19. Pericardial disease
- Introduction. The patterns of pericardial disease have changed over the past 20 to 30 years, with the once common tuberculous pericarditis becoming a rare entity. Uremic pericarditis, formerly one of the most dreaded complications of renal failure, is now managed with relative ease.
Pericarditis can be acute and self-limited, subacute, or chronic. Chronic forms of pericarditis often result in cardiac constriction. A variety of agents cause pericarditis (Table 19-1). Pericarditis is likely to lead to effusion, which may be minor or large enough to interfere with ventricular filling during diastole (tamponade). Chronic forms of pericarditis often are associated with pericardial and even epicardial fibrosis, a condition that can also impede diastolic ventricular filling (restrictive filling). This chapter examines pericarditis, tamponade, and constriction in separate sections.
- History. Much of the historical information obtained from patients with pericarditis varies according to the underlying medical condition. Thus, rheumatoid pericarditis usually accompanies severe rheumatoid arthritis, whereas radiation pericarditis follows large doses of mediastinal radiation, ordinarily administered for control of neoplasm. Systemic symptoms may occur, including fever, sweats, chills, weakness, malaise, weight loss, anxiety, and depression. The pain of pericarditis is characteristic: It is almost always precordial in position, sharp and severe, and increasing in severity, with deep inspiration or recumbency. Occasionally, pain is felt only when the patient lies on the left side and makes a maximum inspiratory effort. The pain not infrequently radiates to the neck or left arm and shoulder.
Dyspnea usually is seen only in individuals with cardiac tamponade or constriction (see Sections III. and IV.). Palpitations are noted commonly. These are caused by atrial arrhythmias, which often accompany pericarditis.
- Physical examination. Patients with pericarditis may have an irregular or rapid pulse secondary to atrial arrhythmias or tamponade (see Section III.). A pericardial friction rub is the hallmark of the disease. This superficial scraping, scratchy, or grating sound is frequently evanescent or intermittent.
Persistent rubs are most often heard with pericarditis secondary to neoplasm, uremia, viral infection, and tuberculosis. Evanescent rubs are common in pericarditis associated with myocardial infarction (MI). Rubs may have one, two, or three components occurring with the following stages of the cardiac cycle: (i) rapid filling in early diastole, (ii) atrial contraction in late diastole, and (iii) systole. On occasion, one- or two-component rubs are confused with systolic or to-and-fro murmurs. Sometimes a patient with pericarditis has an early diastolic sound or pericardial knock, which can be confused with a third heart sound (S3). Other systemic findings in patients with pericarditis depend on the underlying condition.
- ECG. The ECG is often abnormal in patients with pericarditis. ECG findings include diffusely elevated S–T segments, widespread T wave changes, and P–R segment depression. Elevated S–T segments can mimic the ECG findings of acute MI. ECG findings in pericarditis are as follows:
Elevation of S–T segment
Flattening and inversion of T waves
Depression of P–R segment
Differentiation of the ECG changes of pericarditis from the ECG changes of acute MI are listed in Table 19-2. The S–T segment elevation of early repolarization occasionally may be confused with the ECG pattern of pericarditis. However, S–T segment elevation of early repolarization usually is limited to the precordial leads, whereas that of pericarditis occurs throughout limb and precordial leads. Supraventricular arrhythmias are frequently noted in patients with pericarditis.
- Chest x-ray examination. Patients with pericarditis with little or no effusion usually have a normal chest x-ray film. Serial chest films may reveal increasing heart size secondary to accumulation of pericardial fluid (see Section III.). In patients with infectious or hypersensitivity pericarditis, chest roentgenography may show pulmonary infiltrates or pleural effusions.
- Laboratory tests. Laboratory testing may demonstrate striking abnormalities in patients with pericarditis. The nature of these abnormalities depends on the underlying condition producing pericardial irritation. Thus, infectious causes of pericarditis usually are associated with elevated erythrocyte sedimentation rates, white blood cell counts, and various serum globulin fractions; pericarditis secondary to allergic reactions may be associated with eosinophilia; and pericarditis induced by collagen/ vascular disease may be accompanied by positive antinuclear antibody or latex fixation tests.
