WHO AND WHAT SHOULD BE MONITORED? Daniel Lew, D.D.S.
The scope of this presentation is rather forbidding and yet somewhat straightforward. The rhetorical question of who should be monitored is simply answered, "Everyone," especially if one alludes to the dictionary definition of a monitor as that which warns, advises, and instructs. The second part of my assigned topic is, what parameters should be monitored. Again, the obvious answer is, "All those applicable," and therein lies the rub. As a rule, the risk of anesthesia is related to the danger of hypoxemia, cardiac reflexes, hypercarbia, distinct changes in blood pressure, as well as development of cardiac dysrrhythmias. Thus, the major thrust of this discussion will be to identify groups of patients who are liable to present myocardial and/or circulatory complications and to justify appropriate parameters for monitoring. This presentation shall deal with diagnosed pathological entities and the parameters used shall be those available to us all, namely, blood pressure, pulse, and EKG monitoring. Finally, the monitoring is strictly intraoperative and non-invasive. I should like to approach this topic from the vantage point of a practitioner faced with the daily task of delivering emergency care to patients, the majority of whom have diagnosed pathological entities at different levels of compensation. The anesthetic agent and the method of administration are not within the scope of this paper. By far the largest group we have to monitor is the one suffering some degree of coronary-artery disease. About five and a half million American adults, three and a half million under 65, are afflicted with coronary artery disease. Of these, three quarters of a million die yearly.1 They are of interest to us since patients with coronary heart disease are a somewhat higher surgical risk than those without it. Presented at the Annual Scientific Meeting of the American Dental Society of Anesthesiology, February 20, 1977, Chicago, Illinois.
118
There are three basic groups that are of concern: (1) the previously infarcted patient, (2) the patient susceptible to cor-
onary artery disease, (3) the patient suffering assorted endocrine disorders. In 1974, one person in seven had an operation. Thirteen patients per one thousand over 30 years of age underwent surgery with an indication of a previous myocardial infarction.2 Tarhan and his associates at the Mayo Clinic demonstrated recurrent perioperative myocardial infarction incidence rate of 6.5 per cent and a mortality rate of over 50 per cent. The time of anesthesia following the myocardial infarction is rather crucial. Tarhan and his group reported a reinfarction rate of 37.5 per cent in less than three months following an infarct and 5 per cent after six months.3 It is clear that this group of patients is in need of extensive monitoring. What parameters are usefully monitored? (1) A clear and unobstructed airway. A precordial stethoscope is as useful and simple a device as we have to monitor upper airway gaseous exchange. It is crucial to monitor respiratory exchange, for the major concern in coronary artery disease is that myocardial oxygen supply never be insufficient to meet the need imposed upon it.
(2) Blood pressure. Acute hypertension or hypotension in patients with coronary artery disease may precipitate the ultimate problem of an imbalance between myocardial oxygen supply and demand. Hypotension can produce myocardial ischemia by reducing coronary blood flow. Hypertension can increase myocardial oxygen demand by increasing left ventricular wall pressure. Arterial hypotension is potentially the most destructive occurrence in this type of patient for the coronary profusion cannot be maintained to an already partially damaged myocardium. It is crucial that the blood pressure be monitored regularly and frequently and that it be maintained at preoperative levels or slightly below.
ANEsTsEsuA PROGRESS
(3) Pulse. Three potential circulatory problems exist following a myocardial infarction. (1) rate change, usually bradycardia; (2) rhythmic abnormality due to (a) effect of anesthetic agent, (b) ectopic beats, (c) conduction system damage. The bradycardia encountered may be due to (1) drugs such as propranalol and/or digitalis, (2) damage to the conduction system in a posterior infarct, and (3) vagal reflex. Bradycardia poses two potentially serious sequellae: First, because of a diseased myocardium, the heart cannot increase its stroke volume to compensate for the bradycardia, and second, ectopic foci develop from the damaged myocardium during the long diastolic period. The ectopic beats discharged simultaneously with the regular pacemaker render the heart liable to ventricular fibrillation due to an ectopic conduction occurring during repolarization. (4) Arrhythmia. Arrhythmias following myocardial infarction may originate from (a) the damaged and ischemic myocardium, (b) ischemia due to decreased oxygen PO2, hyper- or hypokalemia, digitalis toxicity and quinidine therapy. An EKG monitor is most useful to demonstrate any early ischemic changes. These are seen as an ST depression and, at times, an inversion of the T-wave. Although previously infarcted patients are a distinct surgical risk, the majority of them tolerate surgical procedures and anesthesia quite well. It is essential that one prevent myocardial ischemia, preoperative emotional anxiety, and hypoxia. Electrocardiography is essential to not only demonstrate the presence of a previous myocardial infarction, but also to illustrate and diagnose the presence of severe dysrrhythmias which may be the harbingers of a repeat myocardial infarction. One should be cautioned that the EKG should not be looked for routinely to clinch a diagnosis of an M.I. since changes may not be visible for 24 to 48 hours in a number of cases, and in case of a left bundle branch block, no diagnosis on an EKG is possible. It is perhaps a good time to point out that silent M.I.'s are by no means a rare phenomenon. They occur at
JULY-AUGUST, 1977
the rate of about a third of all clinically diagnosed myocardial infarctions.4 The second group to routinely monitor is made up of those who are susceptible to coronary artery disease. Coronary artery disease is the commonest form of clinical heart disease found in the 40 and above age group. It has become the dominant cause of death and the major culprit in fatal cardiac disease. The two most common manifestations of coronary heart disease are angina pectoris and acute myocardial infarction. It is well known that coronary atherosclerosis progresses with age until it reaches the limit at 60 years in male, and 70 in female.5'6 It has also been demonstrated during the Korean War that among soldiers killed in action with an average age of 22, 77.3 per cent had gross pathological evidence of coronary atherosclerosis. However, only 10 per cent exhibited symptoms of advanced disease.7 It is desirable that we be able to obtain a cardiovascular risk profile on every patient prior to anesthesia. The following are factors implicated in the causation and/ or acceleration of coronary artery disease: Hypercholesteremia, hypertension, smoking, heredity, obesity, age, sex, left ventricular hypertrophy, and finally, endocrine and metabolic disorders. Studies carried out by the National Heart Institute, as well as other studies, have indicated that persons prone to coronary heart disease can be identified due to certain characteristics, etiological factors, and personality traits.8 One of the principle factors appears to be an elevation of serum cholesterol. The Framingham, Albany, and Minneapolis studies have demonstrated that, on the average, men with serum cholesterol values of 260 or over were 4.3 times more susceptible to coronary heart disease than men of the same domicile and age bracket who had a cholesterol level under 200.9,10,11 The relationship of serum cholesterol level to the incidence of coronary artery disease is most dependent on age. This is especially striking in the younger age group and diminishes with age, until in the 60's, the relationship may be insignificant. The pathological lesions and the clinical manifestations of coronary heart disease appear to predominate after 119
