cardiovascular following electro-convulsive · tillotson (1947) have noted increased venous...

CARDIOVASCULAR CHANGES FOLLOWINGELECTRO-CONVULSIVE THERAPY

BY

RALPH KAUNTZE AND GERALD PARSONS-SMITH

From St. George's Hospital

Received January 7, 1948

Electro-convulsive therapy was first used exten-sively in 1939, and with such success that three yearslater Kolb and Vogel (1942) in a survey ofthe UnitedStates reported its use in 42 per cent of mentalhospitals and in the treatment of 2-3 per cent of allmental hospital patients; this latter group wascomprised of the schizophrenias, the manic-depres-sive states, involutional melancholias, and the psycho-neuroses. As convulsant treatment is now ofestablished value in the affective neuroses and aselectric shock has largely superseded insulin andmetrazol as a convulsant, it seemed pertinent toattempt some assessment both clinically and electro-cardiographically of its effect on the cardiovascularsystem. These observations consisted of a clinicalhistory (which by the nature of the psychiatriccondition was not always complete), a routineexamination of the cardiovascular system andelectrocardiograms (standard leads only) bothbefore and after the convulsion. The secondcardiogram was taken in the recovery phase directlyafter the clonic movements had ceased; in someinstances there was slight delay due to uncontroll-able spasmodic movements. The patients in thisseries were not specially selected; a quarter wereobserved during their initial treatments.The convulsant apparatus used was that of Strauss

and MacPhail (1946), which by means of a rapidlydischarging condenser yields the higher voltages atthe start, thereby overcoming the initial resistance,and as only minimal energy is then necessary toinduce the fit, the equally rapid damping minimizessubsequent neuronic bombardment. The timefactor is therefore of less importance and the dosageis reckoned in Joules or total energy rather than inin volts: this varies according to weight and generalfragility; the usual dosage in this series was 18 Joulesdiphasic. A monophasic discharge yields a quieterrecovery but is less certain in inducing a convulsion.The electrodes, soaked in 20 per cent saline, are

applied to the temples, anterior to and a little abovethe external auditory meati. The duration of theshock is, variable, lasting about 0 35 sec.; uncon-sciousness is instantaneous and is succeeded by atonic phase, thence a clonic phase, which in turn isfollowed by exhaustion and relaxation or irritability,from which consciousness is recovered in from fourto fifteen minutes-a consciousness clouded by dis-orientation and amnesia. Occasionally the shockmay produce a " stun" only, the patient remainingconscious. Successive "-stuns " may induce cardio-vascular collapse. The average duration of thetonic phase, as observed in 22 patients, was 16seconds, of the clonic phase 25 seconds. Thelength of the tonic period bore no relationship tothat of the clonic. Directly after the shock oxygenwas administered by mask, and as the tonic phase isshort, cyanosis was not observed.

REsuLTsFifty-one patients, of whom 38 were women and

13 men, were observed before and after 63 electro-convulsions. The presenting psychiatric symptomin 82 per cent was depression. The average findingsin pulse rates and blood pressures are set out inTable I. In seven instances the pulse rate followingthe convulsion remained unchanged or was de-creased; in the main there was considerable increase.The systolic blood pressure following the con-

vulsion was elevated in about a third, showed nosignificant change (systolic ±I10 mm., diastolic ±5mm.) in a third and was actually lowered in theremainder. Where an increase occurred, this layusually between 20 and 35 mm. and was accompaniedin under a third, by a small fall in the diastolic read-ing. The maximum increase .was 55 mm., from135/70 to 190/95 in a man, aged 27, who displayedmarked restlessness and considerable tachycardia.However, restlessness with tachycardia was not in-variably accompanied by a rise in the blood pressure.

57

on April 28, 2020 by guest. P

rotected by copyright.http://heart.bm

j.com/

Br H

eart J: first published as 10.1136/hrt.10.1.57 on 1 January 1948. Dow

nloaded from

http://heart.bmj.com/

BRITISH HEART JOURNAL

TABLE IPULSE RATE AND BLOOD PRESSURE AFTER ELECTRO-CONVULSIVE THERAPY

Age Pulse rates after convulsion Blood pressure

Nos. Ex- In- Un- De- Av. in- iAverage Insigni- De-Nos. ~~Ex- In- Un- De- Av.nn-__De-__Average tremes creased changed creased crease per creased ficant c

minute Before After change t

Women38 433 24-69 34 3 1 23 150/91 147/87 12 12 14

9 47 24-62 7 1 1 17 145/90 135/81 1 4 4

Men13 43-6 26-62 12 - 1 27 129/80 136/75 4 6 3

3 46 27-62 3 - - 32 145/83 173/98 2 1 -

* = Subsequent records t = Systolic pressure IO mm., diastolic +5 mm.

