an evaluation and comparison of effects of alternating and

An Evaluation and Comparison of Effects of Alternating andDirect Current Electrical Discharges on Canine Hearts *

HOWARD N. ANDERSON,* * M.D., DENNIS REICHENBACH, M.D.,GEORGE P. STEINMETZ, JR.,** M.D., K. ALVIN MERENDINO, M.D.

From the Departments of Surgery and Pathology, University of Washington School of Medicine,Seattle, Washington

IntroductionCIRCULATORY ARREST caused by ventricu-

lar fibrillation may occur anywhere withlittle warning. No longer is cardiac resusci-tation restricted to the operating room andpracticed by a limited few. With the effec-tiveness of closed chest cardiac compressionhaving been dramatically documented, itis imperative that all physicians be awareof the problems and equipment involvedin cardiac resuscitation. Effective resuscita-tion almost always requires the use of ex-ternally or internally applied electroshockfor defibrillation. It has been generally ac-cepted that electroshock using alternatingcurrent defibrillators causes some myocar-dial injury. The rediscovery and clinicalapplication of capacitor discharge directcurrent defibrillators raises the question ofwhether direct current may have an advan-tage over alternating current in this respect.

Previous reports have documented myo-cardial injury occurring in canine heartsfollowing repeated shocks from alternatingcurrent defibrillators.9' 18, 20 Two of these re-ports also studied the effects of capacitordischarge direct current shocks on canine

* Submitted for publication August 20, 1963.** Supported in part by U.S.P.H.S. Fellowship

HPD-19,016.** Supported in part by U.S.P.H.S. Fellow-

ship HPD14,658.Supported by U. S. Public Health Service

Grants HE 03379 and HE 03174.

hearts and concluded that direct currentcauses less myocardial injury than alternat-ing current.9' 20 No published histologicstudies compare the effects of alternatingand direct current discharges apart fromthe effects of ventricular fibrillation, manualcardiac massage and vasopressor agents.The purpose of this study was to evaluateand compare the gross and microscopicchanges occurring in canine hearts follow-ing repeated, internally applied shocks byan alternating current and two direct cur-rent, capacitor discharge defibrillators.

Materials and Methods

The alternating current defibrillator usedwas a standard Electrodyne model 33-Vinternal defibrillator which delivered 60-cycle alternating current for 0.150 secondswith voltage adjustable from 50 to 250 voltsin 50-volt steps.The two direct current defibrillators

tested were similar in principle. Each de-livered a single, brief, pulse discharge fromone or more storage capacitors. The firstutilized a 25 microfarad capacitor with atotal discharge duration of 0.005 secondsand measured peak voltages across caninehearts from 340 to 1,000 at 5 to 50 watt-seconds of delivered energy. This defibril-lator is currently used in the University ofWashington operating suite. The seconddefibrillator utilized four 25 microfarad ca-

251

ANDERSON, REICHENBACH, STEINMETZ AND MERENDINO Annals of SurgeryAugust 1964

TABLE 1. Summary of Electroshocks Delivered

Direct AlternatingCurrent Current

No. of dogs shocked 25 27

Total no. of shocks 174 325

No. of times ventricular 14=8.0% 18=5.5%fibrillation occurred

No. of times ventricular 14 17 one failurefibrillation reverted

Average no. of shocks 1.3 2.6required to revertfibrillation

pacitors in parallel with a total dischargeduration of 0.010 seconds and peak voltagesranging from 235 to 650 at 5 to 50 watt-seconds of delivered energy.To test the effects of multiple shocks,

mongrel dogs averaging 14.9 Kg. in weightand with hearts averaging 106 Gm. inweight were anesthetized with intravenouspentobarbital and maintained on positivepressure ventilation through cuffed endo-tracheal tubes. A left thoracotomy was per-formed through the fifth interspace and thepericardium opened anterior to the phrenicnerve. The electrodes were applied firmlyto the surface of the heart and the desirednumber of shocks administered at approxi-mately two to four-minute intervals. Shockswere delivered at random during the car-diac cycle. No attempt was made to avoidthe susceptible phase described by Wig-gers,2' in which ventricular fibrillation ismore apt to occur. Steel electrodes, un-padded, concave, and 5 cm. in diameter,

