Chest Pain

History of present illness should note the location, duration, character, and quality of the pain. The patient should be asked about any precipitating events (eg, straining or overuse of chest muscles), as well as any triggering and relieving factors. Specific factors to note include whether pain is present during exertion or at rest, presence of psychologic stress, whether pain occurs during respiration or coughing, difficulty swallowing, relationship to meals, and positions that relieve or exacerbate pain (eg, lying flat, leaning forward). Previous similar episodes and their circumstances should be noted with attention to the similarity or lack thereof and whether the episodes are increasing in frequency and/or duration. Important associated symptoms to seek include dyspnea, palpitations, syncope, diaphoresis, nausea or vomiting, cough, fever, and chills.

Review of systems should seek symptoms of possible causes, including leg pain, swelling, or both (deep venous thrombosis [DVT] and therefore possible pulmonary embolism) and chronic weakness, malaise, and weight loss (cancer).

Past medical history should document known causes, particularly cardiovascular and gastrointestinal (GI) disorders, and any cardiac investigations or procedures (eg, stress testing, catheterization). Risk factors for coronary artery disease (CAD—eg, hypertension, dyslipidemia, diabetes, cerebrovascular disease, tobacco use) or pulmonary embolism (eg, lower extremity injury, recent surgery, immobilization, known cancer, pregnancy) should also be noted.

Family history should note history of myocardial infarction (particularly among 1st-degree relatives at an early age, ie, < 55 in men and < 60 in women) and hyperlipidemia.

The extent of physical examination is guided by clinical suspicion. Vital signs and weight are measured, and body mass index (BMI) is calculated. Pulses are palpated in both arms and both legs, blood pressure is measured in both arms.

General appearance is noted (eg, pallor, diaphoresis, cyanosis, anxiety).

The neck is inspected for venous distention and hepatojugular reflux. The neck is palpated for carotid pulses, lymphadenopathy, or thyroid abnormality. The carotid arteries are auscultated for bruit.

Lungs are percussed and auscultated for presence and symmetry of breath sounds, signs of congestion (dry or wet crackles, rhonchi), consolidation (pectoriloquy), pleural friction rubs, and effusion (decreased breath sounds, dullness to percussion).

The cardiac examination notes the intensity and timing of the 1st heart sound (S1) and 2nd heart sound (S2), the respiratory movement of the pulmonic component of S2, pericardial friction rubs, murmurs, and gallops. When murmurs are detected, the timing, duration, pitch, shape, and intensity and the response to changes of position, handgrip, and the Valsalva maneuver should be noted. When gallops are detected, differentiation should be made between the 4th heart sound (S4), which is often present with diastolic dysfunction or myocardial ischemia, and the 3rd heart sound (S3), which is present with systolic dysfunction.

The chest is inspected for skin lesions of trauma or herpes zoster infection and palpated for crepitance (suggesting subcutaneous air) and tenderness. The abdomen is palpated for tenderness, organomegaly, and masses or tenderness, particularly in the epigastric and right upper quadrant regions.

The legs are examined for arterial pulses, adequacy of perfusion, edema, varicose veins, and signs of DVT (eg, swelling, erythema, tenderness).

Pulsus paradoxus may be measured if there is clinical concern for pericardial tamponade (distant heart sounds, jugular venous distension, unexplained dyspnea, tachycardia, or hypotension).

Certain findings raise suspicion of a more serious etiology of chest pain:

• Abnormal vital signs (tachycardia, bradycardia, tachypnea, hypotension)

• Signs of hypoperfusion (eg, confusion, ashen color, diaphoresis)

• Shortness of breath

• Hypoxemia on pulse oximetry

• Asymmetric breath sounds or pulses

• New heart murmurs

• Pulsus paradoxus > 10 mm Hg

Symptoms and signs of thoracic disorders vary greatly, and those of serious and nonserious conditions often overlap. Although red flag findings indicate a high likelihood of serious disease, and many disorders have “classic” manifestations (see table Some Causes of Chest Pain), many patients who have serious illness do not present with these classic symptoms and signs. For example, patients with myocardial ischemia may complain only of indigestion or have a very tender chest wall on palpation. A high index of suspicion is important when evaluating patients with chest pain. Nonetheless, some distinctions and generalizations are possible.

Duration of pain can provide clues to the severity of the disorder. Long-standing pain (ie, for weeks or months) is not a manifestation of a disorder that is immediately life threatening. Such pain is often musculoskeletal in origin, although gastrointestinal origin or a cancer should be considered, particularly in patients who are older. Similarly, brief (< 5 seconds), sharp, intermittent pains rarely result from serious disorders. Serious disorders typically manifest pain lasting minutes to hours, although episodes may be recurrent (eg, unstable angina may cause several bouts of pain over 1 or more days).

Patient age is helpful in evaluating chest pain. Chest pain in children and young adults (< 30 years) is less likely to result from myocardial ischemia, although myocardial infarction can occur in people in their 20s. Musculoskeletal and pulmonary disorders are more common causes in these age groups.

Exacerbation and relief of symptoms also are helpful in evaluating chest pain. Although angina can be felt anywhere between the ear and the umbilicus, it is typically consistently related to physical or emotional stress, ie, patients do not experience angina from climbing one flight of stairs one day and tolerate 3 flights the next day. Nocturnal angina is characteristic of acute coronary syndromes, heart failure, or coronary artery spasm.

Pain from many disorders, both serious and minor, can be exacerbated by respiration, movement, or palpation of the chest. These findings are not specific for origin in the chest wall; about 15% of patients with acute myocardial infarction have chest tenderness on palpation.