the age of 40 and thereafter with increasing frequency. Women are not as afflicted as men. The variation is age dependent. The Framingham study found the ratio to decrease with increasing age; thus, in the 30-44 age group, the ratio of male to female was 13 to 1, whereas in the 45-62 age group, the ratio was 2 to 1.12 The incidence at 70 appeared to be equal.13 Hypertension is an important prognosticator of coronary artery disease. Studies from the International Cooperative Study of Cardio-vascular Epidemiology demonstrated that men in the top 20 per cent of the distribution of systolic blood pressure had 2.7 times the coronary death rate of men in the bottom 20 per cent.'4 Hypertension, at any age, and in both sexes, appears to accelerate atherosclerotic changes as reflected by the incidence of coronary heart disease. It is perhaps erroneous to assume that the diastolic component is the ultimate culprit in the consequences of hypertension. Elevated systolic pressure may be as important as diastolic, and particularly, in the elderly. The Framingham study further showed that the presence of coexisting hypertension significantly increased the risk associated with any particular concentration of major lipids; furthermore, that the risk of the clinical entities related to coronary heart disease were intimately related to antecedent blood pressure irrespective of age or sex; finally, that the hazards of elevated lipid concentration were distinctly greater in hypertensives than in normal tensives. Hypertension is found in about 50 per cent of men and about 75 per cent of women with coronary heart disease. Smoking is a factor clearly implicated in coronary heart disease. In the Framingham and Albany studies, heavy cigarette smoking resulted in a three-fold increase in the incidence of coronary heart disease and also in an increased mortality. However, the incidence of angina pectoris appeared to be unrelated to smoking. The Surgeon General, in his report, stated that there is a clear association between cigarette smoking and heart attacks.'5 Heredity has been implicated in the occurrence of coronary heart disease. Thomas and Cohen demonstrated that clinical cor120
onary artery disease was almost four times more frequent in offsprings of persons with coronary disease as among siblings of persons without it.'6 Obesity may be the result of gluttony, metabolic aberration, or a combination of both. It has been demonstated that obesity is accompanied by such atherogenic traits as hypertension and elevation of blood lipids, as well as an impaired glucose tolerance. Thus, it would seem reasonable to expect the obese to demonstrate an excessive risk of coronary heart disease. A particular personality structure and behavior pattern has been implicated in coronary artery disease.17 The personality type commonly referred to as Type A has a higher coronary morbidity and mortality. Type A is characterized by ambition and drive, aggressiveness, competitiveness and one who considers time in short supply. These people are rapid in manner and speech, impatient and restless. Coronary heart disease occurred in 13.5 per thousand of Type A as compared to 5.4 per thousand in Type B, Type B being the more sedentary behavioral type. Finally, electrocardographic evidence of left ventricular hypertrophy is a most disturbing finding for it coincides with a graver prognosis, for all major clinical manifestations of coronary heart disease, a five year mortality of 30 per cent and a tenfold increase of congestive heart failure and sudden death. Patients who are predisposed to coronary heart disease are excellent candidates for intraoperative monitoring, for the clinical manifestations of coronary heart disease, namely, angina pectoris, acute coronary occulsion, myocardial infarction and heart failure, as well as the ultimate catastrophe of sudden death, are all possibilities, in time probabilities, in these patients. We are now faced with the question of what to monitor in this susceptible group. It would seem logical that anticipated changes should be monitored; therefore, if for example, the most common manifestations of coronary heart disease were myocardial infarctions and angina pectoris, the parameters available to demonstrate these pathological changes should be monitored. In addition to close and ANSTHESA PROGRESS
repeated reading of the patient's blood pressure and pulse, an electrocardiogram is essential to demonstrate the presence of a previous myocardial infarction, either diagnosed or silent, the possible emergence of pre-infarct arrhythmias, and to demonstrate the presence of an intraoperative myocardial infarction. The diagnosis of angina pectoris is revealed by a good history, and although an electrocardiagram cannot be used to diagnose the existence of the disease, an active attack will demonstrate changes in many instances. These are ST depression and a T-wave inversion. It is very wise to monitor patients with angina pectoris. As a broad statement, one may say that the prognosis of angina is closely linked to that of the underlying disease, be it coronary artery disease, syphilitic heart disease, etc. Perhaps, also, it can be stated that patients with angina pectoris secondary to syphilis, or those with aortic stenosis or regurgitation, have a more guarded prognosis than those whose etiology is severe atherosclerotic coronary disease. Clearly, the great danger of angina pectoris is the danger of sudden death. This is usually the result of either ventricular fibrillation, cardiac standstill, or myocardial infarction. In a study of 6,882 cases of angina pectoris, about 15 per cent succumbed in the first year after the initial diagnosis.18 The five year survival for this period was 58.4 per cent as compared to a rate of 86.9 per cent for the normal population. This is a condition which demands vigilance on our part. Any disease process that is characterized by onsets of acute M.I.'s and ventricular arrhythmias is an indication for EKG, blood pressure, and pulse monitoring. In summation, although angina pectoris is difficult to diagnose on EKG's unless an actual attack is in progress, the clinical history of the disease should alert us to the possibility of ventricular arrhythmias and/or myocardial infarctions occurring intraoperatively. The frequency of cardiac arrest during surgery has been reported to vary between 1 in 2,382, to 1 in 3,673.19,20 We have no statistics of cardiac arrest during dental outpatient anesthesia. In an arrest, it is important to distinguish
JuLY-AUGUST, 1977
between ventricular fibrillation and asystole, since the treatment for both differs, and unless a diagnosis is clearly made, precious time may be lost. The monitoring should be continued to detect any developing dysrrhythmias following C.P.R. as well as to monitor the efficacy of conversion and treatment. Besides the possibility of intraoperative M.I.'s, potentially lethal arrhythmias and myocardial ischemia, heart failure is the other nagging worry, especially in patients who suffer from rheumatic heart disease, mitral stenosis, chronic lung disease with minimal right sided compensation, and aortic stenosis. These patients have a reduced cardiac output and and reduced cardiac reserve. These patients, too, are fragile and, due to the minimal reserve, must not be overloaded. They are prone to thromboembolic phenomena, for example, pulmonary emboli, and hypoxia and hypocardia can occur very quickly. Finally, surgical stress, fear, or pain may be sufficient to nudge these patients into cardiac failure. These patients need careful monitoring. What are the parameters that one should monitor in patients with borderline failure? ( 1 ) Blood pressure-repeated and frequent readings are mandatory. (2) Pulse-persistent, unexplained tachycardia of around 100 to 110 is a subtle and useful sign of heart failure caused by increased sympathetic activity compensating for the diminished cardiac reserve. Pulsus alternans, more easily detected in the carotid, is a useful diagnostic sign. Neck veins-The external jugular vein may be distended and show prominent pulsations through the overlying skin, extending to the angle of the mandible in an upright patient. This is an indication of increased central venous pressure. Ascultation-A gallop rhythm is a reliable early indicator of heart failure. A precordial stethoscope which should routinely be used is especially desirable for these patients. An EKG is of little value in the detection of failure. Its value is in alerting one to the presence of ischemia, infarction, or rhythmic disturbances. In considering the topic of myocardial 121
