754 IRISH JOURNAL OF MEDICAL SCIENCE

PAROXYSMAL V E N T R I C U L A R T A C H Y C A R D I A .

By I~IE~u~:r MOOR~.

p AROXYSMAL tachycardia is a clinical condition charac- tereised by periods of rapid heart-rate of sudden onset and termination ~ 2: some portion of the heart other

than the sinu-auricular node, the normal pacemaker, takes on the rate-regulating functi.on, discharges a series of rapidly recurring impulses, and therefore itself assumes the rSle of pacemaker; this new pacemaker may be situated in the auricles, in the auriculo-ventricular nodes or in the ventricles. While auricular and nodal tachycardia are comparatively common and easy to diagnose with the aid of electrocardiograms, the ventricular form of paroxysmal tachy- eardia, so far as one can judge from the comparatively few cases reported, appears to be very rare. Less than 40 cases of ventricular tachycardia seem to be described in the literature, but by no means all of them .have been satisfactorily proved to be ventric~lar in origin. The diagnosis of ven~ricular .origin is usually v6ry ~iffi- cult without electrocardiographic examination, and even then may be doubtful. Levine 3, however, believes that slight irregu- larities in the rapid heart rhythm, a changing quality and inten- s i ty of the first sound as heard at the apex, and failure to slow the heart rate by vagal stimulation enable one to make a bedside diagnosis without electrocardiograms. Ventri~ular tachycardia is said to be more serious than that os auricular origin, ~' and in some cases is retated r oec.l~sion of a br, anch of the corormry arteries~., 4, 5; its occurrence is frequently associated with heavy digitalis dosage. To establish the clinical diagnosis of paroxysmal ventricular tachy~ardia the following indications that the im- pulses producing the increased heart rate arise in ~he ventricle are given by Robinson and Hermann ~ :--

(1) An electrocardiogram showing a succession of auricular complexes occurring independently of, and at a slower rate ~han, the complexes of ventricular origin.

(2) The ventrieular complexes are distinctly ~bnormal in form, but this alone cannot be taken as proof of ventri~ular o~igin, as changes in form may be caused by disturbances of intraventricu- lar conduction.

(3) The presence of isolated ectopic ventricular beats before or after a paroxysm is evidence in ~avour of the tachycardia being of ventricular origin, especially when the form of the complexes of ,the isolated b~ats is the same as the form of those of the paroxysms.

Paroxysmal ventricular tachycardia is discussed, amongst others, by Lewis 1, s, r HartS, Butterileld and Hunt s, Willias 1~ Vaughan ~, Cohn and Fraser i2, Hume ta, Gallivardin t~, Singer and Winterberg ~5, Marvin and White ~s, Dieuaide and Davidsonlr

PAROXYSMAL VENTRICULAR TACHYCARDIA 755

Reid TM, Scott 19, Parkinson and Nieholl 2~ Wolferth and McMillan sl, Gilchrist s~, Jones and White s3, Howard s4, Schwensen s~, Marvin an, d White z~, Porter sT, Barker 2s, Strong and Levine sg, Levine and Curtiss zo, Wilson and Finch ~s, Pardee ~, and SmithSL It is often impossible to decide ehe exact origin of ~ paroxysm of ventrieular taehycardia unless its first or last ey~le is recorded eleetroeardio- graphically, or unless auricular beats fall at certain points in the C~2ve 7.

Quinidine has ,been frequently used in recent years as ~ thera- peutic agent in various cardiac arrhythmias. Paz, kinson and Nicholl s~ treated six .cases of paroxysmal tachycardi~, five of w~aich were .auricular and one ventrieular in orig~n, with quinidine given by mouth; they found that in two cases the frequency of the attacks was diminished, but only for a few days. Scott I~ noted tl~at in a ease of paroxysmal ventrieular tachycardia the attacks appeared to be controlled by &ally doses of 0.2 gram of quinidine given by mouth for more than a year. Several cases of auricular tachycardia treated by quinidine with varying results are reported in the literature ~5, 2o, 31 ,On the other hand, the administration of quinidine to .dogs has been followed under cer- tain ciroumstan.ces by the appearance of ventricu~ar tachy- cardia 32, and a few similar cases have been reported occurring in man83, s4. It cannot be sta~ed with' certainty ~ow quinidine acts in controlling ventricu~ar taehycardia, but probably it exerts its influence partly 'by prolonging the refractory perioc~ of the ventricle. Ventricular tachycardia has also been reported in some cases as appearing during digitalis therapy ~8, 24 The present author has recorded 3s a case of paroxysmal ventricular tachycardia occurring in combination with auricular fibrillation and appa- rently due to digitalis intoxication.

