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Observations on Pericardial Disease
Observations on Pericardial Disease FRANCIS C. WOOD, M.D. *
My special interest in diseases of the pericardium began more than a decade ago, when Dr. E. B. Krumbhaar asked me to collaborate with him in writing a review of the subject for Nelson's Loose Leaf Medicine.! In the following discussion I should like to stress certain features of this subject which have been proved by the experience of the intervening years to be especially important. ACUTE NONSPECIFIC PERICARDITIS AND ITS DIFFERENTIATION FROM ACUTE CARDIAC INFARCTION
There are, of course, many considerations of age, past history, and so on, which have a bearing on this differential diagnosis. It must be admitted that sometimes, especially in the early stages, one cannot be sure which of these two conditions the patient has. Under such circumstances we treat for coronary disease, but later on may encourage the patient with the less ominous diagnosis. In many instances the character of the pain has seemed to us the most important differential point. As an example, we shall cite the symptoms of a young colleague who suffered a severe attack of chest pain in the middle of the night. He was thirty-six, possibly a little young for a coronary attack, but it was obvious that he suspected the worst. lIe was comforted considerably when we pointed out the following features of the pain: It throbbed with each heart beat. It was markedly exaggerated by movements of the thorax or of its contents-when the patient changed position, breathed, swallowed or belched. When the blood pressure cuff was pumped up on the arm, the pain became worse. Palpation of the epigastrium and exertion of pressure on the upper abdomen exaggerated the discomfort. We have not collected data in a series of cases to determine how often these symptoms occur in acute nonspecific pericarditis, but they must be rare in cardiac infarction. The point to be stressed is that careful From the Departntent of Medicine, University of Pennsylvania School of Medicine, Philadelphia.
* Professor of Medicine,
University of Pennsylvania School of Medicine.
1639
1640
Francis C. Wood
questioning about the character of the pain may be the most important method of making the diagnosis. One other differential diagnostic feature concerning the location of the pain has been pointed out to me by Dr. Charles C. Wolferth. In nonspecific pericarditis the pain often centers near the left shoulder, especially at a place halfway between the base of the neck and the left shoulder. In cardiac infarction this location of pain is unusual. THE PERICARDIAL FRICTION RUB
The pericardial friction rub may be a noisy, squeaking, crunching sound, heard in the sternal area, which continues when the patient holds his breath. Under such circumstances there is no problem in differentiating it from other sounds. There are, however, a number of instances when a pericardial friction has been mistaken for a murmur. If you are an experienced auscultator, it is quite probable that you recognize a friction in certain instances, as Sir Thomas Lewis once said he recognized mitral stenosis "as you would your dog's bark." You know "instinctively" that it is not the neighbor's dog (aortic insufficiency), but your dog (a pericardial friction). Yet this more or less subconscious differential diagnostic skill must be scrutinized and turned into conscious knowledge if it is to be transmitted to your students. Such scrutinizing has led me to realize that there are few real "to and fro" murmurs, i.e., few instances in which the systolic and the diastolic murmurs at a given place on the precordium have the same quality and pitch. At the base the systolic murmur is apt to be lower pitched and the diastolic murmur higher pitched; at the apex the systolic is apt to be higher pitched and the diastolic lower pitched. (There are, of course, exceptions). Whenever systolic and diastolic "murmurs" are heard at the same location on the precordium, which sound alike, one should stop and ask himself whether this might not be a friction rub. Another important differential point is that the friction often begins "slightly late" in systole and in diastole, when the surface of the heart moves, rather than when the blood moves. It seems to lag a little after both the first and the second sounds, and it tends to be a little louder in systole than in diastole. If, after careful examination, one is still in doubt, and if the patient is not too sick, one may move him from side to side and then listen. This process may change the sound considerably. It may cause the friction to disappear, or occasionally it may cause it to become loud and unmistakable in character. CAREFUL OBSERVATION OF PHENOMENA IN THE CERVICAL VEINS AND LIVER