TABLE 2. Summary of Gross Myocardial Damage in DogsSacrificed 72 Hours After Receiving Electroshocks

AlternatingDirect Current Current

5 Watt-seconds-l+ 100 Volts-1+10 Watt-seconds-1+ 150 Volts-1+20 Watt-seconds-I to 2+ 200 Volts-2+30 Watt-seconds-2+ 250 Volts-3+40 Watt-seconds-2 to 3+50 Watt-seconds-3+

were used for all dogs except several whowere shocked with 8 cm. or gauze-paddedelectrodes soaked in saline. If an arrhyth-mia occurred following electroshock, theheart was allowed to resume a normal-appearing rhythm before the succeedingshocks. If ventricular fibrillation occurred,one or more shocks were delivered rapidlyin an attempt to revert this condition with-out the use of massage and drugs. Follow-ing initial experiments to determine thelimits of energy and number of shocks com-

patible with survival of the animal, it was

evident that results which could be com-

pared were obtained with five shocks.Electrocardiograms were taken imme-

diately on ten dogs given alternating anddirect current shocks. All showed ST seg-

ment and T-wave changes compatible withpatterns of injury and ischemia within sec-

onds after receiving the first shock. No at-tempt was made to classify arrhythmiasfollowing shocks other than to note if ven-

tricular fibrillation occurred.Myocardial temperatures were measured

in four dogs using needle thermistor probesinserted into the ventricular myocardiumunder the electrodes.* No significantchanges in temperature were noted witheither direct or alternating current shocks.The majority of animals were sacrificed

at three days. However, representative ani-mals were sacrificed at weekly intervals toone month.

Microscopic sections were obtained fromall hearts except seven. Sections of forma-lin-fixed tissue were routinely stained byhematoxylin and eosin, Gomori's one-steptrichrome stain and reticulum stain." Rep-resentative selected cases were stained withperiodic acid Schiff (PAS) with and with-out diastase, Sudan black B on paraffin sec-

tion, oil-red-O on frozen section, Masson

Needle Thermistor Probes No. 514; Tele-thermometer Model No. 41TD; Yellow SpringsInstruments Company, Inc., Yellow Springs, Ohio.

252

EFFECTS OF ELECTRICAL DISCHARGES ON CANINE HEARTS

trichrome, toluidine blue, von Kossa andchloranilic acid for calcium.2

Results

Three hundred twenty-five shocks ofalternating current varying from 50 to 250volts were administered to 27 dogs (Table1). Ventricular fibrillation occurred 18times in 15 animals and was reversed withsucceeding alternating current shocks ofthe same or greater magnitude 17 times.One dog could not be defibrillated witheight shocks and expired. Three dogs ex-

pired acutely postoperatively following al-ternating current shocks, presumably frommyocardial failure or arrhythmia as no

other cause of death could be found atpostmortem examination.One hundred seventy-four direct current

capacitor discharge shocks varying from 5to 100 watt-seconds were administered to25 animals (Table 1). Ventricular fibrilla-tion occurred 14 times in nine animals andwas reversed by succeeding direct currentshocks of same or lesser magnitude 14 times.One dog expired acutely postoperativelyafter direct current shocks.

At 72 hours, grossly visible cardiac dam-age was evident in all animals shocked five

FIG. 1A. Minimal gross myocardial injury(1+). Arrows indicate the damage which is linear,arc-shaped and extends up to 3 mm. into the sub-epicardial myocardium.

FIG. 1B. See legend for Figure IA.

or more times at various levels of both al-ternating and direct current. An approxi-mate grading of this damage into threegroups as related to energy levels (Table2) could be accomplished using the follow-ing criteria: 1+ signifies narrow, arc-shapedareas of damage extending up to 3 mm.

into the myocardium; 2+ signifies narrow

and wide, but still arc-shaped, damagedareas extending through the right ventricleand up to 5 to 8 mm. into the left ventricle;3+ signifies wide or confluent damage ex-

tending through the right and/or the leftventricle and in some cases involving thebase of the septal side of the pulmonaryoutflow tract or deep within the interven-tricular septum.

