Chest pain accounts at least 5% of presenting complaints of patients attending the Emergency Department (ED) and as a resident doctor working in the ED, it is vitally important to have a systematic approach to help differentiate between benign and life-threatening presentations.
Contents
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This article is based on the brilliant webinar by EM ST6 Dr Jack Almy – do have a watch!
Approach to the patient with chest pain
There is no one fixed algorithm you must follow, but the following steps can help you identify serious pathology without over-investigating everyone who walks into the department:
- Take an appropriate history
- Thoroughly examine the patient
- Form your differential diagnosis
- Choose the right investigations
- Make your diagnosis
Take an appropriate history
History of presenting complaint (SOCRATES)
Site – can be useful to ask the patient to show you where the pain is:
– If they point with one finger, this type of pinpoint pain is typically more associated with somatosensory receptors located in the skin or musculoskeletal system
– If they gesture to a broader area, this pain is typically more visceral and associated with organs and the vasculature.
Onset – is the pain sudden or gradual?
– Sudden – thinking PE, pneumothorax, dissection MSK injury
– Gradual – thinking ischaemia
Tip: If they can remember precisely what they were doing when the pain started, it is more likely to have been sudden in nature.
Character – Is the pain sharp/stabbing or crushing/heavy?
– Similar to above, sharp/stabbing sensation is more associated with a somatosensory stimulus, such as that from skin or MSK, while a more generalised, crushing pain is associated with a visceral stimulus, such as organ or vasculature injury.
Radiation – It is important to remember that both visceral and somatic sensory receptors converge and synapse in the dorsal horn. As such, the brain often misinterprets a visceral stimulus as somatosensory and perceives the pain as from the associated skin/MSK area.
– Cardiac injury (ACS) – may radiate to the jaw, neck or the upper arms
– Aortic injury (dissection) – may radiate through to the back
Associated symptoms – while not definitive, these can help to differentiate between different similar-sounding presentations. Some examples include:
– Diaphoresis and nausea – cardiac chest pain
– Shortness of breath – PE, pneumothorax
– Fever – pericarditis, myocarditis, LRTI
– Swollen lower limb – PE
– Lower limb neurology – aortic dissection
– Haemoptysis – PE
Timing – if a pain is long-standing, it is likely less life-threatening (it’s worth understanding why they have chosen to present with it now however!), but it is important to ensure it has not progressed over time.
– Does the pain recur, and if so, what are the triggers?
– Does it occur at certain times of day? In certain positions?
– Has the pain increased in severity or frequency over time?
Exacerbating/relieving factors – intertwined with timing
– Has the patient tried anything to relieve the pain, and if so, has it been successful (eg, GTN)?
– As above, do certain positions improve or worsen the pain?
– Does exertion change the pain?
Be mindful of using a response to medication as diagnostic; the placebo effect is real!
Severity – Severity of pain has poor correlation with significance of underlying pathology; mild pain does not mean mild pathology!
– Be mindful of patients with diabetes or advanced age as studies suggest they do not experience pain in the same way as the general population.
Past Medical History
Don’t just rely on what is flagged on your electronic records, as the coding is often inaccurate!
Ask the patient themselves and – where possible – try to explore any diagnoses they have received to a fuller extent eg, Previous MI – did they receive PCI? If so, to which vessels? Have they been followed up?
If there are disparities between your findings and the coding, update the coding for future doctors
Drug History
As above – don’t rely on previous records! Ask the patient themselves which medications they take and explore how compliant they are with them. If they have PRNs, do they use them? How often? Are they purchasing any medications over the counter? Have they used any adjuncts?
Thoroughly examine the patient
All patients will have had a set of observations recorded before you can review them, and these can help to form an impression of both how unwell the patient is, but also what the underlying diagnosis is more likely to be.
Always complete a thorough cardiorespiratory examination of the patient. Things not to forget:
– Look from the end of the bed – is the patient sweaty, pale, clammy? Are there adjuncts around?
– Look at the hands – evidence of smoking?
– Assess fluid status – look at the legs, look for the JVP
Form your differential diagnosis
Always form a differential – even if you feel confident of a certain diagnosis, remain open-minded!
