Electrocardiographic Changes in Head Injuries" HERMAN
FALSETTI, M.D.** AND ROBERT
Burlington, JT ermont
T IS WELL KNOWN THAT PATIENTS WITH
cerebrovascular accidents and cerebral trauma may have a variety of electrocardiographic accidents and cerebral trauma may have a variety of electrocardiographic changes.'......I •• I • These changes may be disturbance of rate, rhythm, p wave or QRS complex. The changes noted in the QRS pattern are: (1) prolonged Q-T interval, (2) R-ST segment elevation or depression, (3) inversion or peaking of the T -wave, and (4) a large positive U wave. Experimentally, these changes have been produced by a number of different investigators. Delgado' has shown that there is cardiovascular representation w hie h includes the tip of the frontal lobe, the orbital cortex, the motor and premotor cortex, the hidden motor areas, the anterior part of the temporal lobe, the insula and the cingular gyrus. Fuster and Weinburg' have delimited experimentally a zone covering most of the lateral and posterior hypothalmus, the zona incerta and tennental fields of Forel, Most often stimulation of the posterior hypothalamus resulted in an acceleration of cardiac rhythm. The more lateral area which included the lateral hypothalamus, the zona incerta and the fields of Forel very often produced the effects of QRS deflection and T-wave changes as well as a high incidence of ventricular premature contractions. Porter" has shown electrocardiographic abnormalities after stimulation of the ventral hippocampus and *From the Department of Medicine and the Department of Nuerosu~ry, University of Vermont College of MedIcine. Supported in part by the John A. Hartford Foundation. ··Fonner trainee in cardiology, USPHS Postgraduate Training Program HTS-5286-C3. Currently Chief of Medicine, 6510 USAF Hospital, Edwards AFB, California. tResident in Neurosurgery.
medial nucleus of the amygdala. Glasser' has found that supramedullary brain stem structures also effect the cardiovascular system. PooI,13 in patients, has noted vasocardiac effects on manipulation of the circle of Willis at surgery. Several other investigators":":":" have confirmed and amplified the above presentations. The exact mechanism of these changes is unknown. It does not appear to be related directly to the extent of head injury, since even routine neurologic procedures can produce electrocardiographic changes.' We have recently investigated the electrocardiograms of 16 patients with severe head injuries. All patients are under 40 years of age, have no evidence of chest trauma and no past history of cardiovascular disease. As can be seen in Table 1, the electrocardiograms appeared to have been of very limited value in localization of the cerebral injury. A single electrocardiogram appeared to be of no particular significance in evaluating the prognosis or clinical course. However, in two cases, case 1 and case 2, serial electrocardiograms appeared to parallel the clinical course and may be a valuable parameter in assessing the clinical course in acute head injuries. CASE REPORTS
1: A 25-year-old white woman, righthanded, was admitted with head trauma following an auto accident. Initial examination revealed a comatose patient with blood pressure of 100/60 and an irregular pulse of 80. Examination of the head showed lacerations of the nose and upper lip. There were a number of fractured loose teeth. Examination of the heart, chest, abdomen and extremities was unremarkable. The neurologic examination revealed a dilated left pupil, fixed to light; the right was pin point and questionably reactive. The retinee appeared unremarkable. CASE
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The jaw was clenched. There was no facial asymmetry and no reaction to sound. Sensory examination revealed that any stimulation resulted in bilateral arm extension, with hands flexed at the wrists and opisthotonos. Motor examination revealed decerebrate rigidity greater in the arms than the legs, equal right with left. Superficial abdominal reflexes were absent. The Hoffman response was positive. All deep tendon reflexes were markedly exaggerated. There was bilateral plantar flexion. The patient was taken at once to the operating room, with increasing bradycardia. An electrocardiogram at this time was abnormal with rate of 57, a wandering atrial pacemaker, peaked T-waves, depressed ST segment and prolonged QT interval (tracing 1). During the course of the operation, her temperature was brought down to 31°e. Under hypothennia and hyperventilation, her pulse was 90 per minute while her blood pressure fell to 75/50. Burr holes placed in the right temporal and parietal areas were negative. On the left, a large subdural hematoma was evacuated via a bone flap. This covered the entire convexity, was one inch in thickness, and the apparent origin was a parietal bridging vein. Although direct control of the bleeding point was not possible, swelling of the brain after removal of the hematoma appeared to control the bleeding. A dural substitute was used to close, and the temperature was allowed to return to normal. Postoperatively the patient did well with stable signs, equal and reactive pupils, and some purposeful movement. The patient appeared to know her name and the hand grips were equal. Over the next two and a half days, she appeared better. On the evening of the third hospital day, the
