Symptoms of pericarditis

Some patients have symptoms of inflammation (acute pericarditis), others have signs of fluid accumulation (pericardial effusion). Manifestations of the disease vary depending on the severity of the inflammation, the number and location of pericardial effusion.

Even large-scale effusion can be asymptomatic if its accumulation is slow (for example, for months).

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Symptoms of acute pericarditis

Acute pericarditis often causes chest pain and pericardial friction noise, sometimes shortness of breath. The first manifestation may be a tamponade with arterial hypotension, shock, or pulmonary edema.

Since innervation of the pericardium and myocardium is the same, pericardial pain in the chest is sometimes similar to pain in inflammation or myocardial ischemia: dull or acute pain in the precardial region or behind the breastbone, capable of radiating to the neck, trapezius muscle (especially the left one) or shoulders. Pain varies from moderate to severe. Unlike ischemic pain in the chest, pain with pericarditis usually increases with chest movements, coughing and breathing; decreases in the sitting position and when tilted forward. Possible tachypnea and unproductive cough. Often there are fever, chills and weakness. In 15-25% of patients with idiopathic pericarditis, symptoms occur periodically for many months or years.

The most important physical symptom is the pericardial friction noise, which coincides with the contraction of the heart. However, this noise is often unstable and short-lived. It can be present only during systole or (more rarely) diastole. A significant amount of effusion in the pericardium can muffle heart tones, increase the area of cardiac dullness, and change the size and shape of the silhouette of the heart.

If suspected of acute pericarditis, it is sometimes necessary to be hospitalized for primary diagnosis. Perform ECG and chest X-ray. If signs of an increase in pressure in the right side of the heart, tamponades or the expansion of the heart contours are found, echocardiography is performed to detect effusion and impaired filling of the heart chambers. In blood tests, leukocytosis and an increase in ESR are possible, but these data are nonspecific.

Diagnosis is based on the presence of typical clinical symptoms and changes in ECG data. To detect changes, an ECG series may be required.

The cardiogram in acute pericarditis can show changes (elevation) of the ST segment and the T wave usually in most leads.

The ST segment in the II or III standard leads is raised, but subsequently returns to the isoline. In contrast to myocardial infarction, acute pericarditis does not cause a reciprocal depression of the segment (except aVR leads), and pathological Q waves do not appear. The PR interval can be shortened. In a few days or later, the teeth can become smoothed and then negative, except for aVR retraction. Inversion of the tooth occurs after the segment returns to the isoline, which distinguishes the data from changes in acute ischemia or MI.

Because pericardial pain can resemble pain in acute MI and pulmonary infarction, additional studies (such as changes in serum cardiac markers, lung scans) may be necessary if the history and findings of the cardiogram are not typical of pericarditis.

Post-pericardiotomy and post-infarction syndromes can present difficulties for diagnosis. They need to be differentiated from recent MI, pulmonary embolism and pericardial infection after surgery. Pain, pericardial friction noise and fever, occurring between 2 weeks to several months after surgery, a quick response to the appointment of acetylsalicylic acid, NSAIDs or glucocorticoids help in diagnosis.

Effusion to the pericardial cavity

The effusion into the pericardial cavity is often painless, but when it develops with acute pericarditis, a pain syndrome is possible. As a rule, heart tones are muffled. You can hear the noise of friction of the pericardium. With extensive exhalation, in some cases, compression of the basal parts of the left lung develops, weakened breathing (near the left scapula) and small bubbling rales (sometimes crepitus). Arterial pulse, jugular venous pulse and blood pressure are normal, if intrapericardial pressure does not increase significantly, causing a tamponade.

With postinfarction syndrome, effusion into the pericardial cavity can be combined with fever, the appearance of pericardial friction noise, fluid accumulation, pleurisy, pleural effusion and pain. This syndrome usually develops in the period from 10 days to 2 months after myocardial infarction. Usually it flows gently, but not always. Sometimes there is a heart rupture after MI, which leads to hemopericardium and tamponade, usually on the 1-10th day after MI, more often in women.

A presumptive diagnosis is made on the basis of clinical data, but often a suspicion of this pathology occurs only after the detection of an enlarged heart contour on the chest X-ray. On the electrocardiogram, the voltage of the QRS complex is often reduced , the sinus rhythm is retained in approximately 90% of patients. With a large amount of effusion, a chronic course of the disease, an electrocardiogram can show an electrical alternative (the amplitude of the P wave, QRS complex or T wave increases and decreases from contraction to contraction). An electrical alternative is associated with changes in the position of the heart. Echocardiography has a high degree of sensitivity and specificity in the detection of pericardial fluid.

Patients with a normal electrocardiogram, a small (<0.5 L) amount of fluid and the absence of suspicious data of anamnesis and objective examination can be left under observation with a consistent performance of a series of examinations and echocardiographies. Another patient showed a further examination to determine the etiology.

Cardiac tamponade

Clinical symptoms are similar to those in cardiogenic shock: reduced cardiac output, low systemic blood pressure, tachycardia and dyspnea. The veins of the neck are markedly enlarged. Severe cardiac tamponade is almost always accompanied by a drop of more than 10 mm Hg. Art. Systolic BP on inspiration (paradoxical pulse). In some cases, the pulse may disappear on inhalation. (However, pulsus paradoxus may also be present in COPD, bronchial asthma, pulmonary embolism, right ventricular infarction and non-cardiogenic shock.) Cardiac tones are muted if the effusion is large enough.

Low voltage and electrical alternative on the electrocardiogram suggest the presence of cardiac tamponade, but these data are not sensitive enough and specific. If a tamponade is suspected, echocardiography is performed, even if a short delay does not pose a threat to life. In the latter case, pericardiocentesis is immediately performed for diagnostic and therapeutic purposes. When echocardiography changes depending on the respiration of transvalvular and venous streams and compression or collapse of the right chambers of the heart in the presence of pericardial effusion confirm the diagnosis.

If you suspect a tamponade, you can perform a catheterization of the right heart (Swan-Ganz). With cardiac tamponade, there is no early diastolic decrease in ventricular pressure. In the pressure curve in the atria, the segment of the pressure curve x is retained, and the segment y is lost. In contrast, with severe failure due to dilated cardiomyopathy or pulmonary artery occlusion, the diastolic pressure in the left ventricle usually exceeds the right atrial pressure, and the mean pressure in the right ventricle is 4 mm Hg. Art. Or more.

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Symptoms of constrictive pericarditis

Fibrosis or calcification is rarely manifested by any symptoms if constrictive pericarditis does not develop. The only early changes are an increase in diastolic pressure in the ventricles, atria, lungs and systemic venous pressure. Symptoms of peripheral venous congestion (eg, peripheral edema, cervical veins, hepatomegaly) may appear together with early diastolic noise (pericardial flick), often better audible in inspiration. This sound is caused by a sharp restriction of diastolic ventricular filling with a dense pericardium. The ventricular systolic function (characterized by the ejection fraction) is usually preserved. A prolonged increase in pulmonary venous pressure leads to dyspnea (especially during exercise) and orthopnea. Weakness can be expressed. Detect the tension of the veins of the neck with an increase in venous pressure on inspiration (Kussmaul's sign), it disappears with a tamponade. Pulsus paradoxus is rarely detected, it is usually less pronounced than with tamponade. The lungs are not full-blooded unless the expressed compression of the left ventricle develops.