Consider the life-threatening diagnoses listed below.
Acute Coronary Syndrome (ACS)
Commonly consists of central, crushing chest pain, radiation to jaw/neck/arms, diaphoresis, nausea and vomiting.
Comprised of three sub-categories:
1. Unstable angina – rupture of a plaque in the coronary arteries causing partial occlusion. There is ischaemia due to reduced oxygen supply but no active infarct. With this, the pain can come on at rest as ischaemia is no longer strictly related to demand. The pain doesn’t typically resolve with GTN.
2. NSTEMI – ruptured plaque causing partial occlusion with evidence of infarct in the subendothelial myocardium. Infarction leads to release of troponin, which we can measure in the blood.
3. STEMI – complete occlusion of a coronary artery causing full transmural infarction of myocardium. There is release of troponin and distinctive changes on the ECG due to poor conduction across the infarcted myocardium.
Risk factors to consider: hypertension, high cholesterol, smoking, diabetes, male, advancing age, South Asian/African-Caribbean descent
Aortic dissection
Presentation commonly consists of sudden-onset, tearing chest pain of maximal intensity radiating to the back +/- pre-syncope/syncope.
Generally categorised using the Stanford classification:
– Type A – tear to the inner layer of the aorta originating from the ascending aorta
– Type B – tear to the inner layer of the aorta originating from the descending aorta
Risk factors to consider: Chronic hypertension but also acute hypertension (eg. following drug use like cocaine), atherosclerosis, advancing age, male, connective tissue disorders eg. Marfans, bicuspid aortic valve, other aortic pathology (eg. coarctation or aneurysm), trauma, pregnancy.
Pulmonary embolism
A classic presentation can involve a combination of the following: sudden-onset, sharp chest pain, shortness of breath and hypoxia, haemoptysis, tachycardia, fevers, wheeze, and presence of swollen calves.
A life-threatening PE will involve haemodynamic instability (hypotension, bradycardia) and can precede cardiac arrest.
Pathology involves clot formation somewhere within the venous system, which gets dislodged and re-occludes in the pulmonary arterial system, causing respiratory dysfunction.
Risk factors are often not all considered, and we have a tendency to incorrectly stratify them:
– High – recent surgery (within last 12 weeks), hospitalisation with heart failure or an MI, previous VTE
– Moderate – Malignancy, pregnancy/post-partum, COCP, lower limb paralysis, thrombophilia (including secondary to autoimmune diseases), IBD and infection, positive family history, advancing age
– Low – prolonged bed-rest, air travel, obesity, varicose veins
Cardiac tamponade
These patients tend to present extremely unwell
Tend to be short of breath and have Beck’s triad – hypotension, muffled heart sounds on auscultation and a raised JVP.
Arises from a pericardial effusion leading to compression of the heart chambers.
Risk factors to consider include: malignancy, pericarditis, recent cardiothoracic surgery, HIV, autoimmune conditions such as SLE or RA, renal disease
Tension pneumothorax
These patients present with ‘pleuritic chest pain’ – sharp and worse on inspiration, difficulty in breathing, tachycardia and hypotension.
Air gets trapped in the pleural space and proceeds to compress the lungs and the heart
Risk factors to be aware of: smoking, chronic lung disease, family history, Marfans, tall and thin build, recent lines inserted in the thorax
Oesophageal rupture
A presentation will involve a severe, central chest pain which radiates to the back and shoulders, pain on swallowing, nausea and vomiting with haematemesis, shortness of breath, fever, and subcutaneous emphysema (crackling under the skin, typically around the collarbones).
Risk factors can include: history of oesophageal disease, foreign body ingestion, severe vomiting, and recent exploration involving the oesophagus (gastroscopy, biopsy, foreign-body retrieval).
Choose the right investigations
Your role as the emergency clinician is to choose the correct tests to rule out the life-threatening diagnoses that could otherwise be missed.
Some tests to consider, from least to most invasive:
– Clinical gestalt (what is your impression?)
