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A MONOPULSE DC CURRENT DEFIBRILLATOR * FOR VENTRICULAR DEFIBRILLATION
A MONOPULSE D C CURRENT FOR VENTRICULAR
DEFIBRILLATION
R. C. Balagot, M.D., W. S. Druz,** E. ]obgen, M. Tomita,
DEFIBRILLATOR*
M. Ramadan**
M. Lopez-Belio,
M.D., and M. S. Sadove, M.D.,
M.D.,
Chicago, III.
B
OTH a capacitor discharge and an alternating current have been shown to be effective in shocking a ventricle out of fibrillation by direct application to the exposed heart. 1 The simplicity, availability, and the successful internal defibrillation of a prolonged ventricular fibrillation in a human subject by Beck2 gained an initial advantage in popular usage for the AC defibrillator. How ever, thoracotomy in an emergency to expose the heart remains a formidable procedure. Further studies showed eventually that defibrillation may be effected through the closed chest provided sufficient voltage and, therefore, current was available.3' *•5 The minimum alternating current necessary to provoke gen eralized intense contraction of the myocardium has been shown to be around 1.0 ampere 3 ' 6 for the exposed heart and around 3 amperes for the closed chest; the resistances encountered average 50 ohms and 90 ohms, respectively. Currents smaller than 1 ampere, applied externally, 3 will frequently throw a normal heart into fibrillation instead of a generalized contraction. Obviously, the effect of an alternating current on the myocardium is excitation and not inhibition. Thus, sufficient current density per unit of weight of myocardium is essential to successful ventricular defibrillation. Such immediately poses two problems, that is, availability of sufficient source voltage to generate the needed AC cur rent, and excessive tissue heat generation with possible thermal damage to the myocardium. For example, a current of 5 amperes across a closed-chest re sistance of 90 ohms will generate heat equivalent to an energy of (W = P R ) 2,250 watts or about 562 joules for 0.25 second optimum period recommended that the stimulus be applied. A similar but lesser amount of energy may be ob tained from a capacitor and applied to the heart for a shorter period of time to achieve possibly better end results. Thermal damages to the myocardium and thoracic wall are thus obviated. Defibrillatory effectiveness of a capacitor discharge depends on the stored energy of the condenser which is equivalent to one half the capacitance times the voltage squared, thus: Wg = % CV2. From the University of Illinois, College of Medicine, Department of Surgery, Division of Anesthesiology, Chicago, 111. Received for publication Aug. 23, 1963. •Developed by the Research Department of Zenith Radio Corporation, Chicago, 111. **Prom the Research Department of Zenith Radio Corporation, Chicago, 111. 487
BALAGOT ET AL.
488
J. Thoracic and Cardiovas. Surg.
I t is evident from Peleska's work in his quest for the optimum defibrillation threshold and other workers 6 , 7 ' 8 - 9 that: (1) myocardial damage is more de pendent on the absolute voltage than the total energy supplied from the capac itor; (2) the defibrillation threshold voltage decreases exponentially as capac itance increases (Fig. 1) and approaches asymptotically a limiting value, about 1.5 kv.; (3) a threshold current has to be exceeded for a required period of time to effect defibrillation. The extent by which the threshold is exceeded deter mines the amount of damage that may be caused various tissues. Based on these considerations, a threshold defibrillating current has been developed which ex ceeds the minimum threshold by a safe margin and which continues at this level for a time sufficient to ensure defibrillation with the least amount of total stored energy. KV
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Description of Unit.—In essence, a delay line discharge pulser10 with two sections of capacitance and inductance having a characteristic impedance Ro = V L/C is employed to provide a defibrillation pulse which has a maximum rise time consistent with the greatest duration at its peak possible for the total value of inductance and capacitance used. It is well known in the theory of radar pulsers that a given value of mutual inductance between inductances which form the individual sections of a delay line is necessary to produce a wave form that has the smallest deviation or dip from the maximum amplitude attained during discharge. The pulse as observed
Vol. 47, No. 4 April, 1964
M O N O P U L S E DC CURRENT
489
DEFIBR1LLATOR
on the oscilloscope has the shape shown in Pig. 2. The energy delivered to the subject is maintained at its peak value and rapidly decreases to zero when the resistance of the subject is equal to the characteristic impedance of the delay line. In case the impedance of the subject is less than the characteristic imped ance, reflections occur at the termination in such a fashion that the peak current through the subject is maintained almost constant but voltage avail able decreases. Such is a property of a delay line constructed of dissipative ele ments. Compared to a critically damped single capacitance and inductance of the same total value, the maximum rate of discharge in this instance is reached much sooner. It then persists for almost the full period in such a manner that the current which exceeds the threshold for defibrillation lasts for a signifi cantly longer period of time for the same value of stored energy (Fig. 3).
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F i g . 2.—Delay line d i s c h a r g e . F i g . 3.—A delay line p u l s e w a v e c o m p a r e d to a c r i t i c a l l y d a m p e d single c a p a c i t a n c e a n d i n d u c t a n c e p u l s e w a v e of t h e s a m e t o t a l v a l u e .
The wave form of voltage available across the terminals connected to a patient with a thoracic resistance of 100 ohms has a duration of approximately 10 milli seconds. With a resistance of 50 ohms, the wave form still has a duration of 10 milliseconds but of smaller voltage amplitude (see Fig. 2). The excess energy is dissipated in the delay line losses. The latter characteristic enables it to be employed for either internal or external defibrillation without any modification or readjustment. The constants of the delay line are: (1) total inductance, 0.4 Henries centertapped; (2) mutual inductance, 0.05 Henries; (3) capacitance per section, 20 microfarads. As a result of the highly efficient solid state switching circuitry (transistors, diode rectifiers, etc.) a large peak current can be supplied to effect charging or recharging in three seconds. Even with an almost totally discharged (about 90 per cent) battery, the charge time does not exceed four seconds. A built-in sensing circuit maintains a nearly constant value of charge on the capacitors and keeps the equipment ready for immediate use. This is accom plished with a minimum drain on the internal battery. The unit is completely portable and weighs 33 pounds. Included in the case is a battery charger for
BALAGOT E T AL.
490
J. Thoracic and Cardiovas. Surg.
OUTPUT
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LINE
POWER
F i g . 4.—DC m o n o p u l s e
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recharging the 12 volt, 4 ampere hour battery. Provisions are incorporated for testing the battery on the same meter used for indicating the watt-seconds of stored energy. The elemental diagram of the equipment is shown in Pig. 4. METHODS
Ventricular fibrillation was produced in dogs by either of two methods: (1) transthoracic application of 100 milliamperes 11 alternating current for 1 to 6 seconds; (2) ligation of the circumflex and anterior descending coronary arteries. Inhalation of chloroform or halothane and subsequent intravenous in jection of epinephrine proved to be an unreliable method for provoking ven tricular fibrillation. Continuous tracings of femoral arterial pressure and elec trocardiogram were recorded except when ventricular fibrillation was provoked (with the small AC current) and the instant the defibrillatory shock was ad ministered transthoracically. The animals were under sodium pentobarbital, 25 mg./Kg. body weight, and artificially respired with a Bird respirator, or a Harvard respirator (for dogs whose circumflex and anterior descending coronaries were ligated). Electrical Fibrillation.—Three types of situations were utilized for this phase of the experimental evaluation. In the first series of dogs (6), fibrillation was effected with the 100 milliampere AC current applied transthoracically for 1 to 6 seconds and the heart was allowed to fibrillate for a period of 2 minutes. This arbitrary time limit was initially selected as an adequate test for the defibrillatory potential of any unit inasmuch as myocardial sensitivity to a defibrillating shock decreased pro gressively with increasing cardiac anoxia. Kouwenhoven's 12 original experiments along the same pattern showed that a 2 minute fibrillation still allowed 93 per cent defibrillation and a 30 per cent survival rate. Our defibrillation rate for
Vol. 47. No. 4 April, 1964
MONOPULSE DC CURRENT D E F I B R I L L A T O R
491
both the monopulse DC defibrillator set at 80 watt-seconds and the AC unit set at 480 volts was 100 per cent. The survival rate was zero. With either unit, defibrillation was accomplished on the first attempt but blood pressure remained at zero level. Myocardial anoxia was obvious in the electrocardiographic trac ing, that is, a ventricular or nodal rhythm developed and with very tall, peaked T waves, almost as tall as the QRS complex. Closed-chest manual systole did not improve the blood pressure, neither did another defibrillatory shock (Fig. 5). In the second series of 6 dogs, a fibrillation-defibrillation sequence was car ried out. Fibrillation was provoked with the 100 milliampere current applied transthoracically for a period of 1 to 6 seconds until fibrillation developed. The dog was then very quickly subjected to the defibrillatory shock, either 80 wattseconds from the monopulse DC or 480 volts AC. This procedure was repeated every 5 minutes for at least twenty times. The harshness of the effects of the alternating current on the heart was outstanding. Immediately after the fibril lation-defibrillation sequence, blood pressure bounded to at least 50 to 100 mm. Hg higher than prefibrillation-defibrillation. The effect was very similar to the injection of 1.0 mg. of epinephrine intravenously. The electrocardiogram showed the greatest changes. Ventricular extrasystoles immediately developed in the first fibrillation-defibrillation sequence. Runs of tachycardia (sinus) are readily apparent. A depressed S-T segment and inversion of the T wave developed very early and became more pronounced with increased repetition of the fibrillationdefibrillation sequence. Signs of infarction and atrial fibrillation were observed at about the twelfth to fifteenth fibrillation-defibrillation sequence. Severe mus-
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BALAGOT E T AL.
