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Electrocardiographic changes following electrically induced convulsions
ELECTROCARDIOGRAPHIC ELECTRICALLY EDWARD M.
XWNE,
CHANGES INDUCED
M.D.,
AND
CONVULSIONS
JOSEPH
CLETELXND,
FOLLOWING
L.
FETTEXMAN,
3l.D.
OHIO
the publication of our report dealing with the electrocardioSINCE graphic changes following metrazol-induced convu1sions,1 a new type of convulsant2 has been introduced for the treatment of certain psychoses. In this method a convulsion is produced by passing a high frequency alternating current between electrodes placed on either temple.” We refer to this technique as eleetro-coma therapy. Certain advantages of this method, such as ease of administration, more uniform reaction, and less violent convulsions, suggest that t,his form of treatment will largely replace metrazol. For this reason it seemedworth while to repeat our observations before and after electrically induced convulsions, and to compare them with those which o+ eurred when metrazol was used as the convulsant agent. Forty-two patients from the private psychiatric practice of one of us (J. I,. E’.) were selected for this study. All were suffering from major psychoses; depressions were the most common because of their favorable response to this form of therapy. The ages ranged from 19 to 71; the distribution by decades is shown in Table I. Electrocardiographic observations were made on each patient before and after a major convulsive seizure (lasting from 30 to 50 seconds). The three standard leads of the electrocardiogram were taken just preceding the application of the rurrent, and Lead II was again recorded immediately upon cessation of the convulsion, and at three, five, and ten minutes after the electric shock. Later in our study. a single apex lead was employed in addition to those ment~ione~l xhore. CHANGES
IX
BLOOD
PRESSURE
Blood pressure measurements were made coincidentally with the electrocardiograms whenever the patient’s cooperation would permit. In all but one instance there was a rise in the systolic pressure, and this was usually accompanied by a smaller increase in the diastolic. The mean increases were 30 mm. Hg for the systolic, and 9 mm. Hg for the diastolic. CHANGE,S
IN
HEART
RATE
An acceleration in cardiac rate was encountered in nearly all instances. If an arbitrary figure of twenty-five cycles per minute is From the Department of Medicine of Western Reservr University School of Mediand the Lakeside Hospital, Cleveland. *The instrument employed in this work was manufactured by Offner Electronics Corporation, Chicago, Illinois. In this machine the “dosage” may be varied by a change in the intensity of the current and the duration of its action. The maximum milliamperage is 700, and the time range from 0.05 to 1.0 second. In all cases the cine,
minimum level and
convulsant gradually
“dose” increasing
is ascertained either the
continued or increased slightly throughout Received for publication April 8, 1942.
by time
the
665
starting below or intensity.
course
the This
of treatments.
ordinary minimum
convulsant “dose”
is
666
AMERICAN
HEART
TABLE
JOURNAL
I
AGE DISTRIBUTION
Age in years Number of eases
10-19 2
20-29 5
30-39 12 TABLE
CHANGES CASE NO.
CONTROL
1.
105/75
2. 3. 4. 5. 6.
12Oj80 150/80 12O;SO
L 9: 10. 11. 12. 13. ii: 16. 17. 18. i: 21: 22. ii: 25. 26. E: 2: E: 2: 2 37: 38. 39. 40. 41. 42.
150/95 125/100 130/90 165/105 120/80 120/80 120/80 125/80 130/80 145/80 135/90 140/80 115/70 135JSO 130/75 120/75 160/85 140/80 135/80 140/75 llOJ60 115/70 HO/50 130/80 120/80 115/60 130/70 140/90 130/80 120/70 110/70 110/80 160/90 160/100 155/80 135/85 120/80
IMnIEDIATELY AFTER CONWLSION
140/75 150/90 210/90 160/80 120/70 185/100 150/105 155/95 215/110 140/85 130/90 140/75 140/85 135,'80 210/100 145/75 140/90 120/75 150/90 170/90 140/90 180/90 160/90 165/80 160/90 135/70 15OJ80 14OJ90 150/90 170/90 180/70 180/100 170/90 160/80 140/60 130/70 180/80 180/f 240/120 170/100 125/80
