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Cardiac Arrest During Urologic Procedures
THE JOURNAL OF UROLOGY
Vol. 77, No. 6, June 1957 Printed in U.S.A.
CARDIAC ARREST DURING UROLOGIC PROCEDURES JOSEPH E. TWIDWELL
AND
GEORGE L. GARSKE
From the Department of Urology, St. Mary's Hospital, Minneap@lis, Minn.
A recent case of cardiac arrest during transurethral prostatectomy in our practice prompted us to review the literature on this subject. Although there are cases reported during a variety of surgical operations, we were surprised at the almost complete lack of reference to cardiac arrest during urologic procedures. All urologists have a knowledge of this dramatic problem, but certainly not all have a working understanding or a routine for its care should such a drastic emergency arise.1- 3 Cardiac arrest, by definition, is the unexpected, sudden onset of cessation of cardiac output. As a surgical emergency it takes precedence over all others, for death, or permanent irreparable cerebral damage ensues if the brain is deprived of adequate oxygenation for a period exceeding approximately four minutes. Resuscitation beyond this time limit can scarcely be deemed successful, even if the patient survives, because almost without exception, it is a vegetative decerebrate existence. This problem is not new, rather it is a problem which has existed since shortly after the first use of general anesthesia, and one that is being attacked continuously with increased vigor in research, in practice and in publicity. Hosler's4 calculation of 10,000 cardiac arrests occurring annually in the United States gives added impetus to the search for more efficient methods of prevention and recognition, and more successful treatment of this catastrophe. The incidence of cardiac arrest is felt by some investigators to be increasing. Briggs et al., 5 in a series covering 189,815 anesthetic and surgical procedures from 1925 to 1954, reported an overall incidence of operating room deaths of 1: 1091, and of cardiac arrests of 1 : 1406. The incidence in the first two decades was 1 : 2458, and from 1945 to 1954, a total incidence of 1: 1038. They conclude that cardiac arrest is the major single cause of death in the operating room, and that there has been an absolute increase in the incidence of cardiac arrest in recent years. Table 1 shows the incidence of cardiac arrest and recovery rate from reports by several authors. ETIOLOGY
The etiologic factors of prime importance are hypoxia (lack of oxygen) and hypercapnea (excess of carbon dioxide). Several excellent reports by experiRead at annual meeting, North Central Section of American Urological Association, Cleveland, Ohio, October 3-5, 1956. 1 Dale, W. A.: Cardiac arrest. Ann. Surg., 135: 3, 1952. 2 Snyder, W. H., Snyder, M. H. and Chaffin, L.: Cardiac arrest in infants and children. A.M.A. Arch. Surg., 66: 714, 1953. 3 Barrett, W. A., Green, J. R., Heinrich, A. N. and Uram, H.: Three minutes in cardiac arrest. J. Int. Coll. Surg., 20: 6, 1953. 4 ~osier, R. M.: Manual on Cardiac Resuscitation. Springfield, Ill.: Charles C. Thomas, publisher, 1954. 5 Briggs, B. D., Sheldon, D. B. and Beecher, H.K.: Cardiac arrest. J.A.M.A., 160: 17, 1956. 783
784
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE TABLE
Author
Ament Bergner Blades Bonica Briggs Hanks Hewlett Johnson L.A. F. B. Miller
Location
Bellevue Hosp., New York City Louisville, Ky. Geo. Wash. Hosp., Wash., D.C. Tacoma, Wash. Mass. Gen. Hosp., Boston, Mass. Presbyterian Hosp., New York City Brooke Army Hosp., San Antonio, Texas Univ. Pennsylvania Hosp., Philadelphia San Antonio, Texas University Hosp., Mpls., Minn.
Reported Arrests
1* Total Cases and Length of Time
Arrest Ratio
% of Survival
9
28,000 (3 yrs.)
1 :3111
75
17 4
35,000 (4 yrs.) 54,579 (5 yrs.)
1:2058 1:13,645
64 50
15 85
90,000 (7 yrs.) 189,815 (30 yrs.)
1:6000 1:1406
not stated not stated
23
49,728 (4 yrs.)
1:2162
43
28
unknown (5 yrs.)
1:2949
50
19
95,000 (7 yrs.)
1:5000
52
6 14
14,809 (2½ yrs.) 12,000 (2½ yrs.)
