diazepam treatment of arrhythmias - Heart · Value ofdiazepam ('Valium') in treatment ofcardiac arrhythmias 829 Inafurtherexperiment,eachof5differentdogs weighing I3-6 to 2I-8 kg.

British Heart journal, 1970, 32, 827-832.

Value of diazepam ('Valium') in treatmentof cardiac arrhythmias

F. H. N. Spracklen, R. J. Chambers, and V. SchrireFrom the Cardiac Clinic, Groote Schuur Hospital, Department of Medicine, University ofCape Town, and the Cardiovascular-Pulmonary Research Group, supported in the Departmentof Medicine by the South African Medical Research Council

Diazepam did not alter the rate or rhythm in iI patients with atrialfibrillation. In 3 out of38 patients with atrialflutter the use of diazepam wasfollowed by an increase in atrioventricularblock. Diazepam restored sinus rhythm in I patient with atrial tachycardia (total 7 patients)and in i patient with ventricular tachycardia (total 8 patients). Experimentally in the dogdiazepam raised the electrically-induced ventricular tachycardia threshold significantly. Pre-treatment with diazepam did not alter significantly the dose of strophanthidin K required toinduce ventricular tachycardia in the dog.

The value of diazepam as a cardiac anti-arrhythmic agent should be further assessed in a

controlled clinical trial, especially in patients with acute myocardial infarction.

It has recently been suggested that diazepam('Valium') has cardiac anti-arrhythmic pro-perties (Van Loon, I968; Papp, I969). Thisdrug has been used alone for heavy sedationbefore electrical conversion of arrhythmias inour department for the past 2 years. We havestudied the anti-arrhythmic properties ofdiazepam in the clinical setting and in experi-mentally-induced arrhythmias in the dog.The purpose of this paper is to report ourfindings.

Clinical studyMaterial and methods Diazepam was givenintravenously (5-75 mg.) to i42 patients on I64different occasions before attempting electricalconversion of an arrhythmia. These arrhythmiaswere atrial fibrillation (iii instances), atrial flutter(38), supraventricular tachycardia (7), and ven-tricular tachycardia (8). Diazepam was given tothese patients for its sedative and hypnotic effect,and its use allowed direct current (DC) shocktherapy to be given without general anaesthesiaand tracheal intubation.

ResultsThe major underlying pathology in our pa-tients was rheumatic heart disease (i I2 cases),ischaemic heart disease (I9 cases), undeter-mined or 'lone' (5 cases), chronic lung disease(4 cases), and treated thyrotoxicosis (3 cases).The remaining I7 patients suffered fromcombinations of these diseases and miscel-

Received 9 March 1970.

laneous other conditions. In none of the i i iepisodes of atrial fibrillation was the rhythminfluenced by the administration of diazepam.Of 38 patients with atrial flutter, there were 3instances of increased atrioventricular blockfollowing diazepam. One patient with supra-ventricular tachycardia (total 7 cases), andone with ventricular tachycardia (total 8 cases)reverted to sinus rhythm immediately afterreceiving diazepam.

Illustrative cases are briefly reported.

Case I: atrial flutter A 73-year-old womanwas admitted to hospital in April i969, with adiagnosis of ischaemic heart disease and left ven-tricular failure. Examination revealed gross car-diomegaly and congestive cardiac failure. Anelectrocardiogram showed atrial flutter with 2:1Iblock and a ventricular rate of 135. Cardioversionwas contemplated and the patient was given 5 mg.diazepam intravenously. After this the rhythmchanged to atrial flutter with 4: i block. Thepatient was therefore not cardioverted but wasdigitalized. The patient reverted to sinus rhythmthree days later.

Case 2: atrial tachycardia A 58-year-old mandeveloped atrial fibrillation after his second myo-cardial infarct in March I967. The patient wasadmitted to hospital in February I969, and aftera test dose (200 mg.), was given quinidine (400mg.) every 2 hours for 3 doses (total I400 mg.).With this, atrial tachycardia occurred. Thisrhythm was unaltered by carotid sinus pressure.The patient was given diazepam (5 mg.) intra-venously with the intention of electrically con-

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828 Spracklen, Chambers, and Schrire

verting his rhythm. Immediately after this injec-tion sinus rhythm was noted.

