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NON-SYNCHRONISED AND SYNCHRONISED DIRECT-CURRENT COUNTERSHOCK IN CARDIAC ARRHYTHMIAS
405
NON-SYNCHRONISED AND SYNCHRONISED DIRECT-CURRENT COUNTERSHOCK IN CARDIAC ARRHYTHMIAS
TABLE I-RESULTS AND COMPLICATIONS IN SYNCHRONISED AND NONSYNCHRONISED CONVERSION ATTEMPTS IN 95 PATIENTS WITH ATRIAL FIBRILLATION
K.-E. KREUS M.D. MEDICAL REGISTRAR
S.
J. SALOKANNEL
E. K. WARIS M.D.
M.D. LECTURER
SENIOR LECTURER
DEPARTMENT OF MEDICINE, UNIVERSITY OF
OULU, OULU,
FINLAND
SINCE Lown et al. (1962a and b, 1963) reported their results, synchronised direct-current (D.c.) shock to terminate cardiac arrhythmias has rapidly gained widespread acceptance (Killip 1963, Brown et al. 1964, Cullhed et al. 1964, Graf and Etkins 1964, Hurst et al. 1964, McDonald et al. 1964, Morris et al. 1964, Oram and Davies 1964, Varnauskas et al. 1964, Korsgren et al. 1965, Reinikainen et al. 1965). Complications have been uncommon, though severe arrhythmias (Graf and Etkins 1964, Ross 1964, Korsgren et al. 1965) and even fatalities (Rabbino et al. 1964) have been reported. According to Lown it is essential to use an electronic synchroniser for the D.C. shock to avoid the vulnerable phase (the initial portion of the T-wave in the cardiac cycle (King 1934). Other workers (Killip 1963, Oram and Davies 1964, Korsgren et al. 1965) share this opinion, and as a result of their experience with completely synchronised D.C. shock have pointed out the importance of synchronisation. The present report describes our experience of nonsynchronised and synchronised D.C. countershock in the treatment of various cardiac arrhythmias. Methods and Patients Countershocks were administered by means of a D.C. defibrillator without a synchronisation device (CorbinFamsworth, Palo Alto, California) and with two apparatuses with synchronisation devices (Corbin-Farnsworth and Electrodyne Inc. C-100 M, D-84 M). The electrodes were placed in the oblique (Lown et al. 1962a) or the transverse (Cullhed et al. 1964) position. A 100 watt-second (joule) discharge was, administered initially with subsequent countershocks of 200, 300, and 400 joules as required. The 400 joule shocks were repeated either until normal sinus rhythm was established or until further attempts were considered futile for the time being. All patients were premedicated (50 mg. pethidine and 0-5 mg. atropine) and anaathetised with 100-250 mg. pentobarbitone sodium in the manner reported earlier (Waris et al. 1965). Each patient was subsequently followed up with repeated estimations of the erythrocyte-sedimentation rate (E.S.R.) and serum-transaminase, serial white-cell-counts, and E.C.G. recordings before defibrillation and on the first, second, and third day thereafter. The series consisted of 95 patients with atrial fibrillation A total of 112 episodes were treated in 76 instances with nonsynchronised D.C. shock and in 36 instances with synchronised D.c. shock. The series included many elderly patients with advanced chronic heart-disease of varying aetiology. Most of them had long-standing atrial fibrillation and nearly all had DR. SHEARMAN AND OTHERS: REFERENCES
Anderson, B. B. (1964) J. clin. Path. 17, 14. Ardeman, S., Chanarin, I. (1963) Lancet, ii, 1350. Girdwood, R. H. (1956) Q. Jl Med. 25, 87. — (1960) Scott. med. J. 5, 10. Irvine, W. J. (1963) Q. Jl exp. Physiol. 48, 427. ’1965) New. Engl. J. Med. 273, 432. Kaplan, H. S., Rigler, L. G. (1945) Am. J. med. Sci. 209, 339. Kay, A. W. (1953) Br. med. J. ii, 77. Mosbech, J., Videbaek, A. (1950) ibid. ii, 390. Schade, R. O. K. (1958) ibid. i, 743. Taylor, K. B., Roitt, I. M., Doniach, D., Couchman, K. G., Shapland, C (1962) ibid. ii, 1347. —
*
1 sudden death.
been previously treated with digitalis and with quinidine for at least three days before the attempted conversion. The the of were for at patients great majority given anticoagulants least three weeks before conversion was attempted. The first 40 episodes were treated with a non-synchronised D.c. defibrillator and, thereafter, every second conversion attempt was made with synchronised D.c. defibrillator until a total of 76 non-synchronised and 36 synchronised defibrillation attempts had been made. In the non-synchronised group, no efforts were made to avoid the so-called vulnerable period. During the initial period of the first 40 treatments, more shocks (up to 9) per attempted conversion were given than later during the study when no more than four to five shocks were given in a single attempt. In addition, 8 episodes of supraventricular and 35 episodes of ventricular tachycardia (in 7 and 13 patients) were treated with non-synchronised countershocks, making a total of 119 non-synchronised D.c. shock treatments. .