1:2468 1:858
85 not stated
* From Martin and Tarrow: Current Res. Anesth.,
35: 147-164, 1956.
mental investigators have shown this to be true. Sloan 6 reported that stimulation of the vagus nerve at the hilum of the lung failed to produce arrest in adequately oxygenated dogs. Animals subjected to marked progressive hypoxia, or asphyxia, showed central cardio-inhibitory impulses which resulted in increased bradycardia and a fall in blood pressure. Under these conditions stimulation of the vagus nerve did produce additional cardiac inhibition, and frequently was followed by arrest. Cardiac arrest occurred more frequently during progressive asphyxia than during hypoxia alone. Young, Sealy, Harris and Botwin7 report that hypercapnea enhances the effect of vagal stimulation on the heart, whereas hypoxia diminishes the effect of vagal stimulation. Stewart, Virtue and Swan8 concluded that hypercapnea significantly enhances vagal cardiac arrest in the normal dog, but not in the chronically hypoxic dog. They also report that vagal stimulation produced ventricular fibrillation in one-third of the chronically hypoxic dogs, but not in previously normal dogs. What is the significance of these findings in relation to cardiac arrest in patients in the urologic service? Chronic cardiovascular disease with its attendant decreased vital capacity can result in unrecognized chronic hypoxia of varying degrees in the preoperative state. Toxemia and fever, such as occur with severe urinary tract infections, anemia and inanition, are also factors which can produce a subclinical hypoxia. Patients with such problems, when subjected to the stress 6 Sloan, H. E.: The vagus nerve in cardiac arrest: The effect of hypercapnea, hypoxia and asphyxia on reflex inhibition of the heart. Surg., Gynec. & Obst., 91: 257, 1950. 7 Young, W. G., Sealy, W. C., Harris, J. and Botwin, A.: The effects of hypercapnea and hypoxia on the response of the heart to vagal stimulation. Surg., Gynec. & Obst., 93: 51, 1951. 8 Stewart, B. D., Virtue, R. W. and Swan, H.: Cardiac arrest and ventricular fibrillation. A.M.A. Arch. Surg., 66: 703, 1953.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
785
of surgery, are likely prospects for cardiac arrest and should be so evaluated preoperatively. The life span of man is increasing yearly and ·with this added longevity, cardiovascular disease assumes increased importance. Genitourinary problems, too, become more prominent in this older age group. Therefore, it is logical to assume that the individual physician responsible for the management of these genitourinary problems must be cognizant of the patient's cardiovascular-respiratory status as well as the urological status. Certain preoperative determinations such as vital capacity, venous pressure and circulation time are helpful. Determination of the patient's serum potassium, sodium, chloride, and carbon dioxide levels prior to surgery provides additional information. Arterial oxygen saturation when indicated can be obtained. Predisposing factors also worth considering are: 1) Preoperative medication. Large doses of narcotics, with their effect of respiratory depression, should be avoided, since they rn.ay further impair ventilation in an individual possibly having chronic hypoxia of some degree. 2) Atropine in sufficient amount, and in proper time relationship to the actual anesthetic procedure, is an aid in controlling abnonnal vagal responses and also diminishes bronchial secretions. 3) Position of the patient during procedure. Positions which may interfere with adequate oxygenation should be avoided, or if such position is absolutely necessary, particular attention must be given to insure proper obstruction-free respiratory exchange by endotracheal intubation. DIAGNOSIS AND TREATMENT
Bradycardia and falling blood pressure in an anesthetized individual, with a previously normal pulse and blood pressure, are signs of progressive asphyxia and impending cardiac arrest. Immediate check must be made to insure that oxygenation is adequate, and that respiratory excursion is sufficient to correct, or prevent, hypercapnea. Cardiac arrest is present when blood pressure and pulse are unobtainable. From. the moment this occurs, the patient has only four critical minutes if he is to be retrieved with any significant degree of success. Time should not be wasted by futile motions looking for stethoscopes to listen for heartbeat, searching for medications and the equipment to inject them into the heart, and by calling for n1ore adequately trained personnel to perform thoracotomy and cardiac massage. As time flies the neuron dies. 9 The responsibility rests with the surgeon, or the individual most capable to perform thoracotomy and cardiac massage. As urologic surgeons, we must be ever aware of our duty in this regard, and must be prepared to deal with this situation promptly and intelligently. Provided sterile thoracotomy instruments are present, they are used, but all that is absolutely essential is a scalpel. Skin asepsis is a matter of little importance at this time. An incision is made medial to lateral in the left fourth or fifth interspace, with several quick strokes of the blade. This approach permits n1ore efficient cardiac massage, and is considered vastly superior to the transdiaphragmatic route. Laceration of the lung can be avoided 9 Turk, L. N. and Glenn, W.W. L.: Cardiac arrest. Results of attempted cardiac resuscitation in 42 cases. New Eng. J. Med., 251: 795-803, 1954.
