‘THE MECHANISM OF ELECTROSURGICAL COAGULATION: STEAM EVOLUTION VERSUS DIELECTRIC BREAKDOWN by STEPHEN F. BART SUBMITTED IN PARTIAL PULPILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF BACHELOR OF SCIENCE at the MASSACHUSETTS INSTITUTE OF TECHNOLOGY May, 1982 Signature of Author eee “peprtment of Efectricai Engineering May 21, 1982 certified by .. a . uv WS mosis Supervisor Accepted by « Chairperson, Departmental Committee on Theses . Archives “7i2 rs, BWwyua WaN¥oo “ ~ 2 92901 asl JassaA 3ynss3ud X3HcHaprER 2 vv cornea into electrical contact with the electrodes. The active electrode consisted of a stainless steel rod which slid into the hole in the center of the cornea holder allowing the distance between it and the cornea to be continuously adjustable. The comnon or return electrode was a piece of platinum foil glued to a square of plexiglass that could be slipped into the trough. In all of our experiments the conducting media used to #111 the cornea trough was 0.15 molar saline. This was chosen because it is approximately isotonic to biological tissues and is also a good conductor. The pressure vessel was pressurized with nitrogen gas. Since it is imperative that we know the temperature versus time charateristics of our specimen given an applied voltage, it was necessary to calculate the electric field density at the specinen for the applied voltage. A simple Electroquasistatic formulation (presented in detail in Appendix 1) yielas: Ey = Ku(e) (ap, where By is the electric field at the specinen site and K is a constant that depends on the geometry of the electrode configuration. From this we can calculate the time average power dissipation density in the region aurrounding the specimen:CHAPTER 2 8 2 PD>, = OK Vg (P1-2), where we have agsuned that the bulk-average conductivity of the specimen and the surrounding saline solution are the same. This approximation is certainly correct to within an order of magnitude, since the increase in tissue conductance due to ite fixed charge groups will compensate to some extent for the decrease in conductance associated with the specimen's fine structure, e.g. cell membranes. From this, thermodynamic argunente (see Appendix 1) yield ADL oKy 2 “ ae” “co Vens: ee where c is the specific heat and ¢ is the mass density? both (e1-3), are assumed to be uniform throughout the fluid and specimen. After evaluating K for the specific geometry (see Appondix 1) we find: 2 4c ar Ma 5.6% 107 y, (pia). ‘This equation gives us our first approximation to the choice of applied vcltages and application times for use in projects 4 and 5. The Valleylab SSB3B Cut #25 (Vpn, * 64v) waveforn (see Figure 2) was chosen because of its relatively low power (the number 25 means that the electrosurgical device would supply 2547 watts (or 158, which ever is larger {1]) to a 3002 resistive oad), thereby yielding an application time long enough to effectively differentiate between boiling and non-boiling stateFIGURE 2 MONOPOLAR OUIPUT WAVEFORMS ‘AS seen cn an oscilloscope Volts/centinetar asCHAPTER 2 2 Project 2) Measurement of Cornea Temperature versus Time During Application of Current The theoretical calculation carried out in project 1 assumes that the conductivity, specific heat, and density of the cornea are the sane as the 0.15M saline bath. It also assumes that the electrosurgical generator will act as a idea! voltage source. Unfortunately it is very difficult to gauge how valid these assumptions are. In fact the output of the Valleylab SSE3B electrosurgical generator is not that of a perfect voltage source: it contains, impedance matching circuitry that cause it to be non-Linear for the first few moments of its operation. Thus the theoretical calculations in project 1 my be significantly in error. Since it is vital that we know the temperature versus time characteristics for ary input that we mey use, direct measurements were made. Procedu The temperature of the cornea was monitered using a thermocouple placed in direct contact with the cornea. The thermocouple was constructed from 3 mil constantin and chromel wires which were soldered into = thermal junction with stainless steel solder. The ends of the leads were soldered to copper wire and immersed in an ice/water bath asCHAPTER 2 a a “zero degree" reference. All thermal junctions were insulated with epoxy. The leads were attached to a Hewlett Packard digital voltmeter from which the junction voltage was read. Note that we tried to record the thermocouple voltage directly using a strip chart, but were unable to isolate the amplifiers from the electrosurgical device's RF fields. The voltage to temperature transformation was accomplished using a published constantin-chromel junction voltage reference [18] (this calibration was double checked by placing the thermocouple in water at the melting point, roon temperature, and the boiling point and checking the juction voltage with the table's value). ate Figure 3 shows the temperature versus time characteristic using the Valleylab SSE9B Pure Cut #25 waveform. (see Figure 2). Note that the slope in the Linear *c *c region is about 2 26 compared to the 2.3 2& value predicted in project 1 (this value is obtained by substituting Veng = 64v for the Cut #25 waveform into equ. (P1-4): see Appendix 1, equ. (Al-21)). The rollofs of the slope in Pigure 3 results from the combination of two effects. As the temperature of the surrounding saline increases, the mobility of its conductive iona increases causing the system resistance to go down. As a consequenceoo er) saxoogs on a os as aWIL o ew 4 Q 22 335 glo 205 90 ous oF feu @~ sd018~ u a a A L v a a a w a LCHAPTER 2 23 of the Valleylab ssE35' design, it tries to keep the input power constant, so it will reduce the applied voltage to compensate. This effect is small; a nore important cause is cal gram vaporization represents the energy needed to change one gram due to water's 540 heat of vaporization (the heat of of Liguid into vapor with no change in temperature). As the slope flattens out, more and nore of the energy being supplied by the electrosurgical current is going into satisfying the heat of vaporization instead of increasing the specimen's temperature. Thus as long as we remain on the slope of 2 portion of the graph no energy is being used to cause vaporization, hence no boiling is occurring even on a local level. We now wish to compute the applied pressure necessary to suppress intracellular boiling in our specimen. Specifically, we will choose the pressure such that the 60 second point is still located on the slope of 2 segnent of the graph so that no local boiling will occur before 60 Seconds. Also, the time necessary to supply enough energy to satisfy the heat of vaporization will cause global boiling to be suppressed well past 110 seconds. In fact since the heat of vaporization is so large compared to the eneray required to increase the tissue temperature we can probably assume that no local boiling will occur at 110CHAPTER 2 4 seconds either (this assumption will not be critical to our results). Tf we extrapolate the slope of 2 section of the graph (figure 3) to intersect the 60 second point we see that the new boiling point must be about 175°C. This