Etiology and morphological changes
In most clinical scenarios, the disease is idiopathic or nonspecific. However, among established causes, special attention is paid to infectious agents, primarily tuberculosis. In addition, systemic connective tissue diseases, various tumor processes, and the consequences of prior radiation therapy (radiation exposure) can lead to the development of this pathology.
The morphological basis of the disease lies in the structural alteration of the pericardial layers. Fusion of the parietal and visceral layers occurs, which can be either complete or partial. The layers themselves significantly thicken, and calcium salts begin to deposit within their tissues, forming pronounced calcinosis (calcification). Signs of cardiac compression can be triggered not only by adhesions and fibrosis, but also by the accumulation of fluid within the enclosed space of the pericardial cavity.
Hemodynamic disorders
The altered, calcified, and rigid pericardium forms a dense framework around the heart that mechanically prevents its normal relaxation during diastole. As a result, diastolic ventricular filling is critically impaired.
It is precisely the inability of the heart to adequately relax and accommodate venous return that triggers a cascade of hemodynamic disorders, resulting in diastolic heart failure. This condition requires clear differential diagnosis, as the contractile (systolic) function of the myocardium may remain preserved for a long time.
Clinical Presentation and Physical Status
The leading clinical syndrome is systemic venous congestion. Patients complain of severe general weakness and rapid fatigue. Examination reveals:
- Early onset of ascites;
- Hepatomegaly (significant enlargement of the liver);
- Peripheral edema;
- A specific symptom — prominent jugular venous distention.
Physical examination findings reveal several characteristic features. Heart size on percussion may remain within normal limits or be enlarged. Precordial pulsation is weakened. On auscultation, heart sounds are muffled. A pathognomonic auscultatory sign (specific only to this pathology) is the appearance of an extra sound immediately following the second heart sound — the so-called pericardial sound or «pericardial knock».
Assessment of hemodynamic parameters reveals pulsus paradoxus, as well as a decrease in arterial and pulse pressure. An increase in left atrial size is frequently observed.
Instrumental diagnostics and treatment
A complex of instrumental methods is used to confirm the diagnosis:
- Chest radiography: allows visualization of pericardial calcification, which is described in classical literature as a "corset heart" or "armored heart".
- Electrocardiography (ECG): records low QRS voltage, signs of left atrial overload, and various rhythm disturbances (most commonly atrial fibrillation).
- Echocardiography (EchoCG): the key sign is the visualization of two separate echo signals originating from the visceral and parietal layers of the thickened pericardium.
Treatment tactics Conservative therapy is largely ineffective once constriction has developed. The method of choice is radical surgical intervention — pericardiectomy. The essence of the operation is the removal of the altered pericardium within the anatomical boundaries between the phrenic nerves. A critically important step of the procedure is the mandatory release of the vena cava orifices from compression, which restores normal venous return to the right side of the heart.
Briefly: answers to topical questions
What is the mechanism of pulsus paradoxus in constrictive pericarditis?
The mechanism of pulsus paradoxus in constrictive pericarditis is related to external compression and restriction of cardiac mobility by the rigid pericardium. Such a pericardium prevents full cardiac relaxation and impairs diastolic ventricular filling. Clinically, pulsus paradoxus manifests as a noticeable decrease in pulse amplitude on inspiration and a drop in systolic blood pressure during deep inspiration by more than 10 mmHg.
What diseases require differential diagnosis with constrictive pericarditis?
Differential diagnosis of constrictive pericarditis is carried out with restrictive cardiomyopathy. EchoCG and Doppler-EchoCG, including the assessment of the "annulus paradoxus" phenomenon, are used for differentiation.
| Sign | Constrictive pericarditis | Restrictive cardiomyopathy |
|---|---|---|
| Ability of the myocardium to lengthen longitudinally | Relatively preserved | Decreases |
| Longitudinal early diastolic velocity (e') | Normal or increases as the disease progresses | Decreases |
| Annulus paradoxus | Septal early diastolic velocity of the mitral annulus is higher than the lateral | Used for differentiation from constrictive pericarditis |
What Doppler echocardiographic signs indicate constrictive pericarditis?
Doppler signs used in assessing constrictive pericarditis include:
- Annulus paradoxus (Annulus Paradox) — early diastolic tissue velocity of the septal mitral annulus is higher than the lateral.
- Preservation or increase of longitudinal early diastolic velocity (e') in constrictive pericarditis.
- Restrictive filling pattern — ratio of early to late peak filling velocity greater than 1.5.
- Respiratory variations in transmitral and transtricuspid blood flow — significant variability in peak ventricular filling velocities depending on the respiratory phase with discordance of left and right heart changes.
Remember the image of the "armored heart": a rigid calcified sac prevents the ventricles from expanding. Because of this, blood cannot enter the heart and "floods" the systemic circulation — leading to ascites, hepatomegaly, and distended jugular veins.
Class and exam questions
What type of heart failure develops in constrictive pericarditis?
Diastolic heart failure develops because the rigid pericardium prevents normal relaxation and ventricular filling.
What is the "pericardial knock"?
This is a pathognomonic extra sound heard after the second heart sound. It is also known as the "pericardial knock".
What surgical operation is the method of choice?
Pericardiectomy is used — the radical removal of the pericardium between the phrenic nerves with obligatory release of the vena cava orifices.
What else to study on this topic
- Mechanism of pulsus paradoxus formation during cardiac compression
- Electrocardiographic signs of left atrial overload
- Topographic anatomy of the phrenic nerves in the context of pericardiectomy
- Differential diagnosis of idiopathic and infectious (tuberculous) pericarditis
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