11/14/24, 10\:48 AM Pulmonary Embolism (PE)

Pulmonary Embolism (PE)

Table of contents
Key points ⚡
Succinct notes to superpower your revision
Pulmonary embolism (PE)\: luminal obstruction of pulmonary arteries by an embolised thrombus, can also be solid, liquid,
or gas.
Incidence\: PE and DVT are the third most common cardiovascular diseases in the UK, with 70,000 hospital episodes and
over 35,000 admissions annually.
Pathophysiology\: embolus detaches, travels through venous system to pulmonary arteries causing luminal obstruction,
ventilation/perfusion mismatch, pulmonary hypertension, pleuritic chest pain.
Risk factors\: diagnosis of DVT, increasing age, previous VTE; venous stasis, hypercoagulable state, endothelial injury.
Symptoms\: dyspnoea, tachypnoea, pleuritic chest pain, features of DVT, haemoptysis, cough, retrosternal chest pain.
Examination
Massive PE\: haemodynamic instability, presyncope/syncope, elevated JVP.
Investigations\: ECG (sinus tachycardia, right ventricular strain), D-dimer (raised), CTPA (de
echocardiography (haemodynamically unstable patients).
Management\: ABCDE approach, two-level PE Wells score, CTPA for high probability, D-dimer for low probability,
anticoagulation therapy (DOACs, LMWH, warfarin).
Complications\: sudden cardiac arrest, pulmonary infarction, right ventricular infarction, recurrence, chronic
thromboembolic pulmonary hypertension (CTEPH).
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A comprehensive topic overview

Introduction

Pulmonary embolism (PE) is 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.
1
Venous thromboembolism (VTE) is an umbrella term encompassing both pulmonary embolism (PE) and deep vein
thrombosis (DVT).
1
In the United Kingdom (UK), PE and DVT together make up the third most common cardiovascular disease (after acute
myocardial infarction and stroke). PE has an overall annual incidence of 53-162 per 100,000 people. Nearly 70,000 hospital
episodes of PE were reported between 2021-2022, resulting in over 35,000 admissions.
2

Aetiology

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.
1
Most PEs originate as thrombi due to deep vein thrombosis, most frequently in the calf veins.
3
Other causes include\:
3
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Fat embolism
Air embolism
Amniotic
Septic emboli
De novo thrombosis (rare)

Pathophysiology

In a PE, an embolus detaches from its origin and embolises to the pulmonary arteries through the systemic venous
system and the right heart,
3,5
Pathological consequences of pulmonary embolism\:
3,5
Ventilation/perfusion mismatch → impaired gaseous exchange → hypoxaemia (type 1 respiratory failure) and
tachypnoea
Pulmonary arterial hypertension (due to increased pulmonary vasculature resistance) → right ventricular overload +/-
dysfunction
Pleural and lung in→ pleuritic chest pain +/- haemoptysis
The diagnosis of PE can be challenging, and these pathological changes do not always manifest with the above clinical
features.
Figure 1. Gross specimen showing a saddle pulmonary embolism

Risk factors

Risk factors for PE include and are not limited to\:
3,4,5
Diagnosis of DVT\: ~45-50% of people with PE have concurrent DVT
Increasing age
Previous VTE
The Virchow's triad for VTE\:
3,4,5
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
Hypercoagulable state\: active malignancy, pregnancy and postnatal period, thrombophilia (e.g. antiphospholipid
syndrome, factor V Leiden mutation), use of combined hormonal contraception and oral hormone replacement therapy.
Endothelial injury\: trauma, surgery, venous harvest, cigarette smoking, obesity.
Concurrent DVT, prolonged immobilisation and previous VTE events are strong risk factors for PE (they form part of the 2-
level PE Wells score).

