- Email: [email protected]
Office Aids in Evaluating Cardiac Function
Office Aids in Evaluating Cardiac Function FRANK R. BOYER, M.D., F.A.C.P. Associate Cardiologist, Pennsylvania Hospital; Assistant Instructor in Medicine, University of Pennsylvania School of Medicine, Philadelphia
IN FEW fields of medicine is it possible for diagnosis to be made with greater accuracy and with such relatively simple and generally available procedures as in cardiovascular disease. Cardiac function or performance can be accurately estimated by utilizing the office procedures of a very carefully taken history and a well performed physical examination with special attention to the cardiovascular system. If this unaided examination is inconclusive, the office aids of electrocardiography and cardiac roentgenography may provide supplemental information. It is the physical examination which points to the particular type of further diagnostic procedure indicated for the individual patient. IMPORTANCE OF THE HISTORY IN CARDIAC DISEASE
The taking of an accurate and relevant history is one of the most difficult and important arts in medicine. Sometimes a complete diagnosis can be made from the history alone, an excellent example being the pain of myocardial ischemia, whether caused by disease of the coronary artery, by aortic stenosis or by insufficiency due to valvular disease, luetic aortitis or anemia. A common mistake is failure to analyze any given symptom sufficiently. In cardiovascular evaluation this applies especially to the symptoms of pain, breathlessness and palpitation. Appropriate but not leading questions are necessary as is intelligent interpretation of the patient's replies. The best history taker is he who can best interpret the answer to an appropriate question. It should always be remembered that severe cardiovascular disease may be present without any symptoms. Good examples of this are coarctation of the aorta, pulmonary stenosis, atrial septal defects, aortic stenosis and even myocardial infarction.
1523
1524
FRANK
R.
BOYER
Pain
MYOCARDIAL ISCHEMIA, ANGINA PECTORIS. Pain of myocardial ischemia or angina pectoris which may severely limit cardiac function is characteristically retrosternal, not precordial. In most cases it tends to appear in the midline of the chest behind the sternum; it may be in the epigastrium or in the throat and may spread centrifugally. It may extend into the lower jaw, to one or both shoulders or to one or both arms. Occasionally it may start in the arms or may be felt only in the wrists and then spread centripetally to the above mentioned areas. The onset and cessation of the pain are related respectively to increase and decrease in cardiac work and thereby are significant indicators of eardiac function. The onset of the attack is abrupt and its duration short, usually less than five minutes. It is usually described as a "pressure, heaviness, squeezing, burning, or like indigestion." It occurs especially on walking, particularly after meals, on a cold day against the wind or up a hill. It forces the patient to stop or slow down, and several minutes later the pain disappears. It is relieved promptly by nitroglycerin sublingually in approximately the time it takes for the tablet to be dissolved. The pain of acute coronary insufficiency occurs at rest, lasts longer-up to 30 minutes-and is often more severe, but the coronary flow is still sufficient to prevent myocardial necrosis. When inquiring about coronary ischemia it is not sufficient to ask about pain alone. Actually, on occasion, the patient may specifically deny pain; one should then ask about "indigestion," tightness, squeezing, burning, heaviness or choking, all of which may be experienced by the patient rather than pain as commonly interpreted. MYOCARDIAL INFARCTION. Pain resulting from myocardial infarction has many of the characteristics of angina of effort. However, it is more severe and more prolonged in most instances. It frequently occurs at rest. It is not relieved by sublingual nitroglycerin. As a prodrome to acute coronary occlusion, a patient with a history of angina may experience a number of frequent and more prolonged attacks of chest pain related to or unrelated to effort and not relieved as readily by nitroglycerin. This has been termed "preinfarction angina" or "pilot angina." The symptoms of myocardial infarction vary from the mild attack of "acute indigestion" to severe seizures. The mild attacks of "acute indigestion" are really episodes of anginal pain lasting 15 to 30 minutes. Severe seizures may last hours and may be associated with all the signs of shock. There may be associated dyspnea, sweating, nausea, vomiting and giddiness, together with an ashen hue of the skin. PERICARDIAL IRRITATION. Pain of pericardial irritation may be fairly widespread over the whole thorax or it may be localized to the substernal, precordial or epigastric area. It may center near the left shoulder at the mid clavicular level, a location unusual for the pain of myocardial infarction. It may throb with each heart beat and may be
Office Aids in Evaluating Cardiac Function
1525
greatly exaggerated by the movement of the thorax or its contents as in a change of position, breathing, swallowing or helching. Inflating the blood pressure cuff on the arm may aggravate the pain as may palpation of the epigastrium or exertion of pressure on the upper abdomen. Breathlessness