The decrease in blood pressure lay within a similarrange: the greatest fall was from 185/100 to 120/80and is probably, in part, a measure of anxiety.

Three patients with severe hypertension showedslight elevation of the systolic or diastolic levels orboth.None of these patients had curare before the

electroplexy and it was not possible to take theblood pressure during the convulsion. As thecardiogram was taken first, there was a slight delaybetween the end of the fit and the recording of theblood pressure, during which it was thought thatthe readings might have been considerably raised.Preliminary observations of patients who have hadcurare and pentothal show a small initial fall andthen following the convulsion there may be no

considerable rise in systolic pressure, or where an

increase occurs, this may be delayed for a minute,or two and has not been excessive (Fig. 1). Withcurare in the usual dosage, there is some movementof the arms in the clonic stage, which makes a bloodpressure reading usually impossible. In one patient,who had five consecutive shocks in twenty minutes,it was possible to record the blood pressure duringone clonic stage (Fig. 2): the systolic level was

raised 20 mm. and remained so for 45 seconds afterthe convulsion had ceased. If sufficient curare isgiven to abolish all movement of the arms, then thelikelihood of anoxia from paralysis of the respiratorymuscles may make the blood pressure readingsunreliable.

Hypertension was the commonest abnormal find-ing in routine examination, being present in 1 man

and 14 women (29 per cent); the upper limit ofnormality was arbitrarily taken as 155/95 at restand on repetition. It may be suggested that these

levels are too low in the circumstances, but thepatients were rarely agitated or indeed alarmed atthe thought of the approaching convulsion forwhich there is subsequent amnesia. Of these 15hypertensives, 12 were mild to moderate and 3 wereconsidered severe (above 220/130); one of theselatter had commencing right ventricular failure.Two patients suffered from bronchial asthma ofmoderate degree. One patient had chronic bron-chitis with early right-sided failure and one was achronic alcoholic. In no patient was there historyof cardiac pain on exertion or suggestive of aprevious infarction.

z

yU

0

a.

y

0

a, 110r )__E1_

L 90-

co

U) 70- _

% UI

% 0i%

Time in minutes

0 2 3 4 5 6 7' 8 9 10_: < W,, Z

0 cc O

Zo O

FIG. 1.-Systolic blood pressure during two convulsionsunder pentothal 0 5 g. and curare 30 mg. in a managed 45. The second record is in dotted lines.

58

-



j.com/

Br H


nloaded from


ELECTRO-CONVULSIVE THERAPY

ISYSTOLIC \

i :8 VU) .

DIASTOLIC ^ () NxICu \

0i X 1(1)Q1 I

1)

O IZO 2(

I

I .

I: e \ cU)

sI

'T'i 2 3 4 s6789 11231116 1718 192 02PENTOTHAL 0.4gm. Time in minutesCURARE 15 mgm

FIG. 2.-Blood pressure records in a girl aged 27 duringfive consecutive convulsions under pentothal 0-4 g.and curare 15 mg.

Although the motor discharge varied considerablyfrom patient to patient, persistently raised cervicalvenous pressure following the convulsion was notobserved. However, Altschule, Sulzbach, andTillotson (1947) have noted increased venous pres-

sure during the convulsiQn and slight elevationsubsequently, less evident in patients given curare.The cardiographic changes following convulsion

are summarized in Table H: the main features areincrease in the height of the P wave in lead II,

prolongation of the P-R interval, increase in theamplitude of the T waves in leads II and III, andless frequently diminution of R I and depressionof S-T II (see Fig. 3).An increase in P II was present in 61 per cent of

patients, the increment ranging from very slight upto 1 5 mm.; this was reflected to a lesser extent inlead III (31 per cent). The P-R interval was

lengthened in 52 per cent; this was invariablyassociated with an elevation of P II, although theconverse was not necessarily so. No gross pro-longation was found, the increase lying between 0 02and 0 06 sec.R I was diminished in size in 29 per cent; the

most marked reduction was -5 mm. This diminu-tion was not accompanied by any constant changein the complex, nor was it consistently present onrepetition of the cardiogram after subsequentconvulsions.

Depression of the S-T segments occurred chieflyin lead II, was slight in extent, and present in 29 percent. Elevation of the T waves was noted in lead IIin 55 per cent and in lead III in 41 per cent; the

LE II

ELECTROCARDIOGRAPHIC CHANGES FOLLOWING ELECTRO-CONVULSIVE THERAPY.