- Echocardiography. Echocardiography is very sensitive in detecting small amounts of pericardial effusion. High-quality echocardiograms may even identify pericardial thickening. Often, confirmation of a diagnosis of pericarditis rests on the demonstration of a small quantity of pericardial fluid by echocardiography.
- Radionuclide studies. Cardiac blood pool scanning after the administration of labeled erythrocytes or albumin can aid in the detection of significant quantities of pericardial effusion; however, echocardiography is more sensitive in detecting pericardial fluid.
- Catheterization and angiography. Hemodynamic measurements are usually normal in patients with uncomplicated pericarditis. As the quantity of pericardial fluid increases, ventricular filling pressures increase (see Section III.). Angiography is less sensitive than echocardiography in detecting small amounts of pericardial fluid.
- Biopsy. Pericardial biopsy can often be performed percutaneously or through a small subxiphoid incision. Pericardial fluid can be collected at the same time. This procedure may be important in confirming the diagnosis of bacterial (especially tuberculous) or neoplastic pericarditis.
- Protocol for the diagnosis of pericarditis
- Testing sequence for the diagnosis. The history, physical examination, ECG, and echocardiogram are central in making the diagnosis of pericarditis.
An appropriate flow chart for making the diagnosis of pericarditis follows:
History (pleuritic, positional chest pain, and precordial rub)
Chest x-ray film and ECG (diffuse S–T and T wave changes)
Echocardiogram (pericardial fluid or thickening or both)
- Criteria for the diagnosis. The diagnosis of pericarditis is made in the following patients:
- Individuals with substernal or precordial pleuritic or positional chest discomfort may have either (i) definite changes of pericarditis on the ECG (diffuse S–T segment elevation with or without diffuse T wave changes and P–R segment depression) or (ii) definite pericardial fluid or thickening by echocardiography.
- Asymptomatic individuals in whom a pericardial rub is heard and who meet either the ECG or the echocardiographic criteria for pericarditis just noted.
- Asymptomatic individuals without audible pericardial friction rub who meet both ECG and echocardiographic criteria for pericarditis just noted.
- Differential diagnosis
- Systolic murmur. Single-component systolic rubs are occasionally mistaken for systolic murmurs. Thus, patients with pericarditis may be thought to have aortic stenosis, mitral regurgitation, or ventricular septal defect. The transient and changing nature of the rub, and associated ECG and echocardiographic evidence of pericarditis, helps to identify the correct diagnosis.
- Unstable angina pectoris. Patients with post-MI pericarditis may be thought to have unstable angina because of recurrent severe substernal chest discomfort. Occasionally, the typical pleuritic or positional nature of the pericarditic discomfort is absent, making it even more difficult to differentiate this pain from that of angina pectoris. In such circumstances, a brief trial of aspirin, indomethacin, or steroids may reveal the true diagnosis by promptly relieving the discomfort.
- Pulmonary infarction. The pleuritic chest pain of pericarditis may be confused with discomfort resulting from pulmonary infarction. The pain of pulmonary infarction is often posterior in location, whereas that of pericarditis is anterior. Associated findings such as abnormal arterial blood gases and pulmonary infiltrates, as well as abnormal lung scan and pulmonary arteriography, point to the diagnosis of pulmonary embolism. ECG and echocardiographic findings suggest the diagnosis of pericarditis.
- Pneumonia. Patients with pneumonia may have pleuritic pain simulating that of pericarditis. Differentiation of these two entities depends on a history of cough, sputum production, and fever and on the presence of an infiltrate on the chest roentgenogram of patients with pneumonia.
- Dissecting aneurysm. Pericarditis with an audible friction rub can occur in patients with aortic dissection secondary to leakage of blood into the pericardial space. Dissection is suspected in patients with severe, nonpleuritic precordial discomfort, abnormal mediastinal widening on the chest x-ray film, loss of one or more arterial pulses, or pulsation of one or both sternoclavicular joints.
