Donna Barto is an advanced practice nurse in the ICU/PCU at Virtua Hospital Marlton in Marlton, N.J.
This article originally appeared in March issue of Nursing2013 Critical Care.
The author has disclosed that she has no financial relationships related to this article.
JM, 30, AN OBESE male with no cardiac history, arrives at the ED complaining of substernal chest pressure. He describes the pain as a squeezing sensation that radiates to his left arm, and rates it as a 7 on a pain intensity rating scale of 0 (no pain) to 10 (worst pain imaginable). The pain doesn't change in intensity with position. JM denies illicit drug use and has no evidence of chest wall trauma. He's pale and diaphoretic. His vital signs are as follows: pulse, 72; respirations, 16; SpO2, 100% on room air; and BP, 168/98 mm Hg. Lung sounds are clear bilaterally, heart sounds are normal, neck veins are flat, and he has no peripheral edema. A 12-lead ECG, obtained within 10 minutes of ED arrival, shows ST-segment elevation in leads II, III, and aVF, which may indicate an inferior wall ST-elevation myocardial infarction (STEMI). (See JM's admission ECG.) A chest X-ray shows no acute infiltrates or pulmonary edema and a heart size in the upper limits of normal.
JM is given chewable aspirin, sublingual nitroglycerin, and I.V. morphine, which reduces his pain intensity level to 3. Stat blood work results include a cardiac troponin I level of 29.8 ng/mL (normal range is less than 0.35 ng/mL), and creatine kinase-MB (CK-MB) of 97.9 ng/mL (normal range, 0.5 to 3.6 ng/mL).
After the healthcare provider reviews JM's history, physical assessment findings, troponin level, and ECG, JM is taken to the cardiac catheterization lab. Coronary arteriography reveals normal coronary arteries. JM's ejection fraction is 60% (normal range, 55% to 70%), indicating normal left ventricular function.
Serial cardiac troponin I results show a peak of 40 ng/mL before beginning a downward trend. His clinical picture and ECG suggest an acute coronary syndrome despite normal coronary arteriography.
A cardiologist speaks with JM and finds out that he had flulike symptoms 2 weeks before the onset of his chest pain and hospital admission. After this conversation, the cardiologist suspects that JM's clinical presentation and ECG abnormalities are caused by viral myocarditis.
ST-segment elevation doesn't always indicate myocardial injury. Electrolyte disorders, pericarditis, and central nervous system abnormalities are a few of the clinical situations in which the ECG can mimic the picture seen with STEMI.1 Acute myocarditis can also mimic STEMI, both in the clinical presentation and ECG changes.
An inflammation of the heart muscle, myocarditis is typically caused by viruses such as adenovirus and enterovirus.2 Other causes of myocarditis include bacteria such as meningococcus and streptococcus, and drugs such as cocaine. Patients may report signs and symptoms of a viral infection, such as fever, fatigue, myalgia, or gastrointestinal symptoms, a few days to weeks before onset of chest pain.3 The clinical presentation of myocarditis can range from mild dyspnea or chest discomfort to dysrhythmias, heart failure, cardiogenic shock, and death.
The patient may have elevated nonspecific serum markers of inflammation, such as the erythrocyte sedimentation rate, C-reactive protein, and leukocyte count. Cardiac biomarkers aren't always elevated in myocarditis, but when they are, troponin I is more likely to be elevated than creatine kinase and CK-MB.1,4 Echocardiography can't specifically diagnose myocarditis, but it can be used to rule out other causes of heart failure if the patient has signs and symptoms of heart failure. Endomyocardial biopsy can be performed as a diagnostic tool, but should be reserved for those who are acutely ill with heart failure because the procedure is invasive and associated with serious risks, including cardiac perforation.
A recent development in diagnosing myocarditis has been the use of cardiac magnetic resonance imaging (MRI). Patients such as JM who have an initial diagnosis of STEMI and normal coronary arteriography can be referred for cardiac MRI to determine if myocarditis is causing the signs and symptoms.5
Treatment of acute viral myocarditis depends on the clinical presentation. Patients with cardiomyopathy are treated with standard heart failure therapy. Treatment with antiviral therapy isn't considered beneficial because most patients with acute viral myocarditis are diagnosed several weeks after the infection. Depending on left ventricular function, patients with acute myocarditis are advised to avoid vigorous exercise for up to 6 months after the onset of signs and symptoms.2
JM's echocardiogram taken the day after cardiac catheterization reveals good left ventricular function. After 36 hours of monitoring in the hospital without any evidence of heart failure or dysrhythmias, he's discharged home on an angiotensin-converting enzyme inhibitor for hypertension he experienced throughout his hospital stay. He'll have a follow-up office visit in 1 week.
Patient education for JM includes teaching him about the importance of getting the seasonal influenza vaccine annually to prevent a recurrence of influenza complications such as acute viral myocarditis.6
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