pulse was again irregular, and the electrocardiogram revealed an ectopic atrial pacemaker, S-T segment depression and normal QT interval (tracing 2). Her blood pressure was stable. The pupils were equal and reactive. The movement of the right arm was definitely less than the left. On the basis of the decreased motion on the right and the again abnormal, electrocardiogram, it was determined to re-explore the patient and a large recurrent subdural hematoma was removed. Immediately following the surgery, the right arm was a little weaker, and the pulse had a sinus respiratory arrhythmia in contra-distinction to the previous ectopic atrial pacemaker. Thirty-six hours later she demonstrated some seizures of the right arm. The blood pressure increased to 158/90 and the pulse was 80 per minute. The electrocardiogram was normal (tracing 3). Pupils were small and equal, with weak reaction to light. The scalp flap was full. She was again re-explored but only 30 ml. of hematoma was removed. Later that evening she was responding to questions and her vital signs were stable. The following day she had a rightsided seizure of her face, and one report of general seizures thought to involve the left side more than the right. Her electrocardiogram remained normal. She was placed on diphenylhydantoin (Dilantin) and no further seizures were observed. The rest of the hospital course was unremarkable and she was discharged approximately one month after her injury with a mild right hemiparesis with right hyperreflexia throughout, bilaterally positive Hoffman response, right greater than left. She still had some memory deficit, but this showed steady signs of improvement. The patient has been followed up as an out-patient
Case 1 2
7 8 9 10
17 35 16
19 17 21
ELECTROCARDIOGRAPHIC CHANGES IN HEAD IN JURIES
*Age in years.
yes yes yes yes yel yea yes yea yel no no no no no no no
left subdural hematoma midbrain contusion hemorrhage left middle cerebral artery multiple lacerations of the brain midbrain contusion midbrain contusion lacerations of the brain stem bilateral cortical hemorrhage hemorrhage of left arterior cerebral artery multi-focal cortical hemorrhage cerebral concussion cerebral concussion occlusion of the left middle cerebral artery cerebral concussion midbrain contusion partial decerebration
recovered expired recovered expired expired expired expired expired expired expired recovered recovered recovered recovered recovered recovered
with complete return of the neurologic signs to normal, with her only remaining deficit being retrograde amnesia for a period of about one month before the accident, and occasional difficulty with some memory functions. She is, however, able to function quite normally in her role as a housewife. CASE
Diseases of the Chest
The second case is that of a 17-year-old boy who was admitted to the hospital following a head injury that occurred after he fell from the hack of a moving car and struck the posterior aspect of his head. He was rendered unconscious immediately. A physician at the scene of the accident noted a small laceration of the posterior occiput, blood pressure of 180/90 and a pulse of 82. Projectile vomiting occurred shortly after the injury. His pupils were noted to be normal and no localizing signs were seen. Upon his arrival at the hospital, he was found to have a pulse rate of 40 and a blood pressure of 170/90. He was a well developed and well nourished white boy in stuporous condition, intermittently arousable by noxious stimuli, spontaneously moving all extremities in a semi-purposeful manner, and demonstrating projectile vomiting of nonbloody material. Examination of the head revealed crusted blood in the left nasal passage, and red blood behind the left tympanic membrane. No blood or fluid was seen in the external auditory canal. There was an abrasion over the occipital region.
Examination of the heart revealed irregular bradycardia. Examination of the chest and abdomen was unremarkable as was the remainder of the general physical examination. On neurologic examination cranial nerves 2-7 were grossly intact. The examination of the cranial nerves 8, 9 and 10 revealed only that the patient was able to swallow and questionably able to hear loud sounds. Cranial nerve 12 was not tested. On reflex examination, the deep tendon reflexes were 2 plus bilaterally with positive Babinski responses. An electrocardiogram done one hour after the accident revealed a wandering atrial pacemaker with a rate of 50, peaked T -waves and prolonged QT interval (tracing 4). Serum electrolyte determinations at this time were normal. The patient was placed on observation, and over the next several days demonstrated excessive urinary output consistent with diabetes insipidus. Approximately two days after his entry to the hospital, following an initial period of some improvement, the patient's level of consciousness suddenly decreased and his vital signs deteriorated. He was taken to the operating room where burr holes were done following the induction of hypothermia. The cerebellum was under extreme tension, but no blood was found. In the occipital area a small collection of blood was found. The patient was then taken to the x-ray department where angiography revealed a depression of the right middle cerebral artery and elevation of the
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1: Serial electrocardiograms in two cases of severe head injury. Tracings 1, 2 and 3 are recorded from a 25-year-old housewife. Tracing one was recorded 30 minutes after admission, tracing two on the third hospital day and tracing three on the fourth hospital day. Tracing 4 and 5 are recorded from a 17year-old boy. Tracing four was recorded 30 minutes after admission and tracing five was recorded 12 days later.
