Chest Pain Differential Diagnosis

Myocardial Ischaemic Pain

The main feature of myocardial ischaemia (impending infarction) is usually prolonged chest pain. Typical characteristics of the pain include:
Duration usually over 20 minutes
Located in the retrosternal area, possibly radiating to the arms (usually to the left arm), back, neck, or the lower jaw
The pain is described as pressing or heavy or as a sensation of a tight band around the chest; breathing or changing posture does not notably influence the severity of the pain.
The pain is continuous, and its intensity does not alter
The symptoms (pain beginning in the upper abdomen, nausea) may resemble the symptoms of acute abdomen. Nausea and vomiting are sometimes the main symptoms, especially in inferoposterior wall ischaemia.
In inferoposterior wall ischaemia, vagal reflexes may cause bradycardia and hypotension, presenting as dizziness or fainting.
Electrocardiogram (ECG) is the key examination during the first 4 hours after pain onset, but normal ECG does not rule out an imminent infarction.
Markers of myocardial injury (cardiac troponins T and I, creatine kinase-MB mass) start to rise about 4 hours after pain onset. An increase of these markers is diagnostic of myocardial infarction irrespective of ECG findings.
Minor signs of myocardial infarction in ECG, see Table 1 in the original guideline document
Nonischaemic Causes of Chest Pain

Illness/condition Differentiating symptoms and signs
Reflux oesophagitis, oesophageal spasm
No ECG changes
Heartburn
Worse in recumbent position, but also while straining, like angina pectoris
The most common cause of chest pain

Pulmonary embolism
Tachypnoea, hypoxaemia, hypocarbia
No pulmonary congestion on chest x-ray
Clinical presentation may resemble hyperventilation.
Both arterial oxygen pressure (PaO2) and partial arterial pressure of carbon dioxide (PaCO2) decreased.
Pain is not often marked.
D-dimer assay positive

Hyperventilation
Hyperventilation Syndrome

The main symptom is dyspnoea, as in pulmonary embolism.
Often a young patient
Tingling and numbness of the limbs, dizziness
PaCO2 decreased, PaO2 increased or normal
Secondary Hyperventilation

Attributable to an organic illness/cause; acidosis, pulmonary embolism, pneumothorax, asthma, infarction, etc.

Spontaneous pneumothorax
Dyspnoea is the main symptom.
Auscultation and chest x-ray

Aortic dissection
Severe pain with changing localization
Type A dissection sometimes obstructs the origin of a coronary artery (usually the right) with signs of impending inferoposterior infarction
Pulses may be asymmetrical
Sometimes broad mediastinum on chest x-ray
New aortic valve regurgitation

Pericarditis
Change of posture and breathing influence the pain.
A friction sound may be heard.
ST-elevation but no reciprocal ST depression

Pleuritis
A stabbing pain when breathing. The most common cause of stabbing pain is, however, caused by prolonged cough

Costochondral pain
Palpation tenderness, movements of chest influence the pain
Might also be an insignificant incidental finding

Early herpes zoster
No ECG changes, rash
Localized paraesthesia before rash

Ectopic beats
Transient, in the area of the apex

Peptic ulcer, cholecystitis, pancreatitis
Clinical examination (inferior wall ischaemia may resemble acute abdomen)

Depression
Continuous feeling of heaviness in the chest, no correlation to exercise
ECG normal

Alcohol-related
A young male patient in a casualty department, inebriated


ST changes resembling those of acute ischaemia
ST segment elevation
Early repolarization in V1–V3. Seen particularly in athletic men ("athlete's heart")
Acute myopericarditis in all leads except V1, aVR. Not resolved with a beta-blocker.
Pulmonary embolism – in inferior leads
Hyperkalaemia
Hypertrophic cardiomyopathy



ECG
ST segment depression
Sympathicotonia
Hyperventilation
Pulmonary embolism
Hypokalaemia
Digoxin
Antiarrhythmics
Psychiatric medication
Hypertrophic cardiomyopathy
Reciprocal ST depression of an inferior infarction in leads V2–V3–V4
Circulatory shock

QRS changes resembling those of Q wave infarction
Hypertrophic cardiomyopathy
Wolff-Parkinson-White (WPW) syndrome
Myocarditis
Blunt cardiac injury
Massive pulmonary embolism (QS in leads V1–V3)
Pneumothorax
Cardiac amyloidosis
Cardiac tumours
Progressing muscular dystrophy
Friedreich's ataxia

ST changes resembling those of a non-Q wave infarction
Increased intracranial pressure – subarachnoid bleed – skull injury
Hyperventilation syndrome
Post-tachyarrhythmia state
Circulatory shock – haemorrhage – sepsis
Acute pancreatitis
Myopericarditis