786
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE
by slipping one's fingers in the pleural space and retracting the lung medially. The costal cartilages above and below are incised to permit ready access to the heart; a rib spreader, if available, facilitates this, and provides for more efficient cardiac massage. The heart is seen to be motionless, contracting feebly, or fibrillating, giving a previously well described sensation of a "bag of worms" in the hand. Massage at the rate of 40 to 60 per minute, or even higher, is begun. Higher rates are difficult for the operator to maintain for any length of time, however. Initially, the pericardium is not opened. Massage, to be effective, is best done with the apex of the heart lying in the palm of the hand. The heart is compressed firmly and rapidly to expel the blood, and allowed to fill during relaxation of the fingers. Care must be exercised to avoid laceration of the heart with the finger tips. Large hearts can be more successfully massaged between the palms of both hands. During periodic momentary rest periods the heart can be observed for evidence of activity. If fibrillation is present, massage is continued for a few minutes until the color of the myocardium is improved since the anoxic myocardium tolerates electric shock poorly, and further damage could result. When the color of the myocardium has improved, de.fibrillation is attempted by use of electric shock techniques such as those described by Wiggers. 10 This form of therapy was developed following observation that passage of strong electric current through the heart produces simultaneous contraction of all the myocardial fibers. Following this massive contraction the heart is in standstill while relaxation follows. Spontaneous beat returns with regular rhythm after the period of asystole. Single shocks delivered by means of a commercial defibrillator are used. The heart is compressed between the sterile electrodes, and a shock of 110 to 130 volts and 2 amperes for 0.1 to 0.5 second may be used. At times, serial shocks of short duration may be of more value than a prolonged single shock. Precautions must be taken to avoid burning the cardiac muscle, and to avoid electrocution of the surgeon and other members of the resuscitation team. It is advisable for all members of the team to remove their hands from the patient, and avoid contact of the patient and the operating table during the period of application of the electrodes. In conjunction with the surgeon's efforts, the anesthesiologist attempts correction of asphyxia by administration of 100 per cent oxygen via endotracheal tube, or if not intubated, by a closed mask until intubation can be accomplished, and provides artificial respiration sufficient to furnish adequate respiratory exchange. Whole blood replacement, rapidly, to correct circulatory volume deficit is useful. However, care should be exercised to avoid overloading the circulatory system. DRUGS
Stimulants to anoxic myocardium should be avoided since they are of questionable value, and may produce additional damage. However, once the condition of the myocardium has improved by massage, certain drugs may be of value. 10 Wiggers, C. J.: Cardiac massage followed by counter-shock in revival of mammalian ventricles from fibrillation due to coronary occlusion. Am. J. Physiol., 116: 161, 1933.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
787
FIG 1. Drug tray with levophed, vasoxyl, calcium chloride, pronestyl, atropine, novocain 1 and 2 per cent, sodium lactate, adrenalin, potassium chloride and isotonic saline solution. Tray is on each anesthesiologist's table and is checked and ready for use before each surgical procedure. ·
FIG. 2. Contents of sterile thoracotomy set. Set is wrapped in red muslin for rapid identification.
These solutions are injected directly into the chamber of the left ventricle so that rapid entrance to the coronary circulation is obtained. If asystole is present, l cc of a solution containing 1 cc of 1: 1000 epinephrine diluted to 10 cc of normal saline is used, and this may be repeated in four to five minutes. If this does not produce a satisfactory response, 2 to 4 cc of a 10 per cent solution of calcium chloride may be used. If ventricular fibrillation is present, the use of epinephrine, and/or calcium chloride is to be avoided since this may make the fibrillation refractory to further treatment. When ventricular fibrillation is present, intracardiac procaine 100 mg.
788
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE
FIG. 3. A, Morris clinical defibrillator, Sterile electrodes are wrapped in red muslin rather than conventional green or white. B, thoracotomy set, sterile electrodes and defibrillator are kept in this portable cabinet.
to 200 mg., or pronestyl 300 mg. to 1000 mg. in 2 per cent to 10 per cent solutions, should be used, accompanied by de-fibrillation by electric shock. 11 Vasopressors such as vasoxyl, neosynephrine, and wyamine may be useful in keeping the blood pressure above shock level. Rapidly acting glucosides (cedilanid and acetyl strophanthin) may be used if spontaneous cardiac activity does not produce a peripheral pulse. 12 If resuscitation is successful, the chest is closed after approximately fifteen minutes of adequate cardiac action. Massage should not be discontinued for a 11 Martin, J. T. and Tarrow, A. B.: A review of cardiac resuscitation. Current Res. Anesth., 35: 147-164, 1956. 12 Sadove, M. S., Wyant, G. M., Julian, 0. C. and Dye, W. S.: Cardiac arrest. Amer. Surg., 20: 5, 1954.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
789
reasonable period of time, even if attempts are unsuccessful to restore action through the use of drugs or other methods. Instances are reported in which cardiac activity returned after thirty to forty minutes of massage. If effective circulation has not returned within one hour, massage may be discontinued. The decision to discontinue massage should not be made on the presence of peripheral cyanosis, because a patient may still be cyanotic and have effective circulation. From the foregoing, it becomes readily apparent that these measures can be accomplished properly only in the presence of a preconceived plan of treatment. Everyone connected with anesthesia, or surgery, should understand his, or her, duties in such a crisis, and be prepared to execute these duties with machinelike precision. Only through such a plan, and by periodic practice will lives be saved, which otherwise would have been lost. The necessary equipment and drugs must be immediately accessible, and must be in proper working condition at all times. The equipment used in one of our hospitals is shown in figures 1 to 3 and is ready for each operation before it begins. CASE REPORT