492
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cular contractions (opisthotonos) developed with each deflbrillation, also micturation, salivation, and defecation. The responses just described occurred very mildly or not at all with the DC unit (Fig. 6). Arterial p 0 2 obtained at prefibrillation, at the fifth fibrillation-defibrillation, and the twentieth fibrillation-defibrillation sequences showed a progressive de crease. Although pC0 2 did not show any significant change, both p H and stan dard H C 0 3 showed a marked tendency to metabolic acidosis. Again, these changes were mild in the DC defibrillated dogs (Table I ) .
TABLE I. ACID-BASE AND p 0 2
CHANGES DURING REPEATED FIBRILLATION-DEFIBRILLATION (F-D) SEQUENCE I N DOGS AC.
BLOOD
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Vol. 47, No. 4 April, 1964
MONOPULSE DC CUERENT D E F I B R I L L A T O R
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Fip. 7.— (Fibrillation—1 min.-deflbrillation ; repeated 20 times.) Toxic effects on the heart are more manifest in these series, particularly with the AC defibrillator. Arrhythmias and atrial fibrillation are readily apparent.
In the third series of dogs (6), a similar procedure was followed as in the first and second series but the fibrillation period was increased to 1 minute. Contrary to other investigators' findings, the dogs very easily survived repeated fibrillation periods of 1 minute, and twenty fibrillation-defibrillation sequences were performed on each dog. The changes in the electrocardiogram were not too greatly different from those in the second series in which the fibrillatory period lasted only a few seconds (Fig. 7). Ligation of the circumflex and the anterior descending coronary arteries (5 dogs) usually resulted in ventricular fibrillation within a period varying from 10 to 30 minutes at the most. This was due to the fact that these dogs were artificially ventilated which probably delayed more generalized myocardial hypoxia and hypercarbia. Upon onset of fibrillation, the ligatures were im mediately released, the chest quickly closed with towel clips, and transthoracic defibrillation attempted. The DC defibrillator was employed on 3 dogs and the AC unit on 2 dogs. All of the dogs survived the fibrillation-defibrillation experi ment for 24 hours or more. Both dogs in the AC group died within 48 hours. In the DC group, one dog died after 24 hours of a pulmonary atelectasis, one died after 48 hours, and the other survived indefinitely until subjected to an other fibrillation-defibrillation sequence with fibrillation induced with the small amperage alternating current. Fibrillation caused by ligature of the circumflex and anterior descending coronary arteries is much more resistant to defibrillation because of the greater hypoxia the heart suffers. Upon ligation of both the circumflex and anterior descending coronaries, the heart is observed to turn into almost one huge infarct. Nevertheless, the DC current proved to be more consistent in its ability to
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Fig. 8.—Ventricular fibrillation induced by ligating circumflex and anterior descending coronary arteries. DC defibrillation (closed chest). Four successive DC shocks at 1,500 volts deflbrillated the heart which reflbrillated spontaneously. A single shock of 2,000 volts DC reverted it to normal rhythm.
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Vol. 47. No. 4
MONOPULSE DC CURRENT D E F I B R I L L A T O R
April, 1964
495
defibrillate than the AC current. Fig. 8 shows a heart that defibrillated after four successive shocks of 1,500 volts DC, 45 watt-seconds, 750 volts at the termi nals. It refibrillated spontaneously, but a single shock of 2,000 volts, 80 wattseconds, 1,000 volts at the terminals, reverted it to normal. On the other hand, Fig. 9 shows repeated AC shocks of 220 volts failing to defibrillate the heart. Finally, three successive shocks of 480 volts defibrillated the heart. Effects of DC and AC Defibrillating Impulses on the Normal Dog Heart.— Since a small AC current will fibrillate a normal heart, either monopulse, DC or AC, was applied transthoracically to the normal dog heart (5 dogs) starting from the lowest voltage setting available to the maximum to see if such exigency might develop. Subdermal temperature readings were obtained at the site of electrode-skin contact. Esophageal temperatures were obtained concurrently. Fig. 10 shows the effects of different voltage settings available from the AC defibrillator on the femoral artery pressure and the electrocardiogram. At the "infant setting" (available voltage about 100 volts), the defibrillatory shock provoked fibrillation. Judging from the femoral artery wave forms, there is a noticeable delay in the ability of the normal heart to recover its original state after an AC defibrillating shock, especially with greater voltages. Subdermal temperature readings (electrode-skin contact) showed a rise of 2° to 4° C , which has also been shown by Kouwenhoven and his associates.13 Esophageal temperature was unaffected. The effects of monopulse DC defibrillator shocks on the normal heart trans thoracically (5 dogs), varying from 100 volts (0.2 watt-seconds) to 2,000 volts (80 watt-seconds) as reflected in the femoral artery pressure and electrocardiographic tracings, are shown in Fig. 11. There were no subdermal or esophageal temperature changes. The amount of resistance encountered across the longi tudinal axis of the chest was measured in 2 dogs that weighed 15 kilograms and was found to vary between a very narrow range of 64 to 70 ohms. Since this narrow range of resistance was found to hold for the different voltage set tings from 100 volts to 2,000 volts, terminal voltages of 50 volts to 1,000 volts, respectively, in the same dog, this more or less establishes the ability of this monopulse DC unit to adjust voltage to resistance encountered or implies its ability to be utilized either as an external or internal defibrillator without any modification or readjustment of voltage setting. TABLE I I .
DC
DEFIBRILLATORY SHOCK APPLIED TRANSTHORACICALLY TO SPECIFIC P H A S E ELECTROCARDIOGRAM ECG P H A S E PWAVE
61 0
No. of shocks No. ventricular fibrillations Interval between shocks—1-2 minutes
Total no. of shocks—470 No. of dogs—10 Energy employed—80 watt-second (joules)
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Fig. 9.—Ventricular fibrillation induced by ligating circumflex and anterior descending coronary arteries. AC deflbrillation (closed chest). Ligatures released upon onset of fibrillation. Deflbrillation attempted with repeated AC shocks set at Adult (Medium) failed—Morris deflbrillator. Three successive shocks set at Adult (High) (about 480 volts) flnally deflbrillated the heart.
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Fig. 10.—Effect of AC deflbrillator shocks on normal dog heart (closed chest). Note that it takes longer for the normal heart to return to its original state after an AC deflbrillating shock. At the Infant setting (about 100 volts) on the AC deflbrillator (Morris), a deflbrillating shock induced fibrillation.