corresponds to an applied pressure of 120 psi [19]. Another way to view the effect of applying this pressure is to note that increasing the boiling point by 75°C simply shifts the graph 32.5 seconds to the right (as well as rescaling the temperature axis). Thus the 60 second samples will be in the same state relative to boiling as the 30 second samples at atmospheric pressure. Project 3 Histological Characterization of Normal Cornea ‘The cornea is the anterior-nost portion of the eye which is responsible for the major part of the refraction of incoming light. It is a slightly elliptical membrane of vlinm mean diameter. Structurally, the cornea consists of 5 layers - (1) the corneal epithelium: (2) the anterior Limiting lamina (Bowman's membrane): (3) the substantia propria or corneal stroma; (4) the posterior Limiting lamina (escenet's membrane): (5) the endothelium of the anterior chamber or mesothelium. Layers (1) through (3) are evident in plate (a) showing a normal bovine cornea. The corneal epithelium covers the front of the corneaCHAPTER 2 25 and consists of three general layers of cells. The deepest cells are columnar; their basal surfaces are flat and their outer surfaces rounded, and they contain large round or oval nuclei. The cells of the second layer are polyhedral with oval nuclei. In the uppermost layer, the cells become progressively flattened with flattened nuclei (see Plate D). Immediately beneath the corneal epithelium is the anterior Limiting lamina or Bownan's membrane. Tt consists of fine closely interwoven collagen fibrils similar to those found in the stroma but contains no fibroblasts (described below). . ‘The substantia propria or corneal stroma is composed of about 200-250 flattened, superimposed lamellae which are made up of bundles of modified connective tissue. The fibers of each lamella are arranged in a roughly parallel orientation. However, the orientations of adjacent lamolla are staggered. Ground substance proteogleans are interspersed between collagen fibrils; connective tissue cells called fibroblasts are found throughout the extraceliular matrix of the stroma (see Plate C). The posterior limiting lamina or Descemet's menbrane covers the posterior surface of the substantia propria, and is a thin, homogeneous membrane. It serves as a basement membrane to the mesothelium, which consists of a singleCHAPTER 2 6 layer of polygonal, flattened, nucleated ces [20]. Procedure Im the course of our study, 7 uneffected, control corneas were obtained and processed in the following manner. Bovine eyes were delivered on ice within 4 hours of slaughtering. The corneas were removed immediately and refrigerated in a bath consisting of their own aqueous humor, All experimental procedures were carried out within 24 hours. After the procedures were completed, the samples were chemically fixed in neutral buffered 108 formalin for a minimum of 26 hours. In preparation for enbedding, the center, treated section of the cornea was trinmed and placed into Tissue Tek IT embedding cassettes. These were put through a series of ethyl alcohol baths to dehydrate the tissue and then cleared with xylene. The samples were then infiltrated with paraffin for 2 hours and mounted in paraffin blocks for microtomy. The paraffin block containig the cornea was mounted and aligned on a microtome for sectioning. The block was iced and 2 5 micrometer thick ribbon was cut. This ribbon was Floated on a 42°C water bath (this procedure deconpresses and flattens the ribbon). The sections were then placed onto slides and dried at 40°C before staining ‘The staining procedure was an autonated one which takesCHAPTER 2 2 the slides through xylene, a graded series of ethanol and finally stains the samples with routine hematoxylin and eosin (which stains nucleic acide purple and cytoplasm pink-red). The slides were coverslipped and dried overnight before handling [21,22]. Photomicrographs of the specimens were taken on a Zeiss Photomicroscope using Kodachrome 25 color slide film. These Photographic slides were then reproduced with a color Xerox machine to obtain the Plates in this document. The color xerox reductions unfortunately do not show the same clarity and detail as the original slides: however, the accompanying discussion should overcome this problem. Results In our work we shall be interested in the cells of the corneal epithelium and the state of the collagen fibers in the corneal stroma. The structures and characteristics described above can be seen in the control (normal) corneas shown in Plates ¢ ané D. Plate D shows the three general epithelial cell types. The parallel lamellae of the corneal sttoma show up as a wavy texture in normal corneas (see Plates C, D and K). Note that the small spaces surrounding the nuclei are an artifact of the histological fixation process. Also as a consequence of microtoming. the lamellae often tear (see Plate C) along their parallel orientation.CHAPTER 2 8 Project 4 Histological Characterization of Cornea which has been subjected to a High Voltage, High Crest-factor Waveform Here, we applied a high voltage, impulsive waveform to the specimen. In this way we could denonstrate whether or not cell damage could occur prior to steam evolution. This experiment therefore tests the possibility of a nigh voltage-induced breakdown mechanism. Procedur ‘The corneas were placed in the frame with the epithelial cell layer fecing the active electrode. The Valleylab Coag #100 setting (peak voltage = 1200 volts) was used to supply the impulsive waveform (see Figure 2) for various lengths of time. Specifically: for 1, 2, and 3 seconds, no boiling will occur: 5 seconds is probably too short for boiling to eccur, but we can not be as sure; and @ seconds was the time necessary for the experimenter to witness boiling (see Figure 3). two specimens were tested for the one second experiment, and one specimen was tested lat each of the other time durations. After the application of current the specinens were processed for histological observation as described in project 3. ResultsCHAPTER 2 ct Plate E represents a specimen which has undergone 1 second of Coag #100 treatment. Although the damage is mild it is evident (more so on the original slide). Note the upper cell layer which has stained more darkly; this effect seems to be characteristic of moderately affected cells. In general, cell menbranes renain intact here. The specimen shown in Plate F was subjected to 2 seconds of Coag #100. Celi damage is much more extensive here. Note the ballooning effect and the large area of cells which have stained more darkly- Plate G is an enlargement of this area and makes it clear that the differentiation between cells has been destroyed in this region. The cells below Were also quite disrupted. The stroma was uneffected. ‘Mt 3 beconds the cell damage is quite severe (Plate H). Many of the cell membranes have ruptured. The entire cell layer seems uniformly disrupted; it has become impossible to differentiate between the three cell types. The stroma shows the randomizing effect over half of its thickness. Keep in mind that no boiling has occurred in any of the specimens seen £0 far. ‘The damage accrued at 5 seconds (Plate T) does not seem