There are a number of things to learn from inspection of the cervical veins. The most important, however, may well be the height of the
Observations on Pericardial Disease
1641
venous pressure. This can be estimated in most patients by the simple expedient of slowly raising and then lowering the head of the bed, and noting the location of the "meniscus." It is helpful to remember that usually the veins pulsate most actively at the level of the "meniscus." It is helpful also to try to fill the cervical vein by obstructing its lower end with a finger to see just where it is, and whether one can fill it. A pulsation in the neck which is seen and not felt is venous. After finding the "meniscus" one can estimate the vertical distance between it and the level of the right auricle. With practice, venous pressure may be estimated with a fair degree of accuracy. The findings in the cervical veins and in the liver must be considered together. When the liver is enlarged and the cervical venous pressure shows an elevation, corresponding in degree to that of hepatic enlargement, heart failure is almost invariably the cause of this combination of findings. When the liver is large and the cervical venous pressure is normal, or when the cervical venous pressure is elevated and the liver is not enlarged, the cause is almost invariably some condition other than cardiac failure. The only exceptions are that (a) when cardiac failure comes on rapidly, the venous pressure may rise before the liver has had time to enlarge; and (b) when cardiac failure clears rapidly, the venous pressure will fall before the liver has had time to return to normal size. These phenomena are discussed at considerable length, because many practicing physicians have gone through their medical lives thus far without having discovered them. Not knowing what to look for in the cervical veins, they often fail to observe the fact that the venous pressure is elevated. Enlargement of the liver accompanied by a high venous pressure is seen in cardiac failure of a variety of types. When these phenomena are found in the absence of murmurs, hypertension or a coronary disease, they often point to pericardial disease (either pericardial effusion under some pressure, or a constricting pericardial scar.) If, on this day, every physician in America would estimate the cervical venous pressure of every patient under his care with large liver and ascites, who has been diagnosed as having "cirrhosis of the liver," a number of patients would be discovered suffering from chronic constrictive pericarditis. THE PULSUS PARADOXUS
This is another physical sign important in pericardial disease. If it is recognized, it helps one to diagnose chronic constrictive pericarditis. It also assists in the diagnosis of pericardial effusion. Moreover, in pericardial effusion it gives some indication as to whether the pressure inside the pericardial sac is high or low. Gauchat and Katz 2 found that they could produce the paradoxic pulse in animals by raising the intrapericardial pressure and that it would disappear if they reduced the pressure
Francis C. Wood
1642
by removing some of the pericardial fluid. There are a number of conditions, other than pericardial effusion or cardiac constriction, which can give rise to a pulsus paradoxus,3 principally bronchial obstruction. and large pleural effusion. When a patient is breathing hard, a pulsus para:doxus is not a reliable sign of pericardial disease. The paradoxic pulse is observed most readily as one takes the blood pressure. The pressure in the cuff should always be allowed to fall slowly as the first beats come through to the ear. Then it is easy to note the "bump, bump, silence, silence, silence, bump, bump, bump" of the paradoxic pulse, and to note that the "bumps" come through with expiration. Incidentally, it should be remembered that the paradoxic pulse is not really a "paradoxical" phenomenon. It is merely an exaggeration of a normally occurring variation in the pulse with inspiration and expiration. PERICARDIAL EFFUSION