Case 3: ventricular tachycardia A 65-year-old man had a long history of peripheral vasculardisease. He was admitted to hospital in MarchI969, with a 6-day story of a painful, cold leftleg. An electrocardiogram showed sinus rhythmand a possible old inferior infarct. The patientresponded well to bed-rest and intravenous hepar-in therapy. The heparin was reduced io days afteradmission and discontinued a day later. On thatmorning the patient complained of the suddenonset of severe, constricting chest pain. This wasaccompanied by breathlessness and sweating. Anelectrocardiogram showed ventricular tachycardia(rate I90 a minute). Lignocaine (ioo mg.) wasgiven intravenously without effect and the patientwas given diazepam (5 mg.) intravenously beforecardioversion. Immediately after the injection hereverted to sinus rhythm. Serial electrocardio-grams and enzyme studies did not show a furthermyocardial infarction.

Experimental studiesMaterial and methods The effect of diazepamon the 'ventricular tachycardia threshold' asdescribed by Lown and associates (Lown, Kleiger,and Williams, I965) was studied. For this studyI2 mongrel dogs of both sexes were used. Thedogs weighed between ii-8 and 23-2 kg. (averageI8-o kg.). Anaesthesia was induced with sodiumpentobarbitone given intravenously (30 mg./kg.).Respiration was maintained with a Harvard pumpusing room air and a cuffed endotracheal tube.The minute volume was adjusted to maintain thearterial oxygen saturation in excess of 95 per cent.At regular intervals 'sighing' was induced manu-ally. Catheters were inserted into the femoralartery and vein. Arterial blood pressure wasmonitored continuously using a Statham P23 Dbstrain gauge.

Direct current shocks were given externallyusing a Corbin-Farnsworth defibrillator. Theelectrode paddles measuring 9 cm. in diameterwere covered with conductive paste and appliedwith pressure on either side of the shaved chestat the level of the cardiac apex beat. The sites weremarked and used on each occasion.The DC shock was synchronized with the elec-

trocardiogram to occur i8 milliseconds after thepeak of the R wave. To determine the ventriculartachycardia threshold, shocks were given everyI0 seconds. The ventricular tachycardia thresholdwas defined as the energy level at which 3 con-secutive DC condensor discharges produced arun of 3 or more consecutive ventricular com-plexes, with abnormal QRS configuration at arate exceeding 60 a minute, and occurring within3 seconds of the shock. The initial shock wasgiven at an energy setting of 40 or 6o watt seconds(w.sec.). If ventricular tachycardia developed(positive response), the energy was reduced to 20,and then I0 w.sec. If it did not occur (negativeresponse), the energy level was increased pro-gressively to 80, I00, 200, 300, and 400 w-sec.

.......

_ *- .Ko A ........... + .4 .................Sv.. \ ,.......... ..............................

...:!' :. . ti1~~~~~......... ...........X

FIG. i Negative response, no ventriculardysrhythmia occurring after a io-watt secondshock. ,_,.+. .*~~~~~~~~~~~~~~~~~~~FI G . 2 Positive response. Ventricular tachy-cardia produced by a 4o-watt second shock.

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C

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Y i4

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FIG. 3 Digitalis intoxication. (A) controltracing; (B) supraventricular tachycardia withaberration; and (C) ventricular tachycardia.

Fig. i and 2 illustrate negative and positiveresponses respectively.

In 8 dogs a stable control period of 6o to 95minutes was established before giving diazepam.The threshold during this period was determinedevery I5 minutes. Diazepam was given rapidlyintravenously as a single dose of 20 mg. Thresh-olds were then measured after 5 minutes, after afurther I0 minutes, and subsequently every i5minutes for a total of go minutes after giving thedrug. In 4 dogs, thresholds were determined atI5-minute intervals for 4 hours without givingdiazepam.



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Value of diazepam ('Valium') in treatment of cardiac arrhythmias 829

In a further experiment, each of 5 different dogsweighing I3-6 to 2I-8 kg. (average I7'3 kg.) werestudied twice at weekly intervals. The dose ofstrophanthidin K ('Strophosid') necessary toproduce toxicity (stable ventricular tachycardia)was determined by infusing the drug at a rate ofzoo ,ug. a minute for 5 minutes, followed by 50 ,ug.every 5 minutes until supraventricular tachycardiaor ventricular ectopic beats occurred. Then 50 ,ug.was given every I0 minutes until ventriculartachycardia occurred (Fig. 3). In one of the twostudies which were performed in random order,the dog was pretreated with diazepam (20 mg.) ISminutes after induction of anaesthesia. After afurther I5 minutes, strophanthidin K was infuseduntil toxicity occurred. In both experiments thestrophanthidin dose schedules were identical.