Clinical features

The signs and symptoms of pulmonary embolism are highly non-speci
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History

Typical symptoms of PE may include\:
2,3,4,9
Dyspnoea\: the most common feature
Tachypnoea (~20-40% cases)
Pleuritic chest pain (~40% of cases)
Features of concurrent DVT (typically unilateral red, painful swollen leg)
Haemoptysis
Other possible symptoms include\:
2,3,4,9
Retrosternal chest pain (due to right ventricular ischaemia)
Cough

Clinical examination

Patients with a suspected PE require a comprehensive respiratory and cardiovascular examination. Acutely unwell
patients will require an ABCDE approach.
Typical clinical
2,3,4,9
Tachycardia
Tachypnoea
Hypoxia
Low-grade fever
Pleural rub
Gallop rhythm, a wide split-second heart sound and tricuspid regurgitant murmur.
Massive pulmonary embolism
Features of a massive PE include\:
2,3,4,9
Haemodynamic instability\: hypotension and cardiogenic shock
Presyncope/syncope
Elevated jugular venous pressure (JVP)

Investigations

Bedside investigations

A 12-lead ECG should always be performed in the context of chest pain. In the context of PE, it should be used to exclude
possible di
Possible ECG
4,11
Sinus tachycardia\: the most common
Right ventricular strain pattern\: T wave inversion in anterior leads (V1-V4) +/- inferior leads (II, III, aVF)
Right bundle branch block (RBBB)
Right axis deviation (RAD)
The classic ‘S1Q3T3’ ECG change is only seen in \<20% patients - large S wave in lead I, large Q wave in lead III, and
inverted T wave in lead III

Laboratory investigations

Relevant laboratory investigations include\:
2,3
D-dimer levels\: often raised, typically >500 ng/mL (see below)
Full blood count (FBC)\: may demonstrate leucocytosis due to acute in
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Urea and electrolytes (U&E)\: often unremarkable, baseline renal function results can be used to guide investigations
and treatment
Liver function tests (LFTs)\: often unremarkable, they can be used to guide treatment
Cardiac biomarkers (troponin and BNP) are not used in diagnosing PE but can provide prognostic information.
Coagulation studies\: should be established before starting treatment and can guide treatment.
D-dimer
D-dimer test has a high sensitivity but low speci
the absence of VTE\:
2,13
Pregnancy
Malignancy
Liver disease
Severe infection or in
Disseminated intravascular coagulation (DIC)
Recent trauma/surgery/hospitalised patients
In these patients, D-dimer testing has no value in diagnosing VTE.

Imaging

Chest X-ray
Chest X-ray should be used to exclude possible dipneumothorax and pneumonia). Most patients
with PE have a normal chest X-ray.
10
Possible chest X-ray in PE include\:
10
Wedge-shaped pulmonary infarction\: wedge-shaped opaci
Atelectasis
Pleural e
Raised hemidiaphragm
CTPA (CT pulmonary angiogram)
CTPA is the preferred investigation for the de
Diagnosis of PE is con
Figure 2. CTPA showing a large pulmonary embolism at the bifurcation of the
pulmonary artery (saddle embolism).
Alternative to CTPA in the diagnosis of PE
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NICE recommends ventilation-perfusion (V/Q) planar scan or SPECT as the investigation of choice instead of CTPA in
the following patients\:
12
2
Severe renal impairment (eGFR \< 30 mL/min/1.73m )
Allergic to contrast media
At high risk from irradiation (e.g. pregnancy)
Both V/Q planar scan and SPECT have a lower e
CTPA.
2
Echocardiography
In haemodynamically unstable patients who are unsuitable for CTPA, echocardiography is recommended to aid the
diagnosis of a suspected PE.
2
Echocardiography may show signs of right ventricular dysfunction that is suggestive of PE, including\:
Abnormal right ventricular ejection pattern – 60/60 sign
McConnel sign – reduced right ventricular free wall contractility compared with the apex
Right ventricular dilation and hypokinesis
Negative echocardiography does NOT exclude a PE. A 40-50% negative predictive value for PE has been reported.
2