By fluoroscopy one cannot always readily differentiate a big effusion from a big heart. The borders do not pulsate very well in either. Fluoroscopy is helpful, however, in the case of a moderate-sized heart. Moderately large hearts pulsate actively as a rule. When a similar moderatesized "cardiac" shadow is produced by pericardial effusion, the pulsation is more apt to be small. We have satisfied ourselves of the accuracy of Williamson's4 observation that, even in the presence of 1000 cc. of fluid in the pericardium, the heart may be right next to the anterior chest wall. The heart sounds may be normally loud, and a friction rub may be audible, even when the patient lies in the supine position. We have rarely seen the posterior thoracic signs of pericardial effusion 5 except when rheumatic fever caused the effusion. Auenbrugger noted that in pericardial effusion the percussion note in the precordium was "flat" rather than "dull."6 Whenever it is easier to determine the position of a cardiac border by percussion than you had expected it to be, stop and consider the possible presence of a pericardial effusion. The striking transition from pulmonary resonance to "cardiac" flatness has given the diagnostic clue in certain cases. Occasionally an angiocardiogram will give real help in diagnosing a pericardial effusion by showing a wide, light gray zone surrounding the more radiopaque cardiac chambers. PERICARDIAL PARACENTESIS
There are many locations on the chest wall at which the pericardium may be tapped. 3 Yet, after considerable experience, we rarely needle a pericardium except at its left margin. We believe it to be the safest and
Observations on Pericardial Disease
1643
easiest place to tap, and the best, unless the fluid is loculated elsewhere. One has less chance of needling the heart. If one does, one usually encounters the thick-walled left ventricle, which, if penetrated, is less likely to continue to bleed than are the thinner-walled chambers. Moreover, with antibiotic therapy available one has less fear of contaminating the pleural cavity, through which the needle must pass, even if one should strike a purulent effusion. One of the most disturbing situations you will encounter will be when the needle is presumably in the pericardial cavity and the fluid which is aspirated looks like blood. The perspiration will start on your forehead. The temptation is great to withdraw the needle. The methods of calming yourself are as follows: (1) If you have tapped along the left border and the point of the needle is in the ventricular cavity, it must have gone through the wall of the left ventricle, which will give it a powerful, unmistakable pull with each systole. If this pull is absent, you should relax and take a few deep breaths. (2) The next move is to centrifuge the fluid and see whether its hematocrit is the same as that of the patient's blood. (3) A more recent suggestion7 is to inject through the needle one of the substances which have been used intravenously to measure circulation time. If the needle point is in the ventricular cavity, the patient should taste the substance without much delay. Recently we saw a patient with "cardiac" enlargement, thought by some to be due to pericardial effusion. A dark red fluid was obtained when the paracentesis needle was inserted into the pericardium (?). The hematocrit of this fluid was definitely lower than that of the patient's blood. When the patient failed to notice any strange taste after Dr. Julian Johnson had injected 2 cc. of Decholin through the paracentesis needle, we felt more comfortable about injecting air to help in subsequent radiographic study, which confirmed the diagnosis of pericardial effusion. Rheumatic pericardial effusion almost never requires tapping. Purulent pericardial effusion has almost disappeared from our experience. PERICARDIAL SCAR
Diagnostic Features
There are three groups of phenomena which seem to us of major importance: 1. The finding of calcium in the pericardium by radiologicexamination. The lateral view usually shows the calcium more clearly than does the posteroanterior view. 2. The finding.of a high venous pressure and enlargement of the liver without obvious cause, Le., without hypertension, coronary' 'history or signs of valvular disease. This finding should start one at once on an ex-
1644
Fra'ncis C. Wood
ploration to prove or disprove the existence of a constricting pericardial scar. One should keep the diagnosis in mind even when the fluoroscopist "rules it out" by finding an active pulsation of the left border of the heart. This pulsation may be occurring at a "window" in the constricting scar. 3. The precordial phenomena described by Skoda:8 The systolic retraction of a segment of the precordium including ribs, when the systolic apex impulse is absent (this proviso is all-important);' and the presence of a diastolisches Spitzenstoss, i.e., a palpable diastolic impulse accompanied by a sound. 9 These phenomena are accompanied by certain electrokymographic phenomena and by a diastolic wave in the ballistocardiogram. Skoda's signs have constituted the leading diagnostic clue in several of our patients. In our experience Broadbent's sign has proved useless for the purpose of diagnosing constricting pericardial scar. Likewise, lack of shift of the position of the cardiac silhouette or of its electrical axis has not been helpful. In an occasional patient with cardiac failure of the "right-sided" type in whom careful diagnostic study has failed to demonstrate the cause, and in whom the presence of a constricting pericardial scar is suspected but cannot be proved, we believe that it is proper to explore the chest surgically to confirm or exclude the diagnosis. Today, in experienced hands such an exploration carries a low mortality, which it is justifiable to accept, because if a constricting scar is found, this discovery can change a hopeless prognosis to an entirely different outlook. Surgical Features