Gross Appearance

At three days, animals given five or more

alternating current shocks at levels of 100and 150 volts showed minimal changes.These consisted of narrow, arc-shaped areas

Volume 160Number 2 253


DC -30

200 Vo.e ts 5 Shoc,s

* )ac r e.c d -it 72 h .w;.i-rJ

FIG. 2A. Intermediate gross myocardial injury(2+). The damage indicated by arrows still fol-lows the outlines of the electrode rims but is be-coming confluent and extends through the rightventricle.

of yellow-brown, firm tissue extending no

deeper than 3 mm. into the myocardium(Fig. la, b). This degree of damage was

classified as 1+. Animals given five 200-volt shocks showed similar lesions (Fig.2a, b) extending through the wall of the

..: 1

/

.. vr..../ ... ...e :.

:

:.

..

: .. Vo.l Ls: 5.S'ock.7 2fa.ci.. e.. e. 7 hE urs.P .

FIG. 2B. See legend for Figure 2A.

right ventricle and partially through theleft ventricle. This degree of damage was

classified as 2+. Animals given five 250-volt shocks showed the same lesions (Fig.3a, b) that tended to be confluent underthe area of the electrodes and in additioninvolved the septal side of the base of thepulmonary outflow tract. In the classifica-tion used, this damage was rated as 3+.

Gross lesions produced by both types ofdirect current defibrillators did not vary

significantly and will be discussed together.At three days, animals given five or more

shocks of 5 and 10 watt-seconds showedminimal or 1+ changes (Fig. 1a,b) simi-lar to those produced by 100 and 150 voltsof alternating current. Damage resultingfrom 20 watt-seconds largely remainedminimal or 1+ in degree (Fig. la,b).However, in one instance, full thicknessdamage of the right ventricle was noted.Thirty and 40 watt-second shocks causedwide to confluent areas of indurated, yel-low-brown myocardium, invariably throughthe right ventricle and deeply involvingthe left ventricle (Fig. 2a,b).This degreeof damage was classed as 2+ and was ap-

proximately equivalent to that noted with200 and 250 volts of alternating current.Five shocks of 50 watt-seconds caused ex-

tensive, confluent areas of damaged myo-

cardium (Fig. 3a,b) extending through bothventricles and deep within the interventric-ular septum. Two animals given 100 watt-second shocks and sacrificed at three daysshowed even more startling changes, in-volving approximately 80 per cent of theentire heart. In these animals, induration,swelling, and discoloration were notedwithin 15 minutes after the shock was

delivered.Delivering the shocks through large or

saline-soaked, padded electrodes made no

significant difference in the amount of dam-

age created. The pattern of injury varied,however, being more confluent and less

confined to the margins of the electrodes.

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Volume 160 EFFECTS OF ELECTRICAL DINumber 2

Minimal, fibrinous pericardial adhesionswere noted in all animals sacrificed at threedays.

Several animals were sacrificed at one-week intervals up to one month. In thoseanimals given five or more shocks of lowvoltage or energy levels, 150 volts and 20watt-seconds or less, minimal gross changeswere noted at one month. These consistedof fine, fibrinous or fibrous pericardial ad-hesions and faintly outlined, arc-shaped,gray, depressed areas involving only theepicardium or sub-epicardial myocardium.Animals which received higher voltagesand energy levels, from 200 volts and 30watt-seconds upwards, showed larger areasof pale, gray, depressed myocardium withdefinite thinning of the wall after onemonth. Animals sacrificed at one, two, andthree weeks showed a gradual transitionfrom the acute lesions to the ones describedabove.Dogs that incurred ventricular fibrillation

with subsequent manual massage, repeatedshocks and in some instances intracardiacepinephrine, showed no significant increasein grossly visible damage compared withthose animals that received shocks alone.

Microscopic AppearanceSignificant microscopic changes involved

both the myocardial cells and the inter-stitial stroma and showed evolution overthe 30-day period of observation. Generally,the changes were confluent in the areas ofgrossly altered myocardium described pre-viously. Frequently, however, foci of in-volvement were seen separated from themain area of damage.