Management

General approach

Acutely unwell patients require an ABCDE approach.
If clinical suspicion of PE is low, the pulmonary embolism rule-out criteria should be used.
12
If PE is suspected, perform a two-level PE Wells score without using pulmonary embolism rule-out criteria. While NICE
(T h e N a t i o n a l I n s t i t u t e f o r H e a l t h a n d C a r e E x c e l l e n c e ) guidelines advocate using the Wells score to aid diagnosis, ESC
( E u r o p e a n S o c i e t y o f C a r d i o l o g y ) guidelines advocate the revised Geneva rule.
Pulmonary Embolism Rule-out Criteria (PERC)
The PERC rule should only be used if the clinical suspicion for PE is low (based on medical history, examination, and
investigations) to avoid the overuse of diagnostic testing for PE.
12
The PERC rule states that if ALL the following criteria are ABSENT, it reduces the probability of PE to \< 2%. 12
cases, an alternative diagnosis should be considered.
In such
Age ≥ 50 y/o
HR ≥ 100 bpm
SpO2 \< 95% on room air
Unilateral leg swelling
Haemoptysis
Recent surgery/trauma ≤4 weeks ago requiring general anaesthesia
Previous DVT / PE
Hormone use (oral contraceptives/hormone replacement/estrogenic hormones)

Two-level PE Wells score-guided investigations

Table 1. The Two-level Wells score for PE.
12
Clinical feature Points
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
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An alternative diagnosis is less likely than PE 3
Heart rate more than 100 beats per minute 1.5
Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1
Malignancy (on treatment, treated in the last 6 months, or palliative) 1
Clinical probability
PE likely PE unlikely More than 4 points
4 points or less
PE is likely (Wells >4)
O
If CTPA cannot be done immediately, o
If CTPA is positive (PE identi
Start or continue therapeutic anticoagulation treatment
If anticoagulation treatment is contraindicated, consider mechanical intervention
If CTPA is negative (PE not identi
Consider a proximal leg vein ultrasound scan if DVT is suspected
If DVT is not suspected → PE is not likely, stop any interim therapeutic anticoagulation but NOT prophylactic
anticoagulation for primary prevention and long-term anticoagulation for secondary prevention, consider alternative
diagnosis
If PE is likely, why not D-dimer?
Remember, the D-dimer test has low speci
because a positive result does not con
conditions.
PE is unlikely (Wells ≤4)
O
If the D-dimer test result cannot be obtained within 4 hours, start interim therapeutic anticoagulation.
If the D-dimer test is positive\:
O
If the D-dimer test is negative\:
PE is not likely
Stop any interim therapeutic anticoagulation but NOT prophylactic anticoagulation and long-term anticoagulation
Consider an alternative diagnosis
If PE is unlikely, why use D-dimer?
Remember, the D-dimer test has high sensitivity for VTE, so if the D-dimer is negative PE can be excluded without
the patient being exposed to radiation from a CTPA.
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Management of con

PE with haemodynamic instability
O
2,12
IV tissue plasminogen activator (tPA) (e.g. alteplase) is often used
Catheter-directed thrombolysis
Open pulmonary embolectomy
Risk assessment (outpatient vs inpatient)
NICE suggest that outpatient treatment for low-risk PE can be considered, using a validated risk strati
determine suitability\:
12,14
NICE guidelines did not include a speci
The British Thoracic Society (BTS) guidelines support the use of the Pulmonary Embolism Severity Index (PESI) score
A key requirement for outpatient treatment is being haemodynamically stable.
Patients with intermediate-risk or high-risk PE should be considered for in-patient treatment.
Anticoagulation
In haemodynamically stable PE, management involves anticoagulation therapy\:
2,12
First line\: apixaban or rivaroxaban, both direct oral anticoagulants (DOACs)
Second line\: low molecular weight heparin (LMWH) followed by dabigatran/edoxaban OR LMWH followed by warfarin
The choice of anticoagulants varies in speci
2,12,14
Pregnant\: LMWH only (DOACs and warfarin contraindicated)
Active cancer\: DOAC preferred over LMWH
2
Severe renal impairment (eGFR \< 15 mL/min/1.73m )\: UFH or dose-adjusted LMWH
Antiphospholipid syndrome (triple positive)\: initial LMWH and warfarin followed by warfarin monotherapy
All forms of anticoagulation contraindicated\: inferior vena cava (IVC)
NICE recommends that all patients should have anticoagulation for at least three months. Further anticoagulation is based
on the patient’s risk of VTE recurrence and risk of bleeding (ORBIT score is recommended to help assess the risk of
bleed).
12
As a rule of thumb\:
12
If VTE was provoked → 3 months of anticoagulation
If VTE was unprovoked → 6 months of anticoagulation
If there is active cancer → 3-6 months of anticoagulation
Provoked vs unprovoked PE
Provoked PE is associated with a recent (within three months) and transient major risk factor (there is no clear-cut
guidance, but NICE CKS give examples of signi
hormonal therapy).
12
Unprovoked PE occurs in the absence of a recent (within three months) major clinical risk factor in a person who is
not using hormonal therapy.
12
It is worth noting that the ESC guidelines no longer support using the terms ‘provoked’ and ‘unprovoked’
. They state
that they are potentially misleading and unhelpful when making a decision about the duration of anticoagulation.
2

