Bauer, A. Robert

Howard, Philip J.

English

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Henry Ford Hospital Medical JournalVolume 10 | Number 4 Article 712-1962The Effect Of Degree Of Hypoxia On TheElectroencephalogram In Infants, IIA. Robert BauerPhilip J. HowardFollow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournalPart of the Life Sciences Commons, Medical Specialties Commons, and the Public HealthCommonsThis Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in HenryFord Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. For more information, please contactacabrer4@hfhs.org.Recommended CitationBauer, A. Robert and Howard, Philip J. (1962) "The Effect Of Degree Of Hypoxia On The Electroencephalogram In Infants, II," HenryFord Hospital Medical Bulletin : Vol. 10 : No. 4 , 573-588.Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol10/iss4/7Henry Ford Hosp. Med. Bull . Vo l . 10, December, 1962 THE EFFECT OF DEGREE OF HYPOXIA ON THE ELECTROENCEPHALOGRAM IN INFANTS, II A . ROBERT BAUER, M . D . A N D P H I L I P J. H O W A R D , M . D . * L E V E L S OF HYPOXIA frequendy occur in newborn or young infants due to birth injury of the central nervous system, congenital deformity of the lungs, or heart, atelectasis or hyaline pneumonia, anemia, or to multiple conditions. Studies have been made to relate the level of oxygenation to the EEG. The purpose of this report is to supplement our original paper with a more complete presentation of the data for those who desire further details.^ M A T E R I A L A N D M E T H O D S Material and methods have been previously described.' Of the 14 cases of degrees of hypoxia described, charts were shown for only cases 3 and 7. Charts for cases I , 2, 4 to 6, and 8 to 14 are therefor included in this report. As stated before, each of these cases showed an increase in oxygen saturation of at least 10 percent between the minimum and maximum levels. Also in addition the electrograms are reproduced for cases 4, 6, 8, 9, 11, 12 and 14. Studies on seven normal newborn infants were carried out for the effect of CO2 on the EEG. Inasmuch as the chart of only one has been published previously,' those of the other six are included here. The type of waves has been shown in the form of a graph expressing the space occupied on an EEG tracing by each type of wave. For instance, a 1 per second wave is a 30 mm wave, a 2 per second wave is a 15 mm wave, etc. To show the space occupied by a given wave, we counted the number occurring in a 10 second sample of the EEG. and multiplied this figure by the number of millimeters characteristic of that wave. The resultant product was designed as summation value and was plotted on the graph as a vertical column using black for the slow (1-4 per sec.) waves, and cross hatched for the more rapid (5-10 per second) waves. No attempt has been made to chart waves over 10 per second, and our conclusions are based on 1-4 per second waves only. The ordinate represents this sum.mation value and the abscissa the wave type. *Department of Pediatrics, Henry Ford Hospital. 573 BAUER AND HOWARD 2 3 4 5 6 8 10 1 2 3 4 5 6 8 10 Number of Waves Per Second Chart 1 Analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 4 days. Lesion low tricuspid valve, divided right ventricle, interauricular defect. Time between observations 14 minutes. I 2 3 4 5 6 8 10 I 2 3 4 5 6 8 10 Number of Waves Per Second Chart 2 .Analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 24 days. Lesion interventricular defect, transposition of great vessels. Time between observations 25 minutes. LOW OXYGEN SAT 7 5 % It 11-4 PER SEC WAVES ";5-lOPER SEC- WAVES HIGH OXYGEN SAT 85 % 1 r ' ; CHART EM 2 3 4 5 6 8 10 I 23 4 5 6 8 10 N u m b e r of Waves Per Second Chart 5 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 16 days. Lesion transposition of great vessels. Time between observations 13 minutes. 