The case which prompted our study of this problem was that of a 73-year-old white, retired policeman (case 228443) in acute urinary retention admitted to St. Mary's Hospital on June 24, 1955. He gave a history of symptoms of progressively increasing vesical neck obstruction for 2 years, especially pronounced the 6 months before hospitalization. Acute urinary retention developed 48 and 24 hours prior to admission, relieved by catheterization by his physician. There were no positive cardiovascular symptoms. A peptic ulcer in 1947 was treated medically with prompt relief, and with no recurrence of symptoms. Positive physical findings were limited to the genitourinary system. Rectal examination revealed a two plus enlargement of the prostate gland. The gland was hard, nodular, irregular, and fixed with induration extending to the seminal vesicles. The lungs were clear to auscultation and percussion. The heart on physical examination was normal in size with regular rhythm, and an apical pulse of 82. Blood pressure was 140/80. Excretory urography revealed architecturally and functionally normal kidneys and ureters bilaterally, and the bladder floor was moderately elevated by the prostatic enlargement. Chest x-ray showed the presence of calcific deposits in the left hilar region, and a diffuse, moderate prominence of bronchovascular markings in both lung fields. Admission urinalysis obtained at the time of vesical decompression contained four tc six leukocytes and twelve to fifteen erythrocytes per high power field. The alkaline phosphatase was 3.6 King-Armstrong units. The acid phosphatase was 1.2 Bodansky units with a prostatic fraction of 0.6. The blood urea nitrogen was 14 mg. per cent. The hemoglobin was was 16.9 gm. and the leukocyte count 10,200 with a normal differential. The electrocardiogram was interpreted as normal except for mild left axis deviation. The patient's condition appeared satisfactory for surgery by the consulting internist, and on June 27, 1955 he was taken to surgery for a transurethral
790
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE
prostatic resection. Blood pressure before anesthetic induction was 190/80. Preoperative medication consisted of subcutaneous sodium luminal, gr. 2 at 6:30 a.m. and subcutaneous morphine sulfate gr. 1/s and atropine sulfate gr. ½oo, given at 7:00 a.m. The anesthetic, intravenous 2.5 per cent pentothal sodium solution containing 5 mg. per cc flaxedil, supplemented by nitrous oxide and oxygen, using the semiclosed technique began at 8:40 a.m. Induction was satisfactory, and resection of the prostate began at 8: 50 a.m. There was moderate amount of prostatic bleeding which was controlled with moderate difficulty because of the sclerotic character of the vascular supply of the prostate and administration of 500 cc of whole blood was started slowly at 9: 05 a.m. The blood pressure and pulse remained stable from the beginning of the procedure until 9:22 a.m. at which time the patient became cyanotic. The anesthetic was immediately discontinued, and an endotracheal tube was inserted at 9: 25 a.m. at which time cardiac arrest was noted. Thoracotomy was accomplished within three minutes. Asystole was present, but after massage for 1 minute active, regular, quite forceful contractions appeared at a rate between 60 to 70 per minute. These persisted for 3 minutes and then ceased. Additional massage was applied, but cardiac action, except for a few incompetent contractions at rare intervals, could not be restored. It was possible to maintain the systolic blood pressure at 90 mm. mercury, but in spite of this and forced respiration with 100 per cent oxygen concentration, there was no improvement in the patient's color at any time. Cardiac massage was maintained for 45 minutes. The defibrillator was used twice during this period without ever restoring cardiac action. The patient was pronounced dead at 10:20 a.m. At autopsy, the heart weighed 460 gm. and revealed moderate left ventricular hypertrophy and patchy atherosclerosis of the coronary vessels. However, the major vessels were not significantly narrowed. The lungs showed no significant gross abnormalities, other than slight apical fibrosis on the left. Microscopic section of the lung revealed interstitial fibrosis. The final diagnosis was 1) cardiac arrest, clinical; 2) carcinoma of the prostate with extension to the seminal vesicles; 3) interstitial fibrosis, pulmonary, etiology undetermined. DISCUSSION
This appears to be a case of true cardiac arrest with pulmonary fibrosis as a possible predisposing factor. Although this patient had no clinical findings or symptoms of cardiorespiratory disease prior to surgery, one wonders if the pulmonary fibrosis, although not marked, was sufficient to diminish his vital capacity and produce a chronic hypoxia of some degree before the operation. Determination of this patient's vital capacity, venous pressure, and circulation time may have provided information to alert us to the possibility of cardiac arrest arising during the course of the surgical procedure. Since clinical and experimental evidence shows the incidence of cardiac arrest to be significantly greater in individuals with chronic hypoxia, it is well to consider the possibility of this situation existing in the older patient even in the absence of significant preoperative symptoms or clinical findings.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
791
SUMMARY
The problem of cardiac arrest is discussed and its relation to chronic hypoxia and hypercapnea is stressed. The possibility of chronic, unrecognized hypoxia due to cardio-respiratory disease in the older patient with genitourinary problems is cited. The salient features in the diagnosis and treatment of this condition, and the responsibility of the urologist as part of the resuscitation team are pointed out. A case of cardiac arrest with chronic pulmonary fibrosis as a possible factor in the production of chronic hypoxia is described. 431 Marquette Bank Building, JJ![inneapolis, JJ![inn.
Vol. 77, No. 6, June 1957 Printed in U.S.A.