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ELECTROCARDIOGRAPHIC CHANGES IN HEAD INJURIES
left middle cerebral artery. He was returned to the operating room where a right craniotomy was done. A small subdural hematoma was found over and just above the region of the island of Reil, The contents of the right temporal lobe were then removed to obtain better exposure, and section of the tentorium was carried out, at which time a subdural hematoma, approximately 2 cm. thick, was found on the surface of the tentorium. The right side was closed and a craniotomy then performed on the left side with only a small epidural hematoma being found, but the undersurface of the temporal lobe on the left was found to be markedly softened and bruised. Following the first surgical procedure, the patient showed slight improvement, and his condition remained extremely critical. Electrolyte changes were noted in the nature of increased serum sodium of 153 mgm. per cent with a serum potassium of 5.2 mgm. per cent. These were thought to be due to dehydration secondary to diabetes insipidus. The patient was maintained on hypothermia. He was also placed on hydrocortisone 21-sodium succinate (Solu-Cortef) therapy. A tracheotomy was done and intermittent positive pressure breathing was given. As the patient continued to show a downhill course, he was taken back to the operating room on the third hospital day and re-explored on the right side. The brain was massively swollen, and the margins of the old temporal lobe incision were greatly edematous. A small catheter was introduced into the ventricle, and brought out for the purpose of constant ventricular drainage via a bag. Decompression of the bone flap was carried out at this time, and the patient was kept on hypothermia. His course from this time continued to be steadily downhill. Serum electrolyte determinations at this time were: serum sodium of 151 mgm. per cent, serum potassium of 4.8 mgm. per cent and blood urea nitrogen of 84 mgm. per cent. On the twelfth hospital day, another electrocardiogram was taken which showed a prolonged QT interval and low T waves (tracing 5). Despite the vigorous supportive therapy, the attempts to regulate his electrolytes, artificial ventilation and hypothermia, the patient died on the fourteenth hospital day. A postmortem examination revealed: multiple skull fractures of the occipital and parietal bones, hemorrhagic necrosis of the frontal, occipital and temporal cortex and focal hemorrhage of the midbrain. DISCUSSION
It is well known that many areas of the brain can affect the electrocardiogram. There are several authors":" who have implicated the hypothalamus as playing a dominant role in cardiac hemodynamics.
While there was evidence of midbrain damage in the two cases reported, the electrocardiogram was only of limited value in localization of the cerebral lesion. The two cases reported are of interest, because the serial electrocardiograms paralleled the clinical course. In the first case, the electrocardiogram was grossly abnormal on admission. The electrocardiogram initially improved after the first craniotomy, but was still abnormal until a second craniotomy was performed and a recurrent hematoma was removed on the third hospital day. The electrocardiogram returned to normal immediately after the second craniotomy. It is on note that on the fourth hospital clay the patient had equivocal signs of progressing cerebral pathology and a normal electrocardiogram. A craniotomy performed at this time was unremarkable and the patient has made a full recovery. In sharp contrast is the second case, where the initial electrocardiogram was grossly abnormal and as the clinical course deteriorated, the electrocardiographic abnormalities were more marked. It is our impression that a single electrocardiogram is not of particular significance in evaluating the site of the lesion or clinical course in a head injury. However, serial electrocardiograms appear to parallel the .clinical course and may be a sensitive index and useful parameter to the physician in the management of these cases. SUMMARY
1. The serial electrocardiogram of two patients with severe head injuries are presented. 2. The electrocardiogram paralleled the clinical course. 3. It is suggested the serial electrocardiogram may be a sensitive index of the clinical course in a patient with head injury. REFERENCES
J. W. AND ROBERTSubarachnoid Hemorrhage Simulating Acute Myocardial Infarction," Amer. Heart I., 58: 755, 1959. 2 BYER, E., ASHMAN, R. AND TOHT, L. A.: "Electrocardiograms with Large Upright T Waves and Long Q-T Intervals," Amer. Heart I., 33: 796, 1947. 1