In animals dying acutely during electricalstimulation, the cytoplasm of the myocar-dial cells showed distinct changes withinminutes of the injury. There was alterationof internal organization manifested by lossof definition of the linear arrangement ofmyofibrils and the appearance of homoge-neous eosinophilic transverse banding or

ISCHARGES ON CANINE HEARTS 255

/

/41 ND)C 27-il5 J:I oc 1 s

'a)4..a t - CS:w. u

FIG. 3A. Severe myocardial injury (3+). Thedamaged areas, indicated by arrows, are confluentbeneath the applied electrode and extend throughthe right and left ventricles as well as into theinterventricular septum.

clumping of the cytoplasm (Fig. 4). Al-though this cytoplasmic alteration was ap-parent on H and E, it was more strikinglybrought out by the Gomori trichrome stainas a bright red, homogeneous, transverseband with intervening areas of red granu-larity. In many of the broader cytoplasmicbands, cross striations could be identifiedwhich were clearly closer together than

:. :.. ... :::..:.:.. ... :. : :

................

.. ... .... .... .. .. ..

~~..... .. . . . . . .. ...

... ......... ....:

FIG. 3B. See legend for Figure 3A.


._ § 'aW...Aft

FIG. 4. The histologic appearance of the myocardium three days after electrical shock. There are

narrow and irregular transverse cytoplasmic bands with intervening granular areas. A relatively normal-appearing cell is present in the bottom of the figure. Gomori trichrome stain (160 x).

cross striations of normal adjacent cells(Fig. 5). In some instances there was

physical separation of the fibers into shortsegments of homogeneous red stainingmaterial without identifiable internal struc-ture, and with intact capillaries maintainingcontinuity and bridging the apparent emptyspaces between segments. When stainedwith Sudan black B, mitochondria were

aggregated between the homogeneousbanded areas in contrast to the orderly ar-

rangement between myofibrils, approxi-mately one per sarcomere and clusteredabout the nucleus in normal cells.The cytoplasmic alteration involved indi-

vidual myocardial cells and in many in-stances was abruptly limited by its modifiedcell membrane, the intercalated disk.'17 19

At the periphery of the lesion, it was notuncommon to find scattered single cellsshowing this cytoplasmic change sur-

rounded by normal-appearing myocardialcells.

In animals dying acutely, the nucleus ofaffected cells showed little change and theonly interstitial reaction consisted of begin-ning accumulation of basophilic edemafluid without significant cellular reaction.

At three days, the cytoplasmic alterationscontinued to be prominent and were essen-

tially the same as those seen acutely. Thetransverse diameters of the affected cellswere smaller than normal and the reticu-lum stain demonstrated an intact but par-

tially collapsed supporting framework (Fig.6).

In occasional animals, there was finebasophilic granular material intracellularlyin the areas of cytoplasmic alteration. Thisgave a positive reaction for calcium andphosphates with chloranilic acid and von

Kossa stains. The presence of this material

256

Volume 160 EFFECTS OF ELECTRICAINumber 2

_ _~~~- - _m_79 . v

FIG. 5. The myoing granular

L DISCHARGES ON CANINE HEARTS 257

-Y~ Y 7-; {iF

kcardial alteration shows broad cytoplasmic bands with close-set striations and interven-r areas. Three days following electrical shock. Gomori trichrome stain (160 X).

did not correlate with the amount or typeof energy discharge.By three days, the nuclei of affected cells

had lost their intensity of staining, hadindistinct internal architecture and ap-

peared to be fading rather than becomingpyknotic. The nuclei of cells adjacent to

those manifesting cytoplasmic alterationwere enlarged, oval and vesicular withsmooth nuclear membranes and containedprominent, enlarged, round nucleoli, in

striking contrast to the small, compact nu-

clei of cells at some distance from the cyto-plasmic alteration, which had small or in-

distinct nucleoli.The interstitial stroma showed a promi-

nent, proliferative, cellular reaction bythree days. The cell infiltrate was composedof slightly elongated cells with plump,round to oval nuclei, moderately prominentnucleoli and slightly basophilic cytoplasm

without identifiable fibrillar structure (Fig.7). The nature of the interstitial cells couldnot always be identified with certainty, butthere were clearly vascular endothelial cellswhich were enlarged and prominent andother cells resembling macrophages, fibro-blasts, sarcolemmic cells and Anitschkowmyocytes. Many mitotic figures were pres-ent in the interstitial reaction includingareas clearly representing vascular chan-nels. None of the cells exhibiting mitoticactivity could be identified as myocardialcells. There was a striking absence of anacute inflammatory reaction. The few poly-morphonuclear leukocytes present werescattered predominately subepicardiallyand were sparsely present throughout theremainder of the lesion. Between the al-tered myocardial cells and muscle bundleswas a prominent accumulation of baso-philic myxoid material which stained meta-chromatically with toluidine blue.


