exist, the CXR is normal and there is no significant symptomatic concurrent cardiopulmonary disease


What do the BTS guidelines recommend about use of D-dimer for diagnosing PE?

  • blood D-dimer assay should only be considered following assessment of clinical probability
  • D-dimer assay should not be performed in those w/ high clinical probability of PE
  • a negative D-dimer test reliably excludes PE in patients w/ low or intermediate clinical probability; such pts do not require imaging for VTE
  • each hospital should provide info on sensitivity + specficitiy of its D-dimer test


What is the urgent, acute management for PE?

  • Assess for signs of haemodynamic instability (ABCDE)
  • if unstable → urgent primary reperfusion
  • ? High-risk (massive/central) PE
  • Seek snr support + escalate to critical care if above suspected
  • If pt peri/cardiac-arrest, PE suspected → thrombolysis immediately without waiting for results of investigations
  • If systolic BP < 90 mmHg +/- JVP elevated 
    • fluids → normal saline / Hartmann's: < 500 mL / 15-30 mins
    • monitor for HF signs (acute RV failure + hypotension leading cause of death in pts w/ high risk of PE)
  • Target O2 94-98%, high-flow + mechanical ventilation if pt extremely unstable - monitor BP
  • Give anticoagulation early if indicated (caution w/ renal impairment, active cancer + pregnancy)


What is the anticoagulation management of pulmonary embolism?

  • high-flow oxygen (60-100%), bed rest, analgesia
  • first-line anti coag → offer apixaban (7d) or rivaroxaban (3w)
  • if DOACs unsuitable → low-molecular-weight heparin 5 days followed by dabigatran or edoxaban OR LMWH concurrently w/ vitamin K antagonist (warfarin) for at least 5 days
  • if haemodynamic instability → unfractionated heparin best
  • aim INR 2.0-3.0 
  • warfarin continued for at least 3/12 -> assess risk + benefits
  • extend warfarin beyond 3/12 for pts w/ unprovoked PE
  • thrombolysis recommended as first-line tx for massive PE where there is circulatory failure - alteplase/reteplase
  • vena cava filter - in pts who develop emboli despite adequate anticoag
  • surgical embolectomy

NICE CKS on how to manage oral anticoagulants


What is the first-line treatment for a massive PE?

  • thrombolysis first-line Rx for massive PE
  • may be instituted on clinical grounds alone if cardiac arrest imminent
  • a 50 mg bolus of alteplase is recommended
  • invasive approaches (thrombus fragmentation and IVC filter insertion) should be considered where facilities and expertise are readily available


The third presentation of pulmonary embolsim is in the form of recurrent small PEs, having mentioned non-massive and massive PEs.

What are recurrent small PEs?

  • each individual episode is usually subclinical (ie does not result in symptoms)
  • but over time, the multiple small emboli occlude arterioles 
  • resulting in gradual occlusion of pulmonary arterial bed
  • leading to gradual development of pulmonary hypertension
  • bc onset is gradual, heart has time to undergo compensatory RVH
  • eventually RV will decompensate + RHF (cor pulmonale) ensues