– Scoring systems
– The ECG
– Blood tests (troponin, d-dimer, inflammatory markers…)
– Chest X-Ray
– POCUS
– CT
ACS
STEMI – diagnosed by history + new ST-elevation on the ECG at the J point in two leads next to each other of more than 1mm (apart from leads V2 and V3, where elevation must be more than 1mm).
Be mindful of presentations which don’t look like ST-elevation but do represent a full transmural infarct eg. Wellens, De Winter & posterior STEMI (it’s worth looking these up and learning to recognise them!)
NSTEMI – diagnosed by history + troponins
The ECG can look variable but may have ST-depression, Q-waves or T-wave inversion. If the ECG is suspicious but you are not sure, get a repeat and look for any dynamic changes; this increases suspicion of an acute, ongoing process.
There are some confounders which can cause an elevated troponin which you should be aware of (eg. CKD, heart failure). A repeat troponin sent three hours after the initial can help to determine if this is the case – a change in either direction of more than 20% suggests a coronary event.
Unstable angina – diagnosed through history and by ruling out the above.
There may be some ischaemic changes on the ECG such as T-wave inversion, but the troponins will be negative. The history, as mentioned, will involve chest pain at rest that is unresolved with GTN spray.
Other cardiac-sounding chest pain can be risk-stratified using the HEART score which which aims to stratify the 6-week risk of a major cardiac event.
PE
The PERC score can help to rule PE OUT if suspicion is low. If the PERC score can’t rule out a PE, then a Wells‘ score should be used which helps to determine which investigation should be done next:
– A high Wells’ score –> straight to imaging (CTPA if good renal function, may need a VQ if poor)
– A low Wells’ score –> do a D-dimer. D-dimer has a high sensitivity but low specificity. It can help rule out a PE out if low, but a D-dimer can be raised for several reasons so further investigation in the form of imaging may be required.
Other investigations are not particularly sensitive but may support the suspected diagnosis:
– An ABG may demonstrate a respiratory alkalosis due to the body’s initial over-compensation to hypoxaemia.
– ECGs may show changes but these are varied – S1Q3T3 is not particularly common.
– A CXR should be performed to rule out other pathologies
– A point-of-care ultrasound (POCUS) is useful if there is someone trained to perform them as it may demonstrate right ventricular heart strain which is a poor prognostic marker and indicates greater clinical urgency.
Aortic Dissection
An aortic dissection can largely be diagnosed on the history as these patients tend to have numerous risk factors and be in a lot of pain.
There is a risk-stratification score called the Aortic Dissection Detection Score but this is only useful if clinical suspicion is very low.
ECGs are largely non-specific, as are blood tests.
A chest X-ray may demonstrate a widened mediastinum, but this is not specific.
A POCUS may show a pericardial effusion or a dilated aortic root.
The definitive diagnosis is with a CT Angiogram of the aorta.
Initial management in the Emergency Department is supportive with analgesia, strict blood pressure control (aim for as close to 120/80 as possible) and early cardiothoracics input.
Type A dissections will require surgical intervention, while Type B are often managed conservatively (though surgery may be used in complicated presentations).
Make your diagnosis
At this point, you have hopefully ruled out the life-threatening causes for chest pain with some degree of certainty. We need to reassure the patient of this, even if we cannot be certain of the underlying cause for their symptoms, and it may be pertinent to arrange some follow-up (eg, with their GP) to ensure the symptoms resolve.
Conclusion
– A detailed history is the cornerstone of determining the likelihood that the problem is serious
– A robust process to rule out the life-threatening issues is essential
– Do not ignore abnormal observations
– Discuss every patient with a senior colleague (ST4 and above) – this is an RCEM standard!
– Always remember to safety net your patients if no concerning pathology is identified – ensure they know that they should return if things worsen or become unmanageable
Resources
- https://www.bmj.com/content/388/bmj.r136
- https://www.rcemlearning.co.uk/reference/chest-pain-syndromes/
- https://www.rcemlearning.co.uk/reference/chest-pain-low-risk-rule-out-pathways/#1568646432127-2dba9437-c8a1
Written by Dr Zara Milner (FY4)
Edited by Dr Eloise Graham (FY2)
With thanks to Dr Jack Almy (Emergency Medicine ST6) for his work on the original webinar