IN DECADES
40-49 11
50-59 6
60-69 5
70-79 1
II
IN BLOOD
PRESSURE
3 MIN.
5 MIN.
AFTER SHOCK
AFTER SHOCK
105/60
100/70 140/70
145/95
120/65
155/85 135/95 2lOJlOO 13OJ80 140/85 135/85 145/75 135/70 145/95 160/90 160/90
160/80 160/90 135/60 190/110 150/80 130/70
190/90 180/80 130180
10 MIN. AFTER SHOCK
180/100 125/75 130/80 170180 140180 130/70 140/90 150/85 140/70 150/90 150/95 130/75 130/80 135/70 160/90 14OJ80 140/70 140/75 110/60 13OJ50 130/70 150/100 175/90 150/80 125/70 - -
145/75 145/80 125/90 180/110 110/80 135190 120/70 125/60 130/70 135/60 120/75 140/90 130/70 15OJ80 145/75 140,'80 125/75 120/70 110/60 110/70 110/70 135/75 130/60 130/80 115/70 110/65 120/80 155/100 190/80 150/85 80/50
assumed to constitute a significant change, there were only ten cases in which the rate was not increased by this amount, and in only one was there a decrease. This is in contrast with the rates after metrasol therapy, when no consistent change occurred. Furthermore, there were none of the extremely .slow rates; the single bradycardia was of nodal origin, with a rate of 58 per minute.
KLINE
AND
FETTERMAN
:
CHANGES
ECG
IN
CHANGES
AND
CONVULSIONS
R,HYTHM
Contrary to the situation after metrazol convulsions, cardiac arrhythmias were not conspicuous. Although there was some change in cardiac rhythm (Fig. 1) in fifteen of the cases, in only two instances was the arrhythmia of a gross nature. These changes were usually present in the record taken immediately after the convulsion, and in all instances the rhythm had returned to normal in the 5-minute record. It can be seen from Table III that the arrhythmias were of two types: those produced by changes in the heart rate and location of the pacemaker; and those resulting from extrasystoles of various types.
668
AMERICAN
HEART
TABLE TYPE
Fig.
AND
FREQUENCY
JOURNAL
III OF ARRHYTHMIAS
Sinus arrhythmia (marked) Shifting pacemaker Atrioventricular rhythm Auricular extrasystoles Atrioventricular extrasystoles Ventricular extrasystoles Number of convulsions after Number of convulsions after
which the above observations which no significant arrhvthmia
Z.-Electrocardiograms
the
in
2 4 3 7
cases in abnormal.
which
the
were made was observed
cardiovascular
system
i 15 26
was
We cannot say definitely from these observations what mechanism is It seems probable that the responsible for the alterations in rhythm. changes in the location of the pacemaker were the result of vagal stimulation induced by the sharp rise in blood pressure which occurred in most instances.
KLINE
AND
FETTERMAN
:
CHANGES
ECG
IN
CHANGES
THE
AND
CONVULSIONS
669
T WAVE’
An increase in the amplitude of the T wave was encountered in all but eight of the eases. This increase in height was accompanied bp a change in contour; the wave hecame more pointed, and narrow at the base. These resembled the T waves after metrazol-induced convulsions. Since these changes are similar to those which occur in acidosiq3 the possibility exists (as in the case of metrazol) that t,here is a temporary acidosis immediately after the convulsion. This might he produced by the extreme muscular activity during a period when respiration is diminished or absent. Contrary to the observations of BelleV and his associates, we had no instances in which the T ware became inverted, or the S-T segment significantly elevated, after treatment. (‘.\SEG
IS
WHICII
THE;
CARDIOVARCUL.\R
SYSTEM
WAS,
AB;h;ORMAT>
There were five cases in this series in which the cardiovascular system was abnormal. In three cases, Nos. 9, 22, and 40, the patients had hypertension, and their electrocardiograms are shown in Fig. 2. Case 1 was that of a fifty-five-year-old woman who had had angina pectoris for many years, in whom Dr. Claude Beck had estahlished a collateral coronary bed by operation on July 30, 1937. In each of these patients the critical nature of the mental condition was such that the risk of treatment seemed justified. All were given the usual course of seizures without complication, and the electrocardiograms after treatment did not differ from those of other patients in this series. In this group we were particularly interested in knowing whether the convulsion might not be followed by a period of myocardia.1 anoxemia. Our attention was, therefore, directed to the S-T segment in the standard ant1 apex leads, but in no instance were these significantly altered Case 42 was that of a fifty-eight-year-old man with chronic valvular disease of rheumatic origin. He had mitral stenosis and insufficiency and moderate cardiac enlargement, hut there were no signs of cardiac failure. This, patient’s mental illness was extremely severe. He refused all food, and, in spite of forced feedings, he lost seven pounds in weight during his first week in the hospital. Twenty minutes