- Pneumothorax. Sudden onset of chest pain associated with a crunching, to-and-fro sound over the precordium can occur in patients with pneumothorax. This loud precordial sound, the result of air in the mediastinum, may be confused with a pericardial friction rub. Pneumothorax is recognized by absence of characteristic ECG changes of pericarditis and presence of air in the pleural space and mediastinum by chest x-ray study.
- Because a number of different conditions can be associated with pericarditis (Table 19-1), it is important to define the etiology of pericarditis once it is identified.
- Medical treatment
- Analgesia. Rarely, the pain of pericarditis requires opiates (meperidine or morphine) for relief. In general, aspirin, indomethacin, or ibuprofen is effective in relieving the discomfort of pericarditis. Two aspirin tablets four times a day, 50 mg of indomethacin four times a day or 400 mg of ibuprofen three or four times a day as needed and tolerated usually suffices to alleviate the discomfort within 24 to 48 hours. If discomfort persists, the dosage may be increased to three aspirin tablets four times a day or 50 mg of indomethacin four times a day. If discomfort still remains after 24 to 48 hours, patients taking aspirin or indomethacin should be given ibuprofen, and vice versa. If this regimen also fails and if the pain is disconcerting to the patient, steroid therapy should be undertaken. It may be difficult to wean patients with pericarditis from steroids once these agents have been prescribed. When steroids are withdrawn, the pain of pericarditis often recurs, so they should be tapered very gradually over weeks or months. The usual starting dose for steroids is 40 to 60 mg of prednisone (or its equivalent) daily. An occasional patient develops recurrent bouts of pain from pericarditis. Some clinicians have had excellent results with chronic oral colchicine (1 to 2 mg per day in divided doses) therapy for these patients, thereby obviating the need for prednisone.
- Anticoagulants. Some authorities warn against using anticoagulants in patients with pericarditis because of the danger of developing hemopericardium and tamponade. Low-dose subcutaneous heparin regimens probably do not result in hemopericardium. Anticoagulation in a patient with pericarditis must be undertaken with extreme caution.
Daily or every-other-day echocardiograms are useful in monitoring such individuals.
- Specific therapy aimed at the underlying condition should be given (e.g., appropriate antibiotics for bacterial pericarditis).
- Surgery. Surgical removal of the pericardium rarely is needed for relief of pain. An occasional patient with intractable discomfort despite repeated courses of steroids will require pericardiectomy. Patients with suppurative pericarditis usually require drainage of the pericardial space together with appropriate antibiotic therapy.
- Pericardial effusion and tamponade. Pericarditis usually is accompanied by pericardial effusion. Often the volume of the effusion is small and does not hinder cardiac function, but larger quantities of fluid sometimes accumulate in the pericardial space, interfering with normal ventricular filling. Low cardiac output and systemic venous congestion result, a condition known as cardiac or pericardial tamponade.
- History. Patients with tamponade complain of dyspnea in addition to the symptoms (e.g., pain) that arise from the pericarditis itself. They may also complain of a dry hacking cough, hoarseness, or dysphagia. These latter symptoms are the result of compression of the trachea, bronchi, lungs, or esophagus by pericardial and, at times, pleural effusion. Patients with tamponade are usually most comfortable when sitting erect and leaning forward.
- Physical examination. A number of physical findings have been associated with the presence of large quantities of fluid in the pericardial space.
- Increased area of cardiac dullness to percussion. Normally, cardiac dullness extends laterally to the apical impulse in the fifth intercostal space. At the base of the heart, the area of dullness is much narrower, extending some 2 to 3 cm to the left of the sternal edge. Patients with large pericardial effusions have an area of increased dullness at the base of the heart in addition to generalized enlargement of the area of cardiac dullness.
- Dullness to percussion, bronchial breath sounds, and egophony posteriorly, below the angle of the left scapula (Pins' or Ewart's sign). These findings are the result of compression of the left lung by the heart, which is pushed posteriorly by retrosternal pericardial effusion.
