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Information ⬇

Author(s): John B. Chambers and David Sprigings

Acute chest pain has a broad differential diagnosis (Box 7.1), ranging from benign to life-threatening disorders. Consider the potentially lethal causes in all patients; these include acute coronary syndrome (ACS), pulmonary embolism and aortic dissection.

The management of acute chest pain is summarized in Figure 7.1.

Priorities ⬆ ⬇

  1. While taking a focused history (Table 7.1), check the pulse and blood pressure, listen over the lungs and:
    • Attach ECG and oxygen saturation monitors.
    • Give oxygen if the patient has severe pain, is breathless, or if arterial oxygen saturation by pulse oximetry is <92%.
    • Put in an IV cannula and take blood for urgent investigation including biomarkers (Table 7.2).
    • Relieve severe pain with morphine 5–10 mg IV plus an antiemetic, for example prochlorperazine 12.5 mg IV.
  2. Correct major arrhythmias (Chapter 39) or hypotension (Chapter 2).
  3. Complete your clinical assessment, record a 12-lead ECG, and compare it with previous ECGs if available. If chest pain persists, repeat the ECG every 15 min. If you suspect ACS but the ECG is normal, include modified leads (lateral and right sided leads) as left circumflex coronary territory or right ventricular ischaemia may not appear with standard lead positions.
    • The working diagnosis is ST-segment elevation acute coronary syndrome (STE-ACS) if there is:
      • ST segment elevation in two or more adjacent leads
      • Left bundle branch block, not known to be old
      • The chest pain is consistent with myocardial ischaemia and has lasted >20 min
    • If the diagnosis is STE-ACS, arrange coronary angiography with a view to primary PCI. If primary PCI is not available, give thrombolysis without delay unless contraindicated (Table 45.2).
    • If the history is not typical of myocardial ischaemia, consider the differential diagnosis (Tables 7.3 and 7.4), and seek urgent advice from a cardiologist before giving thrombolysis.
  4. At this point, you need to review systematically the information you have from clinical assessment, ECG, chest X-ray and biomarkers. Points to note on the chest X-ray are summarized in Table 7.5.
  5. Biomarker results (Table 7.6) must be interpreted in the clinical context. Troponin levels should be checked on admission then at three hours after the onset of chest pain (high-sensitivity cardiac troponin T; hs-cTpT) or after 12 hours (cardiac troponin T; cTpT).
    • Normal levels at three hours after admission of myoglobin, hs-cTpT (12 hours for cTpT) and D-dimer rule out acute coronary syndrome (provided the ECG is normal), pulmonary embolism (in patients at low clinical risk) and aortic dissection (within 24 h of onset of symptoms).
  6. Consider a point-of-care echocardiogram (Table 7.7). This is not widely available and must only be performed by an operator who is trained in echocardiography and subject to the processes of the main echocardiography department (including quality control, continuing education, second opinion):
    • Normal wall motion in the presence of chest pain reduces the likelihood of an ACS. In the presence of ST segment elevation this helps differentiate acute pericarditis from ACS.
    • A dissection flap is visible in up to 90% cases of proximal (Type A) aortic dissection.
    • A pericardial effusion associated with chest pain suggests acute pericarditis or dissection.
    • In clinically suspected pulmonary embolism associated with shock, a dilated RV with raised TR V max is sufficient evidence to give thrombolysis.

Further Management ⬆ ⬇

If the diagnosis is still not obvious, consider other causes (Box 7.7) and ask yourself how closely the clinical picture matches the profile of any of the potentially lethal causes.