ResultsEight dogs were studied to determine the ven-tricular tachycardia threshold before andafter giving diazepam. These dogs main-tained a satisfactory acid base balancethroughout the experiment and had controlthresholds between 40 and 300 w.sec. In one,the threshold did not change after givingdiazepam. The remaining 7 dogs showed arise in threshold after diazepam. The meanthreshold before diazepam was 142 w.sec.(SD 871I). After diazepam the mean thresh-old rose to i87 w.sec. (SD 86-2). The differ-ence in these values is significant at the 5 percent level (t= 2 577). In Fig. 4 a typical riseof ventricular tachycardia threshold after theadministration of diazepam is illustrated. InFig. 5 the mean values for all dogs are de-picted. Four dogs that were not given diaze-pam had thresholds determined every I5minutes over a 4-hour period. No significantchange in threshold was observed during thisperiod.

Five further dogs were each studied twiceto determine the dose of strophanthidin Krequired to produce ventricular tachycardiawith and without pretreatment with diaze-pam. The mean dose of the glycoside withoutdiazepam was I200 t±g. (SD I27-5), while thatafter giving diazepam was II80 jig. (SD266-o). This difference is not statistically sig-nificant. The mean time from the beginningof the strophanthidin infusion to the develop-ment of ventricular tachycardia was 72-4minutes (SD 25 3) in the absence of diaze-pam, and 64-0 minutes (SD 44 3) after pre-treatment with diazepam. The difference inthese values is also not statistically significant.

DiscussionDiazepam, a synthetic benzodiazepine deriva-tive has been used for the control of anxietystates (Randall et al., I961), in tetanus (Hen-

o '-95 -80 -E5 -50 -35 -20 0 5S 30 45 60 75 90Time (min.)

F I G . 4 ' Ventricular tachycardia threshold'before and after giving diazepam.

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F I G. 5 ' Ventricular tachycardia threshold'in 8 dogs before and after giving diazepam.The mean values (± I SD) are shown.

drickse and Sherman, I965), and in the treat-ment of epilepsy and spastic neuromusculardisorders (Gastaut et al., I965; Lombroso,I966; Gordon, I966; Calderon-Gonzalez andMireles-Gonzalez, I968). It has also beenused as premedication for anaesthesia (Brandtand Oakes, i965), for the induction of anaes-thesia (McClish, 1966), and to induce narco-sis before direct current cardioversion (Nutterand Massumi, I965; Kernohan, I966). Mc-Clish (I966) demonstrated transitory minimal



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degrees of hypotension, bradycardia, andrespiratory depression after the use of thisdrug. Lown (I964) reported that diazepamhad no significant effect on respiratory, circu-latory, or autonomic nervous systems.

In epilepsy, associated with post-traumaticscars and expanding lesions, the epileptogenicregion of tissue forms a boundary between thelesion and the histologically normal cortex.The ectopic ventricular impulses that occur

within a few minutes after abrupt occlusionof a coronary artery, arise in partly ischaemictissues which form a margin round a potentialinfarct (Harris, I948). The apparent similari-ties between the origin of ectopic ventricularactivity after coronary occlusion and that offocal epileptic discharges suggest that drugsthat prevent epilepsy might also suppressventricular arrhythmias, especially thoseaccompanying acute myocardial infarction.This thesis was first tested by Harris andKokernot (I950), using diphenylhydantoin.More recently, others have confirmed thevalue of this drug in controlling cardiacarrhythmias, especially those induced bydigitalis (Conn, I965; Ruthen, I965). Intheory, therefore, diazepam, a potent anti-epileptic agent, might be expected to havecardiac anti-arrhythmic properties.

In a case report, Van Loon (I968) describedan 88-year-old man who suffered an anteriormyocardial infarct and had persistent ven-tricular arrhythmias. These arrhythmias couldnot be controlled with lignocaine, diphenyl-hydantoin, antazoline, or procainamide, butboth the multiform ventricular ectopic beatsand ventricular fibrillation were replaced bynormal sinus rhythm within 4 minutes ofgiving IO tO 20 mg. diazepam intravenously.Diazepam was given on 3 separate occasionsand was followed by sinus rhythm whichlasted between I5 and go minutes.

