Pulmonary embolismLast updated: Sep 16, 2019

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Summary
Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by solid, liquid,
or gaseous masses. In most cases, the embolism is caused by blood thrombi, which arise from
the deep vein system in the legs or pelvis (deep vein thrombosis) and embolize to the lungs via
the inferior vena cava. Risk factors include immobility,
inherited hypercoagulability disorders, pregnancy, and recent surgery. The clinical presentation
is variable and, depending on the extent of vessel obstruction, can range from asymptomatic
to cardiogenic shock. Symptoms are often nonspecific, including chest
pain, coughing, dyspnea, and tachycardia. The diagnosis of PE is based primarily on the clinical
findings and is confirmed by detection of an embolism in contrast CT pulmonary
angiography (CTA). Arterial blood gas analysis typically shows evidence of respiratory
alkalosis with low partial oxygen pressure, low partial carbon dioxide pressure, and elevated
pH. Another commonly performed test is the measurement of D-dimer levels, which can rule
out PE if negative. Empiric anticoagulation with heparin is initiated to prevent further
thromboembolisms as well as to promote the gradual dissolution of the embolism and the
underlying thrombosis. Blood-thinning therapy must be continued for at least three months
with oral anticoagulants such as warfarin. In fulminant PE with shock, resolution of
the thrombus with thrombolytic agents or removal in an emergency surgery is attempted.

FEEDBACK

Epidemiology
 Accounts for ∼ 100,000 deaths in the US per year.
 Incidence rises with age.
 Sex: ♂ > ♀
References: [1]

Epidemiological data refers to the US, unless otherwise specified.

FEEDBACK

Etiology
 Deep vein thrombosis (most common cause)
o Risk factors: obesity, hypomobility or immobility,
malignancy, pregnancy, dehydration 
, hypercoagulability, use of contraceptives, previous DVT (see risk
factors for deep vein thrombosis) 
  Fat embolism during major surgical interventions (e.g., endoprosthesis
replacement, osteosynthesis)
 Others: air embolism, amniotic fluid embolism, tissue embolism, cement
embolism, bacterial embolism, tumor embolism
references: [1][2]

FEEDBACK

Pathophysiology
 Mechanism: thrombus formation (see Virchow's triad) → deep vein
thrombosis in the legs or pelvis (most commonly iliac vein) →
embolization to pulmonary arteries via inferior vena cava 
 → partial or complete obstruction of pulmonary arteries
 Pathophysiologic response of the lung to arterial obstruction
o Infarction and inflammation of the lungs and pleura
 Causes pleuritic chest pain and hemoptysis
 Leads to surfactant dysfunction → atelectasis → ↓ PaO 2

 Triggers respiratory
drive → hyperventilation and tachypnea → respiratory
alkalosis with hypocapnia (↓ PaCO2)
o Impaired gas exchange
 Mechanical vessel obstruction → ventilation-perfusion mismatch 
 → arterial hypoxemia (↓ PaO ) and elevated A-a gradient 
2

 (see “Diagnostics” below)

o Cardiac compromise
 Elevated pulmonary artery pressure (PAP) due to blockage →
right ventricular pressure overload → forward failure with
decreased cardiac output 
 → hypotension and tachycardia

References: [3][1]

FEEDBACK

Clinical features
 Acute onset of symptoms, often triggered by a specific event (e.g., on
rising in the morning, sudden physical strain/exercise)
 Dyspnea and tachypnea (> 50% of cases) 
 Sudden chest pain (∼ 50% of cases), worse with inspiration
  Cough and hemoptysis
 Possibly decreased breath sounds, dullness on percussion, split-
second heart sound audible in some cases 
 Tachycardia (∼ 25% of cases), hypotension
 Jugular venous distension 
 Low-grade fever
 Syncope and shock with circulatory collapse in massive PE (e.g., due to
a saddle thrombus)
 Symptoms of DVT: unilaterally painful leg swelling 
Consider PE as a differential diagnosis in recurring or progressive dyspnea of uncertain
etiology!

References: [4]

FEEDBACK

Diagnostics
Initial management according to modified Wells criteria 
 Hemodynamically stable patients (systolic BP > 90 mmHg) with
high probability of PE (Wells score > 4) → CTA for definitive diagnosis
o Unless strongly contraindicated (e.g., high risk of bleeding, recent
surgery), start empiric anticoagulation before conducting a CTA 
o If too unstable for CTA → perform bedside echocardiography obtain a
presumptive diagnosis of PE (right ventricle enlargement/hypokinesis
or visualization of clot) prior to empiric thrombolysis.
 In patients with a low or medium probability of PE (Wells score ≤ 4) →
measure D-dimer levels (+ ABG evaluation + CXR)
o If positive (D-dimers ≥ 500 ng/mL) → CTA → evidence/exclusion of PE
o If negative → PE unlikely → consider other causes of symptoms (see
“Differential diagnosis” below)

Wells criteria for pulmonary embolism

 The Wells score is used as a diagnostic algorithm in stable patients for
assessing the probability of PE. The 2-tier model (modified Wells criteria)
is generally more accepted for use among management guidelines.
  Note that a different version is used for determining
the probability of DVT (see Wells criteria for DVT).