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Fig. 11.—Effect of DC deflbrillator shocks on normal dog heart (closed chest). Recovery from the deflbrillatory shock is quite rapid, as shown by the quick return to the pre-shock wave pattern of the femoral blood pressure impulse. The electrocardiogram exhibits a similar response.
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Vol 47 No. 4
MONOPULSE DC CURRENT D E F I B R I L L A T O R
499
A variable impulse timer geared to the electrocardiogram as observed on an oscilloscope and synchronized with the discharge mechanism of the monopulse defibrillator was devised so any phase of the electrocardiogram, such as the P wave, the QRS complex, the S-T segment, the T wave, may be subjected to a shock from the DC defibrillator at the designated instant. A built-in manu ally operated trigger switch in the unit provided a synchronizing pulse derived from the succeeding R wave which activates the delay circuit causing the defibrillatory discharge. The different phases of the electrocardiogram in 10 dogs were subjected to 80 watt-seconds (energy) from the monopulse defibril lator (Table I I ) . The interval between shocks was at least 60 to 120 seconds and both electrocardiogram and femoral blood pressure were monitored. A total of 470 shocks were administered to these dogs without provoking ven tricular fibrillation. On one dog, 50 shocks of 80 joules were administered transthoracically at 10 second intervals indiscriminately of the electrocardiographic phase. Ventricular fibrillation occurred twelve times. These were easily reversed by another defibrillatory shock. When the interval between shocks was increased to 30 seconds, one ventricular fibrillation occurred once in a successive series of 51 shocks. This occurred when the ninth shock of the series was applied to the R wave. It could not be reproduced. With a longer time interval between shocks, for example 60 to 120 seconds, no ventricular fibrillations developed. DISCUSSION
The objectives of this study are easily noted. First, the ability of the monopulse DC unit to effect a defibrillation was established. Different situations were devised (see Methods) to delineate the parameters of this effectiveness. Aside from just testing its defibrillatory capacity, it was compared to a stan dard AC defibrillator unit under similar circumstances to determine advantages or disadvantages, if any, notwithstanding previous observations that a conden ser discharge is superior to an AC current for defibrillatory purposes. The initial problem was devising methods to provoke ventricular fibril lation. The inhalation of chloroform and subsequent intravenous injection of epinephrine, a technique that was highly regarded by pharmacologists and anesthesiologists, proved to be very inconsistent. The application of a small AC current transthoracically for a variable period of time proved to be most con sistent. A condition which was thought to approximate fibrillation following a myocardial infarct was effected by ligating the circumflex and the anterior descending coronary arteries. This was a formidable surgical procedure. Toxic effects on the presumably normal heart in sinus rhythm were sought for by subjecting this type heart to the different voltages available from both the DC and the AC units. In the series of dogs in which fibrillation was effected with a small mag nitude (100 milliampere) alternating current and the heart was allowed to fibrillate for a 2 minute period, resuscitation was next to impossible although defibrillation was successful. Apparently, a 2 minute period of myocardial and, presumably, brain hypoxia was not conducive to successful resuscitation. It is probable that a more definitive treatment of the shock state in these dogs,
500
BALAGOT ET
AL.
J. Thoracic and Cardiovas. Surg.
such as intra-arterial blood transfusions as suggested by Negovskii,14 might have improved survival rates. After all, Negovskii places 5 minutes as the max imum limit of resuscitability of dogs wherein he induces "clinical d e a t h " exsanguination shock to cardiac arrest. Contrary to observations that 30 seconds was the maximum period during which a dog's ventricle may be allowed to fibrillate and still be successfully resuscitated, we find that this period is prob ably closer to between 1.0 and 1.5 minutes. The discrepancy lies probably in the fact that all dogs utilized in these experiments were ventilated artificially. The differences in electrocardiographic and cardiovascular responses (as moni tored by femoral blood pressure changes), in dogs in which the ventricles were allowed to fibrillate and were immediately defibrillated and those that were al lowed to fibrillate for 1 minute, were very minimal, that is, comparing AC defibrillated dogs (immediately) to AC defibrillated dogs (1 minute) and DC (immediately) to DC (1 minute) defibrillated dogs. However, the differences in response between the DC defibrillated dog and the AC defibrillated dog be came very manifest. The AC defibrillating current is definitely more toxic, not only to the heart but to the animal as a whole. After an AC defibrillating shock of 480 volts, it was not uncommon to find runs of ventricular extrasystoles, a depressed S-T segment, an inverted T wave—signs of myocardial ischemia or infarction—and, with more frequent repetition of the fibrillation-defibrillation sequence atrial fibrillation. These changes were not outstanding with the DC defibrillating impulse of 80 watt-seconds, the most common was a depressed S-T segment and sinus tachycardia. The blood pressure response to the AC defibrillating current was very similar to a rapid intravenous injection of at least 1.0 mg. of epinephrine. One thing that was very noticeable about the blood pressure response after an AC defibrillator shock was the time lag be tween the shock and the response. It frequently takes as much as 0.5 to 1.0 second before the heart starts to beat and cause an effective blood pressure, frequently causing one to wonder whether a defibrillation was effected or not. The DC impulse immediately causes a contraction and an effective blood pres sure if a response is forthcoming. The side effects on the whole animal, such as excessive salivation, severe muscular contractions, defecation, and urination, were rarely seen in the DC defibrillated dog. Most of the toxic effects observed with the AC defibrillation in the pre vious series of dogs were also seen in those in which the coronary arteries (circumflex and anterior descending) were ligated. The DC defibrillator was easily superior to the AC unit in these series of experiments. Except for the absence of coronary atherosclerosis, this experimental situation in a way ap proximates the patient that suddenly develops a myocardial infarct. Certainly, the positive response to the discharge from an external defibrillator, particu larly the monopulse DC type, should encourage greater application of these units in cases of acute, frequently fatal, myocardial infarction. An interesting finding is the progressive decrease of arterial oxygen tension with increasing repetition of the fibrillation-defibrillation sequence. Since these dogs were artificially ventilated, it is not too presumptious to assume that some form of interference with oxygen uptake develops from repetitious ap-
Vol. 47, No. 4 April, 1964
MONOPULSE DC CURRENT D E F I B R I L L A T O R
501
plication of AC and DC currents across the chest. The importance of this observation in human cases of ventricular fibrillation is probably remote, al though it is not uncommon in some situations to apply the defibrillatory shock repeatedly. However, metabolic acidosis, which develops from the hypoxia and catecholamine release, may interfere with successful resuscitation of the subject. Although it has been realized that a capacitor discharge has definite ad vantages over an alternating current for ventricular defibrillation, the proper combination of capacitance and inductance that will give the optimum defibril latory threshold was not established for some time. There is no question, how ever, that a pure capacitor discharge is not as effective as one with inductance inserted in series with the condenser. Kouwenhoven was never enthusiastic for the defibrillatory ability of the condenser discharge because he failed to find the right combination of capacitance and inductance. Nevertheless, and this was probably discouraging to him, he demonstrated pretty well that straight capacitor discharges particularly those with greater energy, for example 80-225 watt-seconds, were more harmful to the heart in that they occasionally caused ventricular fibrillation. Presumably, in the experimental situation cited by Kouwenhoven,9 much of the energy was dissipated in the tissue mass of the chest wall and only a small amount reached the heart, thereby provoking ven tricular fibrillation instead of synchronized contraction of the normal heart. Maekay and Leeds6 calculated that only one third of the total energy spent across the closed chest actually reached the heart. Possibly, without inductance to prolong the discharge current at an effective peak, not even one third of the energy reached the heart. Despite the fact that we were unable to provoke ventricular fibrillation in the normal heart with a maximum available discharge of 80 joules applied for 10 milliseconds, it was disturbing to note that Lown and his associates16 had an incidence of 1.3 per cent with energies of 25 and 50 joules applied for 2.5 milliseconds. The possibility, no matter how remote, that such a phenomenon might occur was explored. Following the studies of Kouwenhoven, the different phases of the electrocardiogram were shocked selectively. Great emphasis was placed on the R wave, the S-T segment, and the T wave. Except in one in stance, where shocks were being administered at 30 second intervals and a ventricular fibrillation developed as a result of a shock administered at the R wave, the other phases were not vulnerable to the monopulse discharge. However, when the interval between shocks was reduced to 10 seconds and ad ministered indiscriminately, irrespective of the electrocardiographic phase, ven tricular fibrillation developed in 12 of 50 shocks, and when the interval between shocks was increased to 30 seconds, one ventricular fibrillation developed in 51 shocks. The fibrillation developed when the shock was applied to the R wave. Attempts to reproduce the phenomenon were unsuccessful. By simply grouping together the total number of dogs with normal hearts that were subjected to the monopulse defibrillator (80 watt-seconds energy) we have 17 dogs that were given a total of 696 shocks, regardless of the time interval between shocks. To reduce this set of data to a number comparable to Lown's and Kouwenhoven's figures, we note 13 fibrillations in 696 shocks, a 1.9 per cent incidence of ven-
BALAGOT E T AL.