Muenster and co-workers (I967) comparedthe use of sodium thiopental with diazepamanaesthesia (I5 tO 20 mg. given intravenouslyover 6o to 90 seconds) for direct current shocktherapy in two similar but small groups ofpatients with atrial fibrillation. After givingsodium thiopental, but before the shock, pre-

mature ventricular systoles occurred fre-quently. No premature ventricular systoleswere observed in the group that receiveddiazepam. After the shock, frequent prema-

ture ventricular systoles persisted in the groupgiven sodium thiopental, whereas the patientswho received diazepam had significantly fewerpremature ventricular systoles. These findingsmay be interpreted as indicating that diaze-pam has an anti-arrhythmic effect. An alterna-tive explanation, however, is that diazepam

has no anti-arrhythmic effect, but that sodiumpentothal induces ventricular ectopic beats.

Winters and associates (I968), using diaze-pam intravenously in doses of io to 40 mg.for 2I elective direct current countershockprocedures for ventricular and supraventricu-lar arrhythmias in i8 patients, found no sig-nificant changes in heart rate, blood pressure,or respiratory rate. One episode of ventriculararrest occurred, however, in a 56-year-oldnegro woman with atrial tachycardia compli-cating an atrial septal defect. The authors didnot relate this episode to the use of diazepam.It seems at least likely, however, that diaze-pam was responsible for this cardiac arrest,and, of course, most anti-arrhythmic agentsare capable of producing cardiac arrest.Papp (i969) stated that diazepam (I0 to 20

mg. intravenously) 'has also been effective inventricular arrhythmias'. No evidence iscited, however, for this conviction. Despitethe widespread use of diazepam in clinicalpractice, no other reports concerning its car-diac anti-arrhythmic properties haveappeared.Our clinical experience has been that

diazepam has no effect on established atrialfibrillation. Unfortunately we have no detailson the incidence of ectopic beats in our pa-tients with atrial fibrillation before and aftercardioversion. Diazepam can, therefore, notbe compared with other anaesthetic agents inthis respect. Our finding that increased atrio-ventricular block occurred after giving di-azepam in 3 out of 38 patients with atrialflutter suggests that diazepam is not quini-dine-like in action. Quinidine in the un-digitalized patient has long been known toreduce the atrial rate in atrial flutter withoutsignificantly reducing atrioventricular con-duction, thereby often paradoxically increas-ing the ventricular rate. A similar effect hasalso been described after the use of ligno-caine, antazoline, and diphenylhydantoin(Dreifus, Rabbino, and Watanabe, I964;Grissom et al., I967; Adamson and Spracklen,I968).A decrease in atrioventricular conduction

would be expected with a propranolol-likedrug. Diazepam, however, did abolish atrialtachycardia in one of our cases. This effect,together with slowing of atrioventricular con-duction in atrial flutter, is found with para-sympathomimetic agents, like edrophoniumchloride (Tensilon) (Moss and Aledort, I966).While coincidence cannot be excluded, ourclinical findings suggest that diazepam mighthave cardiac anti-arrhythmic properties. Cer-tainly controlled trials with diazepam arewarranted, especially with regard to the inci-



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Value of diazepam ('Valium') in treatment of cardiac arrhythmias 831

dence of arrhythmias after myocardial infarc-tion.

For our experiments with diazepam wechose two well-established models, namelyelectrically-induced and digitalis-induced ven-tricular arrhythmias in the dog. We haveclosely followed the technique of Lown andassociates (I965) for inducing ventriculartachycardia with a commercially available ex-ternal defibrillator. Like Lown we found thatthis technique gave stable 'thresholds' overprolonged periods. Attention was paid tosmooth, maintained anaesthesia, adequateventilation, and the avoidance ofhypothermia.With these provisos the preparation was foundto be stable in our hands for at least 4 hours.Lown has reported stability of threshold fora period of 7 hours. A rise in electrically-induced ventricular tachycardia threshold wasfound in 7 out of 8 dogs receiving diazepam.The control thresholds were lower in youngerand smaller dogs. We found a rise, however,after diazepam whether the control value washigh or low. A wide range of thresholds (40to 300 w.sec.) is reflected in the large standarddeviation of the mean values (Fig. 5).While we have shown that diazepam raised