CARDIAC ARREST DURING UROLOGIC PROCEDURES JOSEPH E. TWIDWELL
AND
GEORGE L. GARSKE
From the Department of Urology, St. Mary's Hospital, Minneap@lis, Minn.
A recent case of cardiac arrest during transurethral prostatectomy in our practice prompted us to review the literature on this subject. Although there are cases reported during a variety of surgical operations, we were surprised at the almost complete lack of reference to cardiac arrest during urologic procedures. All urologists have a knowledge of this dramatic problem, but certainly not all have a working understanding or a routine for its care should such a drastic emergency arise.1- 3 Cardiac arrest, by definition, is the unexpected, sudden onset of cessation of cardiac output. As a surgical emergency it takes precedence over all others, for death, or permanent irreparable cerebral damage ensues if the brain is deprived of adequate oxygenation for a period exceeding approximately four minutes. Resuscitation beyond this time limit can scarcely be deemed successful, even if the patient survives, because almost without exception, it is a vegetative decerebrate existence. This problem is not new, rather it is a problem which has existed since shortly after the first use of general anesthesia, and one that is being attacked continuously with increased vigor in research, in practice and in publicity. Hosler's4 calculation of 10,000 cardiac arrests occurring annually in the United States gives added impetus to the search for more efficient methods of prevention and recognition, and more successful treatment of this catastrophe. The incidence of cardiac arrest is felt by some investigators to be increasing. Briggs et al., 5 in a series covering 189,815 anesthetic and surgical procedures from 1925 to 1954, reported an overall incidence of operating room deaths of 1: 1091, and of cardiac arrests of 1 : 1406. The incidence in the first two decades was 1 : 2458, and from 1945 to 1954, a total incidence of 1: 1038. They conclude that cardiac arrest is the major single cause of death in the operating room, and that there has been an absolute increase in the incidence of cardiac arrest in recent years. Table 1 shows the incidence of cardiac arrest and recovery rate from reports by several authors. ETIOLOGY
The etiologic factors of prime importance are hypoxia (lack of oxygen) and hypercapnea (excess of carbon dioxide). Several excellent reports by experiRead at annual meeting, North Central Section of American Urological Association, Cleveland, Ohio, October 3-5, 1956. 1 Dale, W. A.: Cardiac arrest. Ann. Surg., 135: 3, 1952. 2 Snyder, W. H., Snyder, M. H. and Chaffin, L.: Cardiac arrest in infants and children. A.M.A. Arch. Surg., 66: 714, 1953. 3 Barrett, W. A., Green, J. R., Heinrich, A. N. and Uram, H.: Three minutes in cardiac arrest. J. Int. Coll. Surg., 20: 6, 1953. 4 ~osier, R. M.: Manual on Cardiac Resuscitation. Springfield, Ill.: Charles C. Thomas, publisher, 1954. 5 Briggs, B. D., Sheldon, D. B. and Beecher, H.K.: Cardiac arrest. J.A.M.A., 160: 17, 1956. 783
784
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE TABLE
Author
Ament Bergner Blades Bonica Briggs Hanks Hewlett Johnson L.A. F. B. Miller
Location
Bellevue Hosp., New York City Louisville, Ky. Geo. Wash. Hosp., Wash., D.C. Tacoma, Wash. Mass. Gen. Hosp., Boston, Mass. Presbyterian Hosp., New York City Brooke Army Hosp., San Antonio, Texas Univ. Pennsylvania Hosp., Philadelphia San Antonio, Texas University Hosp., Mpls., Minn.
Reported Arrests
1* Total Cases and Length of Time
Arrest Ratio
% of Survival
9
28,000 (3 yrs.)
1 :3111
75
17 4
35,000 (4 yrs.) 54,579 (5 yrs.)
1:2058 1:13,645
64 50
15 85
90,000 (7 yrs.) 189,815 (30 yrs.)
1:6000 1:1406
not stated not stated
23
49,728 (4 yrs.)
1:2162
43
28
unknown (5 yrs.)
1:2949
50
19
95,000 (7 yrs.)
1:5000
52
6 14
14,809 (2½ yrs.) 12,000 (2½ yrs.)
1:2468 1:858
85 not stated
* From Martin and Tarrow: Current Res. Anesth.,
35: 147-164, 1956.