failure, two drugs commonly used in its treatment, namely digitalis and diuretics, is in order. Digitalis, which is not water soluble, is prone to uncertain absorbtion when taken orally. Digitalis toxicity is not an uncommon phenomenon. Of the three traditional categories of intoxication, namely, gastrointestinal, neurological, and cardiac, only the latter is easily monitored during anesthesia. The toxicity can manifest itself by ventricular arrhythmias, such as PVC's, bigeminy, ventricular tachycardia, and ventricular fibrillation, or by atrial arrhythmias such as paroxysmal atrial tachycardia, and finally, a disturbance of the AV conduction mechanism. These are all easily detected by EKG. As a broad statement, it can be said that any dysrrhythmia in a patient on digitalis must be considered digitalis toxicity until proven otherwise. In patients with congestive heart failure who are placed on diuretic therapy, especially on thiazide drugs, hypokalemia is, on occasion, encountered. Hypokalemia predisposes the myocardium to ectopic beats. This is often seen in patients who are on digitalis. Hypokalemia is also commonly encountered in cases of prolonged diarrhea, vomiting, intestinal obstruction, prolonged nasal gastric suction, postoperative infusion of potassium-free intravenous solutions, certain cases of Cushings disease, in primary aldosteronism, as well as occasionally in Addison's disease treated with Desoxycorticosterone. The major culprit in hypokalemia, is, however, inadequate dietary intake of potassium. The physical symptoms of hypokalemia are drowsiness, nausea, muscle weakness, dimunition or loss of the deep tendon reflexes, as well as hypotension and cardiac arrhythmias. Cardiac arrest is not an unknown sequella. Unfortunately, when a patient is under anesthesia, and the condition has not been diagnosed preoperatively, one is pretty much left with the unenviable task of making a differential diagnosis based on cardiac arrhythmias, hypotension, and, alas, on occasion, cardiac arrest. Electrocardiac changes are frequently absent in hypokalemia. However, when the serum potassium concentration falls below 3 mEq/L, EKG changes classical of the con122
dition are noted. They are (1) lowering, flattening, or inversion of the T-wave and depression of the ST segment, (2) prolongation of the QT interval, and (3) presence of an elevated U wave. Therefore, patients who are on digitalis or specific diuretic drug therapy should be routinely monitored. These two drugs have been briefly discussed not only because of their intrinsic interest, but also as an illustration of the necessity of comprehending the pharmacological actions and the physiological changes caused by all drugs. The final group of patients in need of careful monitoring is that group classified as suffering from metabolic disturbances. Of these, diabetes is the most clearly implicated, and diabetics, both overt and latent, are prone to an early and often galloping atherosclerosis. This is illustrated by their higher frequency of coronary artery disease. They are particularly liable to silent mycardial infarctions, and when these occur, they are usually fatal.21'22 Angina pectoris and acute myocardial infarctions have been noted with greater frequency among diabetics than among non-diabetics, and the frequency is to be found equally among males and females.23 Diabetes appears to not only increase the chance of the development of coronary arteriosclerosis, but also seems to hasten its clinical manifestations. It has been noted that among the young with diagnosed premature coronary heart disease, there is an inordinately high percentage of pre-cinical diabetes.24 As already stated, when a myocardial infarction occurs in diabetics, it is frequently fatal. Sixty per cent of all attacks, and 57.8 per cent of all first attacks end fatally.25 There is little doubt that every diabetic is a potential coronary heart disease victim. It should be pointed out that in the United States, diabetes remains undiagnosed in 1.6 million cases.26 Two to 6 percent of the American population over 40 have diabetes, although many do not present with the classical symptoms of polyuria, polydypsia, polyphagia, or weight loss.27 Diabetics, especially brittle ones, always threaten hypoglycemia, and, on occasion, insulin shock is a reality. The trauma and (Continued on page 127)
AsTIEsLA PRoGREss
stress of surgery tend to cause the brittle diabetic to slip into a state of hypoglycemia with moist and pale skin, a normal blood pressure, and a full and bounding pulse indicating impending insulin shock. A diabetic coma, although much rarer and rather slow and insidious in its manifestation may be diagnosed by the dry skin, exaggerated air hunger, the Kusmall breathing, the acetone breath, the weak and rapid pulse together with abdominal cramps. Patients with adrenal insufficiency will often present, in the acute and chronic phase, with striking hypotension. The blood pressure is often between 80 and 100 mm Hg systolic, and 60 to 70 diastolic. The low blood pressure can plummet during a crisis to unmeasurable levels. One should, therefore, keep a close watch on the blood pressure of Addisonians undergoing anesthesia. The patients are prone to syncope due to either postural hypotension or sodium depletion, as well as to hypoglycemia. These patients should be monitored on the EKG to not only detect high serum potassium which normally accompanies Addison's Disease, but also reduced serum potassium which follows treatment with Desoxycorticosterone. Hyperfunction of the adrenal cortexCushing's Syndrome: The important finding with respect to the heart and the cardiovascular system in Cushing's Syndrome is the presence at times, of acute hypertension, as well as an associated cardiac hypertrophy. Glycosuria, as well as hypercholesterolemia, are also noted in this condition. These patients, therefore, appear to qualify for close monitoring, not only for the hypertension, but also for the possibility of coronary artery disease. Hyperthyrodism: The most worrisome sequella of hyperthyroidism is the development of atrial fibrillation, cardiac enlargement, or congestive heart failure. These consequences occur most frequently in the older age group and are rather rare before the age of 40. Females predominate in a ratio of 2 to 1.28 Heart failure due to hyperthyroidism usually occurs in conjunction with pre-existing hypertension. Since congestive heart failure usually develops following a period of atrial fibrillation, it seems wise to monitor the pulse
JULY-AUGUST, 1977
and EKG on all known hyperthyroid patients. In the uncontrolled, the pulse usually runs between 90-120 in a calm patient. The problems become infinitely more difficult if the diagnosis of hyperthyroidism is not made preoperatively. In this case, it is prudent to consider it a possibility in all cases of atrial fibrillation, cardiac enlargement, or heart failure of uncertain
etiology. Myxedema is uncommonly observed and, thus, the myxedematous heart is rather rare. The cardiac, as well as circulatory changes seen in myxedema are not present in the absence of myxedematous skin changes and
mental retardation. The myxedematous heart is a sluggish, enlarged heart seen primarily among women over 40. The most common EKG features one should look for are the flattening or inversion of the T-wave in leads one and two, and generally low voltage of the QRS complex. In advanced cases of myxedema, bradycardia is a characteristic finding. The rate is frequently in the 50 to 60 range. Patients with advanced myxedema are prone to myocardial failure and the disorder is associated with an increased incidence of angina pectoris.29 Blood pressure is usually unchanged. It is generally believed that atherosclerosis prevails earlier and with greater vigor in the myxedematous patient. Therefore, in monitoring a myxedematous patient, symptoms of failure as well as myocardial ischemia should be looked for. Anemia affects the heart in two ways: by either impairing the oxygen supply or increasing the workload. Anemia is particularly dangerous to an arteriosclerotic heart or an enlarged rheumatic heart with its increased oxygen needs. Anemia predisposes these patients to heart failure and/or coronary insufficiency. The outstanding feature of prolonged anemia is an enlarged heart. Heart murmurs are common; these are functional and are usually systolic. The EKG changes noted are those of myocardial anoxia, namely ST segment depression and T-wave flattening or inversion. The patients are prone to high output failure, and one should be alert for that possibility as well as developing angina pectoris in an already diseased heart.
