THE PATIENT WITH ACUTE CHEST PAIN/CHEST DISCOMFORT

THE PATIENT WITH ACUTE CHEST PAIN/CHEST   DISCOMFORT:

Chest pain is one of the most common complaints for which a patient comes to the physi- cian’s office or the emergency department. Patients presenting with chest pain or chest dis- comfort 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 26-year-old medical resident with chest pain that occurred after on-call and who is otherwise healthy is unlikely to have cardiovascular disease, no matter the quality or duration of chest pain. Consider the 58-year-old man with type 2 diabetes and dyslipid- emia with chest discomfort of any type; now the probability for cardiac-related chest pain increases dramatically.

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. Here are a few clinical pearls to remember:

• 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 which resemble acute abdomen (pain in the upper abdomen, nausea) are not uncommon. Nausea and vomiting are sometimes the main symptoms in inferopos- terior wall ischemia. Also, in inferoposterior wall ischemia, 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 nitro- glycerin sometimes occurs with gastroesophageal reflux disease. 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 myo- cardial ischemia and infarction occur in women.

Physical Examination

One of the most important parts of the examination of the chest pain patient is the “initial impression.” Diaphoresis, tachypnea, and anxious expression should alert the clinician to  a potentially life-threatening process. Tachycardia and tachypnea are both nonspecific but occur in almost all cases of pulmonary embolism. Blood pressure should be checked in both arms: a difference of over 20 mm Hg systolic suggests aortic dissection and is present in about 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.

The chest wall should be inspected for tender areas, respiratory motion, respiratory retrac- tions, 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 syn- dromes. Wide physiologic splitting of the second heart sound (splitting wider with inspira- tion) can be found in right bundle branch block or in right ventricular infarction. New para- doxical 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.

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 athero- sclerotic 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 myo- cardial infarction will have an abnormal initial ECG: 50% with acute MI will have diagnostic findings (ST elevation or Q waves), while 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, elec- trolyte abnormalities, aortic dissection).

In interpreting the ECG, every effort must be made to obtain previous ECGs, so that the 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 gastrointestinal tract. This widely available marker has low sensitiv- ity and specificity for cardiac damage. Furthermore, CK levels may be elevated in a number of noncardiac 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 (see Figure 5-1).

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 myo- cardial 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 two 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. 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: 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.

A chest x-ray should be obtained on patients with chest pain. The x-ray may show pneu- mothorax, pneumomediastinum (such as 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 the clinician suspects a noncardiac diagnosis, other tests may be helpful in the evaluation of patients presenting with acute chest pain. Some of the most common ones used are: arterial blood gases, BNP (see pulmonary and heart failure section), spiral CT scan, etc.

Causes of Chest Pain

Aortic Dissection. Pain is sharp, tearing, and extremely severe; typically radiates to back; loss of pulses or aortic insufficiency often develop; mediastinum is widened on chest x-ray; MI may occur if dissection extends into coronary artery; diagnosis confirmed by MRI, CT scan, transesophageal echocardiogram, or aortography.

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 spiral chest CT, lung scan, or pulmonary angiogram.

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.

Myocarditis. May be preceded by viral illness; pain is generally vague and mild if present; the levels of total CK and the MB fraction of CK (CK-MB) are often elevated; conduction abnor- malities and sometimes Q waves occur.

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.

Gastrointestinal 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 infarc- tion; diagnosis may be confirmed by upper GI series, endoscopy, or esophageal manometry; 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.

Pneumothorax. Onset abrupt with sharp pleuritic chest pain and dyspnea; breath sounds absent, chest x-ray confirms.

Pleuritis. Pain is sharp and increases on inspiration; friction rub or dullness may be present; other respiratory symptoms and underlying pulmonary infection usually present.