- Decrease in intensity or absence of the apical impulse and distant or muffled heart sounds. These findings are noted in many, but not all, patients with large pericardial effusions.
- Sinus tachycardia, narrow pulse pressure with low systolic blood pressure, pulsus paradoxus greater than 10 mm Hg, and systemic venous congestion. These findings (Table 19-3) are almost always manifest in patients with cardiac tamponade. Beck's triad of cardiac tamponade is falling systemic arterial pressure, rising systemic venous pressure, and a small quiet heart.
- Jugular venous distension with a prominent X descent but without a Y descent.
- ECG. Besides the ECG findings associated with pericarditis (see above), a diminution in the voltage of the QRS complex may be seen in patients with pericardial effusion. Alternation in the height of every other P wave or QRS complex (electrical alternans) often is seen in patients with large pericardial effusions. Alternation in the height of the QRS complex is seen occasionally in patients with severe heart failure, but P wave alternation occurs only in individuals with pericardial effusion and tamponade.
- Chest x-ray examination. Serial films in the patient with pericarditis may show increasing heart size secondary to accumulation of pericardial fluid. In general, at least 250 ml of pericardial fluid is necessary to produce an enlargement of the cardiac silhouette on the chest film. Roentgenographic findings in patients with pericardial effusion are as follows:
Symmetric cardiac enlargement
Clear lung fields
Obliteration of the normal outlines of the individual cardiac chambers and great vessels, resulting in a pear-shaped or water-bottle cardiac silhouette
Increase in the size of the cardiac silhouette in serial roentgenograms
Systemic venous engorgement with enlargement of the superior vena cava and azygos vein
Fluoroscopic examination of the right-sided heart border of patients lying on their left side after intravenous administration of a small bolus of carbon dioxide can help in the identification of significant quantities of pericardial fluid. Echocardiography has largely replaced this technique as the safest and most sensitive method of identifying pericardial effusion.
- Echocardiography. Pericardial effusion is sensitively detected and roughly quantitated by echocardiography. A characteristic swinging motion of the heart within the pericardial effusion and compression of the right atrium and ventricle are often seen in patients with tamponade. Echocardiography can be used during pericardiocentesis to monitor the position of the needle tip. Occasionally, tumor in the pericardium mimics effusion on the echocardiogram.
Left ventricular ejection times measured from a carotid pulse tracing or an aortic valve echo tracing show marked respiratory variation (50 milliseconds). Individuals without tamponade have a maximum respiratory variation of 10 milliseconds in the left ventricular ejection time.
- Radionuclide studies. Cardiac blood pool scanning can identify pericardial effusion. Echocardiography, however, is a more sensitive technique for recognizing the presence of pericardial fluid.
- Catheterization and angiography. A number of hemodynamic changes can be recorded in patients with cardiac tamponade: Systemic venous pressure is elevated; right and left ventricular filling pressures are equal or nearly so; cardiac output is normal or slightly reduced, but stroke volume is diminished markedly.
The presence of pericardial effusion often can be defined at catheterization by placing a catheter against the lateral right atrial endocardium and noting the distance from the catheter tip to the lung. Patients with pericardial effusion have more than the expected 3- to 5-mm distance from the right atrial endocardium to the lateral border of the heart. Similarly, a right atrial angiogram can be obtained, and the thickness of the free wall of the right heart can be measured. An increase in this measurement of more than 3 to 5 mm suggests pericardial effusion.
- Biopsy. Pericardial fluid can be obtained by pericardiocentesis with a needle or during an open pericardial biopsy. If the etiology of the pericarditis is clear and if signs of tamponade are not present, pericardiocentesis or pericardial biopsy is not required. When the diagnosis is obscure, however, or when tamponade is present, pericardial fluid should be removed. Pericardial fluid should be cultured for bacteria (including those of tuberculosis) and sent for cytologic analysis. Bloody pericardial effusion occurs in a variety of conditions, including tuberculosis, neoplasms, lupus erythematosus, rheumatoid arthritis, and viral infections. Purulent pericardial fluid is highly suggestive of a bacterial infection. Rheumatoid factor or lupus erythematosus cells may be found in pericardial fluid from patients with rheumatoid arthritis or systemic lupus erythematosus.
