|Systemic inflammatory disease|
|Myocardial infarction/Dressler syndrome (pericarditis)|
- Myocarditis is an inflammatory disorder of the cardiac muscle characterized by infiltration of the myocardium by immune cells, and myocyte necrosis.
- The inflammation may be focal or diffuse.
- Any or all cardiac chambers may be involved.
- It may result in regional or global contractile impairment, chamber stiffening, or conduction system disease.
- Clinical manifestation are highly variable depending upon the region of involvement, and include chest pain, acute heart failure, or cardiac arrhythmias.
- Viral illnesses (coxsackievirus, parvovirus, and human herpes virus 6) are the most common causes of myocarditis in the United States.
- Diphtheria is the most common bacterial cause worldwide.
- Chest pain: sharp, pleuritic, and worse with recumbency (95%).
- Pericardial friction rub heard over the left sternal border (15–30%).
- ECG changes: diffuse ST elevations, PR depression in the lateral leads.
- Pericardial effusion.
- Hemodynamic instability secondary to cardiac tamponade.
- Patients may complain of chest pain and dyspnea.
- Heart sounds may be muffled.
- Jugular venous distension.
- ECG demonstrating electrical alternans.
- Large effusion with diastolic right ventricular collapse on bedside echocardiogram.
- Chest pain that may mimic cardiac ischemia.
- Heart failure: dyspnea, fatigue, orthopnea, exercise intolerance.
- Fulminant decompensated heart failure.
- Dysrhythmias, including complete heart block.
- Syncope and sudden cardiac death.
Diagnosis and evaluation
- Acute pericarditis is largely a clinical diagnosis.
- Two of the following four criteria should be met:
- Classic chest pain (sharp, pleuritic, and worse with recumbency).
- Pericardial friction rub.
- ECG changes with new diffuse ST elevation or PR depression in the lateral leads (Table 26.2; Figure 26.1).
- The ST elevations associated with pericarditis can be differentiated from those seen with ST elevation myocardial infarction.
- ST elevations in pericarditis rarely exceed 5 mm.
- ST elevations are diffuse rather than in a vascular distribution.
- Reciprocal ST depression and PR elevation should only be seen in leads aVR and V1.
- Associated temporal changes, such as hyperacute T-waves or Q-waves, are not typically seen in pericarditis.
- Pericardial effusion (Figure 26.2):
- Presence of effusion confirms the diagnosis, though absence does not exclude it.
- Chest radiograph: enlarged cardiac silhouette if effusion is present.
- Inflammatory markers: leukocytes may be normal or elevated, ESR is usually elevated although it is not specific.
- Cardiac markers: may be elevated in myocarditis or postinfarction pericarditis.
- Normal wall motion.
- Evaluate for coexisting effusion; effusion size can be estimated by the distance between the epicardium and the pericardium (<0.5 cm = small effusion; 0.5–2 cm = moderate effusion; >2 cm = large effusion).
- Presence of a large effusion on a bedside echocardiogram with RV collapse during diastole should prompt consideration of impending tamponade.
Table 26.2. ECG manifestations of acute pericarditis
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