574 EFFECT OF DEGREE OF HYPOXIA 70 a z o ^ 6 0 1/) o 7 5 0 X i 4 0 UI _ i a 30 § 2 0 2 10 I 1-4 PER SEC. WAVES 35-10 PER SEC WAVES LOW OXYGEN SAT. 55 7o HIGH OXYGEN SAT, 75 % I 2 3 4 5 6 8 10 12 3 4 5 6 Number of Waves Per Second Chart 10 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 9 days. Le-Sion situs inversus, levocardia. Time between observations 38 minutes. 90 S 80 J 1 70 S 2 60 ° 5 50 = S 5 40 o 2 1 30 I 20 I 10 0 65 SO • |.4 PER SEC WAVES 5-10 PER SEC WAVES LOW OXYGEN SAT 86 % C H A R T 13 HIGH OXYGEN SAT 97 % I 2 3 4 5 6 8 10 ' I '2 '3 '4 '5 '6 '8 ' ld Number of Waves Per Second Chart 13 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 25 days. Lesion ventricular septal defect. Time between observations 4 minutes. 575 BAUER AND HOWARD C H A R T 4 I 1-4 PER SEC WAVES I 5-10 PER SEC. WAVES LOW OXYGEN SAT. 7 5 % HIGH OXYGEN SAT 85 % I 2 3 4 5 e e io Chart 4 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 18 days. Lesion transposition of great vessels. Time between observations 18 minutes. 4 5 6 8T0 Number of Waves Per Second LF LP LO LF LP L3' LT RT E E G # 4 (For Chart 4 ) B. H igh Oxygen 576 B 1-4 PER SEC. WAVES 8 0 ^ 5-10 PER SEC, WAVES LOW OXYGEN SAT 60 °/„ EFFECT OF DEGREE OF HYPOXIA 100 r I C H A R T 6 HIGH OXYGEN SAT 76 % Chart 6 An analysis ot waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 150 days. Lesion transposition of great vessels. Time between observations 12 minutes. . wm 2 3 4 5 6 8 10 I 2 3 4 5 6 8 10 Number of Waves Per Second \f^' 577 i BAUER AND HOWARD 1 1 - 4 PER SEC. WAVES [~]5-I0 PER SEC. WAVES ' 00 80 LOW OXYGEN SAT 65 % HIGH OXYGEN SAT 7 6 % Chart 8 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 16 days. Lesion interauricular defect, pulmonary hy-pertension interventricular defect. Time be-tween observations 26 minutes. I 2 3 4 5 6 8 10 ' \'Z'3'4'5'6'e'ld Number cf Waves Per Second RT E E G # 8 (For Chart 8) A. Low Oxygen RT E E G # 8 (For C h a r t s ) B. High Oxygen 578 90 oBO-J i70 LOW ( SAT o ; 5 0 1^ 40 O S I 30 5 ^ 2 - 2 0 . m m \m 1 10 1 2 3 4 5 6 EFFECT OF DEGREE OF HYPOXIA CHART 9 1-4 PER SEC WAVES 5-10 PER SEC WAVES HIGH OXYGEN SAT 75 % Chart 9 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant same as #8, aged 83 days, time between observations 11 minutes. I 2 3 4 5 6 8 10 Number of Waves Per Second 603 E E G # 9 (ForCharf9) A. Low Oxygen LO \ LT RF EEG#9 (For ChortS) B. High Oxygen^ 579 BAUER AND HOWARD HIGH OXYGEN SAT 99 % Chart 11 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 83 days. Lesion tetralogy of Fallot. Time between observations 5 minutes. I 2 3 45 6 8 10 Number of Waves Per Second LF I? I 2 3 4 56 a 10 EEG #11 (For Chart II) A. Low Oxygen EEG# II (For Chart 1!) B. High Oxygen 580 EFFECT OF DEGREE OF HYPOXIA HIGH OXYGEN SAT 9 5 % Chart 12 An analysis of waves in a 10 second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 88 days. Lesion anomalous venous return. Time be-tween observations 9 minutes. I 2 3 4 5 6 8 10 1 2 3 4 5 6 8 10 Number of Waves Per Second L F RF RP A RT, E E G # 12 (For Chart 12) A. Low Oxygen Lf LP J „>.i,V.T E9J .A.-LD 5AVAy--^^A:V^'AA^>/^.'