mental investigators have shown this to be true. Sloan 6 reported that stimulation of the vagus nerve at the hilum of the lung failed to produce arrest in adequately oxygenated dogs. Animals subjected to marked progressive hypoxia, or asphyxia, showed central cardio-inhibitory impulses which resulted in increased bradycardia and a fall in blood pressure. Under these conditions stimulation of the vagus nerve did produce additional cardiac inhibition, and frequently was followed by arrest. Cardiac arrest occurred more frequently during progressive asphyxia than during hypoxia alone. Young, Sealy, Harris and Botwin7 report that hypercapnea enhances the effect of vagal stimulation on the heart, whereas hypoxia diminishes the effect of vagal stimulation. Stewart, Virtue and Swan8 concluded that hypercapnea significantly enhances vagal cardiac arrest in the normal dog, but not in the chronically hypoxic dog. They also report that vagal stimulation produced ventricular fibrillation in one-third of the chronically hypoxic dogs, but not in previously normal dogs. What is the significance of these findings in relation to cardiac arrest in patients in the urologic service? Chronic cardiovascular disease with its attendant decreased vital capacity can result in unrecognized chronic hypoxia of varying degrees in the preoperative state. Toxemia and fever, such as occur with severe urinary tract infections, anemia and inanition, are also factors which can produce a subclinical hypoxia. Patients with such problems, when subjected to the stress 6 Sloan, H. E.: The vagus nerve in cardiac arrest: The effect of hypercapnea, hypoxia and asphyxia on reflex inhibition of the heart. Surg., Gynec. & Obst., 91: 257, 1950. 7 Young, W. G., Sealy, W. C., Harris, J. and Botwin, A.: The effects of hypercapnea and hypoxia on the response of the heart to vagal stimulation. Surg., Gynec. & Obst., 93: 51, 1951. 8 Stewart, B. D., Virtue, R. W. and Swan, H.: Cardiac arrest and ventricular fibrillation. A.M.A. Arch. Surg., 66: 703, 1953.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
785
of surgery, are likely prospects for cardiac arrest and should be so evaluated preoperatively. The life span of man is increasing yearly and ·with this added longevity, cardiovascular disease assumes increased importance. Genitourinary problems, too, become more prominent in this older age group. Therefore, it is logical to assume that the individual physician responsible for the management of these genitourinary problems must be cognizant of the patient's cardiovascular-respiratory status as well as the urological status. Certain preoperative determinations such as vital capacity, venous pressure and circulation time are helpful. Determination of the patient's serum potassium, sodium, chloride, and carbon dioxide levels prior to surgery provides additional information. Arterial oxygen saturation when indicated can be obtained. Predisposing factors also worth considering are: 1) Preoperative medication. Large doses of narcotics, with their effect of respiratory depression, should be avoided, since they rn.ay further impair ventilation in an individual possibly having chronic hypoxia of some degree. 2) Atropine in sufficient amount, and in proper time relationship to the actual anesthetic procedure, is an aid in controlling abnonnal vagal responses and also diminishes bronchial secretions. 3) Position of the patient during procedure. Positions which may interfere with adequate oxygenation should be avoided, or if such position is absolutely necessary, particular attention must be given to insure proper obstruction-free respiratory exchange by endotracheal intubation. DIAGNOSIS AND TREATMENT
Bradycardia and falling blood pressure in an anesthetized individual, with a previously normal pulse and blood pressure, are signs of progressive asphyxia and impending cardiac arrest. Immediate check must be made to insure that oxygenation is adequate, and that respiratory excursion is sufficient to correct, or prevent, hypercapnea. Cardiac arrest is present when blood pressure and pulse are unobtainable. From. the moment this occurs, the patient has only four critical minutes if he is to be retrieved with any significant degree of success. Time should not be wasted by futile motions looking for stethoscopes to listen for heartbeat, searching for medications and the equipment to inject them into the heart, and by calling for n1ore adequately trained personnel to perform thoracotomy and cardiac massage. As time flies the neuron dies. 9 The responsibility rests with the surgeon, or the individual most capable to perform thoracotomy and cardiac massage. As urologic surgeons, we must be ever aware of our duty in this regard, and must be prepared to deal with this situation promptly and intelligently. Provided sterile thoracotomy instruments are present, they are used, but all that is absolutely essential is a scalpel. Skin asepsis is a matter of little importance at this time. An incision is made medial to lateral in the left fourth or fifth interspace, with several quick strokes of the blade. This approach permits n1ore efficient cardiac massage, and is considered vastly superior to the transdiaphragmatic route. Laceration of the lung can be avoided 9 Turk, L. N. and Glenn, W.W. L.: Cardiac arrest. Results of attempted cardiac resuscitation in 42 cases. New Eng. J. Med., 251: 795-803, 1954.