Results
Atrial Fibrillation
I
The results are shown in table i. The conversion-rate equal in both groups as indicated by the percentages83% and 84% respectively. The mean energy needed for conversion was somewhat higher in the group of nonsynchronised cases, but this group included more advanced cases with longer duration of atrial fibrillation. In both groups atrial, nodal, and ventricular ectopic beats were frequently seen immediately after the countershock. These usually ceased after a few minutes. Again, in both groups instability of conduction-time, first and second degree heart-block, depression or elevation of S.T.segment, inversion of the T-wave, and a u-wave were equally manifest. No changes in the E.S.R. were noted. The frequency of raised serum-glutamic-oxaloacetic-transaminase (S.G.O.T.) levels (up to a maximum of 156 units) was the same for both groups. Raised white-cell counts were not observed. In 1 patient (table i), a 60-year-old obese man with chronic bronchitis, coronary heart-disease, and congestive failure, sinus rhythm was obtained without complications with the second (200 joules) synchronised D.C. shock. He died suddenly twelve hours after the defibrillation, and at necropsy no signs of embolism or myocardial damage were found. He had been given digoxin and diuretics for compensation and, for three days, quinidine 1-2 g. a day before the attempt at conversion. In this patient, the exact cause of cardiac arrest remains obscure.
was
Supraventricular Tachycardia
episodes of supraventricular tachycardia were conto sinus rhythm with a single 100-joule nonsynchronised shock. In 1 patient energy up to 400 joules and 5 shocks were needed; a slight rise in the s.G.o.T. level followed. In another patient an injury current lasting a
The verted
few seconds
arrhythmia
was noted. occurred.
No attacks
of ventricular
406 TABLE II-RESULTS WITH NON-SYNCHRONISED D.C. COUNTERSHOCKS IN 13 PATIENTS WITH VENTRICULAR TACHYCARDIA
tion decreased rapidly when energy levels were increase and was uncommon at a level above 75 joules (Scheinin et al. 1966). On the other hand, very high levels of enert do produce severe arrhythmias and morphological chac irrespective of the period of the cardiac cycle (Pele4
1963). The significance of synchronisation of the D.C. counter. shock in man is not clearly elucidated. Severe post-sh4
Ventricular
Tachycardia
The results and complications are presented in table 11. In 1 patient, a 56-year-old woman (* in table 11) who was in a terminal state-deep shock, hypoxia, pulmonary oedema-D.c. shocks were followed by sinus rhythm which was converted to ventricular fibrillation within a minute or two, but this was readily abolished by a new shock. This happened on three consecutive occasions. After the last shock, the rhythm was converted to atrial fibrillation. The patient is still alive one year after the episode. Another patient (tin table 11) proved to be resistant to 10 D.c. shocks, but thereafter was converted to sinus rhythm with intravenous procainamide. Two days later, she again had ventricular tachycardia which was converted to sinus rhythm after the seventh discharge. A 54-year-old man (t in table 11) with a previous inferior infarction was treated 22 times throughout a period of two years. On 19 occasions conversion was obtained with a single 100-joule discharge, once with 2 shocks, and twice with 5 shocks, without untoward effects of any kind. Anti-arrhythmic drugs in high dosage, such as procainamide, quinidine, ajmaline (rauwolfine), propranolol, antazoline, and diphenylhydantoin, failed to control new attacks of ventricular tachycardia in this patient. Discussion The end of ventricular systole coincident with the T-wave in the electrocardiogram has been demonstrated to be the most vulnerable phase of the cardiac cycle (King 1934, Lown et al. 1962a and b). D.c. defibrillation has been said to be safe, if the impulse is inserted in the cardiac cycle to avoid the vulnerable period (Lown et al. 1962a and b), the optimum position for the impulse being at or near the nadir of the s-wave. In dogs, however, Peleska (1963) found that the arrhythmias caused by a condenser discharge of constant intensity were fewer and milder when the shock was given during the excitation period (corresponding to the p-wave) than during the absolute refractory period (A.R.P.) (corresponding to the s-wave) or the relative refractory period (R.R.P.) (corresponding to the T-wave). The difference in the frequency of arrhythmias between the A.R.P. and R.R.P. was not statistically significant. Moreover, the danger of ventricular fibrillation has been also shown to be related to the energy employed (Lown et al. 1962a and b, King 1934, Peleska 1963, Scheinin et al. 1966). From results in guineapigs (King 1934) increasing the current up to 50 times the threshold value (=the minimum current necessary to cause ventricular fibrillation) still left some danger of fibrillation, but with currents 150 times greater fibrillation was not observed. In dogs, ventricular fibrilla-