BEARD1 E. F., ROBERTSON, SON, R. C.: "Spontaneous
FALSETTI AND MOODY
3 BURCH, G. E., MEYERS, R. AND ABILDSKOV, J. A.: "A New Electrocardiographic Pattern Observed with Cerebrovascular Accidents," Circulation, 9: 719, 1954. 4 CROPP, G. J. AND MANNINO, G. W.: "Electrocardiographic Changes Simulating Myocardial Ischemia and Infarction Associated with Spontaneous Intracranial Hemorrhage," Circulation, 22: 25, 1960. 5 DELGADO, J. M.: "Circulatory Effects of Cortical Stimulation," Physiol. Rev. 40 (suppl. 4), 146, 1960. 6 FENTz, V. AND GORMSEN, J.: "Electrocardiographic Patterns in Patients with Cerebrovascular Accidents," Circulation, 25: 22, 1962. 7 FINKELSTEIN, D. AND NIGAOLIONI, A.: "Electrocardiographic Alterations After Neurosurgical Procedures," Amer. Heart I., 62: 772, 1961. 8 FUSTER, J. M. AND WEINBERG, S. J.: "Bioelectrical Changes of the Heart Cycle Induced by Stimulation of the Diencephalic Regions," Exp. Neurol., 2: 26, 1960. 9 GLASSER, R. L.: "Brain Stem Augmentation of Cardiovascular Activity," Amer. I. Physiol., 198:421, 1960. 10 HERSCH, C.: "Electrocardiographic Changes in Head Injuries," Circulation, 23: 853, 1961. II KORTEWEG, G. C., BOELES, J. T. AND TENCATE, J.: "Influence of Stimulation of Some
Diseases of the Chest
Subcortical Areas on Electrocardiogram," I. Neurophysiol., 20: 100, 1957. MANNINO, J. W., JR. AND PEISS, C. N.: "Cardiovascular Responses to Electrical Stimulation in the Diencephalon," Amer. I. Pkysiol., 198: 366, 1960. POOL, J. L.: "Vasocardiac Effects of the Cicle of Willis," .AMA Arch, Neurol. Psychiat., 78: 355, 1957. PORTER, R. W., KAMIKAWA, K. AND GREENHOOT, J. H.: "Persistent Electrocardiographic Abnormalities Experimentally Induced by Stimulation of the Brain," Amer. Heart I., 64: 815, 1962. ROSEN" A.: "Augmented Cardiac Contraction, Heart Acceleration and Skeletal Muscle Vasodilatation Produced by Hypothalamic Stimulation in Cats," Acta Physiol. Seandinau., 52: 291, 1961. SHUSTER, S.: "The Electrocardiogram in Subarachnoid Hemorrhage," Brit. H earl I., 22: 316, 1960. WEINBERO, S. J. AND FUSTER, J. M.: "Hypothalamic Control of Heart Function as Manifested in an Electrocardiographic Study," .A rch. Int. Phvsiol., 67: 699, 1959.
For reprints, please write: Dr. Falsetti, 6510 USAF Hospital, Edwards AFB, California.
Readers are inyited to submit articles for the Electrocardiogram of the Month. Please submit material to Stephen R. Elek, M.D., 465 North Roxbury Drive, Beverly Hills. Califomia.
EFFECT OF OXYTOCIN ON CARDIAC ARRHYTHMIAS On the basis of clinical and experimental studies
previously published on the abllity of oxytocin to Inhi bit some cardiac arrhythmias. this effect was further Investigated. The experlments were carried out In vivo In various animals and In vitro with Isolated rat and rabbit hearts. Since It would appear that the mechanism of arrhythmia is often adrenergic In nature. the possible Interaction of adrenaline and oxytocin was studied. with reference to a possible Inhibition by oxytocin of the beta receptors. In addition. the effect of oxytocln on blood pressure changes caused by adrenallne and other sympathomimetic amlnes was studied.
The results suggest that the effect of oxytocin Involves an antiadrenergic effect. Oxytocin potentiates the effect of adrenaline and other sympathomimetic amlnes on blood pressure. This can be explained as pharmacologic synergism and not a direct effect on catecholamine release from tissue stores. It would appear that the antiarrhythmic effect of oxytocin is of only limited practical significance. since It applies to some, not all arrhythmias. MORTAaJ, A. AND SIOU, G.: "Recherches sur L'effet de L'ocytocine dans Ies Arythmies Cardiaques;" Cor " VIISII, 7:110, 1965.
LONG TERM ANTICOAGULANT THERAPY A cooperative study to evaluate the effectiveness of long term anticoagulant therapy In patients recovered. from acute myocardial Infarction was begun In 1957 by representatives from a group of Veterans Administration hospitals. The patients were divided at random Into treated and control groups and were subsequently treated and observed aecording to a standard protocol. There were 359 patients In the control group and 388 patients In the anticoagulant
group. Analysis of prellminary results reveals a difference in the mortality rates in favor of those treated with anticoagulants. This difference is significant at probabillty value of 0.05 but not at 0.01. COOPERATIVE SroDY (Veterans Administration): "Longterm Anticoagulant Therapy after Myocardial Infarction," lAMA, 193:929. 1965.