786
JOSEPH E. TWIDWELL AND GEORGE L. GARSKE
by slipping one's fingers in the pleural space and retracting the lung medially. The costal cartilages above and below are incised to permit ready access to the heart; a rib spreader, if available, facilitates this, and provides for more efficient cardiac massage. The heart is seen to be motionless, contracting feebly, or fibrillating, giving a previously well described sensation of a "bag of worms" in the hand. Massage at the rate of 40 to 60 per minute, or even higher, is begun. Higher rates are difficult for the operator to maintain for any length of time, however. Initially, the pericardium is not opened. Massage, to be effective, is best done with the apex of the heart lying in the palm of the hand. The heart is compressed firmly and rapidly to expel the blood, and allowed to fill during relaxation of the fingers. Care must be exercised to avoid laceration of the heart with the finger tips. Large hearts can be more successfully massaged between the palms of both hands. During periodic momentary rest periods the heart can be observed for evidence of activity. If fibrillation is present, massage is continued for a few minutes until the color of the myocardium is improved since the anoxic myocardium tolerates electric shock poorly, and further damage could result. When the color of the myocardium has improved, de.fibrillation is attempted by use of electric shock techniques such as those described by Wiggers. 10 This form of therapy was developed following observation that passage of strong electric current through the heart produces simultaneous contraction of all the myocardial fibers. Following this massive contraction the heart is in standstill while relaxation follows. Spontaneous beat returns with regular rhythm after the period of asystole. Single shocks delivered by means of a commercial defibrillator are used. The heart is compressed between the sterile electrodes, and a shock of 110 to 130 volts and 2 amperes for 0.1 to 0.5 second may be used. At times, serial shocks of short duration may be of more value than a prolonged single shock. Precautions must be taken to avoid burning the cardiac muscle, and to avoid electrocution of the surgeon and other members of the resuscitation team. It is advisable for all members of the team to remove their hands from the patient, and avoid contact of the patient and the operating table during the period of application of the electrodes. In conjunction with the surgeon's efforts, the anesthesiologist attempts correction of asphyxia by administration of 100 per cent oxygen via endotracheal tube, or if not intubated, by a closed mask until intubation can be accomplished, and provides artificial respiration sufficient to furnish adequate respiratory exchange. Whole blood replacement, rapidly, to correct circulatory volume deficit is useful. However, care should be exercised to avoid overloading the circulatory system. DRUGS
Stimulants to anoxic myocardium should be avoided since they are of questionable value, and may produce additional damage. However, once the condition of the myocardium has improved by massage, certain drugs may be of value. 10 Wiggers, C. J.: Cardiac massage followed by counter-shock in revival of mammalian ventricles from fibrillation due to coronary occlusion. Am. J. Physiol., 116: 161, 1933.
CARDIAC ARREST DURING UROLOGIC PROCEDURES
787
FIG 1. Drug tray with levophed, vasoxyl, calcium chloride, pronestyl, atropine, novocain 1 and 2 per cent, sodium lactate, adrenalin, potassium chloride and isotonic saline solution. Tray is on each anesthesiologist's table and is checked and ready for use before each surgical procedure. ·
FIG. 2. Contents of sterile thoracotomy set. Set is wrapped in red muslin for rapid identification.
These solutions are injected directly into the chamber of the left ventricle so that rapid entrance to the coronary circulation is obtained. If asystole is present, l cc of a solution containing 1 cc of 1: 1000 epinephrine diluted to 10 cc of normal saline is used, and this may be repeated in four to five minutes. If this does not produce a satisfactory response, 2 to 4 cc of a 10 per cent solution of calcium chloride may be used. If ventricular fibrillation is present, the use of epinephrine, and/or calcium chloride is to be avoided since this may make the fibrillation refractory to further treatment. When ventricular fibrillation is present, intracardiac procaine 100 mg.
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JOSEPH E. TWIDWELL AND GEORGE L. GARSKE
FIG. 3. A, Morris clinical defibrillator, Sterile electrodes are wrapped in red muslin rather than conventional green or white. B, thoracotomy set, sterile electrodes and defibrillator are kept in this portable cabinet.
to 200 mg., or pronestyl 300 mg. to 1000 mg. in 2 per cent to 10 per cent solutions, should be used, accompanied by de-fibrillation by electric shock. 11 Vasopressors such as vasoxyl, neosynephrine, and wyamine may be useful in keeping the blood pressure above shock level. Rapidly acting glucosides (cedilanid and acetyl strophanthin) may be used if spontaneous cardiac activity does not produce a peripheral pulse. 12 If resuscitation is successful, the chest is closed after approximately fifteen minutes of adequate cardiac action. Massage should not be discontinued for a 11 Martin, J. T. and Tarrow, A. B.: A review of cardiac resuscitation. Current Res. Anesth., 35: 147-164, 1956. 12 Sadove, M. S., Wyant, G. M., Julian, 0. C. and Dye, W. S.: Cardiac arrest. Amer. Surg., 20: 5, 1954.