127
Sickle cell anemia, which is the commonest form seen today, deserves special mention. Oxygen partial pressure should never be allowed to drop below 50 per cent as this may precipitate a crisis. In general, one should strive to maintain a free and unimpeded airway with high oxygen partial pressure to not only prevent the emergence of a crisis, but also to assure adequate oxygen supply to a heart that may already have suffered damage due to anemia. Patients with gouty arthritis have been demonstrated to have a higher incidence rate of coronary heart disease. Finally, the effects of gonadal hormones on atherosclerosis have been demonstrated by the fact that the incidence of coronary heart disease in women who have undergone bilateral oophorectomy before menopause were 4 times greater than in control females, and similarly, the incidence of atherosclerosis was found to be less in men treated with estrogen for carcinoma of the prostate.30
Conclusions Examples of systemic diseases affecting the heart and the circulatory system have been presented. Anticipating path-physiological changes in reality, mandates that all patients be monitored to some extent. Intraoperative monitoring is merely an extension of preoperative monitoring, and the value of intraoperative monitoring is directly proportional to the degree of accuracy one was able to achieve in one's preoperative work up. Intraoperative monitoring is used as a means of identifying anticipated change, and being alert for unexpected change. Unexplained intraoperative tachycardia, for example, could be a manifestation of anoxemia, heart failure, malignant hyperthermia, thyroid storm, or pulmonary embolus, to note but a few possibilities. Monitoring, in this case, is merely one of the tools utilized to arrive at a differential diagnosis. All patients' vital signs must be taken prior to surgery to allow the establishment of a base-line, for further interpretation may offer little unless it can be related to preoperative levels. Intraoperative monitoring, then, has a relative meaning besides an 128
absolute one. The abnormally high blood pressure and the extra systoles noted intraoperatively may be quite normal and well tolerated for that particular patient. However, there is no way of interpreting whether the values determined intraoperatively are within the bounds of tolerance for this patient unless a pre-operative base-line exists. It is my hope that this presentation has brought a little order to the problem of who and what should be monitored. I have taken the liberty of changing the thrust of this presentation by exploring the specific changes imposed on one system by certain disease processes. This same exercise must be applied to all systems, and together with the effect of the anesthetic agent, a totality of expectancy is achieved. REFERENCES 1. Friedberg C K Diseases of the Heart. 3rd ed. Philadelphia: W B Saunders. 2. Tarhan S Moffit E A Taylor W F et al: Myocardial Infarction after general anesthesia. JAMA 220:1451-1454, 1972. 3. Ibid. 4. Kannel W B McNamara P M Feinleib IM et al: The unrecognized myocardial infarction: fourteen year follow-up experience in the Framingham study. Geriatrics 25:75-87, 1970. 5. White N K Edwards J E and Dry T J: Circulation 1:645, 1950. 6. Ackerman R F Dry T J and Edwards J E: Circulation 1:1345, 1950. 7. Enos W F Holmes R H and Beyer J: JAMA 152:1090, 1953. 8. Russerk and Zollman Coronary Heart Diseases. Philadelphia: J P Lippincott, 1971. 9. Doyle J T Heslin A S Hilleboe H E Formel P F et al: Measuring the risk of coronary infant disease in adult population group. Am J of Pub Health 47 (suppl. Apr. 1957):25, 1957. 10. Keys A Taylor H L Blackburn H Broler J Andenjow J T and Simonson E: Coronary Heart Disease among Minnesota business and professional men followed fifteen years. Circulation 28:381, 1963. 11. Kannel W B Dauber R T and McNamara P M: Detection of the coronary prone adult: The Framingham Study. J Iowa Med Soc 52:26, 1866. 1966. 12. Kannel W B Castelli W P and McNamara P IM: Coronary profile: twelve year follow-up: The Framingham Study. J Occup Med 9:611, 1967.
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13. Ibid. 14. Keys A Blackburn H et al: Epidemiological studies related to coronary heart disease: Characteristics of men aged 40-59 in seven countries. Acta Med Scand suppl. 460, 1967, 392. 15. U. S. Dept of Health, Education and Welfare: Office of the Surgeon General. Smoking and Health. Washington, D. C.: GPO, 1964. 16. Thomas C B and Cohen B H: Ann Int Med 42:90, 1955. 17. Friedman M and Rosenmann R H: Association of specific overt patterns with blood and cardiovascular findings, blood cholesterol level, blood clotting time, incidence of arcus senilus and clinical coronary artery disease. JAMA 169:1286-1296, 1959. 18. Block W J Crumpacker E L et al: JAMA 150: 259, 1952. 19. Glenn F: Ann Surg 37:920, 1953. 20. Stephenson H E Reid L D Hinton J W et al: Ann Surg 137:731, 1953. 21. Root H F and Bradley R F: Cardiovascular Disease in the Treatment of Diabetes MeUitus.
22.
23. 24. 25. 26. 27. 28.
10th ed. Joslin, et al. Philadelphia: Lea and Febiger, 1969. Agar J M Silent myocardial infarctions in diabetes mellitus. Med J Austr 49(2):284, 1962. Friedberg C K: Diseases of the Heart. 3rd ed. Philadelphia: W. B. Saunders Co. Herman R V and Gorlin R: Premature coronary artery disease and the preclinical diabetic state. Am J Med 38:481, 1965. Friedberg C K: Diseases of the Hart. 3rd ed. Philadelphia: W. B. Saunders Co. Marble A Bradley R F White P et al: Joslin's Diabetes Mellitus. 11th ed. Philadelphia: Lea and Febiger, 1971. Ibid. Summers and Surtees: Thyrotoxidosity and heart disease. Acta Med Scand 169:661.
29. Ibid. 30. Higens N Robinson R W and Cohen W D: Increased incidence of cardiovascular disease in castrated women. N E J Med 268:1123, 1963.