Breathlessness due to decreasing cardiac capacity and reserve is frequently the first symptom which causes a patient to visit the doctor's office. Cardiac failure is not early when dilatation and enlargement of the heart, systemic and venous congestion and pedal edema are already present. In the progressive decrease in cardiac function these are late phenomena which signify that the heart has failed to such a degree that it no longer has the capacity to do the work required of it while the body is at rest. It is the much earlier diagnosis of decreasing cardiac function that we are interested in, especially in evaluating heart function in the office. Before the signs of venous congestion have appeared, the underlying defect shows itself in a lack of reserve by means of the cardinal symptom of breathlessness on effort. Breathlessness is not in itself abnormal; all people, however healthy, may become breathless on exercise. Abnormality consists in the occurrence of breathlessness in unusual circumstances. Frequently, the first indication of decreasing cardiac function is the limitation of the patient's activities; he notices unusual breathlessness on undertaking some customary activity which previously and perhaps recently could be completed without difficulty. As cardiac reserve wanes, breathlessness continues to occur, but it is experienced in response to decreasing amounts of work as time passes. For example, breathlessness may first occur only on rapid walking or walking uphill; then it occurs when walking on the flat, then on walking more slowly and at shorter and shorter distances; finally, it is present at rest. Thus, the complete course from normal cardiac function to gross cardiac failure is associated with breathlessness ranging from normal breathlessness on exertion to breathlessness when the patient is at rest. Although many exercise tests for cardiac efficiency and inefficiency based upon pulse and blood pressure determinations have been devised, there is none that approaches in delicacy the symptom of breathlessness. Since this is a subjective manifestation, only by a careful history from the patient can its true evaluation be made. No test that we can devise, however carefully graded it may be, will impose the same strain upon different individuals unaccustomed to it. In finally gauging cardiac function, a comparison between a healthy and an unhealthy person is usually far less satisfactory than comparison between the healthy and unhealthy states of the same person. Several types of dyspnea other than breathlessness on effort reflect decreased cardiac function, and they may provide office estimates of
1526
FRANK
R.
BOYER
cardiac function when properly interpreted. These include paroxysmal nocturnal dyspnea, orthopnea and acute pulmonary edema; usually all are caused by variations of the same fundamental mechanism of left ventricular failure, although they can be seen in severe mitral stenosis and in pericardial effusion. Palpitation
Palpitation is a third common symptom in the office patient. Rather naturally it may draw the patient's attention to his heart and he soon may begin to question his cardiac integrity; this leads to anxiety and since emotional turmoil is the commonest cause of the symptom, a vicious cycle ensues. In other patients an awareness of a disturbed feeling of the heart beat may accompany the vigorous action of a hypertrophied heart. Finally, abnormally rapid or irregular heart action may cause unusual sensations. Thus, the symptom is an ambiguous and complex phenomenon requiring thorough analysis to ascertain its basic nature. It is important to learn whether palpitation occurs at rest or with exercise. Palpitation felt on exertion is frequently the first symptom pointing to the presence of a cardiac lesion. As cardiac disease progresses and heart failure ensues with its concomitant rise in heart rate, palpitation commonly occurs with increased intensity and frequency. When palpitation occurs in attacks without apparent cause, even though the patient is at rest, it is necessary to get reliable information about the heart rate. This is not always easy since the patient is often inclined to exaggerate and to speak of a very rapid heart action when the actual rate may have been around 100 per minute. Often it is helpful to have the patient imitate the heart action by beating time with his fingertips on the desk top so that we may obtain a rough approximation of the heart rate and of its regularity or irregularity. If the rate is over 150 per minute, a condition other than simple tachycardia is likely to be present. It is furthermore important to know the mode of onset and cessation of rapid heart action. If the tachycardia did not build up gradually but came suddenly, paroxysmal atrial tachycardia, atrial flutter or atrial fibrillation should be considered. The diagnosis of atrial fibrillation is particularly attractive if the patient reports that the action of his heart was irregular during the attack. Irregularity of the heart beat, with or without tachycardia, is responsible in many instances when the patient complains of palpitation. Frequently the patient is aware of the irregularities and is capable of describing them fairly accurately. He may speak of "skipping of the heart," of long pauses of the heart (in a case of premature contractions) or of a total irregularity of rapid heart action (as in atrial fibrillation). In instances such as these the physician, even without the opportunity