- Protocol for the diagnosis of pericardial effusion and tamponade
- Protocol for making the diagnosis of pericardial effusion. A detailed history and physical examination are followed by an ECG and chest x-ray study.
Pericardial effusion can be suspected on the basis of historical, physical, ECG, or roentgenographic findings. Confirmation of the diagnosis depends on the demonstration of pericardial effusion by echocardiography, radioisotope blood pool scanning, or angiography. Echocardiography is the easiest and most sensitive of these techniques. On occasion, small and even moderate volumes of pericardial fluid are clinically unsuspected until demonstrated by echocardiography. The protocol for making the diagnosis of cardiac tamponade is as follows (dashed arrow indicates optional step):
History and physical diagnosis
ECG and chest x-ray film
Right-sided heart or central venous catheterization
? Pericardial aspiration or biopsy
- Criteria for making the diagnosis of pericardial effusion. The clinical diagnosis of pericardial effusion is based on the presumptive identification of pericardial fluid by echocardiography. In some individuals, a history of positional or pleuritic chest discomfort or the discovery of a friction rub leads to the echocardiographic demonstration of pericardial fluid. In other patients, pericardial effusion is discovered during an echocardiographic examination that was ordered for another reason. Patients with heart failure may develop pericardial effusion without pericardial inflammation. Thus, not all patients with pericardial effusion noted by echocardiography have pericarditis.
- Criteria for making the diagnosis of cardiac tamponade. Two elements must be present to make the diagnosis of cardiac tamponade: pericardial effusion and evidence of restricted ventricular filling. Pericardial effusion is diagnosed as already noted. Evidence suggesting restricted ventricular filling is usually noninvasive and should include at least three of the following: sinus tachycardia, low systolic blood pressure with narrow pulse pressure, marked pulsus paradoxus or jugular venous distention on physical examination; wide respiratory variation in left ventricular ejection times; and a swinging heart or right atrial/ventricular compression on echocardiography. Confirmation of the diagnosis requires the demonstration of elevated right atrial pressure by central venous or right-sided heart catheterization. Right-sided catheterization also documents equalization of right and left ventricular filling pressures (right atrial and pulmonary capillary wedge or pulmonary arterial diastolic pressures) in patients with cardiac tamponade.
- Differential diagnosis of pericardial effusion. Individuals with cardiomyopathy may have enlarged, globular heart outlines on the chest x-ray film that resembles those seen in patients with large pericardial effusions. Differentiation of these two conditions is by echocardiography. Cardiac blood pool scanning and the left lateral decubitus chest x-ray picture after intravenous carbon dioxide injection also can differentiate these conditions when echocardiography is not available.
- Differential diagnosis of pericardial effusion with tamponade. Patients with right ventricular failure resulting in systemic venous congestion and low cardiac output may have clinical features similar to those of patients with cardiac tamponade. For example, a patient with cor pulmonale secondary to chronic obstructive pulmonary disease or an individual with a right ventricular MI may have a low systolic blood pressure, pulsus paradoxus greater than 10 mm Hg, and systemic venous congestion. These conditions can be differentiated by chest roentgenography and echocardiography that show a normal (or even small) cardiac silhouette and absence of pericardial effusion in the patient with right ventricular failure.
- Medical treatment
- Patients with pericardial effusion, but without evidence of tamponade, frequently do not require specific therapy directed at the pericardial effusion. Rather, therapy should be directed to the underlying condition. For example, tuberculous pericarditis with effusion, but without tamponade, is managed appropriately with antituberculous chemotherapy.
- The discomfort of pericarditis is relieved with measures discussed earlier.