502
J. Thoracic and Cardiovas. Surg.
tricular fibrillation. This figure is not too meaningful inasmuch as 12 of the 13 fibrillations occurred in one dog which was subjected to shocks at 10 sec ond intervals indiscriminately of the electrocardiographic phase. One probable explanation for this is the possibility that the electric shock shortens the dura tion of the action potential of the cardiac musculature when applied at very close intervals, for example, 10 seconds. This diminishes this refractory period much more, accelerating the return of excitability and, thus, facilitating the development of ventricular fibrillation.15
I
2
4
8
16
32
50
100
Fig-. 12.—Functional damage to the myocardium in dogs (20-25 Kg.) from single electric discharge: its dependence on source voltage and capacitance. I. Zone without damage. //, Zone of slight damage. III. Zone of medium grave damage. IV. Zone of grave damage. V. Ven tricular fibrillation. Energy curves—25, 50, 100, and 150 watt-seconds. (Modified from Peleska.) The point on the heavily lined curve at which 40 /it. intersects absolute voltage of about 1.8 kv. represents the maximum energy available from the monopulse denbrillator and is out side the zones of myocardial damage (see arrow).
Mackay and Leeds,6 Gurvich and Yuniev 8 have definitely established an inverse relation between capacitance and voltage needed for defibrillation. They have also established that inductance added to the capacitance improved defibrillatory performance by prolonging the duration of the effective discharge peak. Peleska7 virtually mapped out the relationship of source voltage and capacitance in terms of damage to the myocardium in dogs (Fig. 12). By taking advantage of Peleska's observations and utilizing the principle of the delay-line-pulser, a unit that encompasses almost all of the optimum requirements of a good defibrillator has been developed. I t has a low source voltage of about 2,000 volts, a total capacitance of 40 microfarads, and furnishes a wave-form whose peak is reached almost instantaneously, is maintained at a plateau for 10 milli seconds, and regresses very sharply to base line. The maximum energy furnished during this period is 80 watt-seconds across a resistance of 100 ohms. This is the resistance encountered across the longitudinal axis of the average adult human chest, that is, from the suprasternal notch to the left mid-clavicular line at around the fifth intercostal space. This 80 watt-seconds of energy is only
Vol. 47 No. 4 April, 1964
MONOPULSE DC CUBBENT D E F I B B I L L A T O B
503
10 watt-seconds more than the E d 65 of 70 watt-seconds found by Lown and his co-workers (amount of capacitor discharge that will defibrillate 65 per cent of the time). The difference in effectiveness between this unit and Lown's experimental units probably lies in the duration of discharge. The discharge time in Lown's units is 2.5 milliseconds. With this discharge time, his E d 100 is at least 100 watt-seconds. When the monopulse defibrillator is applied across a resistance of 50 ohms, for example the exposed heart, the peak voltage de creases to 650 volts for a minimum dissipated energy of 67.6 watt-seconds, with the wave-form factor taken into account. Since this unit has this capa bility of adjusting voltage to encountered resistance, a determination of the minimal effective defibrillatory discharge (Lown's results) was deemed incon sequential. SUMMARY
A capacitor-type monopulse defibrillator which was developed to take ad vantage of the finding that damage to the myocardium caused by a capacitor discharge is more directly related to the absolute voltage than the capacitance, and which incorporated the principle of the delay-line-pulser, was found to be an excellent defibrillator when applied transthoracically to dogs in which ventricular fibrillation was provoked either by ligation of the anterior descend ing and circumflex coronary arteries or by transthoracic application of a small magnitude AC current, about 100 milliamperes for 1 to 5 seconds. It was superior to a standard external AC defibrillator under the same experimental conditions. In repeated fibrillation-defibrillation sequences over a period of time, toxic effects provoked in the dog were much less and milder as compared to the AC defibrillator. Applied to the normal heart, ventricular fibrillation could not be provoked by shocking definite phases of the electrocardiogram or by al lowing an interval of at least 1 minute between shocks. When the interval between shocks was reduced to 10 seconds, some ventricular fibrillations de veloped. Except for the occasional necessity of recharging the built-in battery which has a capacity of 4 ampere hours from available house current, the unit is com pletely portable. REFERENCES 1. Prevost, J . L., and Battelli, F . : La mort par les courants electriques-courants alternatifs a haute tension, J . physiol. et path. gen. Par. 1: 427, 1889. 2. Beck, C. S., Pritchard, W. H., and Feil, H. S.: Ventricular Fibrillation of Long Duration Abolished by Electric Shock, J . A. M. A. 135: 985, 1947. 3. Hooker, D. E., Kouwenhoven, W. B., and Langworth, O. E . : The Effect of Alternating Electrical Currents on the Heart, Am. J . Physiol. 103: 444, 1933. 4. Guyton, A. C , and Satterfield, J . : Factors Concerned in Electrical Defibrillation of the Heart Particularly Through the Unopened Chest, Am. J . Physiol. 167: 81, 1951. 5. Zoll, P . M., Linenthal, A. J., Gibson, W., Paul, M. H., and Norman, L. E.: Termination of Ventricular Fibrillation in Man by Externally Applied Electrical Countershock, New England J . Med. 254: 727, 1956. 6. Mackay, E. S., and Leeds, 8. E . : Physiological Effects of Condenser Discharges With Application to Tissue Stimulation and Ventricular Defibrillation, J . Appl. Physiol. 6: 67, 1953.
504
BALAGOT E T AL.
J. Thoracic and Cardiovas. Surg.
7. Peleska, B . : The Dependence of the Deflbrillation Threshold of the Heart on the Param eters of Deflbrillation Impulses, International Conf. on Medical Electronics, July, 1961, Sec. 24-25, p. 180. 8. Gurvieh, N . L., and Yuniev, G. S.: Restoration of Heart Rhythm During Fibrillation by a Condenser Discharge, Am. Rev. Soviet Med. 4 : 252, 1947. 9. Kouwenhoven, W. B., and Milnor, W. R.: Treatment of Ventricular Fibrillation Using a Capacitor Discharge, J . Appl. Physiol. 7: 253, 1954. 10. Glasoe, G. N., and Lebacqz, J . V.: Pulse Generators, New York, 1948, McGraw-Hill Co., chap. 6. 11. Kouwenhoven, W. B., Knickerbocker, G. G., Chesnut, R. W., Milnor, W. R., and Sass, D. J . : A-C Shocks of Varying Parameters Affecting the Heart. A I E E — P a r t I . Communications and Electronics 78: 163-169, 1959. 12. Kouwenhoven, W. B., and Milnor, W. R.: Field Treatment of Electric Shock Cases—I. A I E E — P a r t I I I . Power Apparatus and Systems 76: 82-87, 1957. 13. Kouwenhoven, W. B., Milnor, W. R., Knickerbocker, G. G., and Chesnut, W. R.: Closed Chest Deflbrillation of the Heart, Surgery 42: 550, 1957. 14. Negovskii, V. A.: Resuscitation and Artificial Hypothermia, translated from the Russian by Basil Haigh, New York, 1962, Consultants Bureau. 15. Burn, J . H., and Hokovics, S.: Anoxia and Ventricular Fibrillation, With a Summary of Evidence on the Cause of Fibrillation, Brit. J . Pharmacol. 15: 67, 1960. 16. Lown, B., Neuman, J., Amarasingham, R., and Berkovits, B. V.: Comparison of Alter nating Current With Direct Current Electroshock Across the Closed Chest, Am. J. Cardiol. 10: 223-233, 1962.