vastly different from the 2 second case. In the upper cell layer the cytoplasm is gone. The stroma effect reaches through about two thirds of the stroma thickness.CHAPTER 2 30 Plate J shows the case that corresponds to observed boiling (8 seconds of Coag #100). The entire cell layer is gone over much of the cornea's surface. The cells that remain are completely disrupted. The collagen orientation stroma is randomized almost all of the way through. Project 5) ‘Histological Characterization of Cornea which has Been Subjected to Pure Sinusoidal Electrosurgical Current of Various Durations This project will allow us to develop an empirical understanding of the consequences of subjecting corneas to electrosurgical current. From this we will be able to gauge the extent of the damage imparted in the high pressure or high voltage experiments. Procedure Fresh corneas were placed in the experimental frane (see Plate 8) with the epithelial cell layer facing the active electrode. They were then subjected to a 90 volt peak sinusoidal waveform (corresponding to Valleylab setting Pure Cut #25) for 10, 30, 60, or 110 seconds. These times were chosen to place the specinen in certain regions of the corresponding temperature versus time curve (see Figure 3). Specifically, 10 and 30 seconds were short enough toCHAPTER 2 3 preclude boiling: 60 seconds was the borderline for boiling: by 110 seconds, boiling was clearly visible in the fluia within the chamber. One specimen was tested at each of the above durations. Two additional specimens were tested, one ‘at 30 and one at 60 seconds, with a thermocouple in contact with the cornea (see Figure 3). Also, two corneas each were subjected to a 50 volt (peak) 10kiz, sinusoidal voltage for 3, 5, and 10 minutes. Three minutes corresponded to precboiling, 5 and 10 minutes to boiling. These currents were supplied by @ Kepco Bipolar Operational Power Supply. The effects of these lower power, longer duration currents could therefore be compared to the higher power, shorter @uration currents supplied by the Valleylab electrosurgical generator. Results Plate K shows a cornea which has been subjected to 10 seconds of the Cut #25 waveform. It looks essentially normal except in the lover, columnar cell layer. Here we see a greater percentage of open space in the cells; the cytoplasn looks Le homogeneous. This effect is the beginning of an effect called ballooning which is caused by increased osmotic activity due to the fracturing of large cytoplasmic proteins into amaller more osmotically active pieces. In general the cells are still discreet units, implying thatCHAPTER 2 2 coll membranes have not ruptured. Note that the stroma ie essentially normal (compare to Plate C). Plate M shows a cornea which has been subjected to 30 seconds of Cut #25. Here the ballooning effect is much more Pronounced and has effected all but the uppermost layer of cells. The differentiation between cells is beginning to break down. Although it is difficult to see in Plate M, the stroma near the epithelial cell layer has undergone a change. Tt has lost its wavy parallel orientation end has taken on a much more random structure. This is believed to be a consequence of the denaturation of the collagen in the stroma which occurs at 760°C. This collagen denaturation process is very important since it ives us an inherent tomperature marker. Since this denaturation only extends about 1/6 of the way through the stroma, our belief that intracellular boiling is not yet occurring at 30 seconds is strengthened. Plate P is an enlargement of the cell layer from a cornea which has undergone 60 seconds of Cut #25 (this image contains over 80% of the epethelium's cross section). Here all differentiation between cells is gone; the menbranes are completely ruptured. The stromal lamellae have been changed to 2 randomly oriented state over half of the stroma'sCHAPTER 2 3 thickness (not shown in the magnification of Plate P). Plate § shows a cornea which has been subjected to 110 seconds of Cut #25. In this case boiling was actually seen to take place in the saline surrounding the cornea. Again we see oxtensive cell damages cell menbranes have ruptured and much of the cytoplasm has run out to coaguinte in a space between the cell layer and the stroma. Note that the stroma has taken on yet another appearance. No longer can any fine structure be detected: it has become very homogeneous. This effect reaches through the entire stroma. Plate U shows @ cornea which was subjected to a 50 volt (peak), 10kHz sinusoidal voltage for 5 minutes. The damage here is somewhat similar to the 10 second Cut #25 case (Plate k). The ballooning effect is more pronounced, but the stroma still appears normal. Finally, Plate W shows a cornea which has undergone 10 minutes of the 10kilz waveform described above. Ballooning and membrane rupture is extreme. The stroma appears as if it has just barely begun to change to the randomized state. Note that no boiling was observed in the surrounding saline in this case.CHAPTER 2 4 Project 6 Histological Characterization of Cornea which ‘has been Subjected to Blectrosurgical Current under Elevated Pressure In this project we subjected corneas to electrosurgical current for the sane duration as in project 5. However, this time we applied an elevated pressure to stop any boiling of intra-cellular fluid which may have occurred in the previous experiment; specifically, in the 60 and 110 second cases. Procedure ‘In this case ae in the last, fresh corneas were placed in the experimental frame (see Plate 8) with the epithelial coll layer facing the active electrode. The sane 90 volt (peak) Cut #25 sinusoidal waveform was used for the identical durations as in Project 5. The difference was that the samples were sealed inside the pressure vessel, and a pressure of 120 psi was applied (nitrogen was used as the pressurizing agent). After the current was applied, the specimens were allowed to cool down and were then de-pressurized slowly. As in project 5, two samples were run for the 30 and 60 second durations: however, no thermocouple was used. Also, four control corneas were subjected toCHAPTER 2 3 elevated pressure without current application. A few samples Were subjected to the 50 volt, 10kiz waveform described in Project 5 along with 2 100 psi. applied pressure. AlL samp were then processed for histological observation ai described in project 3. Results ‘The pressurized control corneas were indistinguishable from normal cornea as shown in Plates C and D. Plate K shows 2 cornea which was subjected to the Cut #25 waveform for 10 seconds. It ise jentially indistinguishable from the control cornea (compare with Plate C)- Comparison with the 10 second, 1 atmosphere sample (Plate K) shows slightly less Aieruption in the pressurized case. ‘The cornea shown of Plate N was subjected to Cut #25 for 30 seconds at 120 psi. Plate 0 is an enlargenent of the sane specimen. We see a considerable anount of cell damage. cell menbranes have broken down leaving a relatively homogeneous mixture of cytoplasm (see Plate 0). The strona remains unaffected. Comparison with the 30 second, 1 atmosphere sample (Plate M) shows that cellular danage Looks essentially the same in both