- Some authorities feel that anticoagulants (heparin and warfarin) are contraindicated in patients with pericarditis with or without effusion because of the risk of developing hemopericardium with tamponade.
- When the diagnosis of cardiac tamponade is made in the manner outlined earlier, pericardiocentesis should be performed. It is wise to monitor intraarterial blood pressure during and after pericardiocentesis. The procedure can be performed with local anesthesia and needle aspiration.
Some authorities favor leaving a small plastic cannula in the pericardial space for a few days to prevent reaccumulation of fluid. Except in an emergency, pericardiocentesis should be performed by an experienced physician in a catheterization laboratory, operating room, or intensive care unit. If a pericardial biopsy is indicated, simultaneous drainage of pericardial effusion can be performed.
- Specific therapy is directed at the underlying cause of the pericardial effusion. For example, patients with bacterial pericarditis require specific antibiotics, patients with viral (also called benign or idiopathic) pericarditis receive nonsteroidal antiinflammatory agents or corticosteroids, and patients with uremic pericarditis are vigorously dialyzed.
- Patients with neoplastic involvement of the pericardium frequently reaccumulate pericardial fluid after pericardiocentesis. Recurrent episodes of cardiac tamponade may occur. Instillation of tetracycline into the pericardial space often results in its obliteration, with control of recurrent cardiac tamponade. Antineoplastic agents can also be instilled into the pericardial space in such patients.
- Because ventricular contractile function is normal in patients with cardiac tamponade, digitalis administration is of no benefit except to control the ventricular response in those individuals with atrial fibrillation.
Diuresis is contraindicated despite the presence of edema and even ascites because the further reduction in right ventricular filling leads to a further fall in cardiac output. Hypotension with hypoperfusion may result. Patients with cardiac tamponade and hypotension should receive intravenous volume (saline, plasma, dextran) to ensure adequate right ventricular filling and cardiac output until tamponade is relieved by pericardiocentesis. In the event of severe hypotension and hypoperfusion, intravenous isoproterenol, as well as volume, should be administered.
- Surgery. Recurrent tamponade is an indication for surgical drainage of the pericardium. Surgical procedures that can be successful in permanently relieving tamponade include creation of a permanent pericardial window and pericardiectomy. A pericardial window can also be created by a catheter balloon technique, thereby avoiding surgery.
- Constrictive pericarditis. Formerly a common disease, constrictive pericarditis is seen only rarely because the advent of effective antituberculous chemotherapy. Constrictive pericarditis is usually the result of chronic pericardial inflammation and fibrosis that is often the result of a chronic infectious process (bacterial, fungal, or viral), neoplasm, or uremia (Table 19-1).
- History. Patients usually develop symptoms very gradually, with exertional dyspnea, ankle swelling, and abdominal swelling as the main complaints. Many patients note undue fatigue. The chest discomfort noted with acute pericarditis, as well as orthopnea and paroxysmal nocturnal dyspnea, does not usually occur in individuals with constrictive pericarditis.
- Physical examination. Tachycardia, elevated jugular venous pressure, hepatomegaly, ascites, and peripheral edema are noted commonly. The clinical presentation of the patient with constriction resembles that of the individual with tamponade except for normal pulse pressure and lack of pulsus paradoxus in constriction. Inspiratory increase in jugular venous pressure (Kussmaul's sign) is occasionally seen. Sharp X and Y descents are present in the jugular pulse.
- ECG. The ECG findings in constrictive pericarditis include low voltage of the QRS complexes and nonspecific T wave changes. A pattern resembling right ventricular hypertrophy is sometimes seen (Table 19-4).
- Chest x-ray examination. Chest roentgenography in patients with constrictive pericarditis reveals clear lung fields, normal or slightly increased heart size without specific chamber enlargement, and pericardial calcification in 50% of patients. Table 19-4 summarizes these findings.