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Wells score Points

Clinical symptoms of DVT  3

PE more likely than other diagnoses 3

Previous PE/DVT 1.5

Tachycardia (heart rate > 100/min) 1.5

Surgery or immobilization in the past four weeks 1.5

Hemoptysis 1

Malignancy (being treated, in palliative care or diagnosis less than 6 1

months ago)

Wells criteria (clinical probability)

 Total score of 0–1: low probability of PE (∼ 10%)

 Total score of 2–6: moderate probability of PE (∼ 30%)

 Total score of > 6: high probability of PE (∼ 65%)

Modified/simplified Wells criteria (clinical probability)

 Total score of > 4: PE likely

 Total score of ≤ 4: PE unlikely

Blood analysis
 Initial test: measure D-dimer levels (if suspicion for PE low)
o D-dimers: fibrin degradation products detected in the blood
after thrombus resolution via fibrinolysis; normal levels < 500 ng/mL
 o If elevated in patients with low clinical probability of PE → further testing
(see below)
o High sensitivity and negative predictive value: a negative D-dimer test
most likely rules out PE 
o Low specificity: positive results in all forms of fibrinolysis 
o ↑ troponin T and B-type natriuretic peptide (BNP): possible elevation
from right ventricular pressure overload → poor prognosis
 Arterial blood gas (ABG) test
o Respiratory alkalosis 
: ↓ paO  < 80 mmHg, ↓ paCO , ↑ pH
2 2

o ↑ Alveolar-arterial (A-a) gradient : compares the oxygenation status of

alveoli to arterial blood 
o ↓ O saturation
2 

Normal D-dimer values usually rule out PE or DVT in patients with an unremarkable history and
examination for PE! A positive D-dimer is unspecific since it may be elevated anytime
elevated fibrinolysis is occurring.

Imaging
 Helical spiral CT/CT pulmonary angiography (CTPA): best definitive
diagnostic test 
o Contrast-enhanced imaging of the pulmonary arteries
o High sensitivity, specificity and immediate evidence of pulmonary
arterial obstruction
o Visible intraluminal filling defects of pulmonary arteries
o Wedge-shaped infarction with pleural effusion is
almost pathognomonic for PE
 Chest radiograph 
o Initially often performed to rule out other
causes (e.g., pneumonia, pneumothorax, pericarditis, aortic dissection)
o Findings that may indicate PE
 Atelectasis (visible collapse or incomplete expansion of the lung)
 Pleural effusions 
 Signs of pulmonary embolus (rare)
  Hampton's hump: wedge-shaped opacity in the
peripheral lung with its base at the thoracic wall; caused
by pulmonary infarction and not specific for PE 
 Westermark sign: embolus leads to diminished perfusion of
downstream lung tissue, which appears hyperlucent on radiograph.
 Fleischner sign: prominent pulmonary artery caused by
vessel distension due to a large pulmonary embolus (common
in massive PE)
 Cardiomegaly 
 Echocardiography: to detect right atrium pressure (RAP) signs 
o Venous reflux with dilation of inferior vena cava (also liver congestion
in ultrasound of the abdomen)
o Tricuspid regurgitation (tricuspid valve insufficiency) 
o ↑ Pulmonary artery systolic pressure 
o Dilatation and hypokinesis of the right ventricle
 Ventilation/perfusion scintigraphy 
o Indication: alternative to CT angiography in patients with severe renal
insufficiency or contrast allergy
o Method: detects areas of ventilation/perfusion (V/Q) mismatch
via perfusion and ventilation scintigraphy 
o Assessment
 Perfusion failure in normally ventilated affected pulmonary
area (mismatch) suggests PE
 Evidence of normal lung perfusion rules out PE →
ventilation scintigraphy superfluous
 Pulmonary angiography 
o Indications: only conducted if CT angiography unavailable 
o Procedure: right heart catheterization → insertion of a catheter into
a pulmonary artery → radiograph after administration of contrast agent

Other diagnostic measures

 Electrocardiography (ECG)
 o Sinus tachycardia most commonly seen
o Signs of right ventricular pressure overload 
 S Q T  -pattern 
I III III

 New right bundle branch block

 Bradycardia < 50 or tachycardia > 100 bpm
 Right or extreme right axis deviation (30% of cases)
 T negativity in leads V and V  (∼ 30%)
2 3

 Compression Doppler ultrasound: diagnosis of potential underlying deep

vein thrombosis
 Diagnostics for underlying cause
o Thrombophilia workup
o Malignancies