-.A E E G # 12 (For Chart 12) B. High Oxygen 581 BAUER AND HOWARD ^ 1-4 PER SEC WAVES f;"]5-10 PER SEC WAVES C H A R T 14 LOW OXYGEN SAT 8 6 % HIGH OXYGEN SAT 97 % 5 6 8 10 r2 '3 '4 '5 '6 '8TS Number of Waves Per Second Chart 14 .An analysis of waves in a 10 .second EEG in low oxygen compared with a 10 second EEG in high oxygen. Infant aged 30 days. Lesion transposition of great vessels. Time between observations 11 minutes. R-p E E G # 14 (For Chart 14) A. Low Oxygen LP LD 081 RT E E G # 14 (For Chan 14) B. High Oxygen 582 EFFECT OF DEGREE OF HYPOXIA I i -4 PER SEC. WAVES \ 5-10 PER SEC. WAVES CHART IT OXYGEN ONLY 10 45 AM. OXYGEN PLUS CO^ 10:50 AM 1 2 3 4 5 6 8 10 1 2 3 4 5 6 8 10 Number of Waves Per Second lOXYGEN ONLY :00 AM. B1-4 PER SEC. WAVES 5-IC PER SEC WAVES '•'/. OXYGEN PLUS W CO, II 12 AM A j I I 2 3 4 5 6 8 10 "\ '2'3'4 5 ' 6 ' 8 id Number of Waves Per Second 9 0 S 80 C i 70 3 ° 60 5 40 1 ° Si 30 3 z ? « 20 \ 10 0 I 1-4 PER SEC WAVES Q 5-10 PER SEC WAVES OXYGEN ONLY 10 39 A M OXYGEN PLUS CO, 10 4 4 A M 1 2 3 4 5 6 8 10 1 2 3 4 5 6 8 10 Number of Woves Per Second 105 " 80 t 3 70 I " 3 5 60 si °^ ' «. 40 ^ i 3 0 a ^ I ^ 20 * 10 I 1-4 PER SEC WfiVES 1 5-10 PER SEC. WAVES OXYGEN ONLY 10 52 A.M i CHART OXYGEN PLUS CO, II ' 02 A M I Number of Waves Per Second Charts 17, 18, 21, 22 Analyses of waves in a 10 second EEG while giving 100% oxygen compared with a 10 second EEG while giving 95% oxygen and 5% COj. Normal infants. Blood oxygen saturation stable at 99-100% throughout. Improved with COj. 583 BAUER AND HOWARD OXYGEN PLUS CO, 11:30 AM 1 2 3 4 5 6 8 10 1 2 3 4 5 6 1 Number of Waves Per Second I 2 3 4 5 6 a 10 '1 '2'3'4 5 6 B 10 Number of Woves Per Second Charts 19, 20 Analysis of waves in a 10 second EEG while giving 100%' oxygen compared with a 10 second EEG while giving 95% oxygen and 5% CO2. Normal infants. Blood oxygen .saturation stable at 99-100% throughout. Impaired with COj. EEGs Unipolar technique used. Reference point in each case is the symmetric ear, left points to left ear, right points to right ear. The calibration is constant throughout this series of EEGs. EEGs 4, 6, 8, 9, 11, 12, 14 Basic EEGs for corresponding charts. DISCUSSION The variation of the EEG from normal through slow waves to electrical silence may sometimes be seen in a short segment of tracing. These changes from 15 to 30 waves per second through progressively slower waves of 1 to 4 per second to gross irregularity and silence are the accompaniment of increasing hyoxia to a final state of anoxia. Three samples of this series of changes seem so important and interesting that they are reproduced here by permission of the authors and publishers, Borkowski and Bernstine,^ Gastaut and Gastaut,' and Gronquist, Seldon and Falconer.'' Borkowski and Bernstine^ studied immature fetuses by the EEG as the supply of oxygen diminished to none, and demonstrated the progression from normal waves to slow irregular waves, and finally to electrical silence. It is evident as shown in Plate 1, taken with the legend from their report, that there is a deteriorating spectrum of activity in decreasing oxygen supply to the point of electrical silence. Studies during induced cardiac standstill, and during certain anesthetic accidents show also the effect of increasing anoxia although other factors also are involved. Gastaut and Gastaut^ in their study of 174 convulsive children found certain ones in whom a typical seizure could be reproduced by vagal stimulation. This provided a chance to obtain an EEG shown in Plate I I during a prolonged cardiac arrest of 18 seconds. A few seconds of minimal EEG activity were followed by 584 EFFECT OF DEGREE OF HYPOXIA H r Fig. 1 A 77 d«7 old fetus, length 62 EB. Fig. 2 Aatua A5 Jays old, length 16 mm. Fig. 3 SaiT« fetus as f i g . 