cases. Plates @ and R represent 60 seconds of treatment with elevated pressure. Plate Q seems to indicate less damage than the 30 second, 120 psi case described above, yetCHAPTER 2 6 examination of the magnified view (Plate R) shows considerable destruction. However, the integrity of many cell menbranes is still evident. The upper layer cells are more disrupted than the 30 second case and the stroma shows the denaturation effect in the upper third of its thickness. Comparison with the 60 second, 1 atmosphere case (Plate P) indicates considerably less cell randomization and membrane rupture in the pressurized case. Plate T shows @ cornea which has been subjected to 110 seconds of Cut #25. Cell damage is severe: note the long ‘cracks" within the epithelial layer which run parallel to the stroma-cell border. The upper cell layer is completely destroyed. The stroma fiber orientation has been randomized throughout the majority of its bulk. Note however that it does not show the amorphous structure of the specimen in Plate 5, for which boiling was seen to occur. Cell disruption is roughly equivalent in these two cases. Corneas which were subjected to 3 minutes of the 10kHz waveforn (at 100 psi as described above) looked the sane as those that received the treatement without pressure (ive. they both showed damage similar to the 5 minute case shown in Plate U). Corneas that were subjected to 5 minutes of current also looked the same as their unpressurized counterparts (Plate U): however, there was some differenceCHAPTER 2 37 in the uniformity of the cell damage. For example, some sections of the same cornea looked essentially normal, as shown in Plate V. The stroma was unaffected in all cases. A apecimen which underwent 10 minutes of this treatment was virtually indistinguishable from the 10 minute case without pressure (see Plate W); again the stroma was unaffected.CHAPTER 3 38 DISCUSSION: MODELS AND MECHANISMS tm Chapter 2 the results of our experiments were described. Here our task is to interpret these results in terms of the possible mechanisms that could produce initial breakdown of cell membranes, including high voltage-induced @ielectric breakdown and stean evolution due to boiling. Correlations will also be drawn between the cell danage caused by Coag #100, Cut #25 and the lOkHz sinusoidal waveforms used on this study. The dielectric breakdown model will be examined first. A. High Voltage-Induced Dielectric Breakdown ‘The dielectric breakdown model rests on the assumption that there exists some phenomenon which will cause structures such as the cell menbrane to rupture when they are subjected to high voltage. Our goal here is first to review @ model mechanism in order to make such = breakdown Phenonenon plausible and then to assess whether or not the conditions of our experiments’ environment meet the criterion for such a breakdown mechanism. Finally we will review the results of project 4 (Coag #100 waveform) in Light of this understanding and try to determine the role of such a breakdown mechanism in electrosurgical coagulation:CHAPTER 3 29 A model for dielectric cell menbrane breakdown was Proposed by Crowley in 1973 [12]. In this model the cell is treated as an elastic, non-conducting, dielectric surrounded by @ highly conducting medium (see Figure 4). Since the membrane is modeled as a non-conducting dielectric, a voltage applied across it will cause @ compressive electrical stress 7, in the x direction (perpendicular to the plane of the menbrane)+ vt 0 Gn, were V is the applied voltage, ¥ is tne electric field in the nenbrane and ¢ is the dielectric permittivity of the enbrane. The compressive deformations caused by the applied voltage are opposed by the olastic restoring etrest Ty which is related to compressive strain as follows: Ty, = Bn $ (2-2), were £ is Young's modulus, 1 is the original thickness, and ¢ fs the compressed thickness. The term In (f) is a measure of membrane compressive strain for finite deformation, as : a1) cpposed to the uavel infinitesimal strain measure, (E23. Note that Lt is straight-forvard to reformiate thie one imensional equation for more complex geometries40 Crowley's Membrane Model FIGURE 4CHAPTER 3 a By equating these stresses Crowley was able to show [12] that as voltage increases, the compressive deflection increases, approaching infinity ats eve BE + one (3-3). Thus, above sone critical voltage which is a function of the menbrane's electrical and mechanical parameters, an instability results which ruptures the membrane, This result can be reasoned qualitatively by noting that the electrical stress is inversely proportional to the compressed membrane thickness 4 (J-1) while the restoring stress is proportional to 1n (f) from (3-2). ten the applied voltage produces a small enough 1 the electrical compressive stress dominates, tending to reduce 1 even further, and thereby initiating en instability which leads to menbrane rupture. This model was shown to predict the approxinete threshold voltage for the breakdown of artificial 1ipia bilayer fins. We mst now decide whether the voltages we applied in our experiments vere large enough to meet the critical voltage criterion of equation 3-3. Fron Crowley's paper [12] we can obtain the following average values for © Lipid bilayer membrane: Bei 3% ate FE c= = 0.008 5CHAPTER 3 4a Ls 1008 If we substitute these values into equation (3-3) we find: Vv = 270 mv (3-4) In project 4 we applied a Valleylab Coag #100 waveform which has a peak voltage of about 1200 volts. A simple Gerivation (shown in detail in Appendix 2) shows that this waveform will cause a potential difference across the cell membranes of on the order of 1.2 volts. This tells us that the voltages applied in project 6 were in general high enough to cause dielectric breakdown by a mechanism such as Crowley's. Recall from project 2 that 8 seconds of Coag #100 was necessary to produce observed boiling. There may be sone question as to whether intracellular boiling is occurring at 5 seconds, but we may assume that no boiling is occurring at 9 seconds with a large margin for safety. If we review the results of the high voltage experiment (Plate: BF, G, H, I, J) we see that for applications as short as one second duration, cellular changes have occurred. At 2 seconds (Plates: F, G) we see coneiderable cell damage and yet the stroma remains unchanged. This means that the strona has not. reached 60°C, which implies that the intra-cellular fluids id not boil, but damage did occur. By 3 seconds (Plate H)CHAPTER 3 4a serious cell disruption has occurre: membranes have broken down, and differentiation between cell types is gone. From these results we draw the following preliminary evolution may play. when high voltage, high crest factor waveforms are well before intra-celiuiar fluids begin to boil. It seens plausible that the mechanism involved in this cell disruption could be a high voltage-induced dielectric breakdown such as that proposed by Crowley [12]. B. Steam Bvolution ‘The mechanism for menbrane breakdown due to steam evolution is rather straight-forward. As electrosurgical current passes through the tissues, ohmic heating results. When the intra-cellular fluid's boiling point is