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129
The scope of this presentation is rather forbidding and yet somewhat straightforward. The rhetorical question of who should be monitored is simply answered, "Everyone," especially if one alludes to the dictionary definition of a monitor as that which warns, advises, and instructs. The second part of my assigned topic is, what parameters should be monitored. Again, the obvious answer is, "All those applicable," and therein lies the rub. As a rule, the risk of anesthesia is related to the danger of hypoxemia, cardiac reflexes, hypercarbia, distinct changes in blood pressure, as well as development of cardiac dysrrhythmias. Thus, the major thrust of this discussion will be to identify groups of patients who are liable to present myocardial and/or circulatory complications and to justify appropriate parameters for monitoring. This presentation shall deal with diagnosed pathological entities and the parameters used shall be those available to us all, namely, blood pressure, pulse, and EKG monitoring. Finally, the monitoring is strictly intraoperative and non-invasive. I should like to approach this topic from the vantage point of a practitioner faced with the daily task of delivering emergency care to patients, the majority of whom have diagnosed pathological entities at different levels of compensation. The anesthetic agent and the method of administration are not within the scope of this paper. By far the largest group we have to monitor is the one suffering some degree of coronary-artery disease. About five and a half million American adults, three and a half million under 65, are afflicted with coronary artery disease. Of these, three quarters of a million die yearly.1 They are of interest to us since patients with coronary heart disease are a somewhat higher surgical risk than those without it. Presented at the Annual Scientific Meeting of the American Dental Society of Anesthesiology, February 20, 1977, Chicago, Illinois.
118
There are three basic groups that are of concern: (1) the previously infarcted patient, (2) the patient susceptible to cor-
onary artery disease, (3) the patient suffering assorted endocrine disorders. In 1974, one person in seven had an operation. Thirteen patients per one thousand over 30 years of age underwent surgery with an indication of a previous myocardial infarction.2 Tarhan and his associates at the Mayo Clinic demonstrated recurrent perioperative myocardial infarction incidence rate of 6.5 per cent and a mortality rate of over 50 per cent. The time of anesthesia following the myocardial infarction is rather crucial. Tarhan and his group reported a reinfarction rate of 37.5 per cent in less than three months following an infarct and 5 per cent after six months.3 It is clear that this group of patients is in need of extensive monitoring. What parameters are usefully monitored? (1) A clear and unobstructed airway. A precordial stethoscope is as useful and simple a device as we have to monitor upper airway gaseous exchange. It is crucial to monitor respiratory exchange, for the major concern in coronary artery disease is that myocardial oxygen supply never be insufficient to meet the need imposed upon it.
(2) Blood pressure. Acute hypertension or hypotension in patients with coronary artery disease may precipitate the ultimate problem of an imbalance between myocardial oxygen supply and demand. Hypotension can produce myocardial ischemia by reducing coronary blood flow. Hypertension can increase myocardial oxygen demand by increasing left ventricular wall pressure. Arterial hypotension is potentially the most destructive occurrence in this type of patient for the coronary profusion cannot be maintained to an already partially damaged myocardium. It is crucial that the blood pressure be monitored regularly and frequently and that it be maintained at preoperative levels or slightly below.
ANEsTsEsuA PROGRESS
(3) Pulse. Three potential circulatory problems exist following a myocardial infarction. (1) rate change, usually bradycardia; (2) rhythmic abnormality due to (a) effect of anesthetic agent, (b) ectopic beats, (c) conduction system damage. The bradycardia encountered may be due to (1) drugs such as propranalol and/or digitalis, (2) damage to the conduction system in a posterior infarct, and (3) vagal reflex. Bradycardia poses two potentially serious sequellae: First, because of a diseased myocardium, the heart cannot increase its stroke volume to compensate for the bradycardia, and second, ectopic foci develop from the damaged myocardium during the long diastolic period. The ectopic beats discharged simultaneously with the regular pacemaker render the heart liable to ventricular fibrillation due to an ectopic conduction occurring during repolarization. (4) Arrhythmia. Arrhythmias following myocardial infarction may originate from (a) the damaged and ischemic myocardium, (b) ischemia due to decreased oxygen PO2, hyper- or hypokalemia, digitalis toxicity and quinidine therapy. An EKG monitor is most useful to demonstrate any early ischemic changes. These are seen as an ST depression and, at times, an inversion of the T-wave. Although previously infarcted patients are a distinct surgical risk, the majority of them tolerate surgical procedures and anesthesia quite well. It is essential that one prevent myocardial ischemia, preoperative emotional anxiety, and hypoxia. Electrocardiography is essential to not only demonstrate the presence of a previous myocardial infarction, but also to illustrate and diagnose the presence of severe dysrrhythmias which may be the harbingers of a repeat myocardial infarction. One should be cautioned that the EKG should not be looked for routinely to clinch a diagnosis of an M.I. since changes may not be visible for 24 to 48 hours in a number of cases, and in case of a left bundle branch block, no diagnosis on an EKG is possible. It is perhaps a good time to point out that silent M.I.'s are by no means a rare phenomenon. They occur at
JULY-AUGUST, 1977
the rate of about a third of all clinically diagnosed myocardial infarctions.4 The second group to routinely monitor is made up of those who are susceptible to coronary artery disease. Coronary artery disease is the commonest form of clinical heart disease found in the 40 and above age group. It has become the dominant cause of death and the major culprit in fatal cardiac disease. The two most common manifestations of coronary heart disease are angina pectoris and acute myocardial infarction. It is well known that coronary atherosclerosis progresses with age until it reaches the limit at 60 years in male, and 70 in female.5'6 It has also been demonstrated during the Korean War that among soldiers killed in action with an average age of 22, 77.3 per cent had gross pathological evidence of coronary atherosclerosis. However, only 10 per cent exhibited symptoms of advanced disease.7 It is desirable that we be able to obtain a cardiovascular risk profile on every patient prior to anesthesia. The following are factors implicated in the causation and/ or acceleration of coronary artery disease: Hypercholesteremia, hypertension, smoking, heredity, obesity, age, sex, left ventricular hypertrophy, and finally, endocrine and metabolic disorders. Studies carried out by the National Heart Institute, as well as other studies, have indicated that persons prone to coronary heart disease can be identified due to certain characteristics, etiological factors, and personality traits.8 One of the principle factors appears to be an elevation of serum cholesterol. The Framingham, Albany, and Minneapolis studies have demonstrated that, on the average, men with serum cholesterol values of 260 or over were 4.3 times more susceptible to coronary heart disease than men of the same domicile and age bracket who had a cholesterol level under 200.9,10,11 The relationship of serum cholesterol level to the incidence of coronary artery disease is most dependent on age. This is especially striking in the younger age group and diminishes with age, until in the 60's, the relationship may be insignificant. The pathological lesions and the clinical manifestations of coronary heart disease appear to predominate after 119
