Typical angina at any age presents as substernal chest pain, often described as “pressure like,” with radiation to the jaw, neck, or arm. If a patient has experienced an MI in the past, asking the patient if this pain is similar to that experienced during a previous MI can be an important clue. Descriptions of chest pain radiating to the back, may be more suggestive of aortic dissection or gastrointestinal pathology such as esophageal reflux. If patients complain that they feel chest pain after eating or when lying flat, one should consider gastroesophageal reflux as a possible diagnosis.
Features suggesting acute coronary syndrome include diaphoresis, cool clammy skin, new or progressive shortness of breath, and/or exertional shortness of breath. Older patients are typically more likely to delay seeking medical care, or be more inclined to attribute their symptoms to “normal aging,” which can lead to increased adverse outcomes or death if the etiology of the chest pain is serious in nature. Most older adults with acute coronary syndrome present to medical professionals with dyspnea, diaphoresis, nausea/vomiting, and/or syncope, and not necessarily with chest pain. In addition, given that older adults have a higher prevalence of comorbidities, concurrent disease processes may cloud the presentation of acute coronary syndrome. Moreover, patients with delirium or dementia may have trouble communicating their symptoms accurately to their clinician.
Physical examination should begin with vital signs, with special attention to blood pressure, heart rate, and oxygen saturation, to assess the clinical stability of the patient.
Next, the clinician should assess the cardiovascular system. Check blood pressure in both arms, a discrepancy of more than 20 mm Hg systolic between readings, without a history of vascular compromise in either limb should raise suspicion of aortic dissection, especially if the patient describes a “ripping” or “tearing” quality to his chest pain. If heart sounds are muffled on cardiac auscultation, cardiac tamponade should be considered as a cause of distress. Additional signs and symptoms of cardiac tamponade include pulsus paradoxus (a decrease in systolic pressure of >10 mm Hg during inspiration), and hypotension. Cardiac tamponade is more common in the setting of certain chronic illnesses including autoimmune disease, malignancy, or a recent history of acute trauma to the chest. If a cardiac rub is present, a diagnosis of pericarditis should be entertained. A loud new holosystolic murmur, is suggestive of acute coronary pathology and possibly mitral valve papillary dysfunction. Elevated jugular venous pressure and an S3 gallop suggest congestive heart failure. New congestive heart failure in the setting of chest pain should be considered a medical emergency and prompt swift work up to rule out serious diagnoses such as acute coronary syndrome. In the setting of chest pain that varies with respiration with or without the presence of hemoptysis, pulmonary embolism should be considered. Pain on palpation of the chest wall may indicate musculoskeletal pain or costochondritis and can provide reassurance to the clinician and patient. Lower-extremity edema that is symmetric in both limbs and acute or subacute may be suggestive of right heart failure; however, if there is unilateral swelling, one must suspect venous thromboembolism and consider evaluation for pulmonary thromboembolism as a cause of chest pain. In this scenario, chest pain may also be associated with hypoxia and tachycardia and be exacerbated by respiration.
The standard cardiac chemistry panel includes creatinine kinase (CK), creatinine kinase–myocardial bound (CK-MB), and troponin I. CK is leaked out of injured muscle cells and is not specific to myocardial injury. CK-MB as an isoenzyme is more specific to myocardial injury; additionally, when a ratio to CK is performed, if >4.5% of the total CK it is suggestive of myocardial injury. Troponin I is more specific and sensitive to myocardial injury; however, it can take up to 8 hours from initial event to abnormal rise in number. In the case of recurrent injury, CK-MB has a shorter half-life and if it were to rise again in a presumed acute setting, would be a more reliable marker of repeat myocardial injury. Other diagnostic tests that may be of use include D-dimer for work up of pulmonary embolism (see Chapter 32, “Peripheral Arterial Disease & Venous Thromboembolism”).
Diagnostic tests and imaging studies—
Electrocardiogram (ECG) is the first step in the chest pain work up of an older patient. It is important to obtain a previous ECG for comparison; in this age group, patients may already have significant cardiac history, thereby further confounding acute findings, particularly without a comparison study. S-T elevations in a specific coronary territory raises concern for acute coronary plaque rupture and ST-segment elevation MI. Diffuse S-T elevations or depressions may be more suggestive of pericarditis in the appropriate clinical context. ECG findings of cardiac tamponade include blunting of the voltage of QRS complexes, in association with dyspnea and the presence of electrical alternans—a beat to beat variation of QRS complexes in an alternating pattern.
On chest radiography, the presence of a widened mediastinum, if clinical history suggests, should raise suspicion of an aortic dissection. Suspicion for pulmonary thromboembolism or aortic dissection should prompt the clinician to order a CT chest with contrast for diagnostic purposes.
Progressive dyspnea that accompanies chest pain with exertion (angina) should be evaluated with a stress test, either an exercise stress test with an imaging modality such as echocardiogram or nuclear imaging. An imaging modality is absolutely necessary as baseline abnormalities on ECG can confound results during stress testing. Frail older patients may be limited by their functional capacity and unable to complete an exercise stress test. In appropriate patients, using a bicycle instead of a treadmill can sometimes compensate for these functional deficits, for patients who are unable to reach target heart rate with exercise, pharmacologic testing is a viable alternative.
Gastrointestinal causes of chest pain can be mistaken for angina. If the patient notes a correlation of symptoms to food, consider an empiric trial of acid suppression, or if clinically indicated, a barium swallow exam which may show multiple strictures in corkscrew pattern if the patient is suffering from esophageal spasm. Upper endoscopy may be helpful in the diagnosis of esophagitis (see Chapter 35, “Gastrointestinal & Abdominal Complaints,” for further discussion of work-up for esophageal and other gastrointestinal disorders).