arrhythmias-ventricular tachycardia, flutter, or fibrilla. tion-have been reported and attributed to impropc: synchronisation (Killip 1963, Morris et al. 1964, Wilfu 1964, Castellanos et al. 1965), or they have appeared despite adequate synchronisation (Killip 1963, Lown et al, 1964). In addition, a second type of ventricular arrhythmia, appearing after the countershock has established sinus rhythm, may be related to the toxic effects of quinidine or digitalis (Rabbino et al. 1964, Castellanos et al. 1965, De Sanctis 1965) enhanced by countershock. As far as we know (Waris et al. 1965) no series other than the present based on D.C. countershock therapy without synchronisation has been reported. The conversion-rate to sinus rhythm in the present series corresponds in all arrhythmia groups to results reported by other workers using synchronised D.c. shock. The incidence of severe ventricular arrhythmias in the non-synchronised group of the present series is 3/354 (0-84%), which is similar to that reported by Lown et al.(1962) (3/600 [0’5%]) and Castellanos et al. (1965) (6/731 [0-82%]). The only case of ventricular fibrillation occurred in a patient with ventricular tachycardia, and the arrhythmia may have been a result of electric shock given in an anoxaemic and acidotic state of the heart. In the synchronised group, 1 sudden death occurred twelve hours after successful cardioversion, which was perhaps an arrhythmia due to quinidine toxicity (Castellanos et al.
1965). Injury current of a few seconds’ duration was observed in 3 patients after nQn-synchronised and in 1 patient after synchronised shock, a finding reported more or less frequently in completely synchronised D.c.-shock series (Killip 1963, Oram and Davies 1964, Sussman et at. 1964). In the present series, 354 D.C. countershocks without synchronisation were given, and no attempts were made to avoid the so-called vulnerable period. The results and complications do not differ from those reported by others after synchronised D.C. shock. The dangers of nonsynchronised D.c. shocks using the energy levels now in general use (100-400 joules) seem to have been exaggerated. We found no difference in the relapse-rate in the w groups that could be attributed to synchronisation. Reported arrhythmias are probably due to multiple mechanisms, as stated by Killough and Eliades (1965). It is obvious that drugs, metabolic and electrolyte disturbances, and anoxia play some role in the production« arrhythmias. Further investigations are necessary establish the role of the vulnerable period and ott factors that might precipitate severe arrhythmias in the
human heart.
Summary A total of 354 non-synchronised countershocks wert given in various arrhythmias and no attempts made10 avoid the so-called vulnerable period. 272 non-syl1’ chronised direct-current (D.c.) shocks were given in instances of atrial fibrillation. The results and comply tions did not differ from those of a total of 119 countershocks given in 36 instances of atrial fibrillationz this series, and of figures so far reported. No immedi
synchrony
407
complications
in the form of ventricular fibrillation
were
seen.
non-synchronised D.C. shocks were given for 8 episodes of supraventricular tachycardia; they were all readily converted without complications. Of the 35 episodes of ventricular tachycardia treated with non-synchronised D.C. shock, 33 patients were converted to sinus rhythm, 1 to atrial fibrillation, and 1 remained as ventricular tachycardia despite 10 shocks. In 1 patient ventricular fibrillation occurred three times in succession after shocks. In the light of the present series we consider that the dangers of non-synchronised D.c. countershocks have been largely overstated. 12
Requests for reprints should be addressed to K.-E. K., Department of Medicine, University of Oulu, Oulu, Finland. REFERENCES