Office Aids in Evaluating Cardiac Function
1527
to observe the disorder of rhythm, might merely on the basis of the history alone be able to make a correct diagnosis. PHYSICAL EXAMINATION
In this age of precision instruments there is a great tendency for physicians to abandon continued training and skilled use of the unaided senses. It must be emphasized that precise instruments do not necessarily supply precise information. Much that is not obtainable by any other means can be learned about the cardiac status by careful inspection, palpation, percussion and in particular auscultation of the heart, and a careful examination of the patient in general. It has become too routine to "plug the patient into the laboratory" in a futile effort to arrive at a correct cardiac diagnosis. Nevertheless, although much definitive information can be obtained toward making or excluding the diagnosis of organic heart disease by careful physical examination, office procedures are much less helpful in the evaluation of the degree of impairment of the cardiac reserve. This does not mean that certain clues to cardiac function are to be disregarded or overlooked. Pulsus alternans or paradoxical pulse can be detected during routine sphygmomanometry. Moreover, certain signs of cardiac disease such as cardiac enlargement, precordial deformity, arrhythmias, certain abnormalities of heart sounds and murmurs at various precordial and peripheral vascular areas, increased cervical venous pressure, thrills, pericardial rub, and protodiastolic or ventricular gallop rhythm all may yield a degree of information as to probable cardiac function. However, the point to be emphasized is that the most accurate method of determining early impairment of cardiac performance is the careful, precise and detailed history obtained by intelligent interrogation of the patient. The earliest stage of decreased cardiac function is the stage of symptoms such as breathlessness, chest pain and palpitation; the later stage of decreased cardiac function is the stage of signs of congestion such as increased cervical vein pressure and hepatomegaly. Since the signs follow the symptoms the history is paramount. ELECTROCARDIOGRAPHY
The electrocardiogram obtained by the usual method furnishes information only about the electrical forces in the heart muscle; it does not reflect the mechanical forces in the heart muscle which are so important in attempting to evaluate cardiac function. Yet how common it is for physicians to attempt to read into the electrocardiogram, by some intangible thought process, an evaluation of the cardiac function. An electrocardiogram gives no information about the pumping action of the heart. An electrocardiogram is not a substitute for a cardiovascular
1528
FRANK
R.
BOYER
evaluation or a consultation. The electrocardiograph does not have a brain and is not capable of the interpretation and interrogation which are so fundamentally important in attempting to evaluate the early decrease in cardiac function. All too frequent and totally erroneous is the cliehe "How is the electrocardiogram?" when the problem of evaluation of eardiac function, particularly in the preoperative patient, is raised. Generally, the subject is a patient with possible coronary artery disease. What is generally not appreciated, particularly by many surgeons, is that approximately 75 per cent of all patients with angina peetoris due to eoronary atheroselerosis have normal reeords. A normal eleetroeardiogram does not neeessarily indieate a normal heart, and an "abnormal" electroeardiogram does not necessarily indicate an abnormal heart. The problem here is the failure to appreciate the normal range and variation of any biologic information. The greatest hazard in electrocardiography is the tendency to try to read too much into the traeing; too much importance is often attached to minor abnormalities, some of whieh may be due to extracardiac factors. I t must always be remembered that there are wide variations among normal hearts. Little elinieal meaning is to be attached to the fact that a tracing at one time satisfies the criteria for left ventricular hypertrophy and at another time does not; certainly, no accurate interpretation regarding cardiac function can be made from observations such as this. Furthermore, even when certain abnormalities are definitely present in the tracing they transmit no information about heart performance; for example, in acute coronary thrombosis a patient with very little electroeardiographic change may be doing very poorly and may even suddenly die. It is idle to say that "The electrocardiogram is getting better." It is much more important to know how the patient is doing elinically than to know what further changes are occurring in his tracings. Moreover, we are all familiar with attempts to interpret records that have been made when the leads were incorrectly applied, to interpret tracings that have been pasted upside down or to interpret artefacts as pathologic changes.