In this paper a case of paroxysmal taehycardia is re- ported, the electrocardiograms of which are interpreted as show-. ing the paroxysms to .be ventricular in origin; the attacks occurred spontaneously, were readily induced, by the administra- tion of atropine, and, whether spontaneous .or induced by atro- pine, were readily terminated by giving quin~dine orally. Occur- ring spontaneously or after atropine, they usually started with an abrupt change in the form of the QRS complex at an approximately normal heart rate; after a few seconds or minutes of a run of anomalous QRS complexes the rate suddenly rose from 60 or 70 to about 170 per minute, the anomalous form of the complexes remaining the same; towards the end of the attack ~hesc same changes .appeared in the reverse order. Occasionally, a short succession of the anomalous complexes at the slow rate appeared spontaneously or after atropine without subsequently passir~g into the rapid paroxysm, and soon gave place to sinus rhythm;" after atropine, however, the rapid abnormal rhythm appeared later on. The T-wave in the slow atropine paroxysm was upright whenever recorded, whereas it was inverted in the slow spontaneous attacks.

756 IRISH JOURNAL OF MEDICAL SCIENCE.

M.B., schoolboy, aged 12 years. Complaint: " Palpitation," breath- lessness on slight exertion, dyspnoea and (edema of the legs. Admitted to hospital January 20th, 1923.

Family History : Maternal grandfather died suddenly at 61 years of age of " heart-disease " ; one aunt and one uncle died suddenly ~n the sevent)h decade.

Previous history: Asphyxia neonatorum L measles and whooping-cough when betaveen four a n d five years old. No history of rheumatic fever. ,He did not use coffee ; used tea in moderation and smoked an odd cigarette. In August, 1922, he ~vas i,u the nsighhourhood c~ a struggle in which firearms were .used, and he became frightened; during this disturbance, which lasted only a few minutes, he ,noticed that .suddenly his heart began to beat rapidly ; i t continued to do so Sor about half an hour; the rapid ,beating suddenly ceased and was followed ~by a pause of a ~ew moments, during which time he felt that his heart " steed still ," after which he was no longer conscious of any abnormality of the heart or of palpitation.

Present illness: On January 15th, 1923, a similar attack of palpitation and ~adhycardia suddenJy occurred without obvious cause and lasted (so .he said) until I saw him on January 20th.

Physical examination: Pulse rate 166 and regular; respirations 24 per mi,uute ; heart sJightly enlarged to the left, sounds normal and no mur- Inurs; considerable cyanosis of face and hands; moderate (edema of shins and ankles; moist tales and deficient percussion resonance at bases , f lungs; liver edge 2 cms. below costal margi`n and tender on pressure. Blood pressure 100/86. Three carious teeth. Vagal or eyeball pres~sur% deep threath,ing or swallowing did no~. slow the pulse. Urine contained neither albumen nor sugar. T.he right tonsil, and to a lesser degree the left, was hypertrophic. Accessory sinuses of nose transilluminated norm- ally. There were no other abnormalities observed. Blood Wassermann reaction negative. An electrocardiogram (Fig. 1) showed a very abnor- mal tracing which was difficult to .interpret, for although numerous obser- vations .were made, we were not able in this or in subsequent spontaneous .attacks to get a record of the beginning or end of a paroxysm. The QRS complex was anomalous and notched and showed a duration of almost three times the normal. I t was impossible ix) identiaCy P (although i t might possibly be represented by the dips, marked x, before alternate QRS complexes in Lead 1). The case was considered one of peroxysmal taehyc~rdia, probably ventricular in origin.

Treatment: Seventeen grains of powdered digitalis leaves, given over 48 hours, caused no change in heart rate, elimcal condition, or electro- cardiogram. After an interval of two days 0.2 gram of quinidine sul- phate was given by mouth, and as there were no symptoms of idiosyncracy in six hours, 0.4 gram was g~ven by mouth every two hours, nntil 2.6 grams had Ibeen taken. ,WiT)hin half an hour a~ter ~ho ]~s~ dose the patient .reported to the nurse that the palpitation had just then suddenly ceased, and his pulse rate ~as found r ,be 64 per minute .and regular. A`n electrocardiogram taken in a few ,~ hours showed sinus r~y~hm (Fig. 2). The cedema, eyanosis, dyspn0ea and the congestion of the pulmonary bases rapidly disuppeared, the liver .became normal in size, and soon the patient was quite comfortable. He was allowed to leave his bed ,in a .few days in apparently good ~aealt~h.

On returning home he had ~wo or three attacks every month between the end of February, 1923 and November, 1925; they sometimes appeared in a few hours following excessive exercise; when so treated they were stopped in .r to one-and-a-half hours by taking a few doses of quinidine (0.4 gram each), except two which quickly disappeared spon- taneously; otherwise, without quinidine, the attacks usually lasted several, often more than 24, hours. He was re-admitted to hospital for a ~veek's observation in December, 1.925, ~but we were unable to obtain an electrocardiogram of the beginning or end of the only ~spontaneous attack avhich then occurred, and which was quickly t e r m i n a ~ ~by quinidine (Tracings were similar to Fig. 1.)