Brown, K. W. G., Whitehead, E. H., Morrow, J. D. (1964) Can. med. Ass. J. 90, 103. Castellanos, A., Lemberg, L., Gilmore, H., Johnson, D. (1965) Am. J. Med. Sci. 250, 254. Cullhed, I., Holmdahl, M., Malers, E. (1964) Svenska Läkartidn. 61, 742. DeSanctis, R. W. (1965) J. Am. med. Ass. 191, 632. Graf, W. S., Etkins, P. (1964) ibid. 190, 470. Hurst, J. W., Paulk, E. A., Proctor, H. D., Schlant, R. C. (1964) Am. J. Med. 37, 728. Killip, Th. (1963) J. Am. med. Ass. 186, 107. Killough, J. H., Eliades, W. (1965) Med. Clins N. Am. 49, 1341. King, B. G. (1934) Doctoral thesis. New York. Korsgren, M., Leskinen, E., Peterhoff, W., Bradley, E., Varnauskas, E. (1965) Acta med. scand. suppl. 431. Lown, B., Amarasingham, R., Neuman, J. (1962a) Am. J. Cardiol. 10, 223. (1962b) J. Am. med. Ass. 186, 548. Bey, S. K., Perlroth, M. G., Abe, T. (1963) Am. J. Med. Sci. 246, 257. Kleiger, R., Wolf, G. (1964) Am. Heart J. 67, 282. McDonald, L., Resnekov, L., O’Brien, K. (1964) Br. med. J. i, 1468. Morris, J. J., Kong, Y., North, W. C., McIntosh, H. D. (1964) Am. J. Cardiol. 14, 94. Oram, S., Davies, J. P. H. (1964) Lancet, i, 1294. Pele&sbreve;ka, B. (1963) Circulation Res. 12, 21. Rabbino, M. D , Likoff, W., Dreifees, L. S. (1964) J. Am. med. Ass. 190, 417. Reinikainen, M., Koskinen, P., Pöntinen, P., Siitonen, L. (1965) Acta med. scand. suppl. 178. Ross, E. M. (1964) Archs intern. Med. 114, 811. Scheinin, T. M., Kallio, V., Linna, M. I. (1966) Anns med. exp. Biol. Fenn. 44, 74. Sussman, R. M., Woldenburg, D. H., Cohen, M. (1964) J. Am. med. Ass. 189, 739. Varnauskas, E., Korsgren, M., Peterhoff, W., Bradley, E. (1964) Svenska läkartidn. 61, 1166. Waris, E. K., Scheinin, T. M., Kreus, K-E., Salokannel, S. J., Scheinin, B. M. (1965) Acta med. scand. 178, 309. Willis, W. H. (1964) Am. Heart J. 67, 575. —
—
—
—
—
MALIGNANT MELANOMA IN
that all suspicious lesions excised throughout the State have been examined by the panel members. In the first two-year period, 520 new patients with all varieities of malignant melanoma were registered. These included patients with ocular, visceral, and cutaneous lesions besides those who presented with secondaries and no known primary. We have analysed the first 400 cases of cutaneous melanoma on which there has been complete agreement by the panel of pathologists.
Pathological Classification The prognosis of malignant melanoma of the skin may be influenced by the depth of invasion of tumour at the time of removal. Tumours limited to the epidermis or the superficial dermis seem to have a better prognosis than those where the dermis is more deeply invaded (Petersen et al. 1962, Mehnert and Heard 1965). In the survey, the depth of invasion of the dermis by the tumour has been noted, but for the purposes of this paper the lesions have been grouped under three broad headings-malignant melanoma-in-situ, superficial malignant melanoma, and invasive malignant melanoma-comparable to those of Petersen et al. (1962), Lund and Kraus (1962), and Mehnert and Heard (1965). Malignant Melanoma-in-situ These tumours contained cells occurring both individually and in groups which were considered to be cytologically malignant but were restricted to the epidermis. This stage caused the greatest disagreement between the panel of pathologists since the cytology of malignant cells merges with that of actively proliferating but benign junctional neavi. Only those cases which have been clearly labelled malignant by all members of the panel independently are listed. If one or more members of the panel called a tumour borderline or benign, it has been excluded. Serial or step sections to exclude dermal invasion elsewhere in the tissue were not done but transverse and longitudinal blocks were always taken.
Superficial Malignant Melanoma In this group there was definite evidence of dermal invasion limited to the papillary layer or superficial part of the dermis. The tumours ranged from those with only a few clumps of cells in the superficial dermis to larger expansile growths with
QUEENSLAND
ANALYSIS OF 400 SKIN LESIONS M.B.
NEVILLE C. DAVIS Sydney, F.R.C.S., F.R.A.C.S. VISITING SURGEON
M.B.
JOHN J. HERRON Queensland, F.R.C.S., F.R.C.S.E. SENIOR RESEARCH FELLOW
M.B.
G. RODERICK MCLEOD Queensland, F.R.C.S., F.R.C.S.E., F.R.A.C.S. RESEARCH FELLOW
From the
Queensland Melanoma Project, Princess Alexandra Hospital, Brisbane, Australia
A PROSPECTIVE survey into malignant melanoma has been conducted in Queensland since July, 1963 (Davis and Herron 1966). All medical practitioners in the
State have cooperated by notifying new cases of malignant melanoma to a registry at the Princess Alexandra Hospital, Brisbane. Pathologists have referred material for further examination to a panel of pathologists established at this hospital; and their full cooperation has ensured
Fig. 1-Distribution of melanomas.