Nos. PI PII PIII P-R RI I-TII S-T III TI TII TIII

+ +_+ +- - _- +-_ +_ +-_Women

38 2 22A IOA 22 1 3 14 8 6 0 4 18 4 15 2

In subsequentconvulsions

9 1 3 3 3 0 0 5 4 2 1 0 4 1 5 0

Men13 2 9 6 4 0 4 1 7B 4 1 1 10 0 6 0

In subsequentconvulsions

3 0 3 0 1 1 2 0 0 0 0 0 1 1 1 1

TotalsPercentage(51 cases) 8o% 61%| 31% 52% 2% 14% 29% 29% 20% 2% 10% 55% 8% 41% 4%

After standard exercise in healthy young menPercentage(6 cases) 50%0 33% 0% 33% - 17% 67% - - - 67% 0% 50% 0%

ISO.

i45-

140-

135'

130-

125-

|20-

* 110-E 10E ios-- 100-14C, 950 90-

0. 85-

o 80-0

59

A = P 11 and P III were decreased in one patient. B = S-T II was elevated in one patient.



j.com/

Br H


nloaded from


BRITISH HEART JOURNAL

1s1:1-: T I- i:

A C D

FIG. 3.-(A) before, (B) directly after the convulsion showing increase in P II and P III and slight lengtheningof the P-R interval. (C) before, (D) directly after.the convulsion showing increase in T II and T III.

increase in height was usually greater in lead IIvarying between 0 5 and 2-5 mm.Among less frequent changes were increased

prominence of S II and S III in 5 patients, intra-ventricular delay in two patients unassociated withprolongation ofthe P-R interval; 12 patients showedpremature beats, in 4 of whom they were observedonly after the convulsion, these consisted of auri-cular, nodal, and ventricular premature beats.Where subsequent cardiograms were taken the

pattern had reverted to the original ten minuteslater.

DIscUSSIONIncreased amplitude of P II and T II and slight

downward displacement of S-T II together withtachycardia are all encountered in the healthy adultfollowing exercise (Table II), and seem best ex-plained as the result of those processes entailed inmuscular activity. As to the decrease in size ofR I, this with a trend to right axis deviation is alsoan accompaniment of exercise in a proportion(Wood and Wolferth, 1931), perhaps more frequentin the less fit psychiatric patients. P II elevationpresumably indicates some degree of right heartstrain. Some further explanation is necessary forthe slight prolongation of the P-R interval, en-countered in 52 per cent, as opposed to the shorten-ing frequently accompanying increase in the heartrate, as also for the occurrence of intra-ventriculardelay. That this slowing of A-V or bundle branchconduction, in the presence of tachycardia, is dueto vagal action seems most unlikely.

Two patients previously showing some lengthen-ing of the P-R interval following convulsion, weregiven atropine 1/50 of a grain before a subsequentfit and in both instances the P-R delay was againpresent (Fig. 4). Two further possibilities presentthemselves, firstly, that the lowered conductivity iscaused by anoxia or secondly, is an after-effect ofadrenaline. Anoxia produces increase in excursionof the P waves, the P-R interval may be lengthened.the S-T segment may be depressed and the T waves

z+ A -i- L L4-4 f

s75g mSt _ v:~~~~~L

i -I ---- ---

A B

FIG. 4.-Atropine gr. 1/50, followed 20 minutes later byE.C.T. (A) before, (B) directly after the convulsionshowing increase in P II and P III and slight pro-longation of the P-R interval.

L1- II 4f..1iit.T 1: .I"I, - 4 1 i 1. .'k

I I IL ..", : t.,: :1 , :: I ,i:: :,: .' I.R.-

. I

,. r._

4..,

,1 " ,I :1

60

- - - ...... -.1-1 Ir



j.com/

Br H


nloaded from


ELECTRO-CONVULSIVE THERAPY

lowered (Graybiel and White, 1946). Although thetonic phase of the convulsion is short and oxygen isadministered from the beginning, and althoughcyanosis has not been remarkable, the possibilityof anoxia being a factor in the production of thelowered conductivity of the bundle cannot be ex-cluded. Alternatively, adrenaline in the experi-mental animal (cat) may produce partial heart blockand bundle branch block after the preliminaryacceleration; this, of course, in hyper-physiologicalconcentrations. As electric shock produces a syn-chronous discharge such as never occurs naturallyand as the passage of the current is not far removedfrom the prefrontal areas, it is conceivable that a veryhigh adrenaline concentration temporarily results.Adrenaline may also be the cause of cardiac irrit-ability, shown by ectopic beats, as occurred in apatient with a chromaffin adrenal tumour describedby Espersen and J0rgensen (1947). Anoxia, how-ever, seems the more likely factor in producing theP-R prolongation and intraventricular delay.