reached, steam is evolved. Inherent to this steam formation is a large change in volune which causes the cells to rupture. In Projects 5 and 6 we have subjected 2 sets of corneas to equivalent input energies (recall that the temperature change is directly related to the energy input; see Appendix 1) and varied the pressure to see if cell ‘damage could be suppressed. Reviewing the unpressurized corneas (Plates: K, M, P and §) and comparing to their equivalent time, pressurizedCHAPTER 3 44 counterparts (Plates: L, N, 0, 0, R and T), we find that application of pressure id not supress cell damage in a uniform and repeatable way. Plates K and L seem to indicate that damage was suppressed in the 10 second pressurized case. However the damage in both cases is very mild and subsequently hard to quantify. Careful inspection of the original histological specimens does not allow us to make any conclusive statement about suppression of danage in this ease. The same situation is true for the 5 minute, 1OKH2. case (Plates U and V). The 60 second samples seem to show 2 Gefinite reduction of damage in’ the pressurized case (compare Plate P to Plate R) and yet the 30 second samples showing the same type of danage do not (compare Plate M to Plates N and 0). C. Waveform Correlations Given the findings above, it is natural to wonder how the cell damage caused by the different waveforms compares. In order to make such a correlation, we first need to relate the total electrical energy delivered as a function of tine for each waveform. This turns out to be very difficult to quantify: (1) the resistance of the cornea is not known Precisely, (2) the power delivered by the Coag #100 waveform has a tolerance of 15%, and (3) we cannot be sure of the exact time of boiling due to the thermal inertia of the‘CHAPTER 3 4 ‘thermocouple (v1 second) as well ae inaccuractes associated with direct visual observation. We have therefore compared the equivalent energy delivered by Cut #25 and Coag #100 waveforms (see Figure 3) by comparing the measured tissue temperature versus time characteristics for several specimens and then checking these results by comparing the extent of stroma denaturation for each time interval (similar denaturation implies a similar temperature which implies similar energy input). re was found that 3 seconds of Coag #100 is roughly equivalent to 30 seconds of Cut #25 (5 Figure 2). Comparison of these two cases (compare Plate H to Plates N and 0) shows that the damage is quite similar. In no case were we able to quantify any significant differences in the initial phases of cell Gamage caused by these two waveforne. D. Conclusions The results of our study clearly show that some type of sell menbrane breakdown is initiated well before boiling can Qecur. This result was observed with Coag #100 and even with Cut #25 waveforms. As application of current is continued, cell breakdown continues. Significant cell damage has occurred and continues to occur at the onset of boiling: g++ gross morphological changes in the stroma. Similar tissue damage effects after intra-cellular boiling have been‘CHAPTER 3 46 described recently for muscle [15,16]. In the present research, however, we confine ourselves to a description of the initial onset of danage to cells, which is the precursor of such macroscopic changes. As to the mechanien for initial cell membrane breakdown, we conclude that it is very possible that a high voltage dielectric breakdown phenomena such as that proposed by Crowley [12] might be in operation in our situation, certainly for Coag #100 current. due to the nature of the approximations used in Appendix 1, it is conceivable that Crowley's critical voltage was reached even in the cut #25 case. It is possible, however, that a different mechanism for breakdown is at work. In any case, steam evolution is not the sole mechanism for electrosurgical cell disruption. In fact, this study indicates that it may not even be an important factor. When interpreting this last statement it must be Kept in mind that our experiments examined the initial effects of electrosurgical current on the cellular level. They do not necessarily apply to the macroscopic effects on gross tissue morphology. For example, it is understood that the cut and Coaguiate waveforms do indeed have very different effects on the macroscopic scale [1]: our cornea tissue model and specific experimental design were not designed to accentuateCHAPTER 3 47 these macroscopic differences. Im trying to model our tissue we ran into several Problems: working with a biological system for which Physical and electrical characteristics are not well documented, as well as trying to get statistically significant results with only a small number of specimens Thus, while our main conclusion concerning menbrane breakdown rests on firm ground, other correlations betweon Aifferent waveforms must still be considered tentative. There was also sone difficulty using electronic equipment in the presence of the electrosurgical device's RF currents. We have attempted to be as objective as possible. To that ond histological appraisals of researchers not involved in this project were obtained concerning the nature of the cellular Gamage that we have discussed. E. Suggestions for Future Research There are many directons which future work might take to try to develop a working understanding of the microscopic effects of electrosurgical current on biclogical tissues. A replication of this or similar studies might employ more sophisticated temperature probes for accurate, real-tine measurement of specimen temperature using a non-electrical method (e.g. fiber optic probe sensors). In this way, more accurate monitoring of ohmic heating would be enabled,CHAPTER 3 40 without noise or artifacts associated with coupling of sensors and the applied field. Also more samples are needed to draw statistically significant conclusions with regard to waveform correlations. In the study conducted by Chen and Grodzinsky [15,16], real time impedance measurements were made in beef muscle being subjected to electrosurgical current. They found that the admittance versus time plot exhibited a characteristic peak. Initially, the admittance increased because electrolytic mobilities increase with the increased temperature caused by ohmic heating. With time admittance decreased due to the loss of intra-celiular fluide that accompanied boiling. Figure 5 shows a plot of relative admittance of a saline bath versus time quring the application of electrosurgical current. In this study we began a project to replicate this procedure using cornea. In @ preliminary trial done with a slice of beef muscle placed in our cornea rack in saline soloution, we were not able to duplicate the characteristic admittance peak (see Figure 6; relative admittance versus tine). This seemed to be due to the fact that our sample was immersed in a large bath of saline, which prevented it from drying out as intre-celluler Boiling progressed (in the preceding study [15,16], there was no external bathing electrolyte). However, since theCHAPTER 3 4“ corneal strona is so drastically effected by electrosurgical current such a study of impedance versus time may still provide some