A "Diagnostic approach of the adult with chest pain" was made in 2020. It is related to Cardiovascular Medicine.

1. ACUTE CHEST PAIN / DISCOMFORT
̵ Chest pain or discomfort is one of the most common complaints that brings patients
to the physician’s office or emergency department.
̵ Patients presenting with this symptom may have an underlying cause that is benign
and requires only moderate analgesic medication, or they may have a life-threatening
condition such as acute myocardial ischemia or aortic dissection that mandates prompt
diagnosis and treatment.
̵ In the evaluation of chest pain, the focus should be on excluding the more serious
conditions.
History
Assessing the setting in which the chest pain occurs is one of the most important
aspects of the evaluation.
 The healthy 26-year-old medical resident with chest pain that occurred after on-call
is unlikely to have cardiovascular disease, no matter the quality or duration of chest
pain.
 The 58-year-old man who has type 2 diabetes and dyslipidemia with chest
discomfort of any type has a much higher probability for cardiac-related chest pain.
Overall, the chest pain history is more useful than the physical examination. Important
aspects of the history include duration, quality, location, radiation, frequency, alleviating
or precipitating factors (especially exercise), and associated symptoms.
• For both stable angina and acute coronary syndromes, the quality of chest pain
is described by the patient as “tightness, heaviness, or pressure,” but symptoms
resembling acute abdomen (pain in upper abdomen, nausea) are not uncommon.
Nausea and vomiting are sometimes the main symptoms in inferoposterior wall
ischemia (also, vagal reflexes may cause bradycardia and hypotension, presenting as
dizziness or fainting).
• “Sharp” or “knife-like” chest pain and pain which the patient can pinpoint to
an “exact area” are less likely to be related to ischemia or infarction, especially if
the chest pain is reproduced by changes in position or palpation.
• Myocardial infarction is associated with pain that lasts >20–30 minutes in duration.
• Response of chest pain to nitroglycerin (within a few minutes) is most consistent
with transient ischemia or esophageal spasm.
Chest pain that worsens with nitroglycerin sometimes occurs with GERD

2. The response to nitroglycerin is not enough to confirm coronary disease as the
cause of chest pain.
• Acute coronary syndromes in women present with atypical symptoms: dyspnea,
shortness of breath, fatigue. This may be due to the older age group in which
myocardial ischemia and infarction occur in women.
Physical Examination
One of the most important parts in a chest pain examination is “initial impression.”
Diaphoresis, tachypnea, and anxious expression should alert you to a potentially life-
threatening process. Tachycardia and tachypnea are both nonspecific but occur in almost
all cases of pulmonary embolism.
• Check BP in both arms: a difference of >20 mm Hg systolic suggests aortic
dissection and is present in ~70% of cases.
• Hypotension may suggest massive pulmonary embolism or cardiac shock.
• Fever may suggest pneumonia or mediastinitis (esophageal rupture) as the
cause of chest pain.
• Evidence of atherosclerosis (corneal lipid rings, narrowed retinal arteries, and
pigment and hair changes in the legs) is commonly seen in patients with
coronary syndromes.
̵ Inspect the chest wall for tender areas, respiratory motion, respiratory retractions, or
accessory muscle use. If the tender area corresponds to the location of the patient’s
pain and palpation exactly reproduces the pain, consider musculoskeletal chest pain as
the cause of chest pain.
̵ Abnormal heart sounds and new murmurs are commonly found in certain chest pain
syndromes.
➢ Wide physiologic splitting of the second heart sound (splitting wider with
inspiration) can be found in right bundle branch block or in right ventricular
infarction.
➢ New paradoxical splitting is most often due to left bundle branch block (LBBB),
or anterior or lateral infarction.
➢ A new fourth heart sound can occur with angina or infarction.
➢ An S3 is more likely due to underlying heart failure.
➢ A new murmur may be significant: aortic regurgitation occurs in over half of
patients with aortic dissection, while mitral regurgitation can occur in patients
with angina or infarction and is due to papillary muscle dysfunction.