the age of 40 and thereafter with increasing frequency. Women are not as afflicted as men. The variation is age dependent. The Framingham study found the ratio to decrease with increasing age; thus, in the 30-44 age group, the ratio of male to female was 13 to 1, whereas in the 45-62 age group, the ratio was 2 to 1.12 The incidence at 70 appeared to be equal.13 Hypertension is an important prognosticator of coronary artery disease. Studies from the International Cooperative Study of Cardio-vascular Epidemiology demonstrated that men in the top 20 per cent of the distribution of systolic blood pressure had 2.7 times the coronary death rate of men in the bottom 20 per cent.'4 Hypertension, at any age, and in both sexes, appears to accelerate atherosclerotic changes as reflected by the incidence of coronary heart disease. It is perhaps erroneous to assume that the diastolic component is the ultimate culprit in the consequences of hypertension. Elevated systolic pressure may be as important as diastolic, and particularly, in the elderly. The Framingham study further showed that the presence of coexisting hypertension significantly increased the risk associated with any particular concentration of major lipids; furthermore, that the risk of the clinical entities related to coronary heart disease were intimately related to antecedent blood pressure irrespective of age or sex; finally, that the hazards of elevated lipid concentration were distinctly greater in hypertensives than in normal tensives. Hypertension is found in about 50 per cent of men and about 75 per cent of women with coronary heart disease. Smoking is a factor clearly implicated in coronary heart disease. In the Framingham and Albany studies, heavy cigarette smoking resulted in a three-fold increase in the incidence of coronary heart disease and also in an increased mortality. However, the incidence of angina pectoris appeared to be unrelated to smoking. The Surgeon General, in his report, stated that there is a clear association between cigarette smoking and heart attacks.'5 Heredity has been implicated in the occurrence of coronary heart disease. Thomas and Cohen demonstrated that clinical cor120
onary artery disease was almost four times more frequent in offsprings of persons with coronary disease as among siblings of persons without it.'6 Obesity may be the result of gluttony, metabolic aberration, or a combination of both. It has been demonstated that obesity is accompanied by such atherogenic traits as hypertension and elevation of blood lipids, as well as an impaired glucose tolerance. Thus, it would seem reasonable to expect the obese to demonstrate an excessive risk of coronary heart disease. A particular personality structure and behavior pattern has been implicated in coronary artery disease.17 The personality type commonly referred to as Type A has a higher coronary morbidity and mortality. Type A is characterized by ambition and drive, aggressiveness, competitiveness and one who considers time in short supply. These people are rapid in manner and speech, impatient and restless. Coronary heart disease occurred in 13.5 per thousand of Type A as compared to 5.4 per thousand in Type B, Type B being the more sedentary behavioral type. Finally, electrocardographic evidence of left ventricular hypertrophy is a most disturbing finding for it coincides with a graver prognosis, for all major clinical manifestations of coronary heart disease, a five year mortality of 30 per cent and a tenfold increase of congestive heart failure and sudden death. Patients who are predisposed to coronary heart disease are excellent candidates for intraoperative monitoring, for the clinical manifestations of coronary heart disease, namely, angina pectoris, acute coronary occulsion, myocardial infarction and heart failure, as well as the ultimate catastrophe of sudden death, are all possibilities, in time probabilities, in these patients. We are now faced with the question of what to monitor in this susceptible group. It would seem logical that anticipated changes should be monitored; therefore, if for example, the most common manifestations of coronary heart disease were myocardial infarctions and angina pectoris, the parameters available to demonstrate these pathological changes should be monitored. In addition to close and ANSTHESA PROGRESS
repeated reading of the patient's blood pressure and pulse, an electrocardiogram is essential to demonstrate the presence of a previous myocardial infarction, either diagnosed or silent, the possible emergence of pre-infarct arrhythmias, and to demonstrate the presence of an intraoperative myocardial infarction. The diagnosis of angina pectoris is revealed by a good history, and although an electrocardiagram cannot be used to diagnose the existence of the disease, an active attack will demonstrate changes in many instances. These are ST depression and a T-wave inversion. It is very wise to monitor patients with angina pectoris. As a broad statement, one may say that the prognosis of angina is closely linked to that of the underlying disease, be it coronary artery disease, syphilitic heart disease, etc. Perhaps, also, it can be stated that patients with angina pectoris secondary to syphilis, or those with aortic stenosis or regurgitation, have a more guarded prognosis than those whose etiology is severe atherosclerotic coronary disease. Clearly, the great danger of angina pectoris is the danger of sudden death. This is usually the result of either ventricular fibrillation, cardiac standstill, or myocardial infarction. In a study of 6,882 cases of angina pectoris, about 15 per cent succumbed in the first year after the initial diagnosis.18 The five year survival for this period was 58.4 per cent as compared to a rate of 86.9 per cent for the normal population. This is a condition which demands vigilance on our part. Any disease process that is characterized by onsets of acute M.I.'s and ventricular arrhythmias is an indication for EKG, blood pressure, and pulse monitoring. In summation, although angina pectoris is difficult to diagnose on EKG's unless an actual attack is in progress, the clinical history of the disease should alert us to the possibility of ventricular arrhythmias and/or myocardial infarctions occurring intraoperatively. The frequency of cardiac arrest during surgery has been reported to vary between 1 in 2,382, to 1 in 3,673.19,20 We have no statistics of cardiac arrest during dental outpatient anesthesia. In an arrest, it is important to distinguish
JuLY-AUGUST, 1977
between ventricular fibrillation and asystole, since the treatment for both differs, and unless a diagnosis is clearly made, precious time may be lost. The monitoring should be continued to detect any developing dysrrhythmias following C.P.R. as well as to monitor the efficacy of conversion and treatment. Besides the possibility of intraoperative M.I.'s, potentially lethal arrhythmias and myocardial ischemia, heart failure is the other nagging worry, especially in patients who suffer from rheumatic heart disease, mitral stenosis, chronic lung disease with minimal right sided compensation, and aortic stenosis. These patients have a reduced cardiac output and and reduced cardiac reserve. These patients, too, are fragile and, due to the minimal reserve, must not be overloaded. They are prone to thromboembolic phenomena, for example, pulmonary emboli, and hypoxia and hypocardia can occur very quickly. Finally, surgical stress, fear, or pain may be sufficient to nudge these patients into cardiac failure. These patients need careful monitoring. What are the parameters that one should monitor in patients with borderline failure? ( 1 ) Blood pressure-repeated and frequent readings are mandatory. (2) Pulse-persistent, unexplained tachycardia of around 100 to 110 is a subtle and useful sign of heart failure caused by increased sympathetic activity compensating for the diminished cardiac reserve. Pulsus alternans, more easily detected in the carotid, is a useful diagnostic sign. Neck veins-The external jugular vein may be distended and show prominent pulsations through the overlying skin, extending to the angle of the mandible in an upright patient. This is an indication of increased central venous pressure. Ascultation-A gallop rhythm is a reliable early indicator of heart failure. A precordial stethoscope which should routinely be used is especially desirable for these patients. An EKG is of little value in the detection of failure. Its value is in alerting one to the presence of ischemia, infarction, or rhythmic disturbances. In considering the topic of myocardial 121