Complications

Short-term complications of PE include\:
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Sudden cardiac arrest or death can result from ventricular collapse due to massive embolism and occlusion of the
pulmonary vasculature
Pulmonary infarction due to obstruction of arterial blood supply, more common when distal arteries are occluded
Right ventricular infarction, often secondary to pulmonary hypertension and haemodynamic overload
Atelectasis
Exudative pleural e
Long-term complications of PE include\:
3,4
Increased risk of recurrence, history of previous VTE is a signi
Chronic thromboembolic pulmonary hypertension (CTEPH) occurs where
chronic obstruction of the pulmonary vasculature, and hence pulmonary hypertension
CTEPH should be excluded in patients with persistent dyspnoea and poor physical performance three to six months after a
PE.
3,4

References

Kumar V, Abbas AK, Aster JC, Perkins JA. Chapter 4 Haemodynamic Disorders, Thromboembolism, and Shock. Robbins
basic pathology. 10th ed. Philadelphia, PA\: Elsevier; 2018.
Konstantinides SV, Meyer G, Becattini C, Bueno H, Geersing G-J, Harjola V-P, et al. 2019 ESC guidelines for the diagnosis and
management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS).
European Heart Journal. 2019 Aug 31;41(4)\:543–603.
BMJ Best Practice. Pulmonary embolism. Reviewed 2023 Oct; updated 2022 Aug. Available from\: [LINK]
NICE Clinical Knowledge Summaries. Pulmonary embolism. Revised 2023 Sep. Available from\: [LINK]
Turetz M, Sideris A, Friedman O, Triphathi N, Horowitz J. Epidemiology, Pathophysiology, and natural history of pulmonary
embolism. Seminars in Interventional Radiology. 2018 Jun 4;35(02)\:92–8.
Sadeghi A, Brevetti GR, Kim S, Burack JH, Genovese MH, Distant DA, Kodavatiganti R, Lowery RC. Acute massive pulmonary
embolism\: role of the cardiac surgeon. Tex Heart Inst J. 2005;32(3)\:430-3.
Ja
"Management of massive and
submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary
hypertension\: a scienti
RCEM Learning. Pulmonary Embolism. Published in 2023 May 18. Available from\: [LINK]
Walls R, Hockberger R, Gausche-Hill M, Erickson TB, Wilcox SR. Chapter 74 Pulmonary Embolism and Deep Vein
Thrombosis. Rosen's Emergency Medicine\: Concepts and Clinical Practice 10 th
Elsevier Health Sciences; 2022
Jabaz DF. Pulmonary infarction\: Radiology reference article. Radiopaedia.org; 2022. Available from\: [LINK]
Burns E, Buttner R, Buttner EB and R. ECG changes in pulmonary embolism. Published in 2021 Nov 30. Available from\:
[LINK]
National Institute for Health and Care Excellence. Venous thromboembolic diseases\: diagnosis, management and
thrombophilia testing (NICE guideline [NG158]). NICE 2020. Updated 2023 Aug. Available from\: [LINK]
Linkins L‐A., Takach Lapner S. Review of d‐dimer testing\: Good, bad, and ugly. International Journal of Laboratory
Hematology. 2017 Apr 26;39(S1)\:98–103.
Howard LSGE, Barden S, Condli
pulmonary embolism (PE)Thorax 2018 Jun 13;73\:ii1-ii29.

Image references

Figure 1. Bakerstmd.Saddle thromboembolism. License\: [CC BY-SA]
Figure 2. James Heilman, MD. SaddlePE. License\: [CC BY-SA]

Reviewer

Dr Joelle Azzopardi
Respiratory consultant
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Dr Adriano Buontempo
Lecturer in Clinical Communication Skills

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Investigations
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