NON-SYNCHRONISED AND SYNCHRONISED DIRECT-CURRENT COUNTERSHOCK IN CARDIAC ARRHYTHMIAS
TABLE I-RESULTS AND COMPLICATIONS IN SYNCHRONISED AND NONSYNCHRONISED CONVERSION ATTEMPTS IN 95 PATIENTS WITH ATRIAL FIBRILLATION
K.-E. KREUS M.D. MEDICAL REGISTRAR
S.
J. SALOKANNEL
E. K. WARIS M.D.
M.D. LECTURER
SENIOR LECTURER
DEPARTMENT OF MEDICINE, UNIVERSITY OF
OULU, OULU,
FINLAND
SINCE Lown et al. (1962a and b, 1963) reported their results, synchronised direct-current (D.c.) shock to terminate cardiac arrhythmias has rapidly gained widespread acceptance (Killip 1963, Brown et al. 1964, Cullhed et al. 1964, Graf and Etkins 1964, Hurst et al. 1964, McDonald et al. 1964, Morris et al. 1964, Oram and Davies 1964, Varnauskas et al. 1964, Korsgren et al. 1965, Reinikainen et al. 1965). Complications have been uncommon, though severe arrhythmias (Graf and Etkins 1964, Ross 1964, Korsgren et al. 1965) and even fatalities (Rabbino et al. 1964) have been reported. According to Lown it is essential to use an electronic synchroniser for the D.C. shock to avoid the vulnerable phase (the initial portion of the T-wave in the cardiac cycle (King 1934). Other workers (Killip 1963, Oram and Davies 1964, Korsgren et al. 1965) share this opinion, and as a result of their experience with completely synchronised D.C. shock have pointed out the importance of synchronisation. The present report describes our experience of nonsynchronised and synchronised D.C. countershock in the treatment of various cardiac arrhythmias. Methods and Patients Countershocks were administered by means of a D.C. defibrillator without a synchronisation device (CorbinFamsworth, Palo Alto, California) and with two apparatuses with synchronisation devices (Corbin-Farnsworth and Electrodyne Inc. C-100 M, D-84 M). The electrodes were placed in the oblique (Lown et al. 1962a) or the transverse (Cullhed et al. 1964) position. A 100 watt-second (joule) discharge was, administered initially with subsequent countershocks of 200, 300, and 400 joules as required. The 400 joule shocks were repeated either until normal sinus rhythm was established or until further attempts were considered futile for the time being. All patients were premedicated (50 mg. pethidine and 0-5 mg. atropine) and anaathetised with 100-250 mg. pentobarbitone sodium in the manner reported earlier (Waris et al. 1965). Each patient was subsequently followed up with repeated estimations of the erythrocyte-sedimentation rate (E.S.R.) and serum-transaminase, serial white-cell-counts, and E.C.G. recordings before defibrillation and on the first, second, and third day thereafter. The series consisted of 95 patients with atrial fibrillation A total of 112 episodes were treated in 76 instances with nonsynchronised D.C. shock and in 36 instances with synchronised D.c. shock. The series included many elderly patients with advanced chronic heart-disease of varying aetiology. Most of them had long-standing atrial fibrillation and nearly all had DR. SHEARMAN AND OTHERS: REFERENCES
Anderson, B. B. (1964) J. clin. Path. 17, 14. Ardeman, S., Chanarin, I. (1963) Lancet, ii, 1350. Girdwood, R. H. (1956) Q. Jl Med. 25, 87. — (1960) Scott. med. J. 5, 10. Irvine, W. J. (1963) Q. Jl exp. Physiol. 48, 427. ’1965) New. Engl. J. Med. 273, 432. Kaplan, H. S., Rigler, L. G. (1945) Am. J. med. Sci. 209, 339. Kay, A. W. (1953) Br. med. J. ii, 77. Mosbech, J., Videbaek, A. (1950) ibid. ii, 390. Schade, R. O. K. (1958) ibid. i, 743. Taylor, K. B., Roitt, I. M., Doniach, D., Couchman, K. G., Shapland, C (1962) ibid. ii, 1347. —
*
1 sudden death.
been previously treated with digitalis and with quinidine for at least three days before the attempted conversion. The the of were for at patients great majority given anticoagulants least three weeks before conversion was attempted. The first 40 episodes were treated with a non-synchronised D.c. defibrillator and, thereafter, every second conversion attempt was made with synchronised D.c. defibrillator until a total of 76 non-synchronised and 36 synchronised defibrillation attempts had been made. In the non-synchronised group, no efforts were made to avoid the so-called vulnerable period. During the initial period of the first 40 treatments, more shocks (up to 9) per attempted conversion were given than later during the study when no more than four to five shocks were given in a single attempt. In addition, 8 episodes of supraventricular and 35 episodes of ventricular tachycardia (in 7 and 13 patients) were treated with non-synchronised countershocks, making a total of 119 non-synchronised D.c. shock treatments. .