3. ̵ The lungs should be auscultated for crackles and asymmetrical breath sounds.
Asymmetry of breath sounds may be found in patients with spontaneous
pneumothorax.
Absent lung sounds also may occur in pneumothorax and pleural effusions.
̵ The extremities should be examined for pulses, edema, calf tenderness, and signs of
atherosclerotic vessel disease.
➢ Absence of pedal pulses may occur in aortic dissection.
➢ Any swelling of the legs, especially if unilateral, raises the odds of pulmonary
embolism as the cause of chest pain.
Testing
All patients with chest pain should have a 12-lead electrocardiogram (ECG) since the
ECG is the single most important test for the evaluation of the cause of chest pain.
The ECG should be done immediately after initial stabilization and taking of vital signs.
Most patients with myocardial infarction will have an abnormal initial ECG:
• 50% with acute MI will have diagnostic findings (ST elevation or Q waves)
• 35% will have findings consistent with ischemia (ST depression and/or T wave
inversion)
• In patients presenting with acute chest pain who have normal ECG, the chance of
acute MI is much less than 10% (in some studies 1–2.6%).
• An abnormal ECG can be seen in many non-cardiac conditions (pulmonary
embolism, electrolyte abnormalities, aortic dissection).
̵ In interpreting the ECG, make every effort to obtain previous ECGs, so that
abnormalities can be compared with those on the old tracing. Any ECG finding is
assumed to be new unless proven otherwise by an old ECG (if one is available). Also,
in patients with acute coronary syndromes, the ECG is the sole test required to select
patients for emergency reperfusion.
̵ Serum cardiac biomarker determinations play a vital role in the evaluation of patients
who present with acute chest pain and in the diagnosis of acute myocardial infarction.
̵ Serum markers such as aspartate transaminase, lactate dehydrogenase, and lactate
dehydrogenase subforms no longer are used because they lack cardiac specificity and
their delayed elevation precludes early diagnosis.
̵ Creatine kinase (CK) is found in striated muscle and tissues of the brain, kidney, lung,
and GI tract. This widely available marker has low sensitivity and specificity for cardiac
damage. Furthermore, CK levels may be elevated in a number of noncardiac

4. conditions, including trauma, seizures, renal insufficiency, hyperthermia, and
hyperthyroidism.
Currently, the CK marker largely has been replaced by cardiac troponins and CK-MB.
 CK-MB isoenzyme: CK-MB is cardiac specific and is useful for the early diagnosis of
acute myocardial infarction. CK-MB typically is detectable in the serum 4–6 hours after
the onset of ischemia, peaks in 12–24 hours, and normalizes in 2–3 days.
Like the CK level, the peak CK-MB level does not predict infarct size; however, it
can be used to detect early reinfarction. Serial CK-MB levels commonly are obtained
at admission to the emergency department and are repeated in 6–12 hours.
CK-MB subforms: CK-MB may be further characterized into subforms (or isoforms).
CK-MB2 is found in myocardial tissue, and CK-MB1 is found in plasma. The CK-MB
subform is not routinely used.
 Cardiac troponins: Troponins (T, I, C) are found in striated and cardiac muscle.
Because the cardiac and skeletal muscle isoforms of troponin T and I differ, they are
known as the “cardiac troponins.” They are the preferred markers for the diagnosis
of myocardial injury. Troponin T and I generally have similar sensitivity and specificity
for the detection of myocardial injury.
Unlike troponin I levels, troponin T levels may be elevated in patients with renal
disease, polymyositis, or dermatomyositis.
The cardiac troponins typically are measured at emergency department admission and
repeated in 6–12 hours.
Patients with a normal CK-MB level but elevated troponin levels are considered to
have sustained minor myocardial damage, or microinfarction, whereas patients with
elevations of both CK-MB and troponins are considered to have had acute myocardial
infarction.
The cardiac troponins may remain elevated up to 2 weeks after symptom onset, which
makes them useful as late markers of recent acute myocardial infarction.
An elevated troponin T or I level is helpful in identifying patients at increased risk for
death or the development of acute myocardial infarction. Increased risk is related to the
high serum troponin levels. The troponins also can help identify low-risk patients who
may be sent home with close follow-up.