Bellet, Freed, and Dyer (1939) found noteworthycardiographic changes in two-thirds of 58 insulinshock treatments in 40 patients, namely depressionof S-T segments, diminution in the height of the Twaves, prolongation of the Q-T interval and variousarrhythmias including shifting pace-maker, sino-auricular block, auricular extrasystoles, and auricularfibrillation. The auricular fibrillation occurred intwo patients and lasted for four and twenty-fourhours respectively. Similar changes were observedby Hadorn (1937), who in addition found the P-Qinterval lengthened in 10 per cent.Nyman and Silfverskibld (1943) stress the simi-

larity of the electrocardiographic findings afterelectroplexy and those produced by the Valsalvaexperiment, with the exception of the markedlyincreased heart rate in the former. In a series of13 patients they found increased amplitude of P II(69 per cent), diminished R I in all patients andincrease in T 11 (69 per cent), with return to normalafter a few minutes. They postulate that the in-crease in intrathoracic and intra-abdominal pressureoccurring in electric convulsions produces thesechanges.Kolb and Vogel (1942) state that the deaths

resulting from electroconvulsive therapy were 0 5per 1000 compared with 1 per 1000 for metrazoland 6 per 1000 with insulin. Of six fatalitiesreviewed by Napier (1944) one was ascribed tomyocardial degeneration, which was confirmed atautopsy; death occurred half an hour after theconvulsion. Ebaugh, Barnacle, and Neuberger(1943) describe two deaths following electric con-vulsions; the first patient, aged 57 years, had anginalpain directly after the thirteenth treatment and died

an hour and a half later; the autopsy revealedextensive coronary atheroma and a recent throm-bosis. A previous electrocardiogram had beenreported as normal. Their second patient, whohad been treated with curare, died of respiratoryfailure. Death has also resulted from massivepulmonary cedema, two days after the second con-vulsion in a 35-year-old negro, who post-mortemshowed meningo-vascular syphilis (Gralnick, 1945).There was little evidence of cardiac or circulatory

embarrassment resulting from electroplexy, nor wasan important arrhythmia encountered in our cases,the majority of which, however, had normal or nearnormal hearts. None the less, in one patient withchronic bronchitis and early failure, and in the threepatients with severe hypertension nothing untowardoccurred. The dramatic nature of the treatmentmay have over-emphasized its potential dangers;although it is obviously undesirable that a patientwith a history or cardiographic evidence of coronarydisease should be submitted to electro-convulsivetherapy, on occasion psychiatric indications mayoutweigh this consideration. Perhaps the risk fromelectroplexy, off set by curare and the particularavoidance of anoxia, is not so great as at first seemedlikely. Certainly there is less danger of arrhythmiathan from insulin produced convulsions. In thepresence of valvular disease the possibility of pre-cipitating auricular fibrillation exists but is probablyslight.

SUMMARY"Steepwave" electroplexy produces moderate

tachycardia and little sustained change in bloodpressure. With oxygen inhalation there is noobvious cyanosis. The degree of increased venouspressure during the fit is difficult to assess, but ithas not been persistent clinically.The cardiographic changes in 51 patients ob-

served after 63 convulsions consist of elevation ofP II and T II and slight increase in the P-R intervalin half; R I was diminished and S-T II slightlylowered in less than a third; S II and S III were moreprominent in 10 per cent; 2 patients (4 per cent)showed intraventricular delay; 4 patients (8 percent) had heterotopic beats after the convulsiononly.

It is suggested that the changes in P II, T II, R Iand S-T II are the result of " muscular activity "and that the delay in auriculo-ventricular and intra-ventricular conductivity may be the result of anoxia.

Patients of middle age or over should have cardio-grams before electroplexy is undertaken. Althoughevidence of coronary disease is a strong contra-indication, on occasion psychiatric considerationsmay be so imperative as to override this.

61



j.com/

Br H


nloaded from


62 BRITISH HEART JOURNAL

REFERENCESAltschule, M. D., Sulzbach, W. M. Tillotson, K. J. Hadorn, W. (1937). Arch. Kreislauf, 2, 70.

(1947). Arch. Neurol. Psychiat., 58, 193. Kolb, L., Vogel, V. H. (1942). Amer. J. Psychiat, 99,Bellet, S., Freed, H., Dyer, W. W. (1939). Amer. J. med. 90.

Sci., 198, 533. Napier, F. J. (1944). J. Ment. Sci., 90, 875.Ebaugh, F., Barnacle, C., Neuberger, K. (1943). Arch. Nyman, E., Silfverskiold, B. P. (1943). Acta med.

Neurol. Psychiat., 49, 107. Scand., 114, 223.Espersen, T., Jorgensen, J. (1947). Acta. med. Scand., Strauss, E. B., and MacPhail, A. (1946). Lancet, 2,

127, 494. 896.Gralnick, A. (1945). J. Nerv. Ment. Dis., 102, 483. Wood, F. C., Wolferth, C. C. (1931). Arch. intern.Graybiel, A. and White, P. D. (1946). Electrocardio- Med., 47, 339.

graphy in Practice. Philadelphia.



j.com/

Br H


nloaded from


cardiovascular following electro-convulsive · tillotson (1947) have noted increased venous...

Documents