Pulmonary Embolism (PE) | Acute Management | ABCDE

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A pulmonary embolism (PE) is a potentially life-threatening medical emergency which often presents with very few clinical signs or symptoms. As a result, a high index of suspicion is required to diagnose and treat PE in a timely manner.

This guide provides an overview of the recognition and immediate management of PE using an ABCDE approach.

The ABCDE approach can be used to perform a systematic assessment of a critically unwell patient. It involves working through the following steps:

  • Airway
  • Breathing
  • Circulation
  • Disability
  • Exposure

Each stage of the ABCDE approach involves clinical assessment, investigations and interventions. Problems are addressed as they are identified and the patient is re-assessed regularly to monitor their response to treatment.

This guide has been created to assist students in preparing for emergency simulation sessions as part of their training, it is not intended to be relied upon for patient care.

Clinical features of a PE

A study in 2009 reported that in 1 in 4 patients with a PE, the first manifestation will be sudden-unexpected death.¹ PE is an important cause of out-of-hospital and in-hospital cardiac arrest and as such is part of the 4 H’s and 4T’s of reversible causes of cardiac arrest.

The diagnosis of a PE cannot be made on examination alone. In fact, clinical examination is often unremarkable and unless you consider PE as the cause of a patient’s chest pain or shortness of breath, you may miss the diagnosis.

Risk factors

Risk factors for developing a deep vein thrombosis (DVT) or PE include:

  • Recent surgery
  • Recent fractures
  • Recent immobility
  • Personal or family history of a clotting disorder or PE/DVT
  • Obesity
  • Malignancy
  • Infection
  • Pregnancy
  • Medications such as the combined oral contraceptive pill or hormone replacement therapy

A provoked PE refers to a PE developing in an individual who has recognised risk factors for PE.

An unprovoked PE refers to a PE developing in an individual with no known underlying risk factors.


Clinical features of PE include:

  • Shortness of breath
  • Pleuritic chest pain: with each breath, the pleura comes into contact with an ischaemic area of the lung.
  • Cough
  • Haemoptysis: secondary to infarcted lung tissue.
  • Dizziness or syncope: due to haemodynamic instability (i.e. right ventricular strain).


Clinical signs of PE include:

  • Tachypnoea: a respiratory rate of more than 20 breaths per minute.
  • Tachycardia: a heart rate of more than 100 beats per minute.
  • Hypotension: suggestive of right ventricular strain.
  • Evidence of deep vein thrombosis (DVT) such as a red, swollen calf.
  • Pleural rub: a squeaking or grating sound caused by ischaemic lung tissue coming in contact with the pleura.
  • Cyanosis: a late sign that indicates a significant drop in blood oxygen levels (SpO2).
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Tips before you begin

General tips for applying an ABCDE approach in an emergency setting include:

  • Treat all problems as you discover them.
  • Re-assess regularly and after every intervention to monitor a patient’s response to treatment.
  • Make use of the team around you by delegating tasks where appropriate.
  • All critically unwell patients should have continuous monitoring equipment attached for accurate observations.
  • Clearly communicate how often would you like the patient’s observations relayed to you by other staff members.
  • If you require senior input, call for help early using an appropriate SBARR handover structure.
  • Review results as they become available (e.g. laboratory investigations).
  • Make use of your local guidelines and algorithms in managing specific scenarios (e.g. acute asthma).
  • Any medications or fluids will need to be prescribed at the time (in some cases you may be able to delegate this to another member of staff).
  • Your assessment and management should be documented clearly in the notes, however, this should not delay initial clinical assessment, investigations and interventions.

Initial steps

Acute scenarios typically begin with a brief handover from a member of the nursing staff including the patient’s nameagebackground and the reason the review has been requested.

You may be asked to review a patient with a PE due to chest pain or shortness of breath.


Introduce yourself to whoever has requested a review of the patient and listen carefully to their handover.


Introduce yourself to the patient including your name and role.

Ask how the patient is feeling as this may provide some useful information about their current symptoms.


Make sure the patient’s notesobservation chart and prescription chart are easily accessible.

Ask for another clinical member of staff to assist you if possible.

If the patient is an inpatient, check if they have been receiving thromboprophylaxis.

If the patient is unconscious or unresponsive, start the basic life support (BLS) algorithm as per resuscitation guidelines.