ROENTGENOGRAPHY As a method of study of the heart function, roentgenography usually supplies only confirmatory evidence, although at times surprising and useful information may be obtained. Only by this method may the size and shape of the various cardiac chambers be accurately ascertained during life, but it must bc stated that serious heart disease may be present and may be discovered by the previously discussed methods of examination, although no clue to its presence is given by roentgenography. Moreover, early and slight cardiovascular lesions frequently escape notice because there is no roentgenographic evidence of abnormality of
Office Aids in Evaluating Cardiac Function
1529
cardiac size, shape or action. For the most part, roentgenography merely reveals evidence of well established-not early-disease which is difficult or impossible to eradicate. Many roentgenographic findings of the heart are not unequivocal and must be interpretated in the light of the clinical findings. Cardiac function is especially difficult to evaluate by this procedure. In a broad sense, it can be said that the larger the heart the greater the degree of impairment of function. Nevertheless, there are people with considerable cardiac enlargement, as with aortic stenosis or arterial hypertension, who have very satisfactory cardiac function. On the other hand, there are people whose hearts are of normal size by the usual methods of mensuration who have extremely limited cardiac function: for example, patients with coronary artery disease in whom cardiac performance is greatly impaired by the appearance of angina on attempting even very slight effort. CONCLUSIONS
The necessity for proper office evaluation of cardiac function is impelling. Apart from indicating the correct therapeutic measures, it also inevitably entails social, economic and pyschologic adjustments on the part of the patient. As much disability may result from erroneously informing the patient of the nature of his cardiovascular trouble as from failure to recognize it at all. I t is not possible nor is it necessary for the practitioner to be fully conversant with all the newer procedures in cardiology. The oldest and most readily available procedure, that of careful and intelligent history taking, still remains the most important office method of evaluating cardiac function; no other investigation approaches the delicacy and accuracy of this office procedure. To be sure, this may represent a timeconsuming effort, and in a busy practice time is always at a premium. Never1,heless, time so utilized is well invested for the patient who seekH interpretation of chest pain on effort, breathlessness or palpitation since the initial appearance of any of these symptoms may well be the most, significant medical event in the patient's life, particularly the adult male in the coronary artery age. REFERENCES 1. Burch, G. E. and Reaser, P.: Primer of Cardiology. Philadelphia, Lea and
Febiger, 1947. 2. DressIer, William: Clinical Cardiology. New York, Paul B. Hoeber, Inc., 1942. 3. Friedberg, Charles K: Diseases of the Heart. 2nd ed. Philadelphia, W. B. Saunders Co., 1956. 4. Levine, Samuel A.: Clinical Heart Disease. 5th ed. Philadelphia, W. B. Saunders Co., 1958.
1530
FRANK
R.