2. From BorkoMski, Neurology 1955. Plate 1. (From Borkowski)'' Figure 1 A 77 day old fetus, CR length 62 mm. All bipolar readings from fronto-parietal areas. (40) a. recording from surface of head, superficially placed electrodes, (depth of 3 mm). (50) b. irregular rhythm. (57) c. diminished activity. Deeply placed electrodes (depth of I cm). (70) d. usual rhythm. (74) e. usual rhythm. (80) f. diminished activity (85) g. paroxysmal bursts of slow activity. (90) h. end of activity. (Numbers in parenthesis represent time in minutes) after ligation of blood supply to fetus. Figure 2 A fetus 43 to 45 days old, CR length 16 mm. All bipolar leads from fronto-parietal areas. Super-ficially placed electrodes (depth 3 mm). (30) a. usual ihythm. (35) b. paroxysmal discharge of slow activity. (42) c. sleep spindles. (65) d. diminished activity. Electrocardiogram at corresponding time is seen below each line of EEG. Figure 3 Same fetus as Fig. 2. All bipolar readings from fronto-parietal areas. Deeply inserted electrodes (depth of I cm) (72) a. usual activity. (72) b. usual activity. (74) c. paroxysmal discharge of slow activity. (74) d. marked slowing of EKG with irregularity of rhythm. (80) e. diminished activity with occasional fast wave discharge. (77) f. very occasional EK(j seen; (78) g. absence of activity (78) h. absence of EKG. complete recovery. Gronquist, Seldon and Falconer'' give an example of recovery after unexpected breathing arrest as a complication of anesthesia, the EEG tracing of which is reproduced. It shows recovery although the EEG record had progressed to a "considerable decrease in wave forms". This tracing is reproduced in Plate I I I . It will be noted that tracing B is marked only by one 1-per-second wave upon which are superimposed 6 fine waves. There were also two fine waves near the start and 2 near the end, with periods of electrical silence interspersed which constituted most of this record. The patient then went on to a clinical recovery from this serious condition. Torres, Frank, Cohen, Lellehei and Kasper' relate the EEG changes during cardiac arrest to increasing hypoxia in six stages; 1. no slowing below 4-6 per second; 585 BAUER AND HOWARD HENRI GASTAUT and YVETTE GASTAUT E E G C l i n . P h y s i a l . 10:609 1958 Plate 2 (From Gastaut)' With cardiac standstill slow EEG waves increase, become slower, and irregular and stop, and then sf.;rt again as slow irregular waves progressing to normal. 2. occasional slowing below 4-6 per second; 3. slowing to 1-3 per second for short infrequent periods; 4. slowing to 1-3 per second for prolonged or repeated periods; 5. slowing to 1-3 per second for prolonged and repeated periods and showing decreasing amplitude; 6. periods of electrical silence. The EEG spectrum of increasing hypoxia in the newborn infant differs from that obseired in the adult due to relative immaturity of the cerebral cortex in the infant. Because of this the newborn infant has central nervous system functions of 586 EFFECT OF DEGREE OF HYPOXIA Plate 3 (From Gronqvist) A 6-second EEG sample taken in a patient unconscious as a result of an anesthetic accident 1-Vi hours previously in which she was apnoeic and cyanotic for about 6 minutes. Patient made complete clinical recovery. a lower subcortical level which are