Clinical assessment

Can the patient talk?

Yes: if the patient can talk, their airway is patent and you can move on to the assessment of breathing.


  • Look for signs of airway compromise: these include cyanosis, see-saw breathing, use of accessory muscles, diminished breath sounds and added sounds.
  • Open the mouth and inspect: look for anything obstructing the airway such as secretions or a foreign object.
Causes of airway compromise

There is a wide range of possible causes of airway compromise including:

  • Inhaled foreign body: symptoms may include sudden onset shortness of breath and stridor.
  • Blood in the airway: causes include epistaxis, haematemesis and trauma.
  • Vomit/secretions in the airway: causes include alcohol intoxication, head trauma and dysphagia.
  • Soft tissue swelling: causes include anaphylaxis and infection (e.g. quinsy, necrotising fasciitis).
  • Local mass effect: causes include tumours and lymphadenopathy (e.g. lymphoma).
  • Laryngospasm: causes include asthma, gastro-oesophageal reflux disease (GORD) and intubation.
  • Depressed level of consciousness: causes include opioid overdose, head injury and stroke.


Regardless of the underlying cause of airway obstruction, seek immediate expert support from an anaesthetist and the emergency medical team (often referred to as the ‘crash team’). In the meantime, you can perform some basic airway manoeuvres to help maintain the airway whilst awaiting senior input.

Head-tilt chin-lift manoeuvre

Open the patient’s airway using a head-tilt chin-lift manoeuvre:

1. Place one hand on the patient’s forehead and the other under the chin.

2. Tilt the forehead back whilst lifting the chin forwards to extend the neck.

3. Inspect the airway for obvious obstruction. If an obstruction is visible within the airway, use a finger sweep or suction to remove it.

Jaw thrust

If the patient is suspected to have suffered significant trauma with potential spinal involvement, perform a jaw-thrust rather than a head-tilt chin-lift manoeuvre:

1. Identify the angle of the mandible.

2. With your index and other fingers placed behind the angle of the mandible, apply steady upwards and forward pressure to lift the mandible.

3. Using your thumbs, slightly open the mouth by downward displacement of the chin.

Oropharyngeal airway (Guedel)

Airway adjuncts are often helpful and in some cases essential to maintain a patient’s airway. They should be used in conjunction with the maneuvres mentioned above as the position of the head and neck need to be maintained to keep the airway aligned.

An oropharyngeal airway is a curved plastic tube with a flange on one end that sits between the tongue and hard palate to relieve soft palate obstruction. It should only be inserted in unconscious patients as it is otherwise poorly tolerated and may induce gagging and aspiration.

To insert an oropharyngeal airway:

1. Open the patient’s mouth to ensure there is no foreign material that may be pushed into the larynx. If foreign material is present, attempt removal using suction.

2. Insert the oropharyngeal airway in the upside-down position until you reach the junction of the hard and soft palate, at which point you should rotate it 180°. The reason for inserting the airway upside down initially is to reduce the risk of pushing the tongue backwards and worsening airway obstruction.

3. Advance the airway until it lies within the pharynx.

4. Maintain head-tilt chin-lift or jaw thrust and assess the patency of the patient’s airway by looking, listening and feeling for signs of breathing.

Nasopharyngeal airway (NPA)

A nasopharyngeal airway is a soft plastic tube with a bevel at one end and a flange at the other. NPAs are typically better tolerated in patients who are partly or fully conscious compared to oropharyngeal airways. NPAs should not be used in patients who may have sustained a skull base fracture, due to the small but life-threatening risk of entering the cranial vault with the NPA.

To insert a nasopharyngeal airway:

1. Check the patency of the patient’s right nostril and if required (depending on the model of NPA) insert a safety pin through the flange of the NPA.

2. Lubricate the NPA.

3. Insert the airway bevel-end first, vertically along the floor of the nose with a slight twisting action.

4. If any obstruction is encountered, remove the tube and try the left nostril.


If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.


Make sure to re-assess the patient after any intervention.


Clinical assessment


Review the patient’s respiratory rate:

  • normal respiratory rate is between 12-20 breaths per minute.
  • Tachypnoea may be present in PE to compensate for the ventilation-perfusion mismatch typical of the condition.