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reasonable period of time, even if attempts are unsuccessful to restore action through the use of drugs or other methods. Instances are reported in which cardiac activity returned after thirty to forty minutes of massage. If effective circulation has not returned within one hour, massage may be discontinued. The decision to discontinue massage should not be made on the presence of peripheral cyanosis, because a patient may still be cyanotic and have effective circulation. From the foregoing, it becomes readily apparent that these measures can be accomplished properly only in the presence of a preconceived plan of treatment. Everyone connected with anesthesia, or surgery, should understand his, or her, duties in such a crisis, and be prepared to execute these duties with machinelike precision. Only through such a plan, and by periodic practice will lives be saved, which otherwise would have been lost. The necessary equipment and drugs must be immediately accessible, and must be in proper working condition at all times. The equipment used in one of our hospitals is shown in figures 1 to 3 and is ready for each operation before it begins. CASE REPORT
The case which prompted our study of this problem was that of a 73-year-old white, retired policeman (case 228443) in acute urinary retention admitted to St. Mary's Hospital on June 24, 1955. He gave a history of symptoms of progressively increasing vesical neck obstruction for 2 years, especially pronounced the 6 months before hospitalization. Acute urinary retention developed 48 and 24 hours prior to admission, relieved by catheterization by his physician. There were no positive cardiovascular symptoms. A peptic ulcer in 1947 was treated medically with prompt relief, and with no recurrence of symptoms. Positive physical findings were limited to the genitourinary system. Rectal examination revealed a two plus enlargement of the prostate gland. The gland was hard, nodular, irregular, and fixed with induration extending to the seminal vesicles. The lungs were clear to auscultation and percussion. The heart on physical examination was normal in size with regular rhythm, and an apical pulse of 82. Blood pressure was 140/80. Excretory urography revealed architecturally and functionally normal kidneys and ureters bilaterally, and the bladder floor was moderately elevated by the prostatic enlargement. Chest x-ray showed the presence of calcific deposits in the left hilar region, and a diffuse, moderate prominence of bronchovascular markings in both lung fields. Admission urinalysis obtained at the time of vesical decompression contained four tc six leukocytes and twelve to fifteen erythrocytes per high power field. The alkaline phosphatase was 3.6 King-Armstrong units. The acid phosphatase was 1.2 Bodansky units with a prostatic fraction of 0.6. The blood urea nitrogen was 14 mg. per cent. The hemoglobin was was 16.9 gm. and the leukocyte count 10,200 with a normal differential. The electrocardiogram was interpreted as normal except for mild left axis deviation. The patient's condition appeared satisfactory for surgery by the consulting internist, and on June 27, 1955 he was taken to surgery for a transurethral
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prostatic resection. Blood pressure before anesthetic induction was 190/80. Preoperative medication consisted of subcutaneous sodium luminal, gr. 2 at 6:30 a.m. and subcutaneous morphine sulfate gr. 1/s and atropine sulfate gr. ½oo, given at 7:00 a.m. The anesthetic, intravenous 2.5 per cent pentothal sodium solution containing 5 mg. per cc flaxedil, supplemented by nitrous oxide and oxygen, using the semiclosed technique began at 8:40 a.m. Induction was satisfactory, and resection of the prostate began at 8: 50 a.m. There was moderate amount of prostatic bleeding which was controlled with moderate difficulty because of the sclerotic character of the vascular supply of the prostate and administration of 500 cc of whole blood was started slowly at 9: 05 a.m. The blood pressure and pulse remained stable from the beginning of the procedure until 9:22 a.m. at which time the patient became cyanotic. The anesthetic was immediately discontinued, and an endotracheal tube was inserted at 9: 25 a.m. at which time cardiac arrest was noted. Thoracotomy was accomplished within three minutes. Asystole was present, but after massage for 1 minute active, regular, quite forceful contractions appeared at a rate between 60 to 70 per minute. These persisted for 3 minutes and then ceased. Additional massage was applied, but cardiac action, except for a few incompetent contractions at rare intervals, could not be restored. It was possible to maintain the systolic blood pressure at 90 mm. mercury, but in spite of this and forced respiration with 100 per cent oxygen concentration, there was no improvement in the patient's color at any time. Cardiac massage was maintained for 45 minutes. The defibrillator was used twice during this period without ever restoring cardiac action. The patient was pronounced dead at 10:20 a.m. At autopsy, the heart weighed 460 gm. and revealed moderate left ventricular hypertrophy and patchy atherosclerosis of the coronary vessels. However, the major vessels were not significantly narrowed. The lungs showed no significant gross abnormalities, other than slight apical fibrosis on the left. Microscopic section of the lung revealed interstitial fibrosis. The final diagnosis was 1) cardiac arrest, clinical; 2) carcinoma of the prostate with extension to the seminal vesicles; 3) interstitial fibrosis, pulmonary, etiology undetermined. DISCUSSION
This appears to be a case of true cardiac arrest with pulmonary fibrosis as a possible predisposing factor. Although this patient had no clinical findings or symptoms of cardiorespiratory disease prior to surgery, one wonders if the pulmonary fibrosis, although not marked, was sufficient to diminish his vital capacity and produce a chronic hypoxia of some degree before the operation. Determination of this patient's vital capacity, venous pressure, and circulation time may have provided information to alert us to the possibility of cardiac arrest arising during the course of the surgical procedure. Since clinical and experimental evidence shows the incidence of cardiac arrest to be significantly greater in individuals with chronic hypoxia, it is well to consider the possibility of this situation existing in the older patient even in the absence of significant preoperative symptoms or clinical findings.
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SUMMARY
The problem of cardiac arrest is discussed and its relation to chronic hypoxia and hypercapnea is stressed. The possibility of chronic, unrecognized hypoxia due to cardio-respiratory disease in the older patient with genitourinary problems is cited. The salient features in the diagnosis and treatment of this condition, and the responsibility of the urologist as part of the resuscitation team are pointed out. A case of cardiac arrest with chronic pulmonary fibrosis as a possible factor in the production of chronic hypoxia is described. 431 Marquette Bank Building, JJ![inneapolis, JJ![inn.