"W 4

FIG. 6. On the left are a group of normal myocardial cells cut in cross-section outlined by reticu-lum. On the nrght, the reticulum is irregularly collapsed surrounding the damaged cells. Dog myo-cardium, three days following electrical shock, reticulum stain (160 x).

There was no significant accumulation oflipid in the altered fibers, but occasionalcells did manifest a fine, fatty dropletchange. This involved individual cells andwas sharply limited by the intercalateddisks. No PAS positive material was pres-

ent in the involved fibers.By one week, the cytoplasmic alteration

was almost gone; only an occasional iso-lated cell showed any change. The prolif-erative cellular reaction progressed andnow there were large cellular areas inwhich myocardial cells could only occa-

sionally be identified. There was continuedcollapse of the reticulum and minimal col-lagen deposition.

Myocardial cells adjacent to or withinthe interstitial cellular reaction continuedto show enlarged vesicular nuclei and en-

larged nucleoli (Fig. 8). Nuclei with dou-ble nucleoli were frequent as were cells

with double nuclei. The nucleoli were larg-est and surrounded by a clear halo in thecells with the smallest transverse diameters.These fibers had sparse numbers of myo-

fibrils and cross striations were indistinct.At two weeks, the interstitial cellular

reaction had essentially disappeared. Areasof loose connective tissue contained col-lapsed reticulum and pigmented macro-

phages, with a variable amount of fibroustissue adjacent to areas of collapsed reticu-lum. The nuclei and nucleoli were not as

prominent as seen earlier.The residual damage, three and four

weeks following injury, varied from smallsubepicardial zones of loose connective tis-sue with occasional foci of interstitial fibro-sis scattered throughout the myocardium,to more extensive lesions exhibiting focalreplacement by fibrous tissue of the entirethickness of the right ventricular wall from

258

EFFECTS OF ELECTRICAL DISCHARGES ON CANINE HEARTS

epicardium to endocardium. Reticulum was

not evident in areas of residual damageafter three to four weeks, all the fibers tookthe staining reaction of collagen. The lossof stainable reticulum fibers is similar tothe observations of Macpherson.1"

In no instance was the amount of residualdamage at three and four weeks as exten-sive as that produced at three days by a

comparable voltage or energy level. Col-lapse and condensation of the injured area

account for a major portion of this dif-ference.When calcium was deposited in the in-

jured cells, it persisted at three and fourweeks as foci of mineralization with a sur-

rounding foreign body giant cell reactionand fibrosis. Some of the mineralized ma-

terial was present within the cytoplasm ofthe giant cells.

DiscussionCardiac damage following electroshock

is usually assumed to be caused by heatgenerated within the myocardium. In addi-tion, it is commonly stated that direct cur-

rent capacitor discharges cause less myo-

cardial damage than alternating currentdischarges.9' 18, 20 In this study, using needlethermistor probles, no significant tempera-ture elevations were demonstrated in themyocardium directly beneath the elec-trodes. Although it is difficult to compare

the effects of direct and alternating currentdue to their different characteristics, it isevident that marked myocardial damage isproduced in canine hearts by both alter-nating and direct current defibrillators atlevels of energy commonly used for internaldefibrillation of human hearts. To keep thisdamage at a minimum in canine hearts, it

FIG. 7. Three days following electrical shock, there is an interstitial proliferative cellular reactionsurrounding the altered muscle cells. The majority of the cells have plump, round to oval nuclei witha variable amount cytoplasm. There are relatively few polymorphonuclear leukocytes. Hematoxylin andeosin ( 1)00x ).