Review the patient’s oxygen saturation (SpO2):

  • normal SpOrange is 94-98% in healthy individuals and 88-92% in patients with COPD who are at high-risk of COretention.
  • Hypoxaemia is a typical clinical feature of PE.

See our guide to performing observations/vital signs for more details.


Auscultate both lungs:

  • Air entry is typically normal in pulmonary embolism, but may be reduced over an area of infarcted lung tissue.
  • Coarse crackles on auscultation may represent a pleural effusion due to infarcted lung tissue.


Percuss the patient’s chest to identify areas of dullness which may be associated with pleural effusion or lobar collapse secondary to infarcted lung tissue.

Investigations and procedures

Arterial blood gas

Take an ABG if indicated (e.g. low SpO2) to quantify the degree of hypoxia.

Typical ABG findings in PE include low PaO2 and normal/low PaCO2 (a massive PE may also cause metabolic acidosis).

Chest X-ray

In most cases of PE, a chest X-ray will be completely normal. However, it is a useful tool for ruling out other lung pathology (e.g. pneumonia).

CXR findings associated with PE include pleural effusion and/or an area of atelectasis where a small area of lung tissue has collapsed.

Consolidation on the chest X-ray may represent an established area of infarcted lung tissue.

Well’s score

At this stage, without any investigation results, you cannot be certain if you are dealing with a PE or not.

The definitive diagnosis of PE can only be made with a CT pulmonary angiogram (CTPA) or, less commonly, a V/Q scan.

NICE guidance advises calculation of the clinical probability of DVT/PE using a 2-level Wells score.²

A Wells score assigns various clinical features a specific number of points and you need to add up these points to determine the total Wells score.

Clinical feature Points
Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3
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 More than 4 points
PE unlikely 4 points or less

If the Wells score is greater than 4 (i.e. PE is likely), a CTPA is indicated (or V/Q if CTPA is contraindicated):

  • If a CTPA or V/Q scan cannot be performed immediately, offer interim therapeutic anticoagulation with apixaban or rivaroxaban (if no contraindications are present).

If the Wells score is 4 or less (i.e. PE is unlikely) a D-dimer test can be used to rule out a PE (if D-dimer is negative, the likelihood of a PE is very low). If the D-dimer test result cannot be obtained within 4 hours, offer interim therapeutic anticoagulation while awaiting the result. Patients who are deemed low risk on the Wells score do not require CTPA if the D-dimer result is negative.

If the D-dimer result is raised then a CTPA or V/Q scan will be required to rule PE in or out. D-dimer can be raised for a number of different reasons other than the presence of PE or DVT (e.g. infection, recent surgery and malignancy), so a raised D-dimer is not diagnostic for PE or DVT (it is used only to help rule out the diagnosis).

V/Q scans are typically used when CTPA is contraindicated (e.g. renal impairment, contrast allergy, pregnancy).



Administer oxygen to all critically unwell patients during your initial assessment. This typically involves the use of a non-rebreathe mask with an oxygen flow rate of 15L. You can then trial titrating oxygen levels downwards after your initial assessment.

If the patient is conscious, sit them upright as this can also help with oxygenation.

Assisted ventilation

If your patient is unconscious and their respiratory rate is inadequate (too slow or irregular with big pauses), you can provide assisted ventilation through a bag-valve-mask (BVM): ventilate at a rate of 12-15 breaths per minute (roughly one every 4 seconds).

PE treatment

If you can get a CTPA or V/Q scan performed quickly you may be able to wait for a definite diagnosis of PE before commencing treatment. However, in situations where there will be a significant delay before a CTPA or V/Q scan can be performed, anticoagulant therapy (e.g. apixaban or rivaroxaban) should be commenced and then later stopped if PE is ruled out.

Anticoagulation should be continued for at least 3 months for a confirmed PE however treatment duration may be longer if the PE was unprovoked.

For patients with confirmed PE and haemodynamic instability (e.g. massive PE), offer a continuous unfractionated heparin infusion and consider systemic thrombolytic therapy. This is a consultant-led decision and you should seek urgent senior review in this context.

Signs of massive PE occur secondary to right ventricular strain and include:

  • Hypotension
  • Raised jugular venous pressure
  • Heart failure
  • Cardiac arrest 


If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.


Make sure to re-assess the patient after any intervention.