5. Those with a normal or nearly normal ECG and a normal troponin I test 6 hours after
admission had a very low risk of major cardiac events (0.3%) during the next 30 days.
̵ Myoglobin levels begin to rise as early as 1–4 hours after the onset of pain. Normal
myoglobin at 4 hours has a very high negative predictive value.
̵ Chest x-ray should be obtained on patients with chest pain; it may show
pneumothorax, pneumomediastinum (i.e., from esophageal rupture), pleural effusion,
or infiltrates. Aortic dissection can cause widening of the mediastinum. Subtle findings
such as loss of lung volume or unilateral decrease in vascular markings may suggest
pulmonary embolism.
̵ Especially if a noncardiac diagnosis is suspected, arterial blood gases, BNP, and CT
angiogram may be helpful for evaluating acute chest pain.

6. Causes of Chest Pain
1. Aortic Dissection
▪ Pain is sharp, tearing, and extremely severe; typically radiates to back; loss of pulses
or aortic insufficiency often develop
▪ On chest x-ray, mediastinum is widened MI may occur if dissection extends into
coronary artery
▪ Diagnosis confirmed by MRI, CT scan, or transesophageal echocardiogram
2. Pulmonary Embolism
▪ Dyspnea, tachycardia, and hypoxemia are prominent; pain is usually pleuritic,
especially when pulmonary infarction develops.
▪ EKG is usually nonspecific but may show S wave in lead I, Q wave in lead III, or
inverted T wave in lead III
▪ Diagnosis confirmed by CT angiogram
3. Pericarditis
▪ May be preceded by viral illness; pain is sharp, positional, pleuritic, and relieved by
leaning forward.
▪ Pericardial rub often present
▪ Diffuse ST elevation occurs without evolution of Q waves
▪ CK level usually normal
▪ Responds to anti-inflammatory agents
4. Myocarditis
▪ May be preceded by viral illness;
▪ pain is generally vague and mild if present;
▪ total CK and MB fraction of CK (CK-MB) are often elevated;
▪ conduction abnormalities and Q waves may occur.
5. Musculoskeletal Disorders
▪ Most common cause of chest pain.
▪ Includes costochondritis, cervical osteoarthritis, radiculitis;
▪ pain is atypical, stabbing, localized, may be pleuritic; reproduced by motion or
palpation;
▪ EKG changes absent.
6. GI Disorders
▪ Esophageal reflux is often made worse with recumbency or after meals, may be
associated with regurgitation and relieved by antacids; episodes of spasm may be
brought on by cold liquids, relieved by nitroglycerin, and may closely resemble angina
or infarction; diagnosis may be confirmed by upper endoscopy or esophageal
manometry.

7. ▪ Peptic ulcer disease, pancreatitis, and cholecystitis may occasionally mimic
infarction;
Abdominal tenderness is present, with radiation to back and elevated amylase in
pancreatitis;
Sonography can confirm cholecystitis.
7. Pneumothorax
▪ Onset abrupt with sharp pleuritic chest pain and dyspnea;
▪ breath sounds absent;
▪ chest x-ray confirms.
8. Pleuritis
▪ Pain is sharp and increases on inspiration; friction rub or dullness may be present;
▪ other respiratory symptoms and underlying pulmonary infection usually present.

8. Emergency department approach to chest pain
ACS: acute coronary syndrome; ASA: aspirin; CXR: chest x-ray; ECG: electrocardiogram; HF: heart failure; PCI:
percutaneous coronary intervention.