failure, two drugs commonly used in its treatment, namely digitalis and diuretics, is in order. Digitalis, which is not water soluble, is prone to uncertain absorbtion when taken orally. Digitalis toxicity is not an uncommon phenomenon. Of the three traditional categories of intoxication, namely, gastrointestinal, neurological, and cardiac, only the latter is easily monitored during anesthesia. The toxicity can manifest itself by ventricular arrhythmias, such as PVC's, bigeminy, ventricular tachycardia, and ventricular fibrillation, or by atrial arrhythmias such as paroxysmal atrial tachycardia, and finally, a disturbance of the AV conduction mechanism. These are all easily detected by EKG. As a broad statement, it can be said that any dysrrhythmia in a patient on digitalis must be considered digitalis toxicity until proven otherwise. In patients with congestive heart failure who are placed on diuretic therapy, especially on thiazide drugs, hypokalemia is, on occasion, encountered. Hypokalemia predisposes the myocardium to ectopic beats. This is often seen in patients who are on digitalis. Hypokalemia is also commonly encountered in cases of prolonged diarrhea, vomiting, intestinal obstruction, prolonged nasal gastric suction, postoperative infusion of potassium-free intravenous solutions, certain cases of Cushings disease, in primary aldosteronism, as well as occasionally in Addison's disease treated with Desoxycorticosterone. The major culprit in hypokalemia, is, however, inadequate dietary intake of potassium. The physical symptoms of hypokalemia are drowsiness, nausea, muscle weakness, dimunition or loss of the deep tendon reflexes, as well as hypotension and cardiac arrhythmias. Cardiac arrest is not an unknown sequella. Unfortunately, when a patient is under anesthesia, and the condition has not been diagnosed preoperatively, one is pretty much left with the unenviable task of making a differential diagnosis based on cardiac arrhythmias, hypotension, and, alas, on occasion, cardiac arrest. Electrocardiac changes are frequently absent in hypokalemia. However, when the serum potassium concentration falls below 3 mEq/L, EKG changes classical of the con122
dition are noted. They are (1) lowering, flattening, or inversion of the T-wave and depression of the ST segment, (2) prolongation of the QT interval, and (3) presence of an elevated U wave. Therefore, patients who are on digitalis or specific diuretic drug therapy should be routinely monitored. These two drugs have been briefly discussed not only because of their intrinsic interest, but also as an illustration of the necessity of comprehending the pharmacological actions and the physiological changes caused by all drugs. The final group of patients in need of careful monitoring is that group classified as suffering from metabolic disturbances. Of these, diabetes is the most clearly implicated, and diabetics, both overt and latent, are prone to an early and often galloping atherosclerosis. This is illustrated by their higher frequency of coronary artery disease. They are particularly liable to silent mycardial infarctions, and when these occur, they are usually fatal.21'22 Angina pectoris and acute myocardial infarctions have been noted with greater frequency among diabetics than among non-diabetics, and the frequency is to be found equally among males and females.23 Diabetes appears to not only increase the chance of the development of coronary arteriosclerosis, but also seems to hasten its clinical manifestations. It has been noted that among the young with diagnosed premature coronary heart disease, there is an inordinately high percentage of pre-cinical diabetes.24 As already stated, when a myocardial infarction occurs in diabetics, it is frequently fatal. Sixty per cent of all attacks, and 57.8 per cent of all first attacks end fatally.25 There is little doubt that every diabetic is a potential coronary heart disease victim. It should be pointed out that in the United States, diabetes remains undiagnosed in 1.6 million cases.26 Two to 6 percent of the American population over 40 have diabetes, although many do not present with the classical symptoms of polyuria, polydypsia, polyphagia, or weight loss.27 Diabetics, especially brittle ones, always threaten hypoglycemia, and, on occasion, insulin shock is a reality. The trauma and (Continued on page 127)
AsTIEsLA PRoGREss
stress of surgery tend to cause the brittle diabetic to slip into a state of hypoglycemia with moist and pale skin, a normal blood pressure, and a full and bounding pulse indicating impending insulin shock. A diabetic coma, although much rarer and rather slow and insidious in its manifestation may be diagnosed by the dry skin, exaggerated air hunger, the Kusmall breathing, the acetone breath, the weak and rapid pulse together with abdominal cramps. Patients with adrenal insufficiency will often present, in the acute and chronic phase, with striking hypotension. The blood pressure is often between 80 and 100 mm Hg systolic, and 60 to 70 diastolic. The low blood pressure can plummet during a crisis to unmeasurable levels. One should, therefore, keep a close watch on the blood pressure of Addisonians undergoing anesthesia. The patients are prone to syncope due to either postural hypotension or sodium depletion, as well as to hypoglycemia. These patients should be monitored on the EKG to not only detect high serum potassium which normally accompanies Addison's Disease, but also reduced serum potassium which follows treatment with Desoxycorticosterone. Hyperfunction of the adrenal cortexCushing's Syndrome: The important finding with respect to the heart and the cardiovascular system in Cushing's Syndrome is the presence at times, of acute hypertension, as well as an associated cardiac hypertrophy. Glycosuria, as well as hypercholesterolemia, are also noted in this condition. These patients, therefore, appear to qualify for close monitoring, not only for the hypertension, but also for the possibility of coronary artery disease. Hyperthyrodism: The most worrisome sequella of hyperthyroidism is the development of atrial fibrillation, cardiac enlargement, or congestive heart failure. These consequences occur most frequently in the older age group and are rather rare before the age of 40. Females predominate in a ratio of 2 to 1.28 Heart failure due to hyperthyroidism usually occurs in conjunction with pre-existing hypertension. Since congestive heart failure usually develops following a period of atrial fibrillation, it seems wise to monitor the pulse
JULY-AUGUST, 1977
and EKG on all known hyperthyroid patients. In the uncontrolled, the pulse usually runs between 90-120 in a calm patient. The problems become infinitely more difficult if the diagnosis of hyperthyroidism is not made preoperatively. In this case, it is prudent to consider it a possibility in all cases of atrial fibrillation, cardiac enlargement, or heart failure of uncertain
etiology. Myxedema is uncommonly observed and, thus, the myxedematous heart is rather rare. The cardiac, as well as circulatory changes seen in myxedema are not present in the absence of myxedematous skin changes and
mental retardation. The myxedematous heart is a sluggish, enlarged heart seen primarily among women over 40. The most common EKG features one should look for are the flattening or inversion of the T-wave in leads one and two, and generally low voltage of the QRS complex. In advanced cases of myxedema, bradycardia is a characteristic finding. The rate is frequently in the 50 to 60 range. Patients with advanced myxedema are prone to myocardial failure and the disorder is associated with an increased incidence of angina pectoris.29 Blood pressure is usually unchanged. It is generally believed that atherosclerosis prevails earlier and with greater vigor in the myxedematous patient. Therefore, in monitoring a myxedematous patient, symptoms of failure as well as myocardial ischemia should be looked for. Anemia affects the heart in two ways: by either impairing the oxygen supply or increasing the workload. Anemia is particularly dangerous to an arteriosclerotic heart or an enlarged rheumatic heart with its increased oxygen needs. Anemia predisposes these patients to heart failure and/or coronary insufficiency. The outstanding feature of prolonged anemia is an enlarged heart. Heart murmurs are common; these are functional and are usually systolic. The EKG changes noted are those of myocardial anoxia, namely ST segment depression and T-wave flattening or inversion. The patients are prone to high output failure, and one should be alert for that possibility as well as developing angina pectoris in an already diseased heart.