- Echocardiography. The echocardiogram may demonstrate a number of findings in patients with constrictive pericarditis: (i) paradoxical septal motion; (ii) normal or increased diastolic slope of the anterior mitral valve leaflet; (iii) synchronous, parallel movement of the epicardium and parietal pericardium separated by a small echo-free space; (iv) rapid, early diastolic posterior motion of the left ventricular endocardium; (v) thickening of the pericardium; and (vi) normal right ventricular cavity dimensions.
- Magnetic resonance imaging (MRI). MRI may be helpful in distinguishing constrictive pericarditis from restrictive cardiomyopathy. The markedly thickened pericardium is visualized by MRI.
- Catheterization and angiography. Hemodynamic findings include elevated right atrial pressure with a characteristic M-shaped pattern, an early diastolic dip and plateau (square root sign) in the left and right ventricular pressure tracings, and equalization of the following pressures: right atrial, right ventricular and end-diastolic, pulmonary arterial diastolic, pulmonary capillary wedge, and left ventricular end-diastolic. Cardiac output is often normal in patients with constrictive pericarditis. Hemodynamic differentiation of constrictive pericarditis from restrictive cardiomyopathy is dealt with in Table 18-7.
Right atrial angiography may demonstrate a thickened atrial-pericardial heart border and straightening of the right atrial border.
- Biopsy. Open biopsy of the pericardium may be undertaken through a small subxiphoid incision. Biopsy of the pericardium is important in patients suspected of having neoplastic infiltration of the pericardium. In this manner, the diagnosis can be obtained without resorting to a full thoracotomy.
- Protocol for the diagnosis of constrictive pericarditis
- Testing sequence for making the diagnosis. The protocol for making the diagnosis of constrictive pericarditis is the same as that for cardiac tamponade (see above).
- Criteria for making the diagnosis. The diagnosis of constrictive pericarditis is made in symptomatic or asymptomatic patients with findings of elevated systemic venous pressure (jugular venous distention, hepatomegaly, ascites, peripheral edema), low-voltage QRS and nonspecific T wave changes on ECG, clear lung fields on chest x-ray film, a normal-sized right ventricle on echocardiography, equalization of all diastolic pressures (right atrial, right ventricular end-diastolic, pulmonary arterial diastolic, and pulmonary capillary wedge), and a normal cardiac output on right-sided heart catheterization.
- Differential diagnosis. Patients with restrictive myocardial disease (see Chapter 18) may resemble individuals with constrictive pericarditis in clinical presentation and hemodynamic findings. Echocardiography, MRI, and angiography often help to distinguish these two entities: Patients with cardiomyopathy usually demonstrate reduced left ventricular function, whereas individuals with constrictive pericarditis have a thickened pericardium and straightening of the right atrial border (Table 18-7). Occasionally, myocardial biopsy is needed to distinguish these two entities.
- Medical treatment. Because ventricular function is not impaired in patients with constrictive pericarditis, digitalis has no role in the therapy of this condition. Diuresis may result in deterioration by decreasing right ventricular filling further. Diuresis in the patient with constrictive pericarditis can therefore produce a dangerous fall in cardiac output. As noted in Section III, intravenous infusion of saline or generous oral intake of salt and fluids may be required to maintain adequate cardiac output and systemic blood pressure, despite significant ascites and peripheral edema. If hypotension with hypoperfusion occurs in a patient with constrictive pericarditis, the treatment is intravenous infusion of volume (saline, plasma, dextran) and isoproterenol.
- Surgery. The treatment of choice for constrictive pericarditis is surgical removal of the pericardium (pericardiectomy). In some individuals, the pericardium adheres firmly to the epicardium, and pericardiectomy is an arduous procedure. In this event, some epicardium invariably is removed. The operative mortality is higher in patients with densely adherent pericardia.
Cardiac function may not return to normal after successful pericardiectomy, although the patient may experience considerable improvement. Failure of cardiac function to normalize completely after pericardiectomy is usually the result of three factors: (i) extension of the pathologic process that affected the pericardium into the underlying epicardium and myocardium, (ii) incomplete pericardiectomy, and (iii) damage to the epicardium and myocardium during removal of the pericardium.
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