Volume 160Number 2 259

o

of


FIG. 8. Seven days following electrical shock, no cytoplasmic banding or beading is evident andthe transverse diameter of the myocardial cells is narrower than normal. The nuclei are enlarged andoval, with prominent single or double nuclei as indicated by the arrows. These nuclear and nucleolarchanges are not evident after the injury reaction has stabilized. Gomori trichrome stain (160 x).

is necessary to stay below 200 volts ofalternating current and 30 watt-seconds ofdirect current. On the basis of these find-ings, an attempt has been made to use lowenergy levels for clinical internal defibrilla-tion and five watt-seconds has successfullydefibrillated large human hearts followinghypothermic arrest. The lowest possibleenergy levels which will effectively defibril-late should be used.A direct current, capacitor discharge de-

fibrillator is used by preference in the Uni-versity of Washington operating suite. Itis believed that defibrillation is more easilyaccomplished with direct rather than alter-nating current at low energy levels. Experi-mental work by Lown9 indicates that de-fibrillation under acidotic and hypothermicconditions is more easily accomplished withdirect current, rather than alternating cur-

rent. In addition, capacitor discharge, di-rect current defibrillation reduces mass

muscle contractions to a minimum.Although this study involves internal ap-

plication of electroshock, it is felt that thesame advantages listed above apply to ex-

ternal or closed chest defibrillation. Forexternal defibrillation, the direct currentcapacitor discharge defibrillator possesses

the additional advantage of portability andmay be used with storage batteries in am-

bulances and first aid stations.Although the numbers involved are small,

it is evident that direct current capacitordischarges can cause ventricular fibrillationin a normally beating heart. Thus, as withalternating current defibrillators, a definitedanger exists for the operator if he acci-dentally receives the discharged impulse.The distribution of injured areas indi-

260

Volume 160 EFFECTS OF ELECTRICAL DI'Number 2

cated that the most damage occurred inthe area beneath the electrode rims. Thisoccurred despite an attempt to get evencontact between the heart and the elec-trodes and probably represents increasedcurrent flow from the rims as these portionsof the concave electrodes were closest whenthe paddles were applied to the heart.Using larger or padded electrode paddlesdid not affect the quantity of myocardialinjury seen, but did change the distribu-tion so that the areas of injury were patchybeneath the entire area of the appliedelectrode.The gross and microscopic lesions pro-

duced by alternating and direct currentdischarges are similar in nature, differingonly quantitatively with increasing voltageand energy levels. The microscopic appear-ance is quite distinctive and differs fromischemic or thermal coagulation necrosisin several aspects. The cytoplasmic altera-tion is represented by cytoplasmic banding,clumping and alteration of cross-striationsrather than a homogeneous glassy appear-ance and is present in animals dying acutelyduring electrical stimulation in contrast tothe somewhat delayed appearance of thecytoplasmic alteration in coagulation ne-crosis. The myocardial alteration spares thesupporting stroma, vessels and nerves anddoes not stimulate a polymorphonuclearreaction, in contrast to coagulation necro-sis. There is a prominent interstitial cellularreaction composed of macrophages, plumpendothelial cells and fibroblasts with manymitotic figures.Some of the myocardial cells are perma-

nently damaged and their cytoplasm is re-moved, apparently by macrophages, leav-ing a collapsed reticulum associated witha variable amount of fibrous tissue relatedto the severity of the initial damage.The fact that much less damage is noted

at four weeks compared to that at threedays, suggests that the myocardial cellularalteration is in part a reversible one. This

SCJHARGES ON CANINE HEARTS 261

is further suggested by the striking nuclearand nucleolar changes which are presentduring the healing phase of the reactionand may indicate that there has been sub-lethal injury to the cell which is reversibleand results in the restoration of cytoplasmicarchitecture. The large nucleolus may in-dicate active protein synthesis.

This curious myocardial alteration is notspecific for electrical injury. It differs fromcoagulation necrosis and has been seen inhuman hearts 13, 15, 16 hearts of rats3' 4 rab-bits,' dogs,7' 8 and guinea pigs'-5 under awide variety of conditions. For example,it is seen after cardiopulmonary bypass,15in potassium deficiency,5 14 and in hemor-rhagic shock.6' 12 The nature of this lesion,unclear at the present, is under investiga-tion by Reichenbach and Benditt.1"

Conclusions

1. Internally delivered electrical dis-charges from the defibrillators tested pro-duced detectable myocardial injury in ca-nine hearts averaging 106 Gm. in weight.This damage is roughly correlated with theenergy delivered. It is minimal at 100 and150 volts AC and 5 to 20 watt-seconds DC.Levels above these cause increasingly se-vere damage with either alternating or di-rect current.

