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Figure 23.2: X-ray showing a tubular heart with hyperlucent lung-fields

rhythm can be sinus tachycardia, atrial fibrillation or even multifocal atrial tachycardia.

The chest X-ray shows a tubular-shaped heart which appears small because of hyperinflation of the lungs (Fig. 23.2). The main pulmonary artery is often dilated. The lung fields are hyperlucent with prominent broncho-vascular markings. Due to hyperinflation, the intercostal spaces are wide and the domes of the diaphragm are flat and pushed downwards (Table 23.2).

Table 23.2: X-ray chest findings in COPD

•  Tubular heart

•  Hyperinflated lungs

•  Dilated pulmonary artery •  Wide intercostal spaces •  Flat domes of diaphragm

Transthoracic ECHO is sometimes difficult to perform in patients of chronic obstructive lung disease, because of a poor acoustic window due to emphysema. Nevertheless, ECHO may reveal a dilated right ventricle that loses its triangular shape and becomes more globular. There is paradoxical motion of the interventricular septum, that moves away from the left ventricular cavity in systole. On short-axis view, the dilated main pulmonary artery with its right and left branches, gives a “pair of trousers” appearance (Fig. 23.3). On colour flow mapping, a pulmonary regurgitation (PR) jet may be observed in the right ventricular outflow tract (RVOT). The pulmonary artery pressure, estimated from the tricuspid regurgitant velociy, is elevated.

Figure 23.3: ECHO showing dilatation of main pulmonary artery

PERTINENT INVESTIGATIONS

Besides an ECG, X-ray and ECHO, other pertinent investigations in COPD are hematological, biochemical and bacteriological. The hemoglobin is high due to polycythemia while the leucocyte count is elevated with predominant neutrophils, because of the bacterial infection. The ESR is also increased because of chronic pulmonary suppuration but if very high, should alert us to the possibility of pulmonary tuberculosis. Blood glucose and liver and kidney function tests are done to rule out diabetes mellitus and other organ dysfunction. The sputum is examined by Gram staining to identify the causative organism. Sputum is also microscopically examined for acid fast bacilli (AFB) and fungal hyphae. Appropriate cultures are performed to identify suitable antimicrobial therapy. For patients in respiratory distress, arterial blood gas (ABG) analysis is done which may show hypoxemia, hypercapnia and respiratory acidosis.

MANAGEMENT ISSUES

The treatment of acute exacerbation of COPD includes antibiotics to treat the infection and bronchodilators to relieve airway obstruction. The antibiotic choice may be empirical or based on sputum culture report. Bronchodilators are given systemically or by the inhalation route and include theophylline, salbutamol, ipratropium and corticosteroids. Supportive treatment includes antipyretics, expectorants and oxygen therapy. Among the cardiovascular drugs, calcium blockers like verapamil and diltiazem may be used to control the heart rate. Betablockers and digoxin are avoided because of the risk of bronchospasm and ventricular arrhythmias respectively. Pulmonary hypertension can be treated with the phosphodiesterase (PDE) inhibitor sildenafil, prostaglandin (PG) analogue epoprostenol or an endothelin (ET-1) receptor antagonist bosentan.

S E C T I O N

7

Pericardial

Infections

CLINICAL DISCUSSION

When a patient presents with a short febrile illness, clinical signs of heart disease and some ECG abnormalities, possibilities that need to be considered are rheumatic fever, infective endocarditis, acute myocarditis and acute pericarditis. Rheumatic fever generally presents with a migratory polyarthritis, with or without cutaneous nodules or an evanescent skin rash. Infective endocarditis generally follows a dental or surgical procedure with a pre-existing valvular disease or a septal defect. Acute myocarditis is characterized by myocardial dysfunction and clinical signs of heart failure. Our patient presented with chest pain, had an audible pericardial rub and the ECG showed elevation of the S-T segment. Therefore, the most likely diagnosis in this case is acute pericarditis.

The chest pain of acute pericarditis is sharp in character and central in location. Therefore, it resembles the chest pain of myocardial infarction, but lacks the characteristic radiation and accompaniments of ischemic chest pain. The pain increases on deep breathing and coughing and therefore, patients prefer shallow respiration. The pain also worsens on lying supine and hence, the patient prefers to sit and lean forward.

The pericardial friction rub is a high-pitched, scratchy or squeaky sound, audible over the precordium along the lower left sternal border. It is better audible during inspiration, with the patient sitting up and leaning forward. Occasionally, the rub is accompanied by a palpable thrill, especially in patients with uremic pericarditis. The classical pericardial rub is triphasic and has three components, each related to a discrete phase of the cardiac cycle. Accordingly, there is a presystolic rub during atrial systole and a systolic and diastolic component related to ventricular systole and diastole respectively. Sometimes, the rub is a one-component or two-component sound, if there is associated atrial fibrillation or ventricular dysfunction. Sometimes the rub is evanescent and changes its quality on a day-to-day basis.

Table 24.1: Causes of S-T segment elevation

•  Myocardial infarction •  Prinzmetal angina •  Ventricular aneurysm •  Dressler’s syndrome

•  Acute viral pericarditis

•  Early repolarization variant

The most common and significant cause of S-T segment elevation on the ECG is coronary artery disease. S-T elevation occurs in acute myocardial infarction and in coronary vasospasm (Prinzmetal’s angina). In patients with prior myocardial infarction, reasons for S-T segment elevation are Dressler’s syndrome and ventricular aneurysm. S-T elevation also occurs in the early repolarization variant in which case the clinical profile is entirely normal (Table 24.1). The S-T

Table 24.2: ECG features of acute pericarditis

•  S-T segment elevation is concave upwards •  S-T elevation is observed in nearly all leads •  T waves invert after S-T returns to base-line •  Q waves do not appear with ST-T changes •  R wave height is maintained in chest leads •  P-R segment is depressed in the limb leads •  Reciprocal S-T segment depression not seen

•  Sinus tachycardia is almost invariably present

•  Arrhythmias and conduction defects are unusual •  ECG changes do not evolve but resolve rapidly

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.

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 

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.

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

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

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 involvestheQRScomplexaswellasthePandTwaves.Besidescardiactamponade, 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 echofree space. Transudative effusion is sonolucent while sanguinous fluid has high echodensity, sometimes with thrombus formation. Exudative effusion shows