BOYER
5. Lewis, Thomas: Diseases of the Heart. 3rd ed. London, Macmillan and Co., 1944. 6. White, Paul D.: Heart Diseases. 3rd ed. New York, The Macmillan Company, 1946. 7. Wood, Paul: Diseases of the Heart and Circulation. 2nd ed. Philadelphia, J. B. Lippincott Co., 1956. 8. Wood, Francis C.: Observations on Pericardial Disease. M. CLIN. NORTH AMERICA 37: 1639, 1953. 9. Logue, R. B. and Hurst, J. W.: Errors in the Recognition and Treatment of Heart Disease. Circulation 10: 920, 1954. 10. Kossman, Charles E.: The Normal Electrocardiogram. Circulation 8: 920, 1953. 11. Dry, Thomas J.: Types of Dyspnea Associated with Cardiac Disease. Proc. Staff Meet., Mayo Clin. 27(3), January 30, 1952. 12. Harrison, T. R. and Reeves, T. J.: Diagnostic and Therapeutic Value of Reproduction of Chest Pain. Arch. Int. Med. 91: 8, 1953. 530 North 20th Street Allentown, Pennsylvania
IN FEW fields of medicine is it possible for diagnosis to be made with greater accuracy and with such relatively simple and generally available procedures as in cardiovascular disease. Cardiac function or performance can be accurately estimated by utilizing the office procedures of a very carefully taken history and a well performed physical examination with special attention to the cardiovascular system. If this unaided examination is inconclusive, the office aids of electrocardiography and cardiac roentgenography may provide supplemental information. It is the physical examination which points to the particular type of further diagnostic procedure indicated for the individual patient. IMPORTANCE OF THE HISTORY IN CARDIAC DISEASE
The taking of an accurate and relevant history is one of the most difficult and important arts in medicine. Sometimes a complete diagnosis can be made from the history alone, an excellent example being the pain of myocardial ischemia, whether caused by disease of the coronary artery, by aortic stenosis or by insufficiency due to valvular disease, luetic aortitis or anemia. A common mistake is failure to analyze any given symptom sufficiently. In cardiovascular evaluation this applies especially to the symptoms of pain, breathlessness and palpitation. Appropriate but not leading questions are necessary as is intelligent interpretation of the patient's replies. The best history taker is he who can best interpret the answer to an appropriate question. It should always be remembered that severe cardiovascular disease may be present without any symptoms. Good examples of this are coarctation of the aorta, pulmonary stenosis, atrial septal defects, aortic stenosis and even myocardial infarction.
1523
1524
FRANK
R.
BOYER
Pain
MYOCARDIAL ISCHEMIA, ANGINA PECTORIS. Pain of myocardial ischemia or angina pectoris which may severely limit cardiac function is characteristically retrosternal, not precordial. In most cases it tends to appear in the midline of the chest behind the sternum; it may be in the epigastrium or in the throat and may spread centrifugally. It may extend into the lower jaw, to one or both shoulders or to one or both arms. Occasionally it may start in the arms or may be felt only in the wrists and then spread centripetally to the above mentioned areas. The onset and cessation of the pain are related respectively to increase and decrease in cardiac work and thereby are significant indicators of eardiac function. The onset of the attack is abrupt and its duration short, usually less than five minutes. It is usually described as a "pressure, heaviness, squeezing, burning, or like indigestion." It occurs especially on walking, particularly after meals, on a cold day against the wind or up a hill. It forces the patient to stop or slow down, and several minutes later the pain disappears. It is relieved promptly by nitroglycerin sublingually in approximately the time it takes for the tablet to be dissolved. The pain of acute coronary insufficiency occurs at rest, lasts longer-up to 30 minutes-and is often more severe, but the coronary flow is still sufficient to prevent myocardial necrosis. When inquiring about coronary ischemia it is not sufficient to ask about pain alone. Actually, on occasion, the patient may specifically deny pain; one should then ask about "indigestion," tightness, squeezing, burning, heaviness or choking, all of which may be experienced by the patient rather than pain as commonly interpreted. MYOCARDIAL INFARCTION. Pain resulting from myocardial infarction has many of the characteristics of angina of effort. However, it is more severe and more prolonged in most instances. It frequently occurs at rest. It is not relieved by sublingual nitroglycerin. As a prodrome to acute coronary occlusion, a patient with a history of angina may experience a number of frequent and more prolonged attacks of chest pain related to or unrelated to effort and not relieved as readily by nitroglycerin. This has been termed "preinfarction angina" or "pilot angina." The symptoms of myocardial infarction vary from the mild attack of "acute indigestion" to severe seizures. The mild attacks of "acute indigestion" are really episodes of anginal pain lasting 15 to 30 minutes. Severe seizures may last hours and may be associated with all the signs of shock. There may be associated dyspnea, sweating, nausea, vomiting and giddiness, together with an ashen hue of the skin. PERICARDIAL IRRITATION. Pain of pericardial irritation may be fairly widespread over the whole thorax or it may be localized to the substernal, precordial or epigastric area. It may center near the left shoulder at the mid clavicular level, a location unusual for the pain of myocardial infarction. It may throb with each heart beat and may be