after the patient’s first convulsion he perspired profusely, and became pale, cold, and clammy. The blood pressure, which, during the treatment, had heen in the neighborhood of IZS,/SO, fell at this time to 70/30. He was given 0.5 Gm. of caffeine citrate and two 0.3 cc. closes of adrenalin hydrochloride (1 :l,OOO dilution). In another twenty minutes t,he blood pressure had returned to its former level and he appeared normal again. The electrocardiogram at this time was identical wit,h the control record? taken before the seizure had begun. This reaction was different from anything we had seen before, and cannot he satisfactorily explained. Whether the peripheral vascular collapse was associated in some manner
670
AMERICAN
HEART
JOURNAL
with the cardiac lesion cannot be stated with certainty, but it seems rather unlikely. No late untoward results have developed, but treatment was not resumed. CONCLUSIO’NS
The electrically induced convulsion was followed by a rise in both the systolic and diastolic blood pressure, an increase in heart rate, and certain transitory electrocardiographic changes. The T waves of the electrocardiogram were increased in amplitude, and, in some eases, a change in rhythm was observed. These alterations in the cardiovascular system were less marked than those which occurred after metrazol-induced convulsions. R.EFRRENCES
1. Kline,
E. M., Fetterman, J. L., and Williams, G. H., Jr.: Electrocardiographic Changes Following Metrazol-Induced Convulsions, AIX. HEART J. 20: 702, 1940. Electric Convulsion Therapy in Mental 2. Kalinowsky, L., and Berrera, 8. E.: Disorders, Psychiatric Quart. 14: 719, 1940. 3. Barker., P. S., Shrader, E. L., and Ronzoni, E.: The Effects of Alkalosis and Acidosis Upon the Human Electrocardiogram, AM. HEART J. 17: 169, 1939. The tilectroeardiogram During Electric 4. Bellet, S., Kershbaum, A., and Fur&, W.: Shock Treatment of Mental Disorders, Am. J. M. Se. 201: 167, 1941.
XWNE,
CHANGES INDUCED
M.D.,
AND
CONVULSIONS
JOSEPH
CLETELXND,
FOLLOWING
L.
FETTEXMAN,
3l.D.
OHIO
the publication of our report dealing with the electrocardioSINCE graphic changes following metrazol-induced convu1sions,1 a new type of convulsant2 has been introduced for the treatment of certain psychoses. In this method a convulsion is produced by passing a high frequency alternating current between electrodes placed on either temple.” We refer to this technique as eleetro-coma therapy. Certain advantages of this method, such as ease of administration, more uniform reaction, and less violent convulsions, suggest that t,his form of treatment will largely replace metrazol. For this reason it seemedworth while to repeat our observations before and after electrically induced convulsions, and to compare them with those which o+ eurred when metrazol was used as the convulsant agent. Forty-two patients from the private psychiatric practice of one of us (J. I,. E’.) were selected for this study. All were suffering from major psychoses; depressions were the most common because of their favorable response to this form of therapy. The ages ranged from 19 to 71; the distribution by decades is shown in Table I. Electrocardiographic observations were made on each patient before and after a major convulsive seizure (lasting from 30 to 50 seconds). The three standard leads of the electrocardiogram were taken just preceding the application of the rurrent, and Lead II was again recorded immediately upon cessation of the convulsion, and at three, five, and ten minutes after the electric shock. Later in our study. a single apex lead was employed in addition to those ment~ione~l xhore. CHANGES
IX
BLOOD
PRESSURE
Blood pressure measurements were made coincidentally with the electrocardiograms whenever the patient’s cooperation would permit. In all but one instance there was a rise in the systolic pressure, and this was usually accompanied by a smaller increase in the diastolic. The mean increases were 30 mm. Hg for the systolic, and 9 mm. Hg for the diastolic. CHANGE,S
IN
HEART
RATE
An acceleration in cardiac rate was encountered in nearly all instances. If an arbitrary figure of twenty-five cycles per minute is From the Department of Medicine of Western Reservr University School of Mediand the Lakeside Hospital, Cleveland. *The instrument employed in this work was manufactured by Offner Electronics Corporation, Chicago, Illinois. In this machine the “dosage” may be varied by a change in the intensity of the current and the duration of its action. The maximum milliamperage is 700, and the time range from 0.05 to 1.0 second. In all cases the cine,
minimum level and
convulsant gradually
“dose” increasing
is ascertained either the
continued or increased slightly throughout Received for publication April 8, 1942.