The best operative approach to the heart for pericardiectomy seems to us to be Julian Johnson's transverse incision 1o from one midaxillary line to the other. Certain precautions are necessary.3 It is well to open one side first to find out how the patient tolerates positive pressure breathing before the other side is opened. If, however, the patient can tolerate it, the bilateral opening of the pleural cavities offers the surgeon an exposure through which he can manage the accidents which may arise, and through which he can more readily perform a pericardial decortication extensive enough to be effective. We have spent considerable time looking for a patient with a pericardial scar with the following characteristics: (1) It was not constricting the ventricles. (2) It fastened the heart to the ribs and increased cardiac work by making the heart move them with each contraction. (3) The combination of this load plus some other cardiac load (coronary, hypertensive or valvular) was causing congestive heart failure. (4) The cardiac failure could be removed by the "Brauer operation," i.e., remov-
Observations on Pericardial Disease
1645
ing the ribs over the heart. We have not found such a patient. We doubt that one exists. We have operated on several patients hopefully and have improved none of them. SURGERY IN TUBERCULOUS PERICARDITIS
The management of tuberculous pericarditis has been changed by streptomycin and isoniazid. We are learning not to wait too long before operating on these patients. The following situation exemplifies the problem. The patient is found to have cardiac compression probably due to tuberculous pericarditis (often due to a thick pericardium plus some effusion). Treatment with the drugs just mentioned and by other measures results in a disappearance of fever and of some or all of the signs of the cardiac compression. In such instances we used to stop treatment after a considerable time, hoping that the patient would remain well. After a number of disappointments we now tend to operate before therapy is discontinued if we are sure that the patient has tuberculous pericarditis. SUMMARY
We have mentioned certain features which we consider useful in diagnosing and managing the problems presented by patients with pericardial disease: (a) the differential diagnosis between acute nonspecific pericarditis and acute cardiac infarction; (b) certain characteristics of a pericardial friction rub; (c) certain phenomena observable in the veins and liver which help in pericardial diagnosis; (d) the pulsus paradoxus; (e) the diagnosis of pericardial effusion; (j) pericardial paracentesis; (g) certain findings which have helped us to diagnose the presence of a constricting pericardial scar; and a few surgical features which have seemed of interest; (h) a point regarding the management of tuberculous pericarditis. REFERENCES 1. Nelson's Loose Leaf Medicine. New York, Thomas Nelson and Sons, Vo!' 4, pp. 265-306. 2. Gauchat, H. W., and Katz, L. N.: Pulsus Paradoxus (with Special Reference to Pericardial Effusions, Clinical and Experimental). Arch. Int. Med., 33: 350, 371, 1924. 3. Wood F. C., and Krumbhaar, E. B.: Diseases of the Pericardium, in Levy, R. L.: Disorders of the Heart and Circulation. New York, Thomas Nelson and Sons, 1951, Chap. Ill. 4. Williamson, C. S.: Pericarditis with Effusion; Experimental Study. Arch. Int. Med., 25: 206, 1920. 5. Conner, L. A.: On the Diagnosis of Pericardial Effusion. Am. Heart J., 1: 421, 1926. 6. Auenbrugger, L.: On Percussion of the Chest, translated by John Forbes. Baltimore, Johns Hopkins TJnivp.rRity Press, 1936, Twelfth Ohserva,tion (XLVI).
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7. Mills, C. W.: Simple Clinical Aid in Diagnosis of Hemorrhagic Pericardial Effusion. J.A.M.A., 150: 1208, 1952. 8. Skoda, J.: Ueber die Erschienungen, aus denen sich die Verwachsung des Herzens mit dem Herzbeutel an lebenden Menschen erkenne lasst. Zeitschr. d. k. Gesellsch. d. Aerzte zu Wien, 1: 306, 1852. 9. Wood, F. C., Johnson, J., Schnabel, T. G., Jr., Kuo, P., and Zinsser, lie T.: The Diastolic Heart Beat. Tr. A. Am. Phys., 64: 95, 1951. 10. Johnson, J., and Kirby, C. K.: A New Incision for Pericardiectomy. Ann. Surg., 135: 540, 1951.
