Electrocardiographic diagnostics
The pathophysiological basis of ECG changes in acute pericarditis is inflammation of the subepicardial layers of the myocardium. This leads to marked disturbances in ventricular repolarization processes, which is graphically reflected in the ST segment and T wave.
Dynamics of ECG changes:
- Early stage (days 1–2): Characterized by a marked ST-segment elevation. A critical feature is the diffuse nature. Elevation is recorded in almost all standard and chest leads, which differentiates pericarditis from localized ischemic injuries.
- Stage of dynamic changes (several days): The ST segment begins a gradual return to the isoelectric line.
- Stage of negative T wave formation: The formation of a negative T wave occurs strictly after the ST segment has completely returned to the baseline. This is a critically important differential diagnostic sign. At the stage of clinical improvement, the ST segment becomes isoelectric, and the T wave flattens.
Differential diagnostics The main difference between acute pericarditis and myocardial infarction (MI) is that in pericardial inflammation, a pathological Q wave—characteristic of myocardial necrosis—is never formed.
Laboratory findings
The laboratory picture of acute pericarditis is non-specific, but vividly reflects the presence of an acute inflammatory process in the body and myocardial response.
Complete blood count (CBC): Classical signs of systemic inflammation are observed:
- Pronounced leukocytosis;
- Left shift of the leukocyte formula (due to an increase in band neutrophils);
- Elevated erythrocyte sedimentation rate (ESR).
Blood biochemistry: Patients may exhibit an increase in cardiac enzyme levels, specifically transaminases. Pathogenetically, this phenomenon is not associated with cardiomyocyte death (as in infarction), but with concomitant involvement of the superficial layers of the heart muscle adjacent to the pericardium in the inflammatory process.
Principles of treatment
The therapeutic strategy for acute pericarditis is built on two main directions:
- Etiotropic therapy. This is the foundation of treatment. Tactics directly depend on the nature and origin of the underlying disease that served as the trigger for the development of pericarditis (e.g., infection, autoimmune process, or uremia).
- Drug (pathogenetic) therapy. The baseline and most appropriate prescription for suppressing inflammation in the pericardial area is the use of nonsteroidal anti-inflammatory drugs (NSAIDs).
Briefly: answers to topical questions
How does the PR segment change on the ECG in acute pericarditis?
In acute pericarditis, a characteristic change of the acute phase on the ECG can be PR segment depression. Acute pericarditis is also characterized by widespread ST-segment elevation: in the early stage, it is recorded in almost all standard and chest leads, and then gradually returns to the isoelectric line over several days.
What auscultatory signs are characteristic of dry pericarditis?
Acute pericarditis is characterized by a specific sound phenomenon—a pericardial friction rub. It occurs due to pathology and friction of the inflamed pericardial layers.
- Localization — auscultated over the sternum or at its left margin (in the area of absolute cardiac dullness).
- Radiation — the rub is strictly localized, and its intensity drops sharply when moving away from the sternum.
- Components — in the classical variant, the rub has three components (atrial systole, ventricular systole, and diastole), but more frequently only two components or a single systolic component are heard.
How do C-reactive protein (CRP) and troponin levels change in pericarditis?
In acute pericarditis, serum C-reactive protein (CRP) levels are elevated in the majority of patients and serve as the primary marker of inflammation. CRP dynamics are used to monitor disease activity and treatment efficacy; high CRP after acute pericarditis is a predictor of recurrence or a marker of an unidentified underlying disease.
Troponins I and T are elevated in concomitant myocardial involvement. The combination of acute pericarditis criteria with signs of myocardial injury, including elevated troponins I/T or CK-MB, is the basis for diagnosing myopericarditis.
What echocardiographic (EchoCG) signs are characteristic of acute pericarditis?
On EchoCG, clinical and instrumental signs of acute pericarditis include the presence of pericardial effusion and separation of the pericardial layers.
Following acute pericarditis, EchoCG control is mandatory within the first 12 weeks to rule out recurrence without pain syndrome but with exudate formation.
What diseases can act as a trigger for the development of acute pericarditis?
Trigger/etiological factors of acute pericarditis can include various infectious and non-infectious causes:
- Infections — viral infection, including Coxsackie and ECHO viruses; cytomegalovirus pericarditis in immunocompromised individuals and HIV; tuberculosis.
- Systemic connective tissue diseases — systemic lupus erythematosus (SLE) and rheumatoid arthritis.
- Metabolic disorders — uremic pericarditis in chronic kidney disease and myxedematous pericarditis in severe hypothyroidism.
- Coronary heart disease/myocardial infarction — pericarditis in the acute period of myocardial infarction and in the late period as Dressler syndrome.
- Tumors — malignant neoplasms, including paraneoplastic processes or metastasis.
The rule "First descent, then negative": in acute pericarditis, a negative T wave forms only after the ST segment has completely returned to the baseline.
Class and exam questions
How to distinguish pericarditis from myocardial infarction on an ECG?
In pericarditis, ST elevation is diffuse (in all leads), a negative T wave appears only after ST returns to the baseline, and a pathological Q wave is never formed.
What causes the elevation of transaminases in blood biochemistry?
This is pathogenetically related to the spread of the inflammatory process from the pericardial layers to the superficial (subepicardial) layers of the myocardium.
Which group of drugs is baseline for drug therapy?
The prescription of nonsteroidal anti-inflammatory drugs (NSAIDs) is appropriate.
What else to study on this topic
- Etiological factors: infectious and non-infectious causes of pericarditis
- Clinical presentation and features of pain syndrome
- Cardiac auscultation: pericardial friction rub
- Echocardiography (EchoCG) in diagnosing pericardial effusion
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