Million People in This Country

¶ … million people in this country will suffer chest pain related to myocardial infarction this year. Of those people, 50% will die before they ever get to the hospital. Because of this, evaluation of chest pain is possibly one of the most important elements of nursing assessment skills. This paper will review the assessment of myocardial infarction vs. angina.

Clinical paper

Chest pain is notoriously difficult to assess. Depending on the signs and symptoms, findings on the ECG and lab results the management of the patient differs significantly. The classic presenting symptoms of a myocardial infarction (MI) is chest pain or discomfort. Angina pectoris may present the same way but will generally be of shorter duration. Both may be describes as pain, pressure, tightness, heaviness, burning or squeezing. Both may radiate into arms, shoulders, jaw or back. Not all patients will have these classic symptoms.

While any patient with chest pain requires careful evaluation, the presence of risk factors may alert the evaluator to a greater likelihood of cardiac etiology to chest pain. Patients who have a history of smoking, hypertension, hyperlipidemia, obesity, sedentary lifestyle, diabetes or alcoholism all have a greater risk of atherosclerotic coronary artery disease.

Women frequently experience atypical chest discomfort. Patients with diabetes or other neuropathic conditions may experience a silent MI. Angina is most frequently precipitated by activity. An MI may be precipitated by exertion or stress, but most often occur at rest. Intervention for any patient being evaluated for MI vs. angina must be rapid. Vital signs to include pulse oximetry are important parts of the physical assessment, and the patient should receive aspirin immediately (Tough, 2004).

Angina may take many different forms, and therefore may be difficult to discern from the MI. As previously noted, angina is caused by exertion which increases the heart's oxygen demand. Anything which increases the work of the heart - a heavy meal, emotional stress - can lead to angina. Unlike the MI, angina is generally relieved by rest of the administration of nitroglycerine. Prinzmetal variant angina is caused by coronary artery spasm and may occur without increased myocardial oxygen demand. This patient may often report pain in the chest occurring in the morning or when he or she wakes. Unstable angina is another variant, but does not usually respond to rest or nitroglycerine.

All patients should receive supplemental oxygen while being evaluated for chest pain. Oxygen should be provided at a level to keep blood saturation levels at 90% or better (Sommers, 2002). Intravenous access should be obtained and 12 lead ECG/continuous monitoring plus blood draw for enzymes. The patient with angina will respond to sublingual nitroglycerine given 0.3 mg to 0.4 mg repeated every 5 minutes for up to three doses. If pain persists after the third dose, suspicion for MI should be high (Harvey, 2004). An ECG is the next step in assessment of the patient with angina vs. MI, although it should be noted that only 45% of all the patients with MI will have obvious ischemic changes on their ECG. Patients should be monitored for minor changes. ST segment elevations with tall T. waves will usually be the first changes (Docherty, 2003). Evaluators should also be sensitive to ST segment depression in leads which are opposite the site of the injury. T-wave inversion and the development of Q. waves are considered to be pathologic evidence of evolving MI. Changes like these will appear within hours of the infarction and the changes may remain on the ECG indefinitely or eventually resolve. It should be noted that in patients with non-ST segment elevation MI the changes on the ECG will be much less specific.

No one serological test can identify MI from angina. Serological markers can be used to evaluate for myocardial infarction. Troponin T. And Troponin I may be sensitive for the smallest amount of myocardial damage. Troponin levels usually begin to elevate 2-3 hours after the onset of myocardial damage.