Clinical assessment


Patients with PE may be tachycardic, however many patients have a normal pulse rate.

Blood pressure

Significant pain in PE may result in hypertension.

Hypotension is a concerning sign in the context of PE and most likely represents cardiac failure secondary to right heart strain (i.e. massive PE).

Jugular venous pressure (JVP)

An elevated JVP in the context of PE may indicate underlying right heart strain (i.e. massive PE).

Capillary refill time

Capillary refill time may be normal or sluggish due to hypovolaemia.

Auscultation of the heart

Auscultation of the heart may reveal a third heart sound in the context of congestive heart failure.

Fluid balance assessment

Calculate the patient’s fluid balance:

  • Calculate the patient’s current fluid balance using their fluid balance chart (e.g. oral fluids, intravenous fluids, urine output, drain output, stool output, vomiting) to inform resuscitation efforts.
  • Reduced urine output (oliguria) is typically defined as less than 0.5ml/kg/hour in an adult.

Investigations and procedures

Intravenous cannulation

Insert at least one wide-bore intravenous cannula (14G or 16G) and take blood tests as discussed below.

See our intravenous cannulation guide for more details.

Blood tests

Collect blood tests after cannulating the patient including:

  • FBC: to rule out anaemia and to look for a raised white cell count which may indicate an underlying infection.
  • U&Es: to assess renal function to inform fluid resuscitation, investigations (e.g. CTPA) and management (e.g. dose of anticoagulant).
  • LFTs: deranged liver function can directly impact coagulation due to reduced production of clotting factors and abnormal levels of albumin may impact serum drug levels.
  • Coagulation: to screen for clotting abnormalities (e.g. disseminated intravascular coagulation) prior to commencing anticoagulation.
  • CRP: to screen for evidence of inflammation (e.g. pneumonia).
  • Troponin: to screen for myocardial damage which may be due to acute coronary syndrome or secondary to PE (due to right heart strain and prolonged tachycardia).

Record an ECG

The most common ECG finding in PE is sinus tachycardia.

Other ECG findings associated with PE include:

  • T wave inversion
  • New-onset atrial fibrillation
  • Right bundle branch block
  • Right axis deviation
  • S1Q3T3: S waves in lead I, Q waves in lead III, T wave inversion in lead III


Intravenous fluids

Hypovolaemic patients require fluid resuscitation (the below guidelines are for adults):

  • Administer a 500ml bolus Hartmann’s solution or 0.9% sodium chloride (warmed if available) over less than 15 mins.
  • Administer 250ml boluses in patients at increased risk of fluid overload (e.g. heart failure).

After each fluid bolus, reassess for clinical evidence of fluid overload (e.g. auscultation of the lungs, assessment of JVP).

Repeat administration of fluid boluses up to four times (e.g. 2000ml or 1000ml in patients at increased risk of fluid overload), reassessing the patient each time.

Seek senior input if the patient has a negative response (e.g. increased chest crackles) or if the patient isn’t responding adequately to repeated boluses (i.e. persistent hypotension).

See our fluid prescribing guide for more details on resuscitation fluids.


If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.


Make sure to re-assess the patient after any intervention.


Clinical assessment


In the context of PE, a patient’s consciousness level may be reduced secondary to hypoxia or hypovolaemia.

Assess the patient’s level of consciousness using the AVPU scale:

  • Alert: the patient is fully alert, although not necessarily orientated.
  • Verbal: the patient makes some kind of response when you talk to them (e.g. words, grunt).
  • Pain: the patient responds to a painful stimulus (e.g. supraorbital pressure).
  • Unresponsive: the patient does not show evidence of any eye, voice or motor responses to pain.

If a more detailed assessment of the patient’s level of consciousness is required, use the Glasgow Coma Scale (GCS).


Assess the patient’s pupils:

  • Inspect the size and symmetry of the patient’s pupils. Asymmetrical pupillary size may indicate intracerebral pathology.
  • Assess direct and consensual pupillary responses which may reveal evidence of intracranial pathology.

Drug chart review

Review the patient’s drug chart for medications which may cause neurological abnormalities (e.g. opioids, sedatives, anxiolytics).


Blood glucose and ketones

Measure the patient’s capillary blood glucose level to screen for causes of a reduced level of consciousness (e.g. hypoglycaemia or hyperglycaemia). 