Results
Atrial Fibrillation
I
The results are shown in table i. The conversion-rate equal in both groups as indicated by the percentages83% and 84% respectively. The mean energy needed for conversion was somewhat higher in the group of nonsynchronised cases, but this group included more advanced cases with longer duration of atrial fibrillation. In both groups atrial, nodal, and ventricular ectopic beats were frequently seen immediately after the countershock. These usually ceased after a few minutes. Again, in both groups instability of conduction-time, first and second degree heart-block, depression or elevation of S.T.segment, inversion of the T-wave, and a u-wave were equally manifest. No changes in the E.S.R. were noted. The frequency of raised serum-glutamic-oxaloacetic-transaminase (S.G.O.T.) levels (up to a maximum of 156 units) was the same for both groups. Raised white-cell counts were not observed. In 1 patient (table i), a 60-year-old obese man with chronic bronchitis, coronary heart-disease, and congestive failure, sinus rhythm was obtained without complications with the second (200 joules) synchronised D.C. shock. He died suddenly twelve hours after the defibrillation, and at necropsy no signs of embolism or myocardial damage were found. He had been given digoxin and diuretics for compensation and, for three days, quinidine 1-2 g. a day before the attempt at conversion. In this patient, the exact cause of cardiac arrest remains obscure.
was
Supraventricular Tachycardia
episodes of supraventricular tachycardia were conto sinus rhythm with a single 100-joule nonsynchronised shock. In 1 patient energy up to 400 joules and 5 shocks were needed; a slight rise in the s.G.o.T. level followed. In another patient an injury current lasting a
The verted
few seconds
arrhythmia
was noted. occurred.
No attacks
of ventricular
406 TABLE II-RESULTS WITH NON-SYNCHRONISED D.C. COUNTERSHOCKS IN 13 PATIENTS WITH VENTRICULAR TACHYCARDIA
tion decreased rapidly when energy levels were increase and was uncommon at a level above 75 joules (Scheinin et al. 1966). On the other hand, very high levels of enert do produce severe arrhythmias and morphological chac irrespective of the period of the cardiac cycle (Pele4
1963). The significance of synchronisation of the D.C. counter. shock in man is not clearly elucidated. Severe post-sh4
Ventricular
Tachycardia
The results and complications are presented in table 11. In 1 patient, a 56-year-old woman (* in table 11) who was in a terminal state-deep shock, hypoxia, pulmonary oedema-D.c. shocks were followed by sinus rhythm which was converted to ventricular fibrillation within a minute or two, but this was readily abolished by a new shock. This happened on three consecutive occasions. After the last shock, the rhythm was converted to atrial fibrillation. The patient is still alive one year after the episode. Another patient (tin table 11) proved to be resistant to 10 D.c. shocks, but thereafter was converted to sinus rhythm with intravenous procainamide. Two days later, she again had ventricular tachycardia which was converted to sinus rhythm after the seventh discharge. A 54-year-old man (t in table 11) with a previous inferior infarction was treated 22 times throughout a period of two years. On 19 occasions conversion was obtained with a single 100-joule discharge, once with 2 shocks, and twice with 5 shocks, without untoward effects of any kind. Anti-arrhythmic drugs in high dosage, such as procainamide, quinidine, ajmaline (rauwolfine), propranolol, antazoline, and diphenylhydantoin, failed to control new attacks of ventricular tachycardia in this patient. Discussion The end of ventricular systole coincident with the T-wave in the electrocardiogram has been demonstrated to be the most vulnerable phase of the cardiac cycle (King 1934, Lown et al. 1962a and b). D.c. defibrillation has been said to be safe, if the impulse is inserted in the cardiac cycle to avoid the vulnerable period (Lown et al. 1962a and b), the optimum position for the impulse being at or near the nadir of the s-wave. In dogs, however, Peleska (1963) found that the arrhythmias caused by a condenser discharge of constant intensity were fewer and milder when the shock was given during the excitation period (corresponding to the p-wave) than during the absolute refractory period (A.R.P.) (corresponding to the s-wave) or the relative refractory period (R.R.P.) (corresponding to the T-wave). The difference in the frequency of arrhythmias between the A.R.P. and R.R.P. was not statistically significant. Moreover, the danger of ventricular fibrillation has been also shown to be related to the energy employed (Lown et al. 1962a and b, King 1934, Peleska 1963, Scheinin et al. 1966). From results in guineapigs (King 1934) increasing the current up to 50 times the threshold value (=the minimum current necessary to cause ventricular fibrillation) still left some danger of fibrillation, but with currents 150 times greater fibrillation was not observed. In dogs, ventricular fibrilla-