new clues as to the mechanisms occurring during cellular disruption due to electrosurgical current. In Appendix 3 the Fortran and PDP-11 Macro programs used to take real-time voltage, current and temperature data from an analog to digital converter and then convert them to admittance versus time plots are given. The other major avenue for future research is the further development and testing of a high voltage-induced Alelectric breakdown model for cell membranes. This line of work is embryonic? further advances are essential. As the microscopic effects of the electrocoagulation process come into focus they can be correlated with macroscopic effects to yield an overall understanding of the Process. Such an understanding would allow the designers of these devices to tailor waveforms and probes to their specific physiological needs while minimizing the Aiffioulties associated with use in a surgical setting. Ultinately, we would predict the use of microprocessors to monitor the “state” of the tissue in real tine and to adjust the output characteristics of the electrosurgical generator accordingly, allowing it to indicate "good coagulation". In fact, some manufacturers have already made considerable strides towards realizing this goal.50 $ aunora 9 zen ano 1g possegoa NS GeRagelfG “SeQ"BoraRe FIGURE 59 suoota Ea: ano 10 Fokasslte “Ta8 pa FIGUREouexa vousoD WaTH YOROZE =f BAVTEappx ane tvertx puowosaerus euro TewzoN a auwtaayox sme T 905 TooT# Be09 aw suaappx wae Tt 998 z ooT# Seong auWTaaed auousbze Ta we T 988 2 OTe Seo -y aaNTE448 3sec 1 atm coag #109 PLATEapex wyeT 988 § ouT# Buoy =r auvIa9258 ots Broa” Pp aba8yox we T 998 of «Sek aR maT are pe a Wheeavex sd zt 998 of szh ano ot aaa357Brox Fed ozt 998 0c + sek ano oN guwaaappx yd ot 288 09 © sz# ano” Osa |oeex Bustyou peasosqo we T 228 OTT sea ano s amviausex ted ozT 995 OTT sz¥ and Gsappx uwrus wae T zH¥OT 3Tea os codex on auwTax1120 2 atm Kepeo 50 volt, 10 Kitz 10 min PLATE W75 REFERENCES Valleylab SSE3B Service Manual, 1981. 2. Bart, 8. ‘981. + Report to Codman & Shurtleff, April 24, Rook, A.) Wilkingon, B. B., and Elbing, F. J. Ge, eds., Textnook of Dermatology, 3a Edition, Blackwell Scientific Publications+ oxtora, 1979. 4. Honig, Willian M., "The Mechanism of Cutting in Blectrosurgery", IEEE Transactions on Biomedical Engineering, January, 1975, p. 58-62. 5. Drabkin, R. L., "Analysis of Tissue Temperature in Monoactive ‘Electrocoagulation", All-Union Med. Instrum. Res. Inst., Moscow, USSR, 1973; Biomed. Eng., Vol. 12, 1978, p. 80-84. 6. Drabkin, R. L., "Electrocoagulation of the Sclera", All-Union Med. Instrum. Res Inet-, Moscow, USSR, 1973; Biomed. Eng-, Vol. 12, 1978, p. 76-79- Overmyor, K. M., Pearce, J. A. and DeWitt, D. P., "Measurements of ‘Temperature Distributions at Electrosurgical Dispersive Electrode Sites", ASME Paper No. 77-WA/HT-47, Heat Transfer Conference, ASME, August 1977. 8. Vito, R. P., "on Heat Transfer in Biological Tissue", Proc. 29th Annual Conf. Eng. Med. Biol-, Boston, Nov. 6-10, 1976, p-309- 9. Erez, A., and Shitzer, A., "Controlled Destruction and ‘Tenperature Ditributions in Biological Tissues Subjected to Monoactive Flectrocoaguiation", J. Bionech. Eng., Vol- 102, Feb. 1980 p. 42-49.76 10. Aubry-Frize, M., Leduc, As, Marsolais, R., Carrier, Re, "Assessment of Skin Temperature Elevations duc to Electrosurgical Currents", Service Physiqu= Bio-Medicale, Hospital Notre-Dame, 1560 Sherorocks Est. Montreal 133, Que 11. Belov, S. V., “Effects of High Frequency Current Parameters ‘on Tissue Coagulation", All-Union Med- Instrum. Res. Inst., Moscow, USSK, 1973; Biomed. Eng., Vol. 12, 1978, p. 209-211. 12. Crowley, J. M., "Electrical Breakdown of Biomolecilar Lipia’” Membranes as an Electromechanical Instability", Biophysical Journal, Vol- 13, 1973, pe 7d. 13. Vogler, L. J.) and Mylrea, K. C., “Tissue Heating From Electrosurgery Signals",Proc. 3ist Ann. Conf. Eng. Med. Biol-, 20: 34, 1978. 14, Slegel, B., and Dunn, M. Rs, “The Mechanism of Blood Vessel "Closure ky High-Frequency Flectrocoagulation", Surg. Gyn. Obstet., Vol- 121, October 1965, p. 625-831- 15. Chen, TT. Le, "Physical Characterization of Electrosurgical Coagulation", 5.8. Thesis, MIT, 1980. 16. Grodzinsky, A. Js, Chen, T. Le, and Newton, Ds We, “Physical " Characterization of Electrosurgical Coagulation", Journal of Surgical Reaearch, (to appear 1982): 17, Castellan, G. W., Physical Chemistry, 2nd Edition, Adgison-nesley “Publisning-@6-, "Reading! Massachusetts, 1971. 18. omega Pngineering, Inc., Temperature Measurement Handbook, 1981.n 19. CRC Handbook of Chemistry and Physics, 56th Eaition, Press, Cleveland, 1375, pe sie. 20. Warwick, R., and Williams, P. L., ede.) Gray's Anatomy, 35th British Edition, W. B. ‘saunders Conpany, Philadelphia, 1973, p. 1096-1100. 21. Lillie, R. D., Histopathologic Technique and Practical Histochemistry, MeGraw-Hill Book Company, New 22. Mumason G. L., Animal Tissue Techniques, W. H. Freeman ‘and Conpany, San Francisco, 1962, p. 156-164.78 APPENDIX 1 We wish to derive the electric field at the specimen location given a voltage applied at the electrodes. Figure Al-1 shows the geometry of the cornea rack and the placement of the electrodes. ‘The quasi-static form of Faraday's law yields: Vit) = cEge + AB gg + BE gy (area) Since this is a one dimensional derivation we will drop the subscript x. The letter subscript corresponds to the equivalently labeled section of Figure Al-1. Equation (Al-1) can be rewritten in terns of the respective resistances of the regions: v(t) = RACR)0,8, + Ry(aWeQe, + Ro(ert)oB, (Al-2), were: 5 (m1-20) ss tat-2e} 5 Re (aa-2a. Given the assumption that there is no bulk free charge in the system for frequencies of interest, weE=o in each region. We can use Gauss’ Law with the surfaces9 shown in Figure Al-1. 4, Bn dass, eave eB, (aw) + eB, CR!) = 0 (aa) = ek, (RY) + eB, (ret) = 0 (aay Note that we have assumed that the permittivity is the same in all regions since the stroma is © 90% water. Combining (A1-3) and (A1-4) we ge! aw 8,2 B= (ate, = ie, (m-s). Substituting this into (AI-1): v(t) = Cag)? + bE) +e] & (ars). Now wo define: Be toh)? + wey + ot an, wnich allows us to write: = Hele) (are). Defining the current density at the active electrode as 3, we can write 9 statement of conservation of charge: Je egy =O (a9),a0 where: ra (ar-10)- These relations allow us to write a relation for the power Gissipation density in terme of the electric field: Pb(t) = oB(e) +B) (aru). Ppg(t) = eck#v#(t) (a2), where we have used equation (Al-8). Taking the time average (assuming 2 sinusoidal input) yields: Yn" 2 = okt B= ook Ven (aria). ‘The power dissipated into a region (Py) is equal to the power dissipation density times the volume of that region. Thus we can calaculate the time average power dissipated in our sample: cpg = Pdr (arr!) = arztKtov.? (a4), wnere @ is the thickness of the sample. Next we would Like to derive a relation betw sn the power dissipated in the sample and it's temperature as a function of time. The increase in temperature of the sample per second can be related to the time average power dissipation via the specific heat and mass density.ar (nis), Where c is the specific heat and », is the mass density. Substituting equation (Al-13) we get the relation we are looking for: ook? GD, = Mins 2 (ais), wnere y = 0.239 $32 is the conversion factor between calories and joules. For our apparatus’ geometry (see Figure Al-1) we have the following dimensions: = 0.6 om ewneange 1 1 a 3 0.476 cm 1 2 Given these dimensions we can calculate: K = 0.485 cm”! In order to obtain a value for equation (A1-16) we must make certain approximations about the physical parameters of our tissue. We will approximate the tissue as having the same paraneter values as water: © = 1.0 mho/meter = 0.01 mho/ema2 Substituting these values into (Al-16) yields: Bese 10t v4? aan, also: From * 2048 cae) ie 1 2538 (aa-19) R, + 250, (1-20) For the Valleylap Pure cut #25 setting Vj = 90 or Vypme 7 63¥: thus we get (ai-21). When the Kepco supply was used the geometry was slighty @ifferent from that shown in Pigure Al-1. A large electrode such as the right hand one in Figure Al-1 was placed symmetrically on the left side of the specimen. an equivalent computation for this geometry gives the resulta: ease 107 vy? (mite), yoann + 4288 a-188) B+ 258 (a2-20K) Here Vp = SOY OF Ving = 350, which yiera feos 2 ca-aie)FIGURE Al-1 — Plectraie/cornea Geometry FIGURE AZ-1 Coit Membrane/tissue Model84 APPENDIX 2 Our purpose here is to derive the voltage that would develope across a cell menbrane given an applied voltage to the tissue. In order to compute such a voltage we must construct an approximate model for our tissue system. The model we will use is shown in Figure A2-1. Since the corneal cells are closly packed and because the menbrane is very thin compared to the radius of the cell, we will consider only current that flows normal to the membrane. Therefore, we will use a parallel, infinite extent model geometry. Because we neglect (tangential current lines that leak around the cell, this calculation overestimates the membrane voltage drop and thereby provides an upper bound estimate. However, other assumptions to be described below may actually result in an underestimate of transmembrane potential drop. We start by assuming a uniform applied electric fiela, and write the appropriate boundary conditions. Assuming a uniform field in the x direction we can writer Vs ab, + bE, + cF, (a, where the time dependance and x direction notation have been suppressed. The letters a,b, and c refer to the respectivly labled regions in Figure A2-1 when used as subscripts, otherwise they refer to the corresponding dimensions. The85 boundary between region a and b will be refered to as Boundary 1 and the boundary between region b and c: Boundary 2. Region a represents the intra-cellular space. and region © represents the extracellular space. These regions are assumed to be filled with the same type of fluid and thus are characterized by the same physical parameters, © and ¢ (dielectric permittivity and conductivity). Region b is the membrane, which is characterized by the physical parameters Sp and %,. ‘The boundary conditions are as follows. From Gauss’ Law: 0*cE = 0 we find: Beye = ee) = oy, (nz-2a), Bee, = eB) = ee, (n2-28), where ¢,, refers to the surface charge at boundary 1, ete. From 1E = 0 we haver Bah, - 2 = 0 (32-3) which is equavalent to saying: ant (az-4a). at boundary 1. Similarly at boundary 2: tee (x2-40). Conservation of charge yeilde: va+it=o (22-5). Combining this with the relation J = of yields two morea6 conditions: te Beye, - 98) = = et (n2-6), Be (eB, = Oph) = - ee (2-60). Combining (A2-2) with (12-6) (6 + jong, = (a, + 300,8, vara) (oy + Seem = (e+ HE, (n2-70). ‘he charge relaxation in region a and © is given by: refers aot From this we see that + >> T= 1.33410"! sec, which tells us that o >> jue. This allows us to make approximations which transform (A2-7) into: oF, = Jueh, = oF, (nz-8). Tis can be substituted into (A2-1) and solved for the electric field across the nembrane: vie) . E(t) mola (22-9), We can make further simplifications if we note that: BSb | (4.70206) (8-85010") 54 aro" Gey87 where ¢ = «¢,. For a typical cell b » 1008 = 107'm and the > diameter of the cell: a = 107'm. Also we will assume that « is 10 (such a value is typical of lipid dielectrics). These approximations allow us to elliminate a and ¢ in (A2-9) to y, +X = Se : % (a2-10), Pop aw where m is the effective number of menbranes in the entire sample and Vj, is the total voltage drop across the specimen. The constant m can be further subdivided into meNen where n is the number of membranes in the tissue’s cellular layer and N accounts for the underlying tissues. The resistance calculations in Appendix 1 (see equations (Ai-18) and (A1-20)) indicate that about 108 of the applica voltage is dropped across the specimen. Thus for the Vallylab Coag #100 waveform, who's peak applied voltage is approximately 1200 volts, we expect that Vy p 7 20v. The constant m is rather difficult to estimate; the corneal cell layer is about 10 cells thick, so we set n=20. To be on the conservative side we will pick W lerge: N=80. The result of these approximations is that: Epp «2:2 « tor YORE oan) ep. Yap = Epp * 107m # 1.2v (n2-22),88 ‘This derivation rests on many approximations, however it is certainly accurate to within an order of magnitude.39 program difesp Version 4- ‘A sampling and storage program for molecular ‘iffusion and other transient experinents- Sapling is done either synchronously ata prodeternined rate, or asynchronously at Fate determined by variations in the measured signal. Single samples can also be taken. written: March €l by PG edi fied: February 82 by EF ‘3 channel user seletable yee comand byte prnan(10) bre outti1(12),prefix(6) Byte date(10) nt] (64) ,crmt2(64) ,crmt3(64) wre heme(2),crase(2),er1in(2) ~ bre gtline(2),1ine2(9),1ine3(2) yee hal(2) ,bottom(2) integer minits,nsecs,¢ig(3),chan,chnl ineager tuf£0(2000) integer buf 1 (2000) Integer but £2(2000) integer buf#(2000,3) equivalence (boff,buff0) Integer time(2, 2000) commen buff0,buffl, but f2, time a integer nbuft,icount ,ncout ;teount TH integer RRrate, Ft ino, Tet enitim integer tstart,tstop,abflag zal sum rool reine nextim,rate, second « equivalence (prefix(1),outfi1(1)) ‘set constants ISB VE OAs PDT RE 7 date prgmam /'D",'T! data OUEERD JKaeeges R 90 gata count, /5/ Sata home /"033,"110/, erase /*033,"112/ Gata erlin /"033,"113/, geline /"033,"131/ data Line? /"041,"040/, Lines /*042, "040/, data bottom /"067,"040/, half /*053,"080/ logical wit munber for output file sea Tamamn /4/ size of buffers Gata buf /2000/ initialize variables typo 80 heme erase accept 90;prefix type a accept 93,chan type 84! accept S1,delta type accept 92,cmt1 type 83) accept 93,7 call getdat(date) encode (64,85,crrit2) prqnam date, (Out Fi1(X),k=L,10) encode (64,86,cmt3) delta, chan + fomats for this section format (x,28,2a,'sample ID? (six characters) ',$) forrat (x, "nimber of channels to sample? (1) '/8) format (x, "brief description: "y$) format (x, “TRANS threshold? (i)'*,$) format (x, "thickness (microns) of sample? (x) *,$) format ("Gata sampled by: ',10a," ons "10a, > * file: 10a) format (‘thickness (un): *,98-3, > 1 ONTRANS threshold: "£4, > * channets: 1-42)Es 92 93 20 as BRB 300 a format (6a) format. (312.3) format (64a) format (14) nm remnemcut ELL type" NEM’ , FON" UNEUIATIED") write (linn) pronam write (Iunum) Gwitl,comt2,omnt3 accept 290,comand type 285,home,erase,0 call starte to 215 abflag = 0 type 282,gtline, ine?,erLin accept 290, comand! Lf (conand .eq- 'S') go to if (conand eq. 