A blood glucose level may already be available from earlier investigations (e.g. ABG, venepuncture).

The normal reference range for fasting plasma glucose is 4.0 – 5.8 mmol/l.

Hypoglycaemia is defined as a plasma glucose of less than 3.0 mmol/l. In hospitalised patients, a blood glucose ≤4.0 mmol/L should be treated if the patient is symptomatic.

If the blood glucose is elevated, check ketone levels which if also elevated may suggest a diagnosis of diabetic ketoacidosis (DKA).

See our blood glucose measurement, hypoglycaemia and diabetic ketoacidosis guides for more details.


Request a CT head if intracranial pathology is suspected after discussion with a senior.

See our guide on interpreting a CT head for more details.


Maintain the airway

Alert a senior immediately if you have any concerns about the consciousness level of a patient. A GCS of 8 or below warrants urgent expert help from an anaesthetist. In the meantime, you should re-assess and maintain the patient’s airway as explained in the airway section of this guide.


If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.


Make sure to re-assess the patient after any intervention.


It may be necessary to expose the patient during your assessment: remember to prioritise patient dignity and conservation of body heat. 

Clinical assessment

Begin by asking the patient if they have pain anywhere, which may be helpful to guide your assessment.


Inspect the patient’s skin for evidence of bruising which may indicate an underlying clotting abnormality (e.g. disseminated intravascular coagulation).

Assess the patient’s calves for erythema, swelling and tenderness which may suggest a deep vein thrombosis.

Review the output of the patient’s catheter and any surgical drains.


If active bleeding is identified (e.g. disseminated intravascular coagulation):

  • Estimate the total blood loss and the rate of blood loss.
  • Re-assess for signs of hypovolaemic shock (e.g. hypotension, tachycardia, pre-syncope, syncope).


Patients with PE can develop a fever as part of the catecholamine response.


If a DVT is suspected, calculate the patient’s DVT Wells score to determine if an ultrasound scan or D-dimer test should be performed to confirm or exclude the presence of a DVT.


Deep vein thrombosis (DVT)

If DVT is confirmed, consider commencing anticoagulation if not done already in an earlier step (e.g. for PE).


If the patient loses consciousness and there are no signs of life on assessment, put out a crash call and commence CPR.


Make sure to re-assess the patient after any intervention.

Reassess ABCDE

Re-assess the patient using the ABCDE approach to identify any changes in their clinical condition and assess the effectiveness of your previous interventions.

Deterioration should be recognised quickly and acted upon immediately.

Seek senior help if the patient shows no signs of improvement or if you have any concerns.


You should have another member of the clinical team aiding you in your ABCDE assessment, such a nurse, who can perform observations, take samples to the lab and catheterise if appropriate.

You may need further help or advice from a senior staff member and you should not delay seeking help if you have concerns about your patient.

Use an effective SBARR handover to communicate the key information effectively to other medical staff.

Next steps

Well done, you’ve now stabilised the patient and they’re doing much better. There are just a few more things to do…

Take a history

Revisit history taking to identify risk factors for PE and explore relevant medical history. If the patient is confused you might be able to get a collateral history from staff or family members as appropriate.

See our history taking guides for more details.


Review the patient’s notes, charts and recent investigation results.

Review the patient’s current medications and check any regular medications are prescribed appropriately.


Clearly document your ABCDE assessment, including history, examination, observations, investigations, interventions, and the patient’s response.

See our documentation guides for more details.


Discuss the patient’s current clinical condition with a senior clinician using an SBARR style handover.

Questions which may need to be considered include:

  • Are any further assessments or interventions required?
  • Does the patient need a referral to HDU/ICU?
  • Does the patient need reviewing by a specialist?
  • Should any changes be made to the current management of their underlying condition(s)?


The next team of doctors on shift should be made aware of any patient in their department who has recently deteriorated.


  1. Lucena, J., Rico, A., Vazquez, R., Marin, R., Martinez, C., Salguero, M. and Miguel, L. (2009). Pulmonary embolism and sudden-unexpected death: prospective study on 2477 forensic autopsies performed at the Institute of Legal Medicine in Seville. Available from: [LINK].
  2. NICE. Diagnosing and managing venous thromboembolism in primary, secondary and tertiary care. Published 19th August 2020. Available from: [LINK].


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