characterized in the EEG by a production of relatively more slow waves. These in turn are subject to considerable variation being readily influenced by arterial oxygen saturation plasma CO2, blood glucose, level of sleep, and less importantly by factors such as muscular contraction. In fact, Bernstine, Borkowski and Price' have shown in their study of fetal EEGs that 23 of 32 had waves as slow as V2 per second, subjects in whom sleep should not be interfering, but the other factors may be operative. Even though the EEG pattern should parallel the oxygen saturation, within the limits of these observations, based on a 10 percent change in oxygen saturation, the authors were unable to show it in a predictable way. Admittedly none of our cases showed the low oxygen saturation level of 40 percent suggested by Clowes, Kretchmer, McBurney and Simeone' as the level below which EEG changes due to hypoxia become evident. SUMMARY An attempt was made to employ EEG techniques to determine the effect of relative hypoxia on brain cells of newborn or young infants. The cases consisted of fourteen infants aged one week to five months who were suffering from congenital heart disease and had oxygen saturations of 49 percent to 88 percent. Administration of oxygen 587 BAUER AND HOWARD caused an increase of saturation to levels of 65 to 99 percent which reflected an increase of at least 10 percent in each infant from lowest to highest level, over a period of 4 to 38 minutes. EEG tracings were taken at the lowest and highest attained levels. The results showed that 6 infants had a decrease in slow waves (1-4 cps) inter-preted as improvement, whereas eight had an increase interpreted as impairment. The effect of carbon dioxide on the EEG tracing was studied by administering 5 percent carbon dioxide in 95 percent oxygen to infants who were already in 95 percent oxygen. This was done in seven infants, five of whom showed a decrease in 1-4 cps, the other two demonstrating an increase. We concluded that an increase of oxygen saturation of 10 percent at the levels studied did not produce indisputable evidence of improvement in EEG tracings. REFERENCES 1. Howard, P. J., and Bauer, A. R.: The effect of degree of hypoxia on the electroencephalogram infants. J. Pediat. 61:511, 1962. 2. Borkowski, H. J., and Bernstine, R. L.: Electroencephalography of the fetus, Neurology 5:362, 3. Gastaut, H., and Gastaut, Y.: Electroencephalographic and clinical study of anoxic convulsions in children, Electroencept. Clin. Neurophysiol. 10:607, 1958. 4. Gronqvist, Y. K. J., Seldon, T. H., and Faulconer, A., Jr.: Cerebral anoxia during anesthesia, prognostic significance of electroencephalographic changes. Ann. chir. gyn. fenn. 41:149. 1952. 5. Torres, F., Frank, G. S., Cohen, M. M., Lillehei, C. W., and Kaspar, N. : Neurologic and electroencephalographic studies in open heart surgery, Neurology 9:174, 1959. 6. Bernstine, R. L., Borkowski, W. J., and Price, A. H.: Prenatal fetal electroencephalography, Am. J. Obst. & Gynec. 70:623, 1955. 7. Clowes, G. H. A., Jr., Kretchmer, H. E., McBurney, R. W., and Simeone, F. A.: The electro-encephalogram in the evaluation of the effects of anesthetic agents and carbon dioxide accumulation during surgery, Ann. Surg. 138:558, 1953. 588 

The Effect Of Degree Of Hypoxia On The Electroencephalogram In Infants, II

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The Effect Of Degree Of Hypoxia On The Electroencephalogram In Infants, II

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