by time
the
665
starting below or intensity.
course
the This
of treatments.
ordinary minimum
convulsant “dose”
is
666
AMERICAN
HEART
TABLE
JOURNAL
I
AGE DISTRIBUTION
Age in years Number of eases
10-19 2
20-29 5
30-39 12 TABLE
CHANGES CASE NO.
CONTROL
1.
105/75
2. 3. 4. 5. 6.
12Oj80 150/80 12O;SO
L 9: 10. 11. 12. 13. ii: 16. 17. 18. i: 21: 22. ii: 25. 26. E: 2: E: 2: 2 37: 38. 39. 40. 41. 42.
150/95 125/100 130/90 165/105 120/80 120/80 120/80 125/80 130/80 145/80 135/90 140/80 115/70 135JSO 130/75 120/75 160/85 140/80 135/80 140/75 llOJ60 115/70 HO/50 130/80 120/80 115/60 130/70 140/90 130/80 120/70 110/70 110/80 160/90 160/100 155/80 135/85 120/80
IMnIEDIATELY AFTER CONWLSION
140/75 150/90 210/90 160/80 120/70 185/100 150/105 155/95 215/110 140/85 130/90 140/75 140/85 135,'80 210/100 145/75 140/90 120/75 150/90 170/90 140/90 180/90 160/90 165/80 160/90 135/70 15OJ80 14OJ90 150/90 170/90 180/70 180/100 170/90 160/80 140/60 130/70 180/80 180/f 240/120 170/100 125/80
IN DECADES
40-49 11
50-59 6
60-69 5
70-79 1
II
IN BLOOD
PRESSURE
3 MIN.
5 MIN.
AFTER SHOCK
AFTER SHOCK
105/60
100/70 140/70
145/95
120/65
155/85 135/95 2lOJlOO 13OJ80 140/85 135/85 145/75 135/70 145/95 160/90 160/90
160/80 160/90 135/60 190/110 150/80 130/70
190/90 180/80 130180
10 MIN. AFTER SHOCK
180/100 125/75 130/80 170180 140180 130/70 140/90 150/85 140/70 150/90 150/95 130/75 130/80 135/70 160/90 14OJ80 140/70 140/75 110/60 13OJ50 130/70 150/100 175/90 150/80 125/70 - -
145/75 145/80 125/90 180/110 110/80 135190 120/70 125/60 130/70 135/60 120/75 140/90 130/70 15OJ80 145/75 140,'80 125/75 120/70 110/60 110/70 110/70 135/75 130/60 130/80 115/70 110/65 120/80 155/100 190/80 150/85 80/50
assumed to constitute a significant change, there were only ten cases in which the rate was not increased by this amount, and in only one was there a decrease. This is in contrast with the rates after metrasol therapy, when no consistent change occurred. Furthermore, there were none of the extremely .slow rates; the single bradycardia was of nodal origin, with a rate of 58 per minute.
KLINE
AND
FETTERMAN
:
CHANGES
ECG
IN
CHANGES
AND
CONVULSIONS
R,HYTHM
Contrary to the situation after metrazol convulsions, cardiac arrhythmias were not conspicuous. Although there was some change in cardiac rhythm (Fig. 1) in fifteen of the cases, in only two instances was the arrhythmia of a gross nature. These changes were usually present in the record taken immediately after the convulsion, and in all instances the rhythm had returned to normal in the 5-minute record. It can be seen from Table III that the arrhythmias were of two types: those produced by changes in the heart rate and location of the pacemaker; and those resulting from extrasystoles of various types.
668
AMERICAN
HEART
TABLE TYPE
Fig.
AND
FREQUENCY
JOURNAL
III OF ARRHYTHMIAS
Sinus arrhythmia (marked) Shifting pacemaker Atrioventricular rhythm Auricular extrasystoles Atrioventricular extrasystoles Ventricular extrasystoles Number of convulsions after Number of convulsions after
which the above observations which no significant arrhvthmia
Z.-Electrocardiograms
the
in
2 4 3 7
cases in abnormal.
which
the
were made was observed
cardiovascular
system
i 15 26
was
We cannot say definitely from these observations what mechanism is It seems probable that the responsible for the alterations in rhythm. changes in the location of the pacemaker were the result of vagal stimulation induced by the sharp rise in blood pressure which occurred in most instances.