arrhythmias-ventricular tachycardia, flutter, or fibrilla. tion-have been reported and attributed to impropc: synchronisation (Killip 1963, Morris et al. 1964, Wilfu 1964, Castellanos et al. 1965), or they have appeared despite adequate synchronisation (Killip 1963, Lown et al, 1964). In addition, a second type of ventricular arrhythmia, appearing after the countershock has established sinus rhythm, may be related to the toxic effects of quinidine or digitalis (Rabbino et al. 1964, Castellanos et al. 1965, De Sanctis 1965) enhanced by countershock. As far as we know (Waris et al. 1965) no series other than the present based on D.C. countershock therapy without synchronisation has been reported. The conversion-rate to sinus rhythm in the present series corresponds in all arrhythmia groups to results reported by other workers using synchronised D.c. shock. The incidence of severe ventricular arrhythmias in the non-synchronised group of the present series is 3/354 (0-84%), which is similar to that reported by Lown et al.(1962) (3/600 [0’5%]) and Castellanos et al. (1965) (6/731 [0-82%]). The only case of ventricular fibrillation occurred in a patient with ventricular tachycardia, and the arrhythmia may have been a result of electric shock given in an anoxaemic and acidotic state of the heart. In the synchronised group, 1 sudden death occurred twelve hours after successful cardioversion, which was perhaps an arrhythmia due to quinidine toxicity (Castellanos et al.
1965). Injury current of a few seconds’ duration was observed in 3 patients after nQn-synchronised and in 1 patient after synchronised shock, a finding reported more or less frequently in completely synchronised D.c.-shock series (Killip 1963, Oram and Davies 1964, Sussman et at. 1964). In the present series, 354 D.C. countershocks without synchronisation were given, and no attempts were made to avoid the so-called vulnerable period. The results and complications do not differ from those reported by others after synchronised D.C. shock. The dangers of nonsynchronised D.c. shocks using the energy levels now in general use (100-400 joules) seem to have been exaggerated. We found no difference in the relapse-rate in the w groups that could be attributed to synchronisation. Reported arrhythmias are probably due to multiple mechanisms, as stated by Killough and Eliades (1965). It is obvious that drugs, metabolic and electrolyte disturbances, and anoxia play some role in the production« arrhythmias. Further investigations are necessary establish the role of the vulnerable period and ott factors that might precipitate severe arrhythmias in the
human heart.
Summary A total of 354 non-synchronised countershocks wert given in various arrhythmias and no attempts made10 avoid the so-called vulnerable period. 272 non-syl1’ chronised direct-current (D.c.) shocks were given in instances of atrial fibrillation. The results and comply tions did not differ from those of a total of 119 countershocks given in 36 instances of atrial fibrillationz this series, and of figures so far reported. No immedi
synchrony
407
complications
in the form of ventricular fibrillation
were
seen.
non-synchronised D.C. shocks were given for 8 episodes of supraventricular tachycardia; they were all readily converted without complications. Of the 35 episodes of ventricular tachycardia treated with non-synchronised D.C. shock, 33 patients were converted to sinus rhythm, 1 to atrial fibrillation, and 1 remained as ventricular tachycardia despite 10 shocks. In 1 patient ventricular fibrillation occurred three times in succession after shocks. In the light of the present series we consider that the dangers of non-synchronised D.c. countershocks have been largely overstated. 12
Requests for reprints should be addressed to K.-E. K., Department of Medicine, University of Oulu, Oulu, Finland. REFERENCES
