111Case 24 Acute Pericarditis

Table 24.2: ECG features of acute pericarditis

•  S-T segment elevation is concave upwards 

segment elevation of acute pericarditis can be differentiated from that of acute myocardial infarction by several ECG features such as concave upward shape and concomitant depression of the P-R segment (Table 24.2).

PERTINENT INVESTIGATIONS

In patients with chest pain, the most frequently requested test after ECG is cardiac troponin-T. Troponin may be elevated in upto 50% of patients with acute pericarditis, thus limiting its diagnostic value. The total leucocyte count (TLC) and C-reactive protein (CRP) level may be elevated in acute pericarditis. A four-fold rise in antiviral antibody titre may occur, but is not diagnostic and often futile in the absence of specific antiviral therapy. Anti-streptolysin O (ASLO) titre and throat swab culture for beta-hemolytic Streptococcus are appropriate, if rheumatic fever is suspected. Suitable blood cultures are obtained, if the possibility of infective endocarditis is being entertained. In acute pericarditis, ECHO is useful to identify pericardial effusion and features suggestive of associated myocarditis. Usually, only a small rim of effusion is present and the left ventricular systolic function is normal. In myo-pericarditis, the ventricular function is mildly impaired but is generally reversible.

MANAGEMENT ISSUES

Treatment of acute pericarditis should first be targeted against a specific cause, if there is one. Examples include withdrawal of the offending drug in drug-induced pericarditis, hemadialysis for uremic pericarditis, thyroid hormone replacement for myxedema and suitable chemotherapy in malignant disease (Table 24.3).

In most cases, non-steroidal anti-inflammatory drugs (NSAIDs) are first-line treatment, in the absence of a specific cause. In post-infarction Dressler’s syndrome, aspirin is preferable over other NSAIDs. It is given in high-doses to begin with, to be tapered down over a period of time. Concomitant use of a proton pump inhibitor is recommended to reduce the risk of gastrointestinal bleeding.

112 Section 7 Pericardial Infections

Colchicine may be used along with a NSAID in refractory and recurrent cases or alone if NSAIDs are contraindicated. Steroids should only be considered in the context of a systemic inflammatory disease. Steroids should not be used in bacterial or tubercular infection since they cause immunosuppression and in post-MI patients, as they interfere with scar formation. Pericardiocentesis and pericardectomy are rarely required in the treatment of acute pericarditis.

Table 24.3: Causes of acute pericarditis

•  Infective: viral, bacterial, tubercular 

•  Traumatic: accidental, cardiac surgery 

•  Malignant: metastasis, radiotherapy 

•  Autoimmune: rheumatoid arthritis, SLE 

•  Metabolic: uremia and myxedema

•  Drug-induced: procainamide, hydrallizine 

•  Infarction: post-MI Dressler’s syndrome 

C A S E

25 Pericardial

Effusion

CASE PRESENTATION

A 66-year old gentleman visited the out-patient department of a tertiary-care hospital, with two months history of progressively worsening exertional breathlessness and increasing ankle swelling. There was no history of orthopnea or nocturnal dyspnea and he denied complaints of fever, productive cough, chest pain or hemoptysis. The patient was a known case of long-standing diabetes and hypertension. Recently, he was diagnosed to have chronic kidney disease and was advised peritoneal dialysis.

His daily medication included lisinopril, frusemide, digoxin and glimepiride. There was no past history of angina pectoris or myocardial infarction, although he was told to have an “enlarged heart”.

On examination, the patient was pale and mildly tachypneic, but not in any distress. The pulse was rapid, regular and low in volume, with an appreciable fall in pulse volume during inspiration. The pulse rate was 110 beats/min. with a BP of 104/66 mm Hg and respiratory rate of 24/min. The JVP was elevated without any noticeable descent during inspiration and there was pitting ankle edema. The precordium was silent and the apex beat was not visible but could be located only on palpation. On percussion, the area of cardiac dullness extended beyond the cardiac apex. The S₁ and S₂ were faintly audible on auscultation, but no murmur, gallop rhythm or friction rub was appreciated. Breath sounds were diminished over the left lung base posteriorly, with an area of bronchial breathing just above it. The rest of the lung fields were clear.

CLINICAL DISCUSSION

From the case history and particularly from the physical examination, the most likely diagnosis in this case is pericardial effusion. ECG showed sinus tachycardia with generalized low QRS voltages. The R wave amplitude varied on a beat-to-beat basis. X-ray chest findings were a markedly enlarged globular cardiac silhouette with a narrow basal vascular pedicle, giving the heart a “money-bag”

appearance. The pulmonary broncho-vascular markings were normal. ECHO revealed a 2.5 cm wide echo-free space around the heart. There was noticeable collapse of the right atrium and right ventricle during diastole. The left ventricular function was normal.

In retrospect, there were several clinical pointers towards the diagnosis of pericardial effusion. A decline in pulse volume (fall in systolic BP>10 mm) during

114 Section 7 Pericardial Infections

inspiration, is known as pulsus paradoxus. Increase in venous return shifts the interventricular septum towards the left ventricle, thereby reducing stroke volume. Besides pericardial effusion with cardiac tamponade, other reasons for pulsus paradoxus are constrictive pericarditis and status asthmaticus. A raised JVP without noticeable descent, indicates inadequate venous emptying during inspiration. Besides pericardial effusion, a raised and fixed JVP is a feature of superior vena caval obstruction.

A silent precordium with a non-palpable apex beat and muffled heart sounds indicate some intervening substance, may be fluid (pericardial effusion), air (pulmonary emphysema) or fat (morbid obesity). The combination of low BP, raised JVP and muffled heart sounds is known as Beck’s triad and is characteristic of cardiac tamponade. The area of diminished breath sounds, dull percussion note and bronchial breathing just above it, indicate compression of the left lower lobe by the pericardial effusion. This constitutes the Ewart’s sign.

On ECG, the beat-to-beat variability of QRS amplitude is known as electrical alternans. Its clinical counterpart is pulsus alternans. Total electrical alternans involves the QRS complex as well as the P and T waves. Besides cardiac tamponade, electrical alternans is also observed in severe left ventricular dysfunction. The

“money-bag” heart, with enlarged cardiac silhouette and narrow vascular pedicle, is characteristic of pericardial effusion (Fig. 25.1). When cardiomegaly is due to heart failure, there is cephalization of pulmonary veins, along with hilar congestion, Kerley B lines and pulmonary edema.

Echocardiography is extremely valuable not only to confirm the presence of pericardial effusion (Fig. 25.2), but also to assess its magnitude and to identify signs of cardiac tamponade. It is also useful to exclude other causes of heart failure and to guide drainage of pericardial fluid. The quantity of pericardial fluid can be gauged from the width of the echo-free space around the heart (Table 25.1).

The nature of pericardial fluid can be judged from careful analysis of the echo-free space. Transudative effusion is sonolucent while sanguinous fluid has high echodensity, sometimes with thrombus formation. Exudative effusion shows

Figure 25.1: X-ray showing large cardiac silhouette with a narrow basal vascular pedicle

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