DEFIBRILLATION
R. C. Balagot, M.D., W. S. Druz,** E. ]obgen, M. Tomita,
DEFIBRILLATOR*
M. Ramadan**
M. Lopez-Belio,
M.D., and M. S. Sadove, M.D.,
M.D.,
Chicago, III.
B
OTH a capacitor discharge and an alternating current have been shown to be effective in shocking a ventricle out of fibrillation by direct application to the exposed heart. 1 The simplicity, availability, and the successful internal defibrillation of a prolonged ventricular fibrillation in a human subject by Beck2 gained an initial advantage in popular usage for the AC defibrillator. How ever, thoracotomy in an emergency to expose the heart remains a formidable procedure. Further studies showed eventually that defibrillation may be effected through the closed chest provided sufficient voltage and, therefore, current was available.3' *•5 The minimum alternating current necessary to provoke gen eralized intense contraction of the myocardium has been shown to be around 1.0 ampere 3 ' 6 for the exposed heart and around 3 amperes for the closed chest; the resistances encountered average 50 ohms and 90 ohms, respectively. Currents smaller than 1 ampere, applied externally, 3 will frequently throw a normal heart into fibrillation instead of a generalized contraction. Obviously, the effect of an alternating current on the myocardium is excitation and not inhibition. Thus, sufficient current density per unit of weight of myocardium is essential to successful ventricular defibrillation. Such immediately poses two problems, that is, availability of sufficient source voltage to generate the needed AC cur rent, and excessive tissue heat generation with possible thermal damage to the myocardium. For example, a current of 5 amperes across a closed-chest re sistance of 90 ohms will generate heat equivalent to an energy of (W = P R ) 2,250 watts or about 562 joules for 0.25 second optimum period recommended that the stimulus be applied. A similar but lesser amount of energy may be ob tained from a capacitor and applied to the heart for a shorter period of time to achieve possibly better end results. Thermal damages to the myocardium and thoracic wall are thus obviated. Defibrillatory effectiveness of a capacitor discharge depends on the stored energy of the condenser which is equivalent to one half the capacitance times the voltage squared, thus: Wg = % CV2. From the University of Illinois, College of Medicine, Department of Surgery, Division of Anesthesiology, Chicago, 111. Received for publication Aug. 23, 1963. •Developed by the Research Department of Zenith Radio Corporation, Chicago, 111. **Prom the Research Department of Zenith Radio Corporation, Chicago, 111. 487
BALAGOT ET AL.
488
J. Thoracic and Cardiovas. Surg.
I t is evident from Peleska's work in his quest for the optimum defibrillation threshold and other workers 6 , 7 ' 8 - 9 that: (1) myocardial damage is more de pendent on the absolute voltage than the total energy supplied from the capac itor; (2) the defibrillation threshold voltage decreases exponentially as capac itance increases (Fig. 1) and approaches asymptotically a limiting value, about 1.5 kv.; (3) a threshold current has to be exceeded for a required period of time to effect defibrillation. The extent by which the threshold is exceeded deter mines the amount of damage that may be caused various tissues. Based on these considerations, a threshold defibrillating current has been developed which ex ceeds the minimum threshold by a safe margin and which continues at this level for a time sufficient to ensure defibrillation with the least amount of total stored energy. KV
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Description of Unit.—In essence, a delay line discharge pulser10 with two sections of capacitance and inductance having a characteristic impedance Ro = V L/C is employed to provide a defibrillation pulse which has a maximum rise time consistent with the greatest duration at its peak possible for the total value of inductance and capacitance used. It is well known in the theory of radar pulsers that a given value of mutual inductance between inductances which form the individual sections of a delay line is necessary to produce a wave form that has the smallest deviation or dip from the maximum amplitude attained during discharge. The pulse as observed
Vol. 47, No. 4 April, 1964
M O N O P U L S E DC CURRENT
489
DEFIBR1LLATOR
on the oscilloscope has the shape shown in Pig. 2. The energy delivered to the subject is maintained at its peak value and rapidly decreases to zero when the resistance of the subject is equal to the characteristic impedance of the delay line. In case the impedance of the subject is less than the characteristic imped ance, reflections occur at the termination in such a fashion that the peak current through the subject is maintained almost constant but voltage avail able decreases. Such is a property of a delay line constructed of dissipative ele ments. Compared to a critically damped single capacitance and inductance of the same total value, the maximum rate of discharge in this instance is reached much sooner. It then persists for almost the full period in such a manner that the current which exceeds the threshold for defibrillation lasts for a signifi cantly longer period of time for the same value of stored energy (Fig. 3).
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F i g . 2.—Delay line d i s c h a r g e . F i g . 3.—A delay line p u l s e w a v e c o m p a r e d to a c r i t i c a l l y d a m p e d single c a p a c i t a n c e a n d i n d u c t a n c e p u l s e w a v e of t h e s a m e t o t a l v a l u e .
The wave form of voltage available across the terminals connected to a patient with a thoracic resistance of 100 ohms has a duration of approximately 10 milli seconds. With a resistance of 50 ohms, the wave form still has a duration of 10 milliseconds but of smaller voltage amplitude (see Fig. 2). The excess energy is dissipated in the delay line losses. The latter characteristic enables it to be employed for either internal or external defibrillation without any modification or readjustment. The constants of the delay line are: (1) total inductance, 0.4 Henries centertapped; (2) mutual inductance, 0.05 Henries; (3) capacitance per section, 20 microfarads. As a result of the highly efficient solid state switching circuitry (transistors, diode rectifiers, etc.) a large peak current can be supplied to effect charging or recharging in three seconds. Even with an almost totally discharged (about 90 per cent) battery, the charge time does not exceed four seconds. A built-in sensing circuit maintains a nearly constant value of charge on the capacitors and keeps the equipment ready for immediate use. This is accom plished with a minimum drain on the internal battery. The unit is completely portable and weighs 33 pounds. Included in the case is a battery charger for
BALAGOT E T AL.
490
J. Thoracic and Cardiovas. Surg.
OUTPUT
©—I
CONTROL
LINE
POWER
F i g . 4.—DC m o n o p u l s e
deflbrillator.