KLINE
AND
FETTERMAN
:
CHANGES
ECG
IN
CHANGES
THE
AND
CONVULSIONS
669
T WAVE’
An increase in the amplitude of the T wave was encountered in all but eight of the eases. This increase in height was accompanied bp a change in contour; the wave hecame more pointed, and narrow at the base. These resembled the T waves after metrazol-induced convulsions. Since these changes are similar to those which occur in acidosiq3 the possibility exists (as in the case of metrazol) that t,here is a temporary acidosis immediately after the convulsion. This might he produced by the extreme muscular activity during a period when respiration is diminished or absent. Contrary to the observations of BelleV and his associates, we had no instances in which the T ware became inverted, or the S-T segment significantly elevated, after treatment. (‘.\SEG
IS
WHICII
THE;
CARDIOVARCUL.\R
SYSTEM
WAS,
AB;h;ORMAT>
There were five cases in this series in which the cardiovascular system was abnormal. In three cases, Nos. 9, 22, and 40, the patients had hypertension, and their electrocardiograms are shown in Fig. 2. Case 1 was that of a fifty-five-year-old woman who had had angina pectoris for many years, in whom Dr. Claude Beck had estahlished a collateral coronary bed by operation on July 30, 1937. In each of these patients the critical nature of the mental condition was such that the risk of treatment seemed justified. All were given the usual course of seizures without complication, and the electrocardiograms after treatment did not differ from those of other patients in this series. In this group we were particularly interested in knowing whether the convulsion might not be followed by a period of myocardia.1 anoxemia. Our attention was, therefore, directed to the S-T segment in the standard ant1 apex leads, but in no instance were these significantly altered Case 42 was that of a fifty-eight-year-old man with chronic valvular disease of rheumatic origin. He had mitral stenosis and insufficiency and moderate cardiac enlargement, hut there were no signs of cardiac failure. This, patient’s mental illness was extremely severe. He refused all food, and, in spite of forced feedings, he lost seven pounds in weight during his first week in the hospital. Twenty minutes after the patient’s first convulsion he perspired profusely, and became pale, cold, and clammy. The blood pressure, which, during the treatment, had heen in the neighborhood of IZS,/SO, fell at this time to 70/30. He was given 0.5 Gm. of caffeine citrate and two 0.3 cc. closes of adrenalin hydrochloride (1 :l,OOO dilution). In another twenty minutes t,he blood pressure had returned to its former level and he appeared normal again. The electrocardiogram at this time was identical wit,h the control record? taken before the seizure had begun. This reaction was different from anything we had seen before, and cannot he satisfactorily explained. Whether the peripheral vascular collapse was associated in some manner
670
AMERICAN
HEART
JOURNAL
with the cardiac lesion cannot be stated with certainty, but it seems rather unlikely. No late untoward results have developed, but treatment was not resumed. CONCLUSIO’NS
The electrically induced convulsion was followed by a rise in both the systolic and diastolic blood pressure, an increase in heart rate, and certain transitory electrocardiographic changes. The T waves of the electrocardiogram were increased in amplitude, and, in some eases, a change in rhythm was observed. These alterations in the cardiovascular system were less marked than those which occurred after metrazol-induced convulsions. R.EFRRENCES
1. Kline,
E. M., Fetterman, J. L., and Williams, G. H., Jr.: Electrocardiographic Changes Following Metrazol-Induced Convulsions, AIX. HEART J. 20: 702, 1940. Electric Convulsion Therapy in Mental 2. Kalinowsky, L., and Berrera, 8. E.: Disorders, Psychiatric Quart. 14: 719, 1940. 3. Barker., P. S., Shrader, E. L., and Ronzoni, E.: The Effects of Alkalosis and Acidosis Upon the Human Electrocardiogram, AM. HEART J. 17: 169, 1939. The tilectroeardiogram During Electric 4. Bellet, S., Kershbaum, A., and Fur&, W.: Shock Treatment of Mental Disorders, Am. J. M. Se. 201: 167, 1941.