Office Aids in Evaluating Cardiac Function
1525
greatly exaggerated by the movement of the thorax or its contents as in a change of position, breathing, swallowing or helching. Inflating the blood pressure cuff on the arm may aggravate the pain as may palpation of the epigastrium or exertion of pressure on the upper abdomen. Breathlessness
Breathlessness due to decreasing cardiac capacity and reserve is frequently the first symptom which causes a patient to visit the doctor's office. Cardiac failure is not early when dilatation and enlargement of the heart, systemic and venous congestion and pedal edema are already present. In the progressive decrease in cardiac function these are late phenomena which signify that the heart has failed to such a degree that it no longer has the capacity to do the work required of it while the body is at rest. It is the much earlier diagnosis of decreasing cardiac function that we are interested in, especially in evaluating heart function in the office. Before the signs of venous congestion have appeared, the underlying defect shows itself in a lack of reserve by means of the cardinal symptom of breathlessness on effort. Breathlessness is not in itself abnormal; all people, however healthy, may become breathless on exercise. Abnormality consists in the occurrence of breathlessness in unusual circumstances. Frequently, the first indication of decreasing cardiac function is the limitation of the patient's activities; he notices unusual breathlessness on undertaking some customary activity which previously and perhaps recently could be completed without difficulty. As cardiac reserve wanes, breathlessness continues to occur, but it is experienced in response to decreasing amounts of work as time passes. For example, breathlessness may first occur only on rapid walking or walking uphill; then it occurs when walking on the flat, then on walking more slowly and at shorter and shorter distances; finally, it is present at rest. Thus, the complete course from normal cardiac function to gross cardiac failure is associated with breathlessness ranging from normal breathlessness on exertion to breathlessness when the patient is at rest. Although many exercise tests for cardiac efficiency and inefficiency based upon pulse and blood pressure determinations have been devised, there is none that approaches in delicacy the symptom of breathlessness. Since this is a subjective manifestation, only by a careful history from the patient can its true evaluation be made. No test that we can devise, however carefully graded it may be, will impose the same strain upon different individuals unaccustomed to it. In finally gauging cardiac function, a comparison between a healthy and an unhealthy person is usually far less satisfactory than comparison between the healthy and unhealthy states of the same person. Several types of dyspnea other than breathlessness on effort reflect decreased cardiac function, and they may provide office estimates of
1526
FRANK
R.
BOYER
cardiac function when properly interpreted. These include paroxysmal nocturnal dyspnea, orthopnea and acute pulmonary edema; usually all are caused by variations of the same fundamental mechanism of left ventricular failure, although they can be seen in severe mitral stenosis and in pericardial effusion. Palpitation
Palpitation is a third common symptom in the office patient. Rather naturally it may draw the patient's attention to his heart and he soon may begin to question his cardiac integrity; this leads to anxiety and since emotional turmoil is the commonest cause of the symptom, a vicious cycle ensues. In other patients an awareness of a disturbed feeling of the heart beat may accompany the vigorous action of a hypertrophied heart. Finally, abnormally rapid or irregular heart action may cause unusual sensations. Thus, the symptom is an ambiguous and complex phenomenon requiring thorough analysis to ascertain its basic nature. It is important to learn whether palpitation occurs at rest or with exercise. Palpitation felt on exertion is frequently the first symptom pointing to the presence of a cardiac lesion. As cardiac disease progresses and heart failure ensues with its concomitant rise in heart rate, palpitation commonly occurs with increased intensity and frequency. When palpitation occurs in attacks without apparent cause, even though the patient is at rest, it is necessary to get reliable information about the heart rate. This is not always easy since the patient is often inclined to exaggerate and to speak of a very rapid heart action when the actual rate may have been around 100 per minute. Often it is helpful to have the patient imitate the heart action by beating time with his fingertips on the desk top so that we may obtain a rough approximation of the heart rate and of its regularity or irregularity. If the rate is over 150 per minute, a condition other than simple tachycardia is likely to be present. It is furthermore important to know the mode of onset and cessation of rapid heart action. If the tachycardia did not build up gradually but came suddenly, paroxysmal atrial tachycardia, atrial flutter or atrial fibrillation should be considered. The diagnosis of atrial fibrillation is particularly attractive if the patient reports that the action of his heart was irregular during the attack. Irregularity of the heart beat, with or without tachycardia, is responsible in many instances when the patient complains of palpitation. Frequently the patient is aware of the irregularities and is capable of describing them fairly accurately. He may speak of "skipping of the heart," of long pauses of the heart (in a case of premature contractions) or of a total irregularity of rapid heart action (as in atrial fibrillation). In instances such as these the physician, even without the opportunity