recharging the 12 volt, 4 ampere hour battery. Provisions are incorporated for testing the battery on the same meter used for indicating the watt-seconds of stored energy. The elemental diagram of the equipment is shown in Pig. 4. METHODS
Ventricular fibrillation was produced in dogs by either of two methods: (1) transthoracic application of 100 milliamperes 11 alternating current for 1 to 6 seconds; (2) ligation of the circumflex and anterior descending coronary arteries. Inhalation of chloroform or halothane and subsequent intravenous in jection of epinephrine proved to be an unreliable method for provoking ven tricular fibrillation. Continuous tracings of femoral arterial pressure and elec trocardiogram were recorded except when ventricular fibrillation was provoked (with the small AC current) and the instant the defibrillatory shock was ad ministered transthoracically. The animals were under sodium pentobarbital, 25 mg./Kg. body weight, and artificially respired with a Bird respirator, or a Harvard respirator (for dogs whose circumflex and anterior descending coronaries were ligated). Electrical Fibrillation.—Three types of situations were utilized for this phase of the experimental evaluation. In the first series of dogs (6), fibrillation was effected with the 100 milliampere AC current applied transthoracically for 1 to 6 seconds and the heart was allowed to fibrillate for a period of 2 minutes. This arbitrary time limit was initially selected as an adequate test for the defibrillatory potential of any unit inasmuch as myocardial sensitivity to a defibrillating shock decreased pro gressively with increasing cardiac anoxia. Kouwenhoven's 12 original experiments along the same pattern showed that a 2 minute fibrillation still allowed 93 per cent defibrillation and a 30 per cent survival rate. Our defibrillation rate for
Vol. 47. No. 4 April, 1964
MONOPULSE DC CURRENT D E F I B R I L L A T O R
491
both the monopulse DC defibrillator set at 80 watt-seconds and the AC unit set at 480 volts was 100 per cent. The survival rate was zero. With either unit, defibrillation was accomplished on the first attempt but blood pressure remained at zero level. Myocardial anoxia was obvious in the electrocardiographic trac ing, that is, a ventricular or nodal rhythm developed and with very tall, peaked T waves, almost as tall as the QRS complex. Closed-chest manual systole did not improve the blood pressure, neither did another defibrillatory shock (Fig. 5). In the second series of 6 dogs, a fibrillation-defibrillation sequence was car ried out. Fibrillation was provoked with the 100 milliampere current applied transthoracically for a period of 1 to 6 seconds until fibrillation developed. The dog was then very quickly subjected to the defibrillatory shock, either 80 wattseconds from the monopulse DC or 480 volts AC. This procedure was repeated every 5 minutes for at least twenty times. The harshness of the effects of the alternating current on the heart was outstanding. Immediately after the fibril lation-defibrillation sequence, blood pressure bounded to at least 50 to 100 mm. Hg higher than prefibrillation-defibrillation. The effect was very similar to the injection of 1.0 mg. of epinephrine intravenously. The electrocardiogram showed the greatest changes. Ventricular extrasystoles immediately developed in the first fibrillation-defibrillation sequence. Runs of tachycardia (sinus) are readily apparent. A depressed S-T segment and inversion of the T wave developed very early and became more pronounced with increased repetition of the fibrillationdefibrillation sequence. Signs of infarction and atrial fibrillation were observed at about the twelfth to fifteenth fibrillation-defibrillation sequence. Severe mus-
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BALAGOT E T AL.
492
after 5
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cular contractions (opisthotonos) developed with each deflbrillation, also micturation, salivation, and defecation. The responses just described occurred very mildly or not at all with the DC unit (Fig. 6). Arterial p 0 2 obtained at prefibrillation, at the fifth fibrillation-defibrillation, and the twentieth fibrillation-defibrillation sequences showed a progressive de crease. Although pC0 2 did not show any significant change, both p H and stan dard H C 0 3 showed a marked tendency to metabolic acidosis. Again, these changes were mild in the DC defibrillated dogs (Table I ) .
TABLE I. ACID-BASE AND p 0 2
CHANGES DURING REPEATED FIBRILLATION-DEFIBRILLATION (F-D) SEQUENCE I N DOGS AC.
BLOOD
Before F-D sequence After 5th F-D After 20th F-D
po 2 107 94 93.5
|
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21.8 20.5
107 97
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7.46
36.3
24.9
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36 37
24.4 23.0
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Vol. 47, No. 4 April, 1964
MONOPULSE DC CUERENT D E F I B R I L L A T O R
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In the third series of dogs (6), a similar procedure was followed as in the first and second series but the fibrillation period was increased to 1 minute. Contrary to other investigators' findings, the dogs very easily survived repeated fibrillation periods of 1 minute, and twenty fibrillation-defibrillation sequences were performed on each dog. The changes in the electrocardiogram were not too greatly different from those in the second series in which the fibrillatory period lasted only a few seconds (Fig. 7). Ligation of the circumflex and the anterior descending coronary arteries (5 dogs) usually resulted in ventricular fibrillation within a period varying from 10 to 30 minutes at the most. This was due to the fact that these dogs were artificially ventilated which probably delayed more generalized myocardial hypoxia and hypercarbia. Upon onset of fibrillation, the ligatures were im mediately released, the chest quickly closed with towel clips, and transthoracic defibrillation attempted. The DC defibrillator was employed on 3 dogs and the AC unit on 2 dogs. All of the dogs survived the fibrillation-defibrillation experi ment for 24 hours or more. Both dogs in the AC group died within 48 hours. In the DC group, one dog died after 24 hours of a pulmonary atelectasis, one died after 48 hours, and the other survived indefinitely until subjected to an other fibrillation-defibrillation sequence with fibrillation induced with the small amperage alternating current. Fibrillation caused by ligature of the circumflex and anterior descending coronary arteries is much more resistant to defibrillation because of the greater hypoxia the heart suffers. Upon ligation of both the circumflex and anterior descending coronaries, the heart is observed to turn into almost one huge infarct. Nevertheless, the DC current proved to be more consistent in its ability to
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Vol. 47. No. 4
MONOPULSE DC CURRENT D E F I B R I L L A T O R
April, 1964
495
defibrillate than the AC current. Fig. 8 shows a heart that defibrillated after four successive shocks of 1,500 volts DC, 45 watt-seconds, 750 volts at the termi nals. It refibrillated spontaneously, but a single shock of 2,000 volts, 80 wattseconds, 1,000 volts at the terminals, reverted it to normal. On the other hand, Fig. 9 shows repeated AC shocks of 220 volts failing to defibrillate the heart. Finally, three successive shocks of 480 volts defibrillated the heart. Effects of DC and AC Defibrillating Impulses on the Normal Dog Heart.— Since a small AC current will fibrillate a normal heart, either monopulse, DC or AC, was applied transthoracically to the normal dog heart (5 dogs) starting from the lowest voltage setting available to the maximum to see if such exigency might develop. Subdermal temperature readings were obtained at the site of electrode-skin contact. Esophageal temperatures were obtained concurrently. Fig. 10 shows the effects of different voltage settings available from the AC defibrillator on the femoral artery pressure and the electrocardiogram. At the "infant setting" (available voltage about 100 volts), the defibrillatory shock provoked fibrillation. Judging from the femoral artery wave forms, there is a noticeable delay in the ability of the normal heart to recover its original state after an AC defibrillating shock, especially with greater voltages. Subdermal temperature readings (electrode-skin contact) showed a rise of 2° to 4° C , which has also been shown by Kouwenhoven and his associates.13 Esophageal temperature was unaffected. The effects of monopulse DC defibrillator shocks on the normal heart trans thoracically (5 dogs), varying from 100 volts (0.2 watt-seconds) to 2,000 volts (80 watt-seconds) as reflected in the femoral artery pressure and electrocardiographic tracings, are shown in Fig. 11. There were no subdermal or esophageal temperature changes. The amount of resistance encountered across the longi tudinal axis of the chest was measured in 2 dogs that weighed 15 kilograms and was found to vary between a very narrow range of 64 to 70 ohms. Since this narrow range of resistance was found to hold for the different voltage set tings from 100 volts to 2,000 volts, terminal voltages of 50 volts to 1,000 volts, respectively, in the same dog, this more or less establishes the ability of this monopulse DC unit to adjust voltage to resistance encountered or implies its ability to be utilized either as an external or internal defibrillator without any modification or readjustment of voltage setting. TABLE I I .