Brown, K. W. G., Whitehead, E. H., Morrow, J. D. (1964) Can. med. Ass. J. 90, 103. Castellanos, A., Lemberg, L., Gilmore, H., Johnson, D. (1965) Am. J. Med. Sci. 250, 254. Cullhed, I., Holmdahl, M., Malers, E. (1964) Svenska Läkartidn. 61, 742. DeSanctis, R. W. (1965) J. Am. med. Ass. 191, 632. Graf, W. S., Etkins, P. (1964) ibid. 190, 470. Hurst, J. W., Paulk, E. A., Proctor, H. D., Schlant, R. C. (1964) Am. J. Med. 37, 728. Killip, Th. (1963) J. Am. med. Ass. 186, 107. Killough, J. H., Eliades, W. (1965) Med. Clins N. Am. 49, 1341. King, B. G. (1934) Doctoral thesis. New York. Korsgren, M., Leskinen, E., Peterhoff, W., Bradley, E., Varnauskas, E. (1965) Acta med. scand. suppl. 431. Lown, B., Amarasingham, R., Neuman, J. (1962a) Am. J. Cardiol. 10, 223. (1962b) J. Am. med. Ass. 186, 548. Bey, S. K., Perlroth, M. G., Abe, T. (1963) Am. J. Med. Sci. 246, 257. Kleiger, R., Wolf, G. (1964) Am. Heart J. 67, 282. McDonald, L., Resnekov, L., O’Brien, K. (1964) Br. med. J. i, 1468. Morris, J. J., Kong, Y., North, W. C., McIntosh, H. D. (1964) Am. J. Cardiol. 14, 94. Oram, S., Davies, J. P. H. (1964) Lancet, i, 1294. Pele&sbreve;ka, B. (1963) Circulation Res. 12, 21. Rabbino, M. D , Likoff, W., Dreifees, L. S. (1964) J. Am. med. Ass. 190, 417. Reinikainen, M., Koskinen, P., Pöntinen, P., Siitonen, L. (1965) Acta med. scand. suppl. 178. Ross, E. M. (1964) Archs intern. Med. 114, 811. Scheinin, T. M., Kallio, V., Linna, M. I. (1966) Anns med. exp. Biol. Fenn. 44, 74. Sussman, R. M., Woldenburg, D. H., Cohen, M. (1964) J. Am. med. Ass. 189, 739. Varnauskas, E., Korsgren, M., Peterhoff, W., Bradley, E. (1964) Svenska läkartidn. 61, 1166. Waris, E. K., Scheinin, T. M., Kreus, K-E., Salokannel, S. J., Scheinin, B. M. (1965) Acta med. scand. 178, 309. Willis, W. H. (1964) Am. Heart J. 67, 575. —
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MALIGNANT MELANOMA IN
that all suspicious lesions excised throughout the State have been examined by the panel members. In the first two-year period, 520 new patients with all varieities of malignant melanoma were registered. These included patients with ocular, visceral, and cutaneous lesions besides those who presented with secondaries and no known primary. We have analysed the first 400 cases of cutaneous melanoma on which there has been complete agreement by the panel of pathologists.
Pathological Classification The prognosis of malignant melanoma of the skin may be influenced by the depth of invasion of tumour at the time of removal. Tumours limited to the epidermis or the superficial dermis seem to have a better prognosis than those where the dermis is more deeply invaded (Petersen et al. 1962, Mehnert and Heard 1965). In the survey, the depth of invasion of the dermis by the tumour has been noted, but for the purposes of this paper the lesions have been grouped under three broad headings-malignant melanoma-in-situ, superficial malignant melanoma, and invasive malignant melanoma-comparable to those of Petersen et al. (1962), Lund and Kraus (1962), and Mehnert and Heard (1965). Malignant Melanoma-in-situ These tumours contained cells occurring both individually and in groups which were considered to be cytologically malignant but were restricted to the epidermis. This stage caused the greatest disagreement between the panel of pathologists since the cytology of malignant cells merges with that of actively proliferating but benign junctional neavi. Only those cases which have been clearly labelled malignant by all members of the panel independently are listed. If one or more members of the panel called a tumour borderline or benign, it has been excluded. Serial or step sections to exclude dermal invasion elsewhere in the tissue were not done but transverse and longitudinal blocks were always taken.
Superficial Malignant Melanoma In this group there was definite evidence of dermal invasion limited to the papillary layer or superficial part of the dermis. The tumours ranged from those with only a few clumps of cells in the superficial dermis to larger expansile growths with
QUEENSLAND
ANALYSIS OF 400 SKIN LESIONS M.B.
NEVILLE C. DAVIS Sydney, F.R.C.S., F.R.A.C.S. VISITING SURGEON
M.B.
JOHN J. HERRON Queensland, F.R.C.S., F.R.C.S.E. SENIOR RESEARCH FELLOW
M.B.
G. RODERICK MCLEOD Queensland, F.R.C.S., F.R.C.S.E., F.R.A.C.S. RESEARCH FELLOW
From the
Queensland Melanoma Project, Princess Alexandra Hospital, Brisbane, Australia
A PROSPECTIVE survey into malignant melanoma has been conducted in Queensland since July, 1963 (Davis and Herron 1966). All medical practitioners in the
State have cooperated by notifying new cases of malignant melanoma to a registry at the Princess Alexandra Hospital, Brisbane. Pathologists have referred material for further examination to a panel of pathologists established at this hospital; and their full cooperation has ensured
Fig. 1-Distribution of melanomas.