Office Aids in Evaluating Cardiac Function
1527
to observe the disorder of rhythm, might merely on the basis of the history alone be able to make a correct diagnosis. PHYSICAL EXAMINATION
In this age of precision instruments there is a great tendency for physicians to abandon continued training and skilled use of the unaided senses. It must be emphasized that precise instruments do not necessarily supply precise information. Much that is not obtainable by any other means can be learned about the cardiac status by careful inspection, palpation, percussion and in particular auscultation of the heart, and a careful examination of the patient in general. It has become too routine to "plug the patient into the laboratory" in a futile effort to arrive at a correct cardiac diagnosis. Nevertheless, although much definitive information can be obtained toward making or excluding the diagnosis of organic heart disease by careful physical examination, office procedures are much less helpful in the evaluation of the degree of impairment of the cardiac reserve. This does not mean that certain clues to cardiac function are to be disregarded or overlooked. Pulsus alternans or paradoxical pulse can be detected during routine sphygmomanometry. Moreover, certain signs of cardiac disease such as cardiac enlargement, precordial deformity, arrhythmias, certain abnormalities of heart sounds and murmurs at various precordial and peripheral vascular areas, increased cervical venous pressure, thrills, pericardial rub, and protodiastolic or ventricular gallop rhythm all may yield a degree of information as to probable cardiac function. However, the point to be emphasized is that the most accurate method of determining early impairment of cardiac performance is the careful, precise and detailed history obtained by intelligent interrogation of the patient. The earliest stage of decreased cardiac function is the stage of symptoms such as breathlessness, chest pain and palpitation; the later stage of decreased cardiac function is the stage of signs of congestion such as increased cervical vein pressure and hepatomegaly. Since the signs follow the symptoms the history is paramount. ELECTROCARDIOGRAPHY
The electrocardiogram obtained by the usual method furnishes information only about the electrical forces in the heart muscle; it does not reflect the mechanical forces in the heart muscle which are so important in attempting to evaluate cardiac function. Yet how common it is for physicians to attempt to read into the electrocardiogram, by some intangible thought process, an evaluation of the cardiac function. An electrocardiogram gives no information about the pumping action of the heart. An electrocardiogram is not a substitute for a cardiovascular
1528
FRANK
R.
BOYER
evaluation or a consultation. The electrocardiograph does not have a brain and is not capable of the interpretation and interrogation which are so fundamentally important in attempting to evaluate the early decrease in cardiac function. All too frequent and totally erroneous is the cliehe "How is the electrocardiogram?" when the problem of evaluation of eardiac function, particularly in the preoperative patient, is raised. Generally, the subject is a patient with possible coronary artery disease. What is generally not appreciated, particularly by many surgeons, is that approximately 75 per cent of all patients with angina peetoris due to eoronary atheroselerosis have normal reeords. A normal eleetroeardiogram does not neeessarily indieate a normal heart, and an "abnormal" electroeardiogram does not necessarily indicate an abnormal heart. The problem here is the failure to appreciate the normal range and variation of any biologic information. The greatest hazard in electrocardiography is the tendency to try to read too much into the traeing; too much importance is often attached to minor abnormalities, some of whieh may be due to extracardiac factors. I t must always be remembered that there are wide variations among normal hearts. Little elinieal meaning is to be attached to the fact that a tracing at one time satisfies the criteria for left ventricular hypertrophy and at another time does not; certainly, no accurate interpretation regarding cardiac function can be made from observations such as this. Furthermore, even when certain abnormalities are definitely present in the tracing they transmit no information about heart performance; for example, in acute coronary thrombosis a patient with very little electroeardiographic change may be doing very poorly and may even suddenly die. It is idle to say that "The electrocardiogram is getting better." It is much more important to know how the patient is doing elinically than to know what further changes are occurring in his tracings. Moreover, we are all familiar with attempts to interpret records that have been made when the leads were incorrectly applied, to interpret tracings that have been pasted upside down or to interpret artefacts as pathologic changes.