DC
DEFIBRILLATORY SHOCK APPLIED TRANSTHORACICALLY TO SPECIFIC P H A S E ELECTROCARDIOGRAM ECG P H A S E PWAVE
61 0
No. of shocks No. ventricular fibrillations Interval between shocks—1-2 minutes
Total no. of shocks—470 No. of dogs—10 Energy employed—80 watt-second (joules)
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Vol 47 No. 4
MONOPULSE DC CURRENT D E F I B R I L L A T O R
499
A variable impulse timer geared to the electrocardiogram as observed on an oscilloscope and synchronized with the discharge mechanism of the monopulse defibrillator was devised so any phase of the electrocardiogram, such as the P wave, the QRS complex, the S-T segment, the T wave, may be subjected to a shock from the DC defibrillator at the designated instant. A built-in manu ally operated trigger switch in the unit provided a synchronizing pulse derived from the succeeding R wave which activates the delay circuit causing the defibrillatory discharge. The different phases of the electrocardiogram in 10 dogs were subjected to 80 watt-seconds (energy) from the monopulse defibril lator (Table I I ) . The interval between shocks was at least 60 to 120 seconds and both electrocardiogram and femoral blood pressure were monitored. A total of 470 shocks were administered to these dogs without provoking ven tricular fibrillation. On one dog, 50 shocks of 80 joules were administered transthoracically at 10 second intervals indiscriminately of the electrocardiographic phase. Ventricular fibrillation occurred twelve times. These were easily reversed by another defibrillatory shock. When the interval between shocks was increased to 30 seconds, one ventricular fibrillation occurred once in a successive series of 51 shocks. This occurred when the ninth shock of the series was applied to the R wave. It could not be reproduced. With a longer time interval between shocks, for example 60 to 120 seconds, no ventricular fibrillations developed. DISCUSSION
The objectives of this study are easily noted. First, the ability of the monopulse DC unit to effect a defibrillation was established. Different situations were devised (see Methods) to delineate the parameters of this effectiveness. Aside from just testing its defibrillatory capacity, it was compared to a stan dard AC defibrillator unit under similar circumstances to determine advantages or disadvantages, if any, notwithstanding previous observations that a conden ser discharge is superior to an AC current for defibrillatory purposes. The initial problem was devising methods to provoke ventricular fibril lation. The inhalation of chloroform and subsequent intravenous injection of epinephrine, a technique that was highly regarded by pharmacologists and anesthesiologists, proved to be very inconsistent. The application of a small AC current transthoracically for a variable period of time proved to be most con sistent. A condition which was thought to approximate fibrillation following a myocardial infarct was effected by ligating the circumflex and the anterior descending coronary arteries. This was a formidable surgical procedure. Toxic effects on the presumably normal heart in sinus rhythm were sought for by subjecting this type heart to the different voltages available from both the DC and the AC units. In the series of dogs in which fibrillation was effected with a small mag nitude (100 milliampere) alternating current and the heart was allowed to fibrillate for a 2 minute period, resuscitation was next to impossible although defibrillation was successful. Apparently, a 2 minute period of myocardial and, presumably, brain hypoxia was not conducive to successful resuscitation. It is probable that a more definitive treatment of the shock state in these dogs,
500
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AL.
J. Thoracic and Cardiovas. Surg.
such as intra-arterial blood transfusions as suggested by Negovskii,14 might have improved survival rates. After all, Negovskii places 5 minutes as the max imum limit of resuscitability of dogs wherein he induces "clinical d e a t h " exsanguination shock to cardiac arrest. Contrary to observations that 30 seconds was the maximum period during which a dog's ventricle may be allowed to fibrillate and still be successfully resuscitated, we find that this period is prob ably closer to between 1.0 and 1.5 minutes. The discrepancy lies probably in the fact that all dogs utilized in these experiments were ventilated artificially. The differences in electrocardiographic and cardiovascular responses (as moni tored by femoral blood pressure changes), in dogs in which the ventricles were allowed to fibrillate and were immediately defibrillated and those that were al lowed to fibrillate for 1 minute, were very minimal, that is, comparing AC defibrillated dogs (immediately) to AC defibrillated dogs (1 minute) and DC (immediately) to DC (1 minute) defibrillated dogs. However, the differences in response between the DC defibrillated dog and the AC defibrillated dog be came very manifest. The AC defibrillating current is definitely more toxic, not only to the heart but to the animal as a whole. After an AC defibrillating shock of 480 volts, it was not uncommon to find runs of ventricular extrasystoles, a depressed S-T segment, an inverted T wave—signs of myocardial ischemia or infarction—and, with more frequent repetition of the fibrillation-defibrillation sequence atrial fibrillation. These changes were not outstanding with the DC defibrillating impulse of 80 watt-seconds, the most common was a depressed S-T segment and sinus tachycardia. The blood pressure response to the AC defibrillating current was very similar to a rapid intravenous injection of at least 1.0 mg. of epinephrine. One thing that was very noticeable about the blood pressure response after an AC defibrillator shock was the time lag be tween the shock and the response. It frequently takes as much as 0.5 to 1.0 second before the heart starts to beat and cause an effective blood pressure, frequently causing one to wonder whether a defibrillation was effected or not. The DC impulse immediately causes a contraction and an effective blood pres sure if a response is forthcoming. The side effects on the whole animal, such as excessive salivation, severe muscular contractions, defecation, and urination, were rarely seen in the DC defibrillated dog. Most of the toxic effects observed with the AC defibrillation in the pre vious series of dogs were also seen in those in which the coronary arteries (circumflex and anterior descending) were ligated. The DC defibrillator was easily superior to the AC unit in these series of experiments. Except for the absence of coronary atherosclerosis, this experimental situation in a way ap proximates the patient that suddenly develops a myocardial infarct. Certainly, the positive response to the discharge from an external defibrillator, particu larly the monopulse DC type, should encourage greater application of these units in cases of acute, frequently fatal, myocardial infarction. An interesting finding is the progressive decrease of arterial oxygen tension with increasing repetition of the fibrillation-defibrillation sequence. Since these dogs were artificially ventilated, it is not too presumptious to assume that some form of interference with oxygen uptake develops from repetitious ap-
Vol. 47, No. 4 April, 1964
MONOPULSE DC CURRENT D E F I B R I L L A T O R
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plication of AC and DC currents across the chest. The importance of this observation in human cases of ventricular fibrillation is probably remote, al though it is not uncommon in some situations to apply the defibrillatory shock repeatedly. However, metabolic acidosis, which develops from the hypoxia and catecholamine release, may interfere with successful resuscitation of the subject. Although it has been realized that a capacitor discharge has definite ad vantages over an alternating current for ventricular defibrillation, the proper combination of capacitance and inductance that will give the optimum defibril latory threshold was not established for some time. There is no question, how ever, that a pure capacitor discharge is not as effective as one with inductance inserted in series with the condenser. Kouwenhoven was never enthusiastic for the defibrillatory ability of the condenser discharge because he failed to find the right combination of capacitance and inductance. Nevertheless, and this was probably discouraging to him, he demonstrated pretty well that straight capacitor discharges particularly those with greater energy, for example 80-225 watt-seconds, were more harmful to the heart in that they occasionally caused ventricular fibrillation. Presumably, in the experimental situation cited by Kouwenhoven,9 much of the energy was dissipated in the tissue mass of the chest wall and only a small amount reached the heart, thereby provoking ven tricular fibrillation instead of synchronized contraction of the normal heart. Maekay and Leeds6 calculated that only one third of the total energy spent across the closed chest actually reached the heart. Possibly, without inductance to prolong the discharge current at an effective peak, not even one third of the energy reached the heart. Despite the fact that we were unable to provoke ventricular fibrillation in the normal heart with a maximum available discharge of 80 joules applied for 10 milliseconds, it was disturbing to note that Lown and his associates16 had an incidence of 1.3 per cent with energies of 25 and 50 joules applied for 2.5 milliseconds. The possibility, no matter how remote, that such a phenomenon might occur was explored. Following the studies of Kouwenhoven, the different phases of the electrocardiogram were shocked selectively. Great emphasis was placed on the R wave, the S-T segment, and the T wave. Except in one in stance, where shocks were being administered at 30 second intervals and a ventricular fibrillation developed as a result of a shock administered at the R wave, the other phases were not vulnerable to the monopulse discharge. However, when the interval between shocks was reduced to 10 seconds and ad ministered indiscriminately, irrespective of the electrocardiographic phase, ven tricular fibrillation developed in 12 of 50 shocks, and when the interval between shocks was increased to 30 seconds, one ventricular fibrillation developed in 51 shocks. The fibrillation developed when the shock was applied to the R wave. Attempts to reproduce the phenomenon were unsuccessful. By simply grouping together the total number of dogs with normal hearts that were subjected to the monopulse defibrillator (80 watt-seconds energy) we have 17 dogs that were given a total of 696 shocks, regardless of the time interval between shocks. To reduce this set of data to a number comparable to Lown's and Kouwenhoven's figures, we note 13 fibrillations in 696 shocks, a 1.9 per cent incidence of ven-
BALAGOT E T AL.