My special interest in diseases of the pericardium began more than a decade ago, when Dr. E. B. Krumbhaar asked me to collaborate with him in writing a review of the subject for Nelson's Loose Leaf Medicine.! In the following discussion I should like to stress certain features of this subject which have been proved by the experience of the intervening years to be especially important. ACUTE NONSPECIFIC PERICARDITIS AND ITS DIFFERENTIATION FROM ACUTE CARDIAC INFARCTION
There are, of course, many considerations of age, past history, and so on, which have a bearing on this differential diagnosis. It must be admitted that sometimes, especially in the early stages, one cannot be sure which of these two conditions the patient has. Under such circumstances we treat for coronary disease, but later on may encourage the patient with the less ominous diagnosis. In many instances the character of the pain has seemed to us the most important differential point. As an example, we shall cite the symptoms of a young colleague who suffered a severe attack of chest pain in the middle of the night. He was thirty-six, possibly a little young for a coronary attack, but it was obvious that he suspected the worst. lIe was comforted considerably when we pointed out the following features of the pain: It throbbed with each heart beat. It was markedly exaggerated by movements of the thorax or of its contents-when the patient changed position, breathed, swallowed or belched. When the blood pressure cuff was pumped up on the arm, the pain became worse. Palpation of the epigastrium and exertion of pressure on the upper abdomen exaggerated the discomfort. We have not collected data in a series of cases to determine how often these symptoms occur in acute nonspecific pericarditis, but they must be rare in cardiac infarction. The point to be stressed is that careful From the Departntent of Medicine, University of Pennsylvania School of Medicine, Philadelphia.
* Professor of Medicine,
University of Pennsylvania School of Medicine.
1639
1640
Francis C. Wood
questioning about the character of the pain may be the most important method of making the diagnosis. One other differential diagnostic feature concerning the location of the pain has been pointed out to me by Dr. Charles C. Wolferth. In nonspecific pericarditis the pain often centers near the left shoulder, especially at a place halfway between the base of the neck and the left shoulder. In cardiac infarction this location of pain is unusual. THE PERICARDIAL FRICTION RUB
The pericardial friction rub may be a noisy, squeaking, crunching sound, heard in the sternal area, which continues when the patient holds his breath. Under such circumstances there is no problem in differentiating it from other sounds. There are, however, a number of instances when a pericardial friction has been mistaken for a murmur. If you are an experienced auscultator, it is quite probable that you recognize a friction in certain instances, as Sir Thomas Lewis once said he recognized mitral stenosis "as you would your dog's bark." You know "instinctively" that it is not the neighbor's dog (aortic insufficiency), but your dog (a pericardial friction). Yet this more or less subconscious differential diagnostic skill must be scrutinized and turned into conscious knowledge if it is to be transmitted to your students. Such scrutinizing has led me to realize that there are few real "to and fro" murmurs, i.e., few instances in which the systolic and the diastolic murmurs at a given place on the precordium have the same quality and pitch. At the base the systolic murmur is apt to be lower pitched and the diastolic murmur higher pitched; at the apex the systolic is apt to be higher pitched and the diastolic lower pitched. (There are, of course, exceptions). Whenever systolic and diastolic "murmurs" are heard at the same location on the precordium, which sound alike, one should stop and ask himself whether this might not be a friction rub. Another important differential point is that the friction often begins "slightly late" in systole and in diastole, when the surface of the heart moves, rather than when the blood moves. It seems to lag a little after both the first and the second sounds, and it tends to be a little louder in systole than in diastole. If, after careful examination, one is still in doubt, and if the patient is not too sick, one may move him from side to side and then listen. This process may change the sound considerably. It may cause the friction to disappear, or occasionally it may cause it to become loud and unmistakable in character. CAREFUL OBSERVATION OF PHENOMENA IN THE CERVICAL VEINS AND LIVER