2. No qualitative difference could be de-tected between damage caused by director alternating current.

3. The damage observed was not asso-ciated with significant elevations of myo-cardial temperature and is probably relatedto a direct effect of electrical energy onmyocardial cells rather than thermal injury.

4. Microscopic changes in damaged areasare characterized by striking cytoplasmicchanges in muscle cells and a proliferativeinterstitial reaction. These changes are ap-parently in part degenerative and may pro-gress to necrosis with variable amounts ofreticulum collapse and fibrosis. This lesionprobably represents a nonspecific though

262 ANDERSON, REICHENBACH, STEINMETZ AND MERENDINO Annals of SurgeryAugust 1964

characteristic response of myocardial cellsto injury, and is similar to experimentalcardiac necrosis produced in several speciesof animals with a variety of agents.

AcknowledgmentsThe authors wish to express thanks to Dr.

Earl P. Benditt, Professor and Chairman of theDepartment of Pathology, for his invaluable helpin the evaluation of the gross and microscopicfindings.

References1. Berfenstam, R. and L. Zettergren: Myocardial

Changes Following Oxygen Inhalation. ActaPediat., Suppl., 117:89, 1959.

2. Carr, L. B., 0. N. Rambo and T. V. Feicht-meir: A Method of Demonstrating Calciumin Tissue Sections Using Chloranilic Acid.J. Histochem. Cytochem., 9:415, 1961.

3. Chappel, C. I., G. Rona, T. Balazs and R.Gaudry: Comparison of Cardiotoxic Actionsof Certain Sympathomimetic Amines. Canad.J. Biochem., 37:35, 1959.

4. Danilova, K. M.: Adrenalin Myocarditis.Translated abstract in I.C.R.S. Medical Re-ports, Vol. 4, 1962.

5. French, J. E.: A Histological Study of theHeart Lesions in Potassium-Deficient Rats.A.M.A. Arch. Path., 53:485, 1952.

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8. Jennings, R. B., H. M. Sommers, G. A. Smyth,H. A. Flack and H. Linn: Myocardial Ne-crosis Induced by Temporary Occlusion of aCoronary Artery in the Dog. Arch. Path.,79:68, 1960.

9. Lown, B., J. Neuman, R. Amarasingham andB. V. Berkovits: Comparison of Alternating

Current with Direct Electroshock Across theClosed Chest. Amer. J. Cardiol., 10:223,1962.

10. Macpherson, C. R.: Myocardial Necrosis in thePotassium-Depleted Rat; A Reassessment.Brit. J. Exp. Path., 37:279, 1956.

11. Alanual of Histologic and Special StainingTechnics. U. S. Armed Forces Institute ofPathology, Washington, D. C., 1957.

12. Martin, A. M., Jr. and D. B. Hackel: TheMyocardium of the Dog in HemorrhagicShock. Lab. Invest., 12:77, 1963.

13. McFarland, J. A., L. B. Thomas, J. W. Gil-bert and A. G. Morrow: Myocardial NecrosisFollowing Elective Cardiac Arrest Inducedwith Potassium Citrate. J. Thorac. Cardiov.Surg., 40:200, 1960.

14. Molnar, Z., K. Larsen and B. Spargo: CardiacChanges in the Potassium-Depleted Rat.Arch. Path., 74:339, 1962.

15. Reichenbach, D. and E. P. Benditt: Unpub-lished data, 1963.

16. Rodriguez, C. E., A. L. Wolfe and V. W.Bergstrom: Hypokalemic Myocarditis. Amer.J. Clin. Path., 20:1050, 1950.

17. Spiro, D.: The Ultrastructure of Heart Mus-cle. Trans. N. Y. Acad. Sci., Series 2, 24:879, 1962.

18. Stearns, N. S., G. L. Maison and J. W. Stutz-man: Cardiac Resuscitation from InducedVentricular Fibrillation; Influence of Mas-sage, Procaine and Electric Shock. Amer. J.Physiol., 164:601, 1951.

19. Stenger, R. J. and D. Spiro: Structure of theCardiac Muscle Cell. Amer. J. Med., 30:653,1961.

20. Tedeschi, C. G. and C. W. White, Jr.: Morph-ologic Study of Canine Hearts Subjectedto Fibrillation, Electrical Defibrillation andManual Compression. Circulation, 9:916,1954.

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an evaluation and comparison of effects of alternating and

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