ROENTGENOGRAPHY As a method of study of the heart function, roentgenography usually supplies only confirmatory evidence, although at times surprising and useful information may be obtained. Only by this method may the size and shape of the various cardiac chambers be accurately ascertained during life, but it must bc stated that serious heart disease may be present and may be discovered by the previously discussed methods of examination, although no clue to its presence is given by roentgenography. Moreover, early and slight cardiovascular lesions frequently escape notice because there is no roentgenographic evidence of abnormality of
Office Aids in Evaluating Cardiac Function
1529
cardiac size, shape or action. For the most part, roentgenography merely reveals evidence of well established-not early-disease which is difficult or impossible to eradicate. Many roentgenographic findings of the heart are not unequivocal and must be interpretated in the light of the clinical findings. Cardiac function is especially difficult to evaluate by this procedure. In a broad sense, it can be said that the larger the heart the greater the degree of impairment of function. Nevertheless, there are people with considerable cardiac enlargement, as with aortic stenosis or arterial hypertension, who have very satisfactory cardiac function. On the other hand, there are people whose hearts are of normal size by the usual methods of mensuration who have extremely limited cardiac function: for example, patients with coronary artery disease in whom cardiac performance is greatly impaired by the appearance of angina on attempting even very slight effort. CONCLUSIONS
The necessity for proper office evaluation of cardiac function is impelling. Apart from indicating the correct therapeutic measures, it also inevitably entails social, economic and pyschologic adjustments on the part of the patient. As much disability may result from erroneously informing the patient of the nature of his cardiovascular trouble as from failure to recognize it at all. I t is not possible nor is it necessary for the practitioner to be fully conversant with all the newer procedures in cardiology. The oldest and most readily available procedure, that of careful and intelligent history taking, still remains the most important office method of evaluating cardiac function; no other investigation approaches the delicacy and accuracy of this office procedure. To be sure, this may represent a timeconsuming effort, and in a busy practice time is always at a premium. Never1,heless, time so utilized is well invested for the patient who seekH interpretation of chest pain on effort, breathlessness or palpitation since the initial appearance of any of these symptoms may well be the most, significant medical event in the patient's life, particularly the adult male in the coronary artery age. REFERENCES 1. Burch, G. E. and Reaser, P.: Primer of Cardiology. Philadelphia, Lea and
Febiger, 1947. 2. DressIer, William: Clinical Cardiology. New York, Paul B. Hoeber, Inc., 1942. 3. Friedberg, Charles K: Diseases of the Heart. 2nd ed. Philadelphia, W. B. Saunders Co., 1956. 4. Levine, Samuel A.: Clinical Heart Disease. 5th ed. Philadelphia, W. B. Saunders Co., 1958.
1530
FRANK
R.
BOYER
5. Lewis, Thomas: Diseases of the Heart. 3rd ed. London, Macmillan and Co., 1944. 6. White, Paul D.: Heart Diseases. 3rd ed. New York, The Macmillan Company, 1946. 7. Wood, Paul: Diseases of the Heart and Circulation. 2nd ed. Philadelphia, J. B. Lippincott Co., 1956. 8. Wood, Francis C.: Observations on Pericardial Disease. M. CLIN. NORTH AMERICA 37: 1639, 1953. 9. Logue, R. B. and Hurst, J. W.: Errors in the Recognition and Treatment of Heart Disease. Circulation 10: 920, 1954. 10. Kossman, Charles E.: The Normal Electrocardiogram. Circulation 8: 920, 1953. 11. Dry, Thomas J.: Types of Dyspnea Associated with Cardiac Disease. Proc. Staff Meet., Mayo Clin. 27(3), January 30, 1952. 12. Harrison, T. R. and Reeves, T. J.: Diagnostic and Therapeutic Value of Reproduction of Chest Pain. Arch. Int. Med. 91: 8, 1953. 530 North 20th Street Allentown, Pennsylvania