He returned to the country, and took quinidine by mouth daily (0.2-0.4 gram thrice daily) for a year. The attacks during 1926 were infrequent and ~su,ally of Short duration, and, if they lasted longer than an ~our, appeared to be readily terminated .by an extra dose or two of quinidine. The patient was able to live ~h,is ordinary life and play gashes ~n modera- tion except during the attacks. No ill effects were at any time noticed from the quinidine.

}~LA~ I.

Time m a r k e r shows fifths and gwenty-fif ths of a second; 1 cm. excurs ion of s t r i n g is equ iva len t to one millivolt . The t rac ings are reduced for

publ ica t ion .

E~

PAROXYSMAL VENTRICULAR TACHYCARDIA 757

He re-entered hospital again in January, 1927, for further observation. By electrocardiogrephic study wJth the paper camera the following facts were observed: the spontaneous attacks began and ended with a period of a few seconds' to a few minutes' duration, during which the anomalous QRS complexes replaced the normal ones, with a hear t ra te not at all or only slightly increased, the abnormal complexes being of the same type as those of the rapid paroxysm; these " s l o w " spontaneous attacks abrupt ly gave place to the rapid paroxysms; these might last several hours or even days, and each of the la t ter in i ts tu rn was suddenly replaced by a run of the slow anomalous complexes once again, this being succeeded by normal rhythm; the changes from the nomnal to slow @hnormal rhythm, ~rom the la t ter to the rapid abnormal, from the rapid @bnorm.al to the slow ~bnormal once again, and from the slow a)bnormal to ~he normal r~yth.m "took ,place ~bruptly and in this order; the patient was ,~mmediately conscious of each change, and could give warning to the electrocardiogra,phic operator; the administration of 1/100 to 1/75 of a grain of ~tropine sulphate intramnscularly (~with the consent of the patient and his parents) caused an attack to appear on each of four occasions in from 12 to 45 minutes, ~ and in the rapid

doses); untreated, ~wo atropine attacks lasted several hours, until finaUy chocke<l ,by quinidine. These various findings are illustrated in Figs. 4 to 15 ; ~he transition from a moderately slow " atropine " atback, suc- ceeding the abnormal rapid rhythm, to the normal rhythm induced by quinidine is shown in Fig. 9, and the transition from nor~nal rhythm to that.of the s!o~ " atropine " attack i.s shown in Fig. 13. The T-wave was ~nver~ m the slow spontaneous attacks (Fig. 14), and ~n the abnor- mal complexes of slo~ rate induced by quinidJne towards the end of a rapid spontaneous ~aroxy.szn before normal rhyt~n appeared (Fig. II), vzhile T ~was upright in the abnormal complexes of the ~Iow atropine attacks (Figs. 6, 6a, 6b and 7) ; i t is therefore open to some doubt whet~her one can draw conclusions relative ~o the nature of the spontaneous paroxysms from a study of the tracJng.s of the slow atropine attacks, although QRS seemed to be generally of the same type in both. In the rapid paroxysms, whether s,pontaneoue or due to atropine, T was upright (Figs. 1, 8 "and 10). The dl"rection of T~ however, may ,be comparatively easily 5nfluenced, e.g., by digitalis, qumidine, drinking of iced water, urmmia, ,morphine, etc. (9,9, 30), and possibly may .'be influenced by atropine in this case. I t is frequently difficult to be sure whether a given wave i.s T owing to its changing position ~vJth reference ~ the end of QRS (compare Figs�9 9, 10, 11, 13 and 14).

D I 2 0 U 2 8 I O N .

T h a t the new r h y t h m was v e n t r i e u l a r in o r ig in is shown b y t h e eye l e s m a r k e d ~ in F i g s . 6a a n d 6b; t he se a r e t r a n s i t i o n a l , Q R S b e i n g p r e e e d e d b y p1 a t too shor t an i n t e r v a l fo r fu l l a u r i c u l a r response on the p a r t of the ventr icle---- the ven t r i c l e r e s p o n d s in p a r t to i ts own impu l se a n d in p a r t to the a u r i c u l a r one. T h e same e x p l a n a t i o n ho lds f o r the l a s t a b n o r m a l eyele in F i g . 9, in which i t is a lso no t iced t h a t when n o r m a l r h y t h m a p p e a r s t h e r e

The first " atropine " a t tack occurred 45 minutes after 1[100 grain of ~,tropine sulphate given intramuscularly; the second 14 minu~s, the ~hird 17 m~nutes and the fourth 12 minutes, after 1/75 grain .intrarnuscularly. Atropine was given with the idea tha t if the nature of ~Lhe tachycardia could .be elucidated a clue to mere effcient t reahnent might be obtained.