References: [5][4][6][3]

FEEDBACK

Treatment
Acute management

General measures
 45° reclining sitting posture
  Oxygen supplementation and intubation if respiratory failure
 IV fluids and/or vasopressors in patients with hypotension
 Analgesics and sedatives

Specific measures

Non-life-threatening pulmonary embolism: therapeutic anticoagulation

 Empiric anticoagulation in patients with no absolute contraindication until
definitive diagnosis has been made 
An absolute contraindication for empiric anticoagulation is a high risk of bleeding (e.g., recent
surgery, hemorrhagic stroke, active bleeding)!
1. Initial anticoagulation (0–10 days)
o Low molecular weight heparin (LMWH) or fondaparinux in stable
patients without renal insufficiency, especially in cancer patients 
o Unfractionated heparin (UFH) in patients with renal failure and those
who may still require thrombolysis 
2. Long-term anticoagulation and prophylaxis (3–6 months)
o Anticoagulation treatment is indicated for a minimum of three months
after PE (see “Therapy” in deep vein thrombosis). The following agents
may be used:
 Warfarin (target INR 2–3)
 LMWH
 Direct oral
anticoagulants (rivaroxaban, apixaban, edoxaban, dabigatran) 
o Patients with a hypercoagulable state with DVT or PE: heparin followed
by 3–6 months of warfarin for the first event, 6–12 months for the
second, and lifelong anticoagulation for further events

Massive, life-threatening pulmonary embolism: recanalization

 Thrombolytic therapy
o Indications
 In cases of massive PE causing right heart failure
 In hemodynamically unstable patients requiring resuscitation
 Alternative to PTCA for patients with STEMI if PTCA cannot be
performed within 90–120 minutes (see “Treatment algorithm based
on ECG findings” in the acute coronary syndrome learning card)
 o Procedure: fibrinolysis, preferably with recombinant tissue-
type plasminogen activator (tPA), e.g., alteplase
 Most commonly systemic infusion via IV catheter
 Alternatively, direct infusion of tPA into pulmonary artery via
pulmonary arterial catheter 
 Administration of anticoagulants discontinued
during thrombolysis
o Complications
 Risk of hemorrhage during thrombolytic treatment 
 Observe contraindications for thrombolytic therapy 
 Embolectomy
o Treatment of last resort when thrombolysis is contraindicated or
unsuccessful
o Surgical or catheter-based thrombus removal
There is no contraindication for systemic thrombolysis if the patient requires resuscitation!

Further measures
 Inferior vena cava filter 
o Indications
 In recurrent DVTs despite anticoagulation
 If anticoagulation is contraindicated (e.g., high-risk of bleeding) in
patients with a documented lower leg DVT
 DVT prophylaxis: (subcutaneous heparin or LMWH for all immobile
patients, early ambulation, and compression stockings)
References: [7][5][3][8]

FEEDBACK

Complications
 High risk of recurrence: without anticoagulant treatment ∼ 10% in the
first year, ∼ 5% per year after 
 Right ventricular failure
 Sudden cardiac death due to pulseless electrical activity
 Atelectasis (∼ 20% of cases) 
 Pulmonary effusion
 Pulmonary infarction (∼ 10% of cases)
 o Embolisms of smaller segmental arteries can lead to wedge-
shaped hemorrhagic pulmonary infarctions 
o Right ventricular failure, increased bronchial venous pressure, and
preexisting pulmonary diseases increase the risk.
 Pneumonia from pulmonary infarction: peripheral infiltration on chest X-
ray (typically wedge-shaped = Hampton's hump)

References: [1][9]

We list the most important complications. The selection is not exhaustive.

FEEDBACK

Differentials
 See differential diagnosis of acute chest pain.
 Post-surgery atelectasis
 Anxiety disorders
FEEDBACK

References
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2.
Bauer KA, Lip GY. Overview of the causes of venous thrombosis. In: Post TW, ed. UpToDate. Waltham,
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Ouellette DR. Pulmonary Embolism. In: Pulmonary Embolism. New York,
NY: WebMD.http://emedicine.medscape.com/article/300901. June 6, 2016. Accessed February 2, 2017.
4.
Thompson BT. Clinical presentation, evaluation, and diagnosis of the adult with suspected acute
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Tapson VF. Treatment, prognosis, and follow-up of acute pulmonary embolism in adults. In: Post TW,
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Fedullo PF, Roberts A. Placement of vena cava filters and their complications. In: Post TW,
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Lip GYH, Hull RD. Rationale and indications for indefinite anticoagulation in patients with venous
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Accessed February 27, 2017.
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Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014
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Kenneth A Bauer, MD Gregory YH Lip, MD. Overview of the causes of venous thrombosis. In: Post TW,
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