the ventricular tachycardia threshold signifi-cantly (p<o os), the interpretation of thisfinding is difficult. Lown and associates (I965)have shown that digitalis dramatically lowersthe ventricular tachycardia threshold. Witten-berg and Lown (I969) showed that dextro-propranolol (a drug with a non-specific anti-arrhythmic action, but with virtually no betaadrenergic blocking effect) and propranololrestored the ventricular tachycardia thresholdto normal after it had been reduced withouabain. ICI 50,I72, a pure beta-blockingagent, did not have this effect. The effect ofother anti-arrhythmic agents on this thresholdhas not been reported. It would be prudentat this stage, therefore, not to assume that anagent which raises the ventricular tachycardiathreshold is necessarily anti-arrhythmic in theclinical setting. Bacaner (I966, I968a), how-ever, has shown that the vulnerability of thedog heart to ventricular fibrillation provokedby directly-applied electric shocks is reducedby treatment with bretylium tosylate. Thesame author has also found this agent to beeffective clinically in the treatment of ven-tricular fibrillation and other ventriculararrhythmias (Bacaner, I968b).Our finding that diazepam is ineffective in

the prophylaxis of digitalis-induced ventricu-lar tachycardia in anaesthetized dogs shouldnot exclude this agent from further trials inthe management of digitalis-induced arrhyth-mias. Diphenylhydantoin and beta-adrenergic

blocking agents are of proven value in thetreatment of digitalis-induced arrhythmias inman (Conn, I965; Ruthen, I965; Lang et al.,I965). Experimentally, however, there is con-flicting evidence whether pretreatment withdiphenylhydantoin and beta-adrenergic block-ing agents protect against digitalis-inducedarrhythmias (Vaughan Williams and Sekiya,I963; Lucchesi, I964; Aroesty and Cohen,I966; Scherlag et al., I968; Zeft et al.,I969). Nevertheless both diphenylhydantoinand beta-adrenergic blocking agents signi-cantly shorten the duration of digitalis-in-duced ventricular tachycardia when givenshortly after the onset of the arrhythmia (Zeftet al., I969). Further work is therefore neededto determine if diazepam is of value in the ther-apy of digitalis-induced arrhythmias in man.

We wish to thank Dr. J. G. Burger, MedicalSuperintendent of Groote Schuur Hospital, forpermission to publish. The Corbin-Farnsworthdefibrillator and monitoring equipment was kindlysupplied by Mr. B. J. Kirby of Keatings Pharma-ceuticals, Ltd., Cape Town. For this we are ex-tremely grateful.Our thanks are also due to the South African

Medical Research Council and the City CouncilofCapeTown fortheir continued financial support.

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Bacaner, M. (1966). Bretylium tosylate for suppressionof induced ventricular fibrillation. American3Journalof Cardiology, 17, 528.

- (I968a). Quantitative comparison of bretyliumwith other antifibrillatory drugs. American J7ournalof Cardiology, 2I, 504.

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Grissom, J. H., Sy, B. G., Duffy, J. P., and Dunea, G.(I967). Dangerous consequence from use of pheny-toin in atrial flutter. British Medical Journal, 4, 34.

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, and Kokernot, R. H. (I950). Effects of diphenyl-hydantoin sodium (dilantin sodium) and pheno-barbital sodium upon ectopic ventricular tachy-cardia in acute myocardial infarction. AmericanJournal of Physiology, I63, 505.

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Muenster, J. J., Rosenberg, M. S., Carleton, R. A.,and Graettinger, J. S. (I967). Comparison betweendiazepam and sodium thiopental during DCcountershock. Journal of the American MedicalAssociation, 199, 758.

Nutter, D. O., and Massumi, R. A. (I965). Diazepamin cardioversion. New EnglandJournal of Medicine,273, 650.

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Randall, L. O., Heise, G. A., Schallek, W., Bagdon,R. E., Banziger, R., Boris, A., Moe, R. A., andAbrams, W. B. (I96I). Pharmacological and clinicalstudies on Valium: a new psychotherapeutic agentof the benzodiazepine class. Current TherapeuticResearch, Clinical and Experimental, 3, 405.

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diazepam treatment of arrhythmias - Heart · Value ofdiazepam ('Valium') in treatment ofcardiac arrhythmias 829 Inafurtherexperiment,eachof5differentdogs weighing I3-6 to 2I-8 kg.

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