There are a number of things to learn from inspection of the cervical veins. The most important, however, may well be the height of the
Observations on Pericardial Disease
1641
venous pressure. This can be estimated in most patients by the simple expedient of slowly raising and then lowering the head of the bed, and noting the location of the "meniscus." It is helpful to remember that usually the veins pulsate most actively at the level of the "meniscus." It is helpful also to try to fill the cervical vein by obstructing its lower end with a finger to see just where it is, and whether one can fill it. A pulsation in the neck which is seen and not felt is venous. After finding the "meniscus" one can estimate the vertical distance between it and the level of the right auricle. With practice, venous pressure may be estimated with a fair degree of accuracy. The findings in the cervical veins and in the liver must be considered together. When the liver is enlarged and the cervical venous pressure shows an elevation, corresponding in degree to that of hepatic enlargement, heart failure is almost invariably the cause of this combination of findings. When the liver is large and the cervical venous pressure is normal, or when the cervical venous pressure is elevated and the liver is not enlarged, the cause is almost invariably some condition other than cardiac failure. The only exceptions are that (a) when cardiac failure comes on rapidly, the venous pressure may rise before the liver has had time to enlarge; and (b) when cardiac failure clears rapidly, the venous pressure will fall before the liver has had time to return to normal size. These phenomena are discussed at considerable length, because many practicing physicians have gone through their medical lives thus far without having discovered them. Not knowing what to look for in the cervical veins, they often fail to observe the fact that the venous pressure is elevated. Enlargement of the liver accompanied by a high venous pressure is seen in cardiac failure of a variety of types. When these phenomena are found in the absence of murmurs, hypertension or a coronary disease, they often point to pericardial disease (either pericardial effusion under some pressure, or a constricting pericardial scar.) If, on this day, every physician in America would estimate the cervical venous pressure of every patient under his care with large liver and ascites, who has been diagnosed as having "cirrhosis of the liver," a number of patients would be discovered suffering from chronic constrictive pericarditis. THE PULSUS PARADOXUS
This is another physical sign important in pericardial disease. If it is recognized, it helps one to diagnose chronic constrictive pericarditis. It also assists in the diagnosis of pericardial effusion. Moreover, in pericardial effusion it gives some indication as to whether the pressure inside the pericardial sac is high or low. Gauchat and Katz 2 found that they could produce the paradoxic pulse in animals by raising the intrapericardial pressure and that it would disappear if they reduced the pressure
Francis C. Wood
1642
by removing some of the pericardial fluid. There are a number of conditions, other than pericardial effusion or cardiac constriction, which can give rise to a pulsus paradoxus,3 principally bronchial obstruction. and large pleural effusion. When a patient is breathing hard, a pulsus para:doxus is not a reliable sign of pericardial disease. The paradoxic pulse is observed most readily as one takes the blood pressure. The pressure in the cuff should always be allowed to fall slowly as the first beats come through to the ear. Then it is easy to note the "bump, bump, silence, silence, silence, bump, bump, bump" of the paradoxic pulse, and to note that the "bumps" come through with expiration. Incidentally, it should be remembered that the paradoxic pulse is not really a "paradoxical" phenomenon. It is merely an exaggeration of a normally occurring variation in the pulse with inspiration and expiration. PERICARDIAL EFFUSION
By fluoroscopy one cannot always readily differentiate a big effusion from a big heart. The borders do not pulsate very well in either. Fluoroscopy is helpful, however, in the case of a moderate-sized heart. Moderately large hearts pulsate actively as a rule. When a similar moderatesized "cardiac" shadow is produced by pericardial effusion, the pulsation is more apt to be small. We have satisfied ourselves of the accuracy of Williamson's4 observation that, even in the presence of 1000 cc. of fluid in the pericardium, the heart may be right next to the anterior chest wall. The heart sounds may be normally loud, and a friction rub may be audible, even when the patient lies in the supine position. We have rarely seen the posterior thoracic signs of pericardial effusion 5 except when rheumatic fever caused the effusion. Auenbrugger noted that in pericardial effusion the percussion note in the precordium was "flat" rather than "dull."6 Whenever it is easier to determine the position of a cardiac border by percussion than you had expected it to be, stop and consider the possible presence of a pericardial effusion. The striking transition from pulmonary resonance to "cardiac" flatness has given the diagnostic clue in certain cases. Occasionally an angiocardiogram will give real help in diagnosing a pericardial effusion by showing a wide, light gray zone surrounding the more radiopaque cardiac chambers. PERICARDIAL PARACENTESIS