502
J. Thoracic and Cardiovas. Surg.
tricular fibrillation. This figure is not too meaningful inasmuch as 12 of the 13 fibrillations occurred in one dog which was subjected to shocks at 10 sec ond intervals indiscriminately of the electrocardiographic phase. One probable explanation for this is the possibility that the electric shock shortens the dura tion of the action potential of the cardiac musculature when applied at very close intervals, for example, 10 seconds. This diminishes this refractory period much more, accelerating the return of excitability and, thus, facilitating the development of ventricular fibrillation.15
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Fig-. 12.—Functional damage to the myocardium in dogs (20-25 Kg.) from single electric discharge: its dependence on source voltage and capacitance. I. Zone without damage. //, Zone of slight damage. III. Zone of medium grave damage. IV. Zone of grave damage. V. Ven tricular fibrillation. Energy curves—25, 50, 100, and 150 watt-seconds. (Modified from Peleska.) The point on the heavily lined curve at which 40 /it. intersects absolute voltage of about 1.8 kv. represents the maximum energy available from the monopulse denbrillator and is out side the zones of myocardial damage (see arrow).
Mackay and Leeds,6 Gurvich and Yuniev 8 have definitely established an inverse relation between capacitance and voltage needed for defibrillation. They have also established that inductance added to the capacitance improved defibrillatory performance by prolonging the duration of the effective discharge peak. Peleska7 virtually mapped out the relationship of source voltage and capacitance in terms of damage to the myocardium in dogs (Fig. 12). By taking advantage of Peleska's observations and utilizing the principle of the delay-line-pulser, a unit that encompasses almost all of the optimum requirements of a good defibrillator has been developed. I t has a low source voltage of about 2,000 volts, a total capacitance of 40 microfarads, and furnishes a wave-form whose peak is reached almost instantaneously, is maintained at a plateau for 10 milli seconds, and regresses very sharply to base line. The maximum energy furnished during this period is 80 watt-seconds across a resistance of 100 ohms. This is the resistance encountered across the longitudinal axis of the average adult human chest, that is, from the suprasternal notch to the left mid-clavicular line at around the fifth intercostal space. This 80 watt-seconds of energy is only
Vol. 47 No. 4 April, 1964
MONOPULSE DC CUBBENT D E F I B B I L L A T O B
503
10 watt-seconds more than the E d 65 of 70 watt-seconds found by Lown and his co-workers (amount of capacitor discharge that will defibrillate 65 per cent of the time). The difference in effectiveness between this unit and Lown's experimental units probably lies in the duration of discharge. The discharge time in Lown's units is 2.5 milliseconds. With this discharge time, his E d 100 is at least 100 watt-seconds. When the monopulse defibrillator is applied across a resistance of 50 ohms, for example the exposed heart, the peak voltage de creases to 650 volts for a minimum dissipated energy of 67.6 watt-seconds, with the wave-form factor taken into account. Since this unit has this capa bility of adjusting voltage to encountered resistance, a determination of the minimal effective defibrillatory discharge (Lown's results) was deemed incon sequential. SUMMARY
A capacitor-type monopulse defibrillator which was developed to take ad vantage of the finding that damage to the myocardium caused by a capacitor discharge is more directly related to the absolute voltage than the capacitance, and which incorporated the principle of the delay-line-pulser, was found to be an excellent defibrillator when applied transthoracically to dogs in which ventricular fibrillation was provoked either by ligation of the anterior descend ing and circumflex coronary arteries or by transthoracic application of a small magnitude AC current, about 100 milliamperes for 1 to 5 seconds. It was superior to a standard external AC defibrillator under the same experimental conditions. In repeated fibrillation-defibrillation sequences over a period of time, toxic effects provoked in the dog were much less and milder as compared to the AC defibrillator. Applied to the normal heart, ventricular fibrillation could not be provoked by shocking definite phases of the electrocardiogram or by al lowing an interval of at least 1 minute between shocks. When the interval between shocks was reduced to 10 seconds, some ventricular fibrillations de veloped. Except for the occasional necessity of recharging the built-in battery which has a capacity of 4 ampere hours from available house current, the unit is com pletely portable. REFERENCES 1. Prevost, J . L., and Battelli, F . : La mort par les courants electriques-courants alternatifs a haute tension, J . physiol. et path. gen. Par. 1: 427, 1889. 2. Beck, C. S., Pritchard, W. H., and Feil, H. S.: Ventricular Fibrillation of Long Duration Abolished by Electric Shock, J . A. M. A. 135: 985, 1947. 3. Hooker, D. E., Kouwenhoven, W. B., and Langworth, O. E . : The Effect of Alternating Electrical Currents on the Heart, Am. J . Physiol. 103: 444, 1933. 4. Guyton, A. C , and Satterfield, J . : Factors Concerned in Electrical Defibrillation of the Heart Particularly Through the Unopened Chest, Am. J . Physiol. 167: 81, 1951. 5. Zoll, P . M., Linenthal, A. J., Gibson, W., Paul, M. H., and Norman, L. E.: Termination of Ventricular Fibrillation in Man by Externally Applied Electrical Countershock, New England J . Med. 254: 727, 1956. 6. Mackay, E. S., and Leeds, 8. E . : Physiological Effects of Condenser Discharges With Application to Tissue Stimulation and Ventricular Defibrillation, J . Appl. Physiol. 6: 67, 1953.
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7. Peleska, B . : The Dependence of the Deflbrillation Threshold of the Heart on the Param eters of Deflbrillation Impulses, International Conf. on Medical Electronics, July, 1961, Sec. 24-25, p. 180. 8. Gurvieh, N . L., and Yuniev, G. S.: Restoration of Heart Rhythm During Fibrillation by a Condenser Discharge, Am. Rev. Soviet Med. 4 : 252, 1947. 9. Kouwenhoven, W. B., and Milnor, W. R.: Treatment of Ventricular Fibrillation Using a Capacitor Discharge, J . Appl. Physiol. 7: 253, 1954. 10. Glasoe, G. N., and Lebacqz, J . V.: Pulse Generators, New York, 1948, McGraw-Hill Co., chap. 6. 11. Kouwenhoven, W. B., Knickerbocker, G. G., Chesnut, R. W., Milnor, W. R., and Sass, D. J . : A-C Shocks of Varying Parameters Affecting the Heart. A I E E — P a r t I . Communications and Electronics 78: 163-169, 1959. 12. Kouwenhoven, W. B., and Milnor, W. R.: Field Treatment of Electric Shock Cases—I. A I E E — P a r t I I I . Power Apparatus and Systems 76: 82-87, 1957. 13. Kouwenhoven, W. B., Milnor, W. R., Knickerbocker, G. G., and Chesnut, W. R.: Closed Chest Deflbrillation of the Heart, Surgery 42: 550, 1957. 14. Negovskii, V. A.: Resuscitation and Artificial Hypothermia, translated from the Russian by Basil Haigh, New York, 1962, Consultants Bureau. 15. Burn, J . H., and Hokovics, S.: Anoxia and Ventricular Fibrillation, With a Summary of Evidence on the Cause of Fibrillation, Brit. J . Pharmacol. 15: 67, 1960. 16. Lown, B., Neuman, J., Amarasingham, R., and Berkovits, B. V.: Comparison of Alter nating Current With Direct Current Electroshock Across the Closed Chest, Am. J. Cardiol. 10: 223-233, 1962.