127
Sickle cell anemia, which is the commonest form seen today, deserves special mention. Oxygen partial pressure should never be allowed to drop below 50 per cent as this may precipitate a crisis. In general, one should strive to maintain a free and unimpeded airway with high oxygen partial pressure to not only prevent the emergence of a crisis, but also to assure adequate oxygen supply to a heart that may already have suffered damage due to anemia. Patients with gouty arthritis have been demonstrated to have a higher incidence rate of coronary heart disease. Finally, the effects of gonadal hormones on atherosclerosis have been demonstrated by the fact that the incidence of coronary heart disease in women who have undergone bilateral oophorectomy before menopause were 4 times greater than in control females, and similarly, the incidence of atherosclerosis was found to be less in men treated with estrogen for carcinoma of the prostate.30
Conclusions Examples of systemic diseases affecting the heart and the circulatory system have been presented. Anticipating path-physiological changes in reality, mandates that all patients be monitored to some extent. Intraoperative monitoring is merely an extension of preoperative monitoring, and the value of intraoperative monitoring is directly proportional to the degree of accuracy one was able to achieve in one's preoperative work up. Intraoperative monitoring is used as a means of identifying anticipated change, and being alert for unexpected change. Unexplained intraoperative tachycardia, for example, could be a manifestation of anoxemia, heart failure, malignant hyperthermia, thyroid storm, or pulmonary embolus, to note but a few possibilities. Monitoring, in this case, is merely one of the tools utilized to arrive at a differential diagnosis. All patients' vital signs must be taken prior to surgery to allow the establishment of a base-line, for further interpretation may offer little unless it can be related to preoperative levels. Intraoperative monitoring, then, has a relative meaning besides an 128
absolute one. The abnormally high blood pressure and the extra systoles noted intraoperatively may be quite normal and well tolerated for that particular patient. However, there is no way of interpreting whether the values determined intraoperatively are within the bounds of tolerance for this patient unless a pre-operative base-line exists. It is my hope that this presentation has brought a little order to the problem of who and what should be monitored. I have taken the liberty of changing the thrust of this presentation by exploring the specific changes imposed on one system by certain disease processes. This same exercise must be applied to all systems, and together with the effect of the anesthetic agent, a totality of expectancy is achieved. REFERENCES 1. Friedberg C K Diseases of the Heart. 3rd ed. Philadelphia: W B Saunders. 2. Tarhan S Moffit E A Taylor W F et al: Myocardial Infarction after general anesthesia. JAMA 220:1451-1454, 1972. 3. Ibid. 4. Kannel W B McNamara P M Feinleib IM et al: The unrecognized myocardial infarction: fourteen year follow-up experience in the Framingham study. Geriatrics 25:75-87, 1970. 5. White N K Edwards J E and Dry T J: Circulation 1:645, 1950. 6. Ackerman R F Dry T J and Edwards J E: Circulation 1:1345, 1950. 7. Enos W F Holmes R H and Beyer J: JAMA 152:1090, 1953. 8. Russerk and Zollman Coronary Heart Diseases. Philadelphia: J P Lippincott, 1971. 9. Doyle J T Heslin A S Hilleboe H E Formel P F et al: Measuring the risk of coronary infant disease in adult population group. Am J of Pub Health 47 (suppl. Apr. 1957):25, 1957. 10. Keys A Taylor H L Blackburn H Broler J Andenjow J T and Simonson E: Coronary Heart Disease among Minnesota business and professional men followed fifteen years. Circulation 28:381, 1963. 11. Kannel W B Dauber R T and McNamara P M: Detection of the coronary prone adult: The Framingham Study. J Iowa Med Soc 52:26, 1866. 1966. 12. Kannel W B Castelli W P and McNamara P IM: Coronary profile: twelve year follow-up: The Framingham Study. J Occup Med 9:611, 1967.
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13. Ibid. 14. Keys A Blackburn H et al: Epidemiological studies related to coronary heart disease: Characteristics of men aged 40-59 in seven countries. Acta Med Scand suppl. 460, 1967, 392. 15. U. S. Dept of Health, Education and Welfare: Office of the Surgeon General. Smoking and Health. Washington, D. C.: GPO, 1964. 16. Thomas C B and Cohen B H: Ann Int Med 42:90, 1955. 17. Friedman M and Rosenmann R H: Association of specific overt patterns with blood and cardiovascular findings, blood cholesterol level, blood clotting time, incidence of arcus senilus and clinical coronary artery disease. JAMA 169:1286-1296, 1959. 18. Block W J Crumpacker E L et al: JAMA 150: 259, 1952. 19. Glenn F: Ann Surg 37:920, 1953. 20. Stephenson H E Reid L D Hinton J W et al: Ann Surg 137:731, 1953. 21. Root H F and Bradley R F: Cardiovascular Disease in the Treatment of Diabetes MeUitus.
22.
23. 24. 25. 26. 27. 28.
10th ed. Joslin, et al. Philadelphia: Lea and Febiger, 1969. Agar J M Silent myocardial infarctions in diabetes mellitus. Med J Austr 49(2):284, 1962. Friedberg C K: Diseases of the Heart. 3rd ed. Philadelphia: W. B. Saunders Co. Herman R V and Gorlin R: Premature coronary artery disease and the preclinical diabetic state. Am J Med 38:481, 1965. Friedberg C K: Diseases of the Hart. 3rd ed. Philadelphia: W. B. Saunders Co. Marble A Bradley R F White P et al: Joslin's Diabetes Mellitus. 11th ed. Philadelphia: Lea and Febiger, 1971. Ibid. Summers and Surtees: Thyrotoxidosity and heart disease. Acta Med Scand 169:661.
29. Ibid. 30. Higens N Robinson R W and Cohen W D: Increased incidence of cardiovascular disease in castrated women. N E J Med 268:1123, 1963.
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