There are many locations on the chest wall at which the pericardium may be tapped. 3 Yet, after considerable experience, we rarely needle a pericardium except at its left margin. We believe it to be the safest and
Observations on Pericardial Disease
1643
easiest place to tap, and the best, unless the fluid is loculated elsewhere. One has less chance of needling the heart. If one does, one usually encounters the thick-walled left ventricle, which, if penetrated, is less likely to continue to bleed than are the thinner-walled chambers. Moreover, with antibiotic therapy available one has less fear of contaminating the pleural cavity, through which the needle must pass, even if one should strike a purulent effusion. One of the most disturbing situations you will encounter will be when the needle is presumably in the pericardial cavity and the fluid which is aspirated looks like blood. The perspiration will start on your forehead. The temptation is great to withdraw the needle. The methods of calming yourself are as follows: (1) If you have tapped along the left border and the point of the needle is in the ventricular cavity, it must have gone through the wall of the left ventricle, which will give it a powerful, unmistakable pull with each systole. If this pull is absent, you should relax and take a few deep breaths. (2) The next move is to centrifuge the fluid and see whether its hematocrit is the same as that of the patient's blood. (3) A more recent suggestion7 is to inject through the needle one of the substances which have been used intravenously to measure circulation time. If the needle point is in the ventricular cavity, the patient should taste the substance without much delay. Recently we saw a patient with "cardiac" enlargement, thought by some to be due to pericardial effusion. A dark red fluid was obtained when the paracentesis needle was inserted into the pericardium (?). The hematocrit of this fluid was definitely lower than that of the patient's blood. When the patient failed to notice any strange taste after Dr. Julian Johnson had injected 2 cc. of Decholin through the paracentesis needle, we felt more comfortable about injecting air to help in subsequent radiographic study, which confirmed the diagnosis of pericardial effusion. Rheumatic pericardial effusion almost never requires tapping. Purulent pericardial effusion has almost disappeared from our experience. PERICARDIAL SCAR
Diagnostic Features
There are three groups of phenomena which seem to us of major importance: 1. The finding of calcium in the pericardium by radiologicexamination. The lateral view usually shows the calcium more clearly than does the posteroanterior view. 2. The finding.of a high venous pressure and enlargement of the liver without obvious cause, Le., without hypertension, coronary' 'history or signs of valvular disease. This finding should start one at once on an ex-
1644
Fra'ncis C. Wood
ploration to prove or disprove the existence of a constricting pericardial scar. One should keep the diagnosis in mind even when the fluoroscopist "rules it out" by finding an active pulsation of the left border of the heart. This pulsation may be occurring at a "window" in the constricting scar. 3. The precordial phenomena described by Skoda:8 The systolic retraction of a segment of the precordium including ribs, when the systolic apex impulse is absent (this proviso is all-important);' and the presence of a diastolisches Spitzenstoss, i.e., a palpable diastolic impulse accompanied by a sound. 9 These phenomena are accompanied by certain electrokymographic phenomena and by a diastolic wave in the ballistocardiogram. Skoda's signs have constituted the leading diagnostic clue in several of our patients. In our experience Broadbent's sign has proved useless for the purpose of diagnosing constricting pericardial scar. Likewise, lack of shift of the position of the cardiac silhouette or of its electrical axis has not been helpful. In an occasional patient with cardiac failure of the "right-sided" type in whom careful diagnostic study has failed to demonstrate the cause, and in whom the presence of a constricting pericardial scar is suspected but cannot be proved, we believe that it is proper to explore the chest surgically to confirm or exclude the diagnosis. Today, in experienced hands such an exploration carries a low mortality, which it is justifiable to accept, because if a constricting scar is found, this discovery can change a hopeless prognosis to an entirely different outlook. Surgical Features