#f No a t tempt was made to determine exactly when quinidine became effective after the initiation of the " atropine " attack�9

758 I R I S H J O U R N A L OF M E D I C A L S C I E N C E .

is a gradual slowing of the sinus rate. The curves suggest tha t the case m a y possibly be one of a " parasystol ic " rhythm. The cycle marked y in Fig. 6a is a normal one, QRS not being anomalous, of pract ica l ly normal dura t ion and responding to a normal P wae wi th a normal P R interval , and the same is t rue of the first normal cycle in Fig. 9. I n any of the anomalous complexes when P can be identified (Figs. 6a, 6b, and 9) the notch in the abnorma l QRS complex is least no t iceable ; it m a y therefore be tha t this notch represents re t rograde conduc- tion to the auricle, but the explanat ion is doubtful, as P can be identified jus t before the first abnormal complex in Fig. 13 (p1) a t a point where P is expected. Occasionally the notch in the abnormal QRS completely d isappeared (Figs. 6 and 10) and then the succeeding wave (T) showed a sl ightly higher voltage which m a y possibly mean a coincident P and T, but, again, this is doubtful . I n Figs. 5, 6 and 10 (at ropine attacks) the notch in QRS is inconstant in its position.

The second criterion of Robinson and H e r m a n n relat ing to vent r icu lar tachycard ia is present in the t racings of the present case; while their th i rd character is t ic- - isola ted anomalous beats independent ly of the p a r o x y s m - - i s not present ; however, short series of anomalous vent r icu la r complexes do occur in in t ra- pa roxysmal periods (Fig. 14, Lead II) . Their first indication is not present, namely, a succession of aur icu lar complexes occurr ing independent ly of, and a t a slower rate than, complexes of ~en t r icu la r or igin; aur icular complexes can, however, be separa ted ~rom the vent r icu la r ones and are marked x in Figs. 6a, 6b, and Fig. 13 (p1), and doubtfu l ly in Fig. 1 (x, Lead 1,) leaving abnormal QRS complexes which seem in Figs. 6a and 6b (x) to be definitely t ransi t ional in origin, the ventricle responding pa r t l y ~rom the aur icu lar and p a r t l y f rom the ectopie vent r icu la r focus.

Subsequent His tory . - - In February, 1927, when the patient was leaving hospital, he was advised ~o take 0.4 gram of quinidine ~hree thnes daily. He reported on Sept. 16th, 1927, Vhat since February of that year he had been taking 0.2 gram of quinidine ,by mouth, twice daily after food; the atbacks .of tachycardia occurred every t~wo or Lhree weeks; sametimes ~hey lasted only 5 or 6 minutes, but if their duration was longer they termi- nated wit~hin ,an hour on almost all occasions after taking an extra dose of 0.4 gram of quinidine. From Sept. 29th, 1927 to Dec. 26th, 1927. he took 0.4 .gram of quinidino thrice daily, and Ja~d seven .attae.ks, eac~ of w~ieh lasted from 45 to 150 irdnutes; two to three extra cal~sules of quinidino (0.4 gram each) were taken at intervals from half an hour of ~aho beginning of each attack. The routine use of quinidine was discontinued on Dec. 26th, 1927, .and since Vhen u.p to l~Iay 8th, ]928, the patient experienced fifteen attacks, each of w~iah lasted a minute and a half or less and ceased spontaneously. For the five months prior to the time of writing (Oct. 18th, 1928)'he reported that, although he had not been taking quinidine, he has noticed only occasional attacks, that all ceased spontaneously, and that none exceeded two minubes' duration. Since the end of 1923 the patient has been at a boarding-school, lives a normal life, and plays games in moderation, except during and for a short time after the attacks.

In this case of paroxysmal vent r icular tachycardia the condition did not seem to have been associated with grave hear t disease

P A R O X Y S M A L V E N T R I C U L A R T A C H Y C A R D I A 759

(as is f requent ly stated to be the case) judging f rom the subse- quent history.

S U M M A R Y .

A case of paroxysmal tachycardia is described; the tachycardia we in terpre t as ventr ieular in origin. I t was possible to terminate the longer at tacks b y the adminis t ra t ion of quinidine by mouth, but it is not clear whether the oral routine adminis t ra t ion of quinine in dai ly doses of 0.4 t.o 1.2 g r a m rendered the occurrence of the paroxysms less frequent . I t is now more than 56 months since the pat ient was first s tudied; the at tacks have become less f requent and of shorter duration, al though no special t r ea tmen t was under taken for more than the last 9 months.

Bibliography.

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Beat, London, 1925. 8. Har~: Heart, 1912-13, 4, 128. 9. Butterfield and Hunt: Q~art. Jo. Med., 1914, 7, 209.

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