Acute pericarditis typically presents as sharp central chest pain that worsens with recumbency and deep breathing and is relieved by leaning forward. The pathognomonic physical finding is the pericardial friction rub, which is usually auscultated along the lower left sternal border. The ECG is useful in the diagnosis of acute pericarditis, with abnormalities found in approximately 90 per cent of cases. Changes on ECG classically occur in four stages. All cases of acute pericarditis do not show all the 4 stages. In fact, all four stages are present in only 50 per cent of patients or less.
The stage I occurs during the first few days of pericardial inflammation and is characterized by diffuse ST-segment elevation. This stage may last up to two weeks. Stage II is characterized by return of the ST-segments to baseline and flattening of the T-wave and may last from days to several weeks. Stage III usually begins at the end of the second or third week and is characterized by inversion of the T-waves in the opposite direction of the ST-segment;this stage may last several weeks. Stage IV represents the gradual resolution of the T-wave changes and may last up to three months. The most sensitive ECG change characteristic of acute pericarditis is ST-segment elevation, which reflects the abnormal repolarization that develops secondary to pericardial inflammation. The following features differentiate the pericarditis and acute myocardial ST elevations.
1) The ST-segment elevation that occurs during acute pericarditis is usually “concave”,compared with the “convex” appearance of the ST-segment that occurs during the acute injury stage of a myocardial infarction.
2) In acute pericarditis there is widespread ST-segment elevation not corresponding with any specific arterial territory, which usually occurs in association with acute myocardial infarction.
3) Reciprocal changes are absent in acute pericarditis, while they are frequent with acute myocardial infarction.
4) The ST-segments in acute pericarditis return to baseline in a few days and are followed by diffuse T-wave inversion, in conjunction with the ST-segment at baseline. In contrast, T inversion in infarction occurs before ST-segment returns to baseline.
5) Another feature that may aid in differentiating acute pericarditis from acute myocardial infarction is the absence of Q-waves.
6) Loss of R-wave progression may occur with acute myocardial infarction, but this feature is not present with acute pericarditis.
There may also be ST-segment depression in leads aVR and V1. In the absence of underlying cardiac disease, the P-wave and QRS complexes are normal. Depression of the PR-segment is very specific of acute pericarditis and is attributed to subepicardial atrial injury and occurs in all leads except aVR and V1. These leads may exhibit PR-segment elevation. Symptoms subside within two weeks and ECG changes resolve over a period of weeks to months. Development of atrial and ventricular arrhythmias, heart blocks and fascicular blocks does not occur in acute pericarditis. Presence of these changes in the setting of acute pericarditis indicates the presence involvement.
The stage I occurs during the first few days of pericardial inflammation and is characterized by diffuse ST-segment elevation. This stage may last up to two weeks. Stage II is characterized by return of the ST-segments to baseline and flattening of the T-wave and may last from days to several weeks. Stage III usually begins at the end of the second or third week and is characterized by inversion of the T-waves in the opposite direction of the ST-segment;this stage may last several weeks. Stage IV represents the gradual resolution of the T-wave changes and may last up to three months. The most sensitive ECG change characteristic of acute pericarditis is ST-segment elevation, which reflects the abnormal repolarization that develops secondary to pericardial inflammation. The following features differentiate the pericarditis and acute myocardial ST elevations.
1) The ST-segment elevation that occurs during acute pericarditis is usually “concave”,compared with the “convex” appearance of the ST-segment that occurs during the acute injury stage of a myocardial infarction.
2) In acute pericarditis there is widespread ST-segment elevation not corresponding with any specific arterial territory, which usually occurs in association with acute myocardial infarction.
3) Reciprocal changes are absent in acute pericarditis, while they are frequent with acute myocardial infarction.
4) The ST-segments in acute pericarditis return to baseline in a few days and are followed by diffuse T-wave inversion, in conjunction with the ST-segment at baseline. In contrast, T inversion in infarction occurs before ST-segment returns to baseline.
5) Another feature that may aid in differentiating acute pericarditis from acute myocardial infarction is the absence of Q-waves.
6) Loss of R-wave progression may occur with acute myocardial infarction, but this feature is not present with acute pericarditis.
There may also be ST-segment depression in leads aVR and V1. In the absence of underlying cardiac disease, the P-wave and QRS complexes are normal. Depression of the PR-segment is very specific of acute pericarditis and is attributed to subepicardial atrial injury and occurs in all leads except aVR and V1. These leads may exhibit PR-segment elevation. Symptoms subside within two weeks and ECG changes resolve over a period of weeks to months. Development of atrial and ventricular arrhythmias, heart blocks and fascicular blocks does not occur in acute pericarditis. Presence of these changes in the setting of acute pericarditis indicates the presence involvement.
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