The best operative approach to the heart for pericardiectomy seems to us to be Julian Johnson's transverse incision 1o from one midaxillary line to the other. Certain precautions are necessary.3 It is well to open one side first to find out how the patient tolerates positive pressure breathing before the other side is opened. If, however, the patient can tolerate it, the bilateral opening of the pleural cavities offers the surgeon an exposure through which he can manage the accidents which may arise, and through which he can more readily perform a pericardial decortication extensive enough to be effective. We have spent considerable time looking for a patient with a pericardial scar with the following characteristics: (1) It was not constricting the ventricles. (2) It fastened the heart to the ribs and increased cardiac work by making the heart move them with each contraction. (3) The combination of this load plus some other cardiac load (coronary, hypertensive or valvular) was causing congestive heart failure. (4) The cardiac failure could be removed by the "Brauer operation," i.e., remov-
Observations on Pericardial Disease
1645
ing the ribs over the heart. We have not found such a patient. We doubt that one exists. We have operated on several patients hopefully and have improved none of them. SURGERY IN TUBERCULOUS PERICARDITIS
The management of tuberculous pericarditis has been changed by streptomycin and isoniazid. We are learning not to wait too long before operating on these patients. The following situation exemplifies the problem. The patient is found to have cardiac compression probably due to tuberculous pericarditis (often due to a thick pericardium plus some effusion). Treatment with the drugs just mentioned and by other measures results in a disappearance of fever and of some or all of the signs of the cardiac compression. In such instances we used to stop treatment after a considerable time, hoping that the patient would remain well. After a number of disappointments we now tend to operate before therapy is discontinued if we are sure that the patient has tuberculous pericarditis. SUMMARY
We have mentioned certain features which we consider useful in diagnosing and managing the problems presented by patients with pericardial disease: (a) the differential diagnosis between acute nonspecific pericarditis and acute cardiac infarction; (b) certain characteristics of a pericardial friction rub; (c) certain phenomena observable in the veins and liver which help in pericardial diagnosis; (d) the pulsus paradoxus; (e) the diagnosis of pericardial effusion; (j) pericardial paracentesis; (g) certain findings which have helped us to diagnose the presence of a constricting pericardial scar; and a few surgical features which have seemed of interest; (h) a point regarding the management of tuberculous pericarditis. REFERENCES 1. Nelson's Loose Leaf Medicine. New York, Thomas Nelson and Sons, Vo!' 4, pp. 265-306. 2. Gauchat, H. W., and Katz, L. N.: Pulsus Paradoxus (with Special Reference to Pericardial Effusions, Clinical and Experimental). Arch. Int. Med., 33: 350, 371, 1924. 3. Wood F. C., and Krumbhaar, E. B.: Diseases of the Pericardium, in Levy, R. L.: Disorders of the Heart and Circulation. New York, Thomas Nelson and Sons, 1951, Chap. Ill. 4. Williamson, C. S.: Pericarditis with Effusion; Experimental Study. Arch. Int. Med., 25: 206, 1920. 5. Conner, L. A.: On the Diagnosis of Pericardial Effusion. Am. Heart J., 1: 421, 1926. 6. Auenbrugger, L.: On Percussion of the Chest, translated by John Forbes. Baltimore, Johns Hopkins TJnivp.rRity Press, 1936, Twelfth Ohserva,tion (XLVI).
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7. Mills, C. W.: Simple Clinical Aid in Diagnosis of Hemorrhagic Pericardial Effusion. J.A.M.A., 150: 1208, 1952. 8. Skoda, J.: Ueber die Erschienungen, aus denen sich die Verwachsung des Herzens mit dem Herzbeutel an lebenden Menschen erkenne lasst. Zeitschr. d. k. Gesellsch. d. Aerzte zu Wien, 1: 306, 1852. 9. Wood, F. C., Johnson, J., Schnabel, T. G., Jr., Kuo, P., and Zinsser, lie T.: The Diastolic Heart Beat. Tr. A. Am. Phys., 64: 95, 1951. 10. Johnson, J., and Kirby, C. K.: A New Incision for Pericardiectomy. Ann. Surg., 135: 540, 1951.