Associated findings may also suggest a cause. Fever is nonspecific but, if accompanied by cough, suggests a pulmonary cause. Patients with Raynaud syndrome or migraine sometimes have coronary spasm.

The presence or absence of risk factors for CAD (eg, hypertension, hypercholesterolemia, smoking, obesity, diabetes, positive family history) alters the probability of underlying CAD but does not help diagnose the cause of a given episode of acute chest pain. Patients with those factors may well have another cause of chest pain, and patients without them may have an acute coronary syndrome. However, known CAD in a patient with chest pain raises the likelihood of that diagnosis as the cause (particularly if the patient describes the symptoms as “like my angina” or “like my last heart attack”). A history of peripheral vascular disease also raises the likelihood that angina is the cause of chest pain.

For adults with acute chest pain, immediate life threats must be ruled out. Most patients should initially have pulse oximetry, ECG, and chest x-ray. In patients with hemodynamic instability, a bedside echocardiogram can also be useful in further evaluating potential life-threatening causes. Echocardiography can be particularly useful in identifying left ventricular or right ventricular dysfunction, evidence of RV pressure overload, valvular pathology, pericardial effusions, and signs of pericardial tamponade.

If symptoms suggest an acute coronary syndrome or if no other cause is clear (particularly in at-risk patients), troponin levels are measured. Expeditious evaluation is essential because if myocardial infarction or other acute coronary syndrome is present, the patient should be considered for urgent heart catheterization (when available). Immediate catheterization is indicated in patients with ST-elevation on ECG or non–ST-segment elevation myocardial infarction (NSTEMI) causing hypotension, ventricular arrhythmias, or persistent chest pain despite optimal medical management.

Some abnormal findings on these tests confirm a diagnosis (eg, acute myocardial infarction, pneumothorax, pneumonia). Other abnormalities suggest a diagnosis or at least the need to pursue further investigation (eg, abnormal aortic contour on chest x-ray suggests need for testing for thoracic aortic dissection). Thus, if these initial test results are normal, thoracic aortic dissection, tension pneumothorax, and esophageal rupture are highly unlikely. However, in acute coronary syndromes, ECG may not change for several hours or sometimes not at all, and in pulmonary embolism, oxygenation may be normal. Thus, other studies may need to be obtained based on findings from the history and physical examination (see table Some Causes of Chest Pain).

Because a single normal set of cardiac markers does not rule out a cardiac cause, patients whose symptoms suggest an acute coronary syndrome should have serial measurement of the cardiac marker troponin and ECGs. Drug treatment for suspected acute coronary syndrome

Troponin will be elevated in acute coronary syndromes except unstable angina, and often in other disorders that damage the myocardium (eg, myocarditis, pericarditis, aortic dissection involving coronary artery flow, pulmonary embolism, heart failure, severe sepsis). Creatine kinase (CK) may be elevated due to damage to any muscle tissue, but creatine kinase-MB isoenzyme (CK-MB) elevation is specific to damage to the myocardium. However, troponin is the standard marker of cardiac muscle injury. Advances in high-sensitivity troponin assays allow for more rapid serial evaluation of a possible acute coronary syndrome. With improved negative predictive value, high sensitivity troponin also has the potential to decrease the necessity of further testing in patients with negative biomarkers and has been demonstrated to allow patients to be discharged more quickly (1). Recent guidelines recommend using normal troponin levels and negative coronary CT scanning as a reliable strategy to exclude acute coronary syndrome in patients with chest pain and no red flags (2 ). ST-segment abnormality on the ECG may be nonspecific or due to antecedent disorders, so comparison with previous ECGs is important. Some clinicians follow initial testing (acutely or within several days) with a stress ECG or a stress imaging test.

If a pulmonary embolism (PE) is considered possible, D-dimer testing is done in low- and intermediate-risk patients. The likelihood of pulmonary embolism is affected by a number of clinical factors, which can be used to derive an approach to testing. Many of these factors are included in scoring systems that help determine the probability of PE such as the Wells Scoring System, the Revised Geneva Scoring System, and the Pulmonary Embolism Rule Out Criteria (PERC—3–5).

In patients with chronic chest pain, immediate threats to life are unlikely. Most clinicians initially obtain a chest x-ray and do other tests based on symptoms and signs.

1. 1. Neumann JT, Sorensen NA, Schwemer T, et al: Diagnosis of myocardial infarction using a high sensitivity troponin I 1-hour algorithm. JAMA Cardiol 1(4):397–404, 2016. doi: 10.1001/jamacardio.2016.0695

2. 2. Gulati M, Levy PD, Mukherjee D, et al: 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 144(22):e368–e454, 2021. doi: 10.1161/CIR.0000000000001029

3. 3. Wells PS, Anderson DR, Rodger M, et al: Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med 135(2):98–107, 2001. doi: 10.7326/0003-4819-135-2-200107170-00010

4. 4. Le Gal G, Righini M, Roy PM, et al: Prediction of pulmonary embolism in the emergency department: the revised Geneva score. Ann Intern Med 144(3):165–171, 2006. doi: 10.7326/0003-4819-144-3-200602070-00004

5. 5. Kline JA, Mitchell AM, Kabrhel C, et al: Clinical criteria to prevent unnecessary diagnostic testing in emergency department patients with suspected pulmonary embolism. J Thromb Haemost 2(8):1247–1255, 2004. doi: 10.1111/j.1538-7836.2004.00790.x