Could you be missing an acute coronary syndrome (Chapters 45 and 46)?Could you be missing an acute coronary syndrome (Chapters 45 and 46)?
  • Remember that the pain of myocardial ischaemia and oesophageal pain (due to acid reflux or spasm) may be indistinguishable. Both may radiate to the back or arms, and both may be burning or gripping in quality. Both may be relieved transiently by belching. Angina may occur after meals, but usually during exercise after meals.
  • The presence of ST segment depression or T wave inversion strongly favours an acute coronary syndrome rather than oesophageal pain. A normal ECG does not exclude unstable angina. The differential diagnosis of ST segment changes is given in Table 7.1.
  • The first sign of acute myocardial infarction may be hyperacute peaking of the T wave, which is often overlooked. If present, give aspirin and nitrate, and repeat the ECG in 20–30 min.
  • If the history is compatible with myocardial ischaemia, or the patient is at moderate or high risk of ischaemic heart disease, admit for observation. Repeat the ECG initially after 1 h and await cTpT levels.
  • A normal hs-cTpT on admission and after three hours excludes an ACS, provided the ECG is normal. If there are cardiac risk factors and there is no alternative cause for the pain, a cardiology referral should be made for consideration of secondary prophylaxis and further outpatient investigation. A coronary CT scan can be considered for patients with a low QRisk (<20%). Stress echocardiography or a myocardial perfusion scan are indicated for those with an intermediate risk (20–65%)
Could you be missing pulmonary embolism (Chapter 56)?Could you be missing pulmonary embolism (Chapter 56)?
  • One or more risk factors for venous thromboembolism (Table 56.1) are found in 80–90% of patients with pulmonary embolism. In the absence of these, pleuritic chest pain is more likely to be caused by pneumonia or pleurisy.
  • In patients at low clinical risk, pulmonary embolism is excluded by a normal D-dimer level.
Could you be missing aortic dissection (Chapter 50)?Could you be missing aortic dissection (Chapter 50)?
  • Aortic dissection must be excluded by contrast CT if:
    • The chest pain was instantaneous in onset.
    • There are associated neurological abnormalities.
    • The patient has Marfan syndrome, known dilated aortic root or bicuspid aortic valve, or is pregnant.
  • Remember that the pulses and chest X-ray are normal in at least 50% of patients with aortic dissection. If you suspect aortic dissection, seek urgent advice on further management from a cardiologist.
  • An acute dissection is very unlikely with a normal D-dimer level (within 24 h of onset of symptoms).
Could you be missing oesophageal rupture (Chapter 75)?Could you be missing oesophageal rupture (Chapter 75)?

Spontaneous oesophageal rupture is very rare. Typically the pain follows vomiting (while, in acute myocardial infarction, vomiting follows pain).

  • Check the chest X-ray for mediastinal gas (a crescentic radiolucent zone, which may be retrocardiac or along the right cardiac border), a pleural effusion or a widened mediastinum.
  • If you suspect oesophageal rupture, put the patient nil by mouth and start antibiotic therapy with coamoxiclav and metronidazole. Discuss further management with a gastroenterologist or surgeon.
Could you be missing a pneumothorax (Chapter 64)?Could you be missing a pneumothorax (Chapter 64)?

This usually causes breathlessness rather than chest pain resembling myocardial ischaemia. Look again at the chest X-ray. It is easy to miss a small apical pneumothorax.

Further Reading ⬆

Chambers JB, Marks EM, Hunter MS (2015) The head says yes but the heart says no: what is non-cardiac chest pain and how is it managed? Heart 101, 1240–1249. DOI: 10.1136/heartjnl-2014-306277.

Pollak P, Brady W (2012) Electrocardiographic patterns mimicking ST Segment elevation myocardial infarction. Cardiol Clin 30, 601–615. http://dx.doi.org/10.1016/j.ccl.2012.07.012.

Rybicki FJ, Udelson JE, Peacock WF, et al. (2016) Appropriate utilization of cardiovascular imaging in emergency department patients with chest pain: a joint report of the American College of Radiology Appropriateness Criteria Committee and the American College of Cardiology Appropriate Use Criteria Task Force. J Am Coll Cardiol 67, 853–879.

Vafaie M, Biener M, Mueller M, et al. (2014) Analytically false or true positive elevations of high sensitivity cardiac troponin: a systematic approach. Heart 100, 508–514.