'T') go to 400 if (comand Leg. 'R') 99 £0 500 if (conan ‘eq. 'E') go to goto 210) format (/x, "comands are as follows?! [ox,'5 ~ SINGLE SOLE" J6x,'8 = exit program’ > ix, 'enter coerand: ",$) format (x,28,28,23, ‘enter comand (S,T,RE): ',8) fomat (x,2a,2a, elapsed tine +',16," min',22, 'DIPSSP.VO4" ) formt (al) call getine(rinits,rtime)92 © * call sampling macro a cont. = neount call tensim(-1, chan buff0,buf fl butf2, tine, > ‘eoount smimiest2,0) e * calculate sarple 0320 k= 1, chan 5 sum = 0. S310 3 = L,tcont 310 Sin = sum + lone (bafe(3,%)) / 2.048 320 sighh) = ifix(sun / float (tcount)) e + display & store sample weite (Itt) time, (sig(k) kel chan) Tooune = foot +1 type 380.geLine bottom, icount,reime, (isig() kel ;chan) type 285,hone,erlin,minits gto 20 * fomats for this section 380 fomat (x,23,2a/x, "sample. i 10%, £12.3," seconds" > PG, channel 2)" : "ae," awe) ) 400 type 480, gt Line, Line2erlin 490, Trt TP (eweim st. 0) go to 400 call getine(ninits,rtine) Gaitin = minits + Tein + 2 410. type 285,hone,erlin,minits type 486, gel ine, 1ine2,erLin,endtin, 1H Af (abflag sme. 0) gp to. 10 © * call sampling macro ‘eoount = nbuff call trnsan(Ti, chan buf£0,bufF buf £2, time, . ‘ecount ,endtim,abéTaa) . * calgulate & store data totart = icount +1 5420 j= 1 toot Becond = Float(tine(2,3)) * 001 Gf (eccond sIt- 0.) Second = 65.536 + second ‘Peine = second + Float (time(2,$))%60-93 0 415 k= 1, chan as Big(k) = i¢ix(Floae(euFe($,%)) / 2.048) B write (lunum) reine, (sigik) ket, chan) 420 Heount = feount +1 tatop = feount type 487, gt Line bottom, tstart, tstop, > ‘tstop, time, (kysig(k) Kel, chan) ~ e 1 chock tine & repeat call to sampling nacro if necessary call getine(ninits, tine) Gf (miniee -1e- endtine) to Alo e * retura to command gection type 285,hare,erlinyminits 90 to 210 * formats for this section 480 format (x,2a,2a,2a, ‘enter duration (min) for TRANS" > rose (4):""58) 496 format (2a, 28,20, "TRANS mode ends ats *,16, a > rin! 10e, ‘thresholds ',45,) 487 format (x, 24,2a, ‘samples "15," "through "15, > yore taken in TRS node" > Jxytsample ",i6,10x,£12.3," seconds’ > (3i5x, "channel iL 56," mse) ) 490 format (45) 500 type 580, gtline, ine2,erLin accept 590; FtRrate Gf (Rate ‘it. 1) qo to 500, 505 type S81, gtlino, Line2,erlin accept $90, sRtime ~ if (RRtime sit. 0) goto 505, rate = float (rtrate) call getine(ninits, time) hextim = reine + rate fendtim = minies + RRtime + 1 type 285,hare,erlin,minits type 586, getline, 1ine2,erLin,endtin,RRrate * sampling loop 510 if (abflag ane. 0) goto 210 call getine(ninits,rtine)520 530 570 Af (rtime sits nextin) 94 else 4 530 to 570 * take eample toount = neount call trnsan(-1,chan,buff0,buffl,buff2,tine, ‘ecoont yminies#2,0) * calculate sarple k= 1, chan m=O. 0 520 | = 1,tooint sum = sun + float (buft(3,k)) / 2.048 Sig(k) = ifix(sum / float (count) ) + aisplay & store sample write (umm) reine, (sigh) e=L,chan) feount count + 1 380,gel.ine bottom, fcount tine, (X, sig) kel chan) 288; hone er Lin rinits 586, gel ine, Line2,er1in,endtin,RRrate + upiate next saple tine if (reine s1t, noxtin)| gto 570 Lf (apfiag ne. 0) gto 210 nextim = nextim + rate gto 540) if (minits .1t. endtin) pio 510 else return to conrand section pte 210 + formate for this section fomat format * close pe cul endfiie (x,2a,2a,22, "enter sampling rate in seconds (i): ',$) (5:22,2a,2a, ‘enter duration (min) for REGULAR RATE, rode (i)2''48) ((6,2a, 2a, 2a, 'REGUIAR RATE node ends ats 156, win! 1x, rater "15," sec") (3) file & stop 780, heme, erase stope Tour lose (unit=lnum) type stop ‘aL "ind of Sampling Run!95 > + somats for this section format. (x,2a,2a,"closing output file") format (x,"done") end a8 > ‘subroutine getine(minits,rtime) Returns the elapeed tine both in minates (integer) and in seconds (real). written: 20 dansary edi fied: 30 January integer minitsmsocs real reiie, second ‘call gote(minits,msocs) Second = Float(msecs) * .001 (nsecs «1. 0) Second = 65.536 + second reine = secend + Float (minits)*60. return end96 venabl le “Gtle trea version 2 ‘globl tunsan,starte, stope,gete ‘Takes a/8 converter sample every 16 milliseconds, but only saves sample hen it differs from previous sample by a minimum threshold. written: 13 October 81 by PC edi fied: 31 January 81 By PC modified 2 February 62 by EF 3 channels weer select register definitions aaccsr = 176770 adore = (176772 adoveo = 000130, Gao = «176760, ‘acl = 376762 ac? 676s rtecer = 370420 toa = 170422 Htevec = 000440 @ovice comants rtcsta = 000200 go = 000001 he = oco040 meie2 = 00004 model = 00002 mogeo = 000000 mmest2 = 01000, intov 00109 ovflag = 000200, sdesta ‘200200 extrig = 000002 intena = 0100 vmxl = 000000 vmaxl0 = 900030, chan = 900000 Ganl = 000400starter ” chan? = 001000, cen00l = gotintanatunarl O4chand como] = gotintenatermselOschan? carol = gotintenstmaLOschand comdl0 = gotintenatymaxl+chan0 ‘comll0 gotintenatmax]schan] con210 = © gotintenatmaslvchan? useful numbers gacnin = 374000 caomx = 003777 argurent List offsets 2 4 6 men = 10 buff? = 2 bates = 4 aimber = 16 finlim = 20 abflag = 22 hitine = 2 lotine 4 start clock routine mov @fadodbr, x} sdumy read to clear ade nov fadcint, Btadevec mov Fadesta,Efadoveot? start up real tine clock clr @trtcesr mov #1, €brtodbe: cle rtentlh clr tenth clr tflag mov frtcint, @prtevee nov drtesta,@hrtcvect? mv fhe, temp rset rate to 1 Kile pis go, Lemp Heat go bie, bie frodel, camp set to mode 1 bis fintov, temp fallow interr upon rte overflow nov temp, Girtccer fstart clock rts pe read clock routinegete: stope: ‘emneane oopet: sample: ocpe: waiter obins 98 nov rtentH,@hitime(1ist) mov reentL,@lotine(1ist) rs ps stop clock routine clr Otrtccer stop clock rts pe sampling routine nov Gtinlim(List),Limit get. parameters nov @nurber(1ist) scount. mov Blnemne (ist), Inc mov @chan(1ist),chnls asl ine Bel ine asl ine asl ine nov chnls,chnl Cir chniak clr @dachan(chniax) rset DACs to zero. clr indac(chniax) ine chia inc enix fob hn Joopel mov baff0(List) cho rset up buffers mov Boffl(1ist) ,chl mov buf£2(list) ,ch2 mov buff3(List) time ake samples chnts,chnt clr cmiax #Ladfiag dSors(chnidx), @fadccsr :coarse sample ~ channel chnidx bdflag fweit for ade to sample dcout, indac(chnidx) indaclchnidx),Adacrin :2er0 out offaet. with DAC okmin ‘enowin, indac(ehnidx) instac, tac aegiga ayaea oles {aacnax, indac(amnix)roopl6: first: nowait oope: waite: clr clr aaa ga 98 9 G86 GRRE F F aad 99 {indac(chnidx) , @dachan(chnix) cnniax, chnicte nl, loops Hinitilaize variables chats, cant chniase pewarv(chnidx) oldav(ehniax) Geils ‘cinid eal, Toop 436,point nowt point point, Eelag first tflag duis.cint chniase point, save ‘#Ladfiag 2acfin(chnide) ,@tadcesr +Fine sample ~ channel 0 bates Hwait for ede to sample waite ‘acout ,oldav( ehnigx) fdcout spew (chnids) ‘doout jelret point) #40,c0int enna. ennids, ent, Loope save, point, point, Looplé reentl,@time precord data & time reentL, @eine ‘tine einemov chins, cn clr chniaxe oopmy: mov indac(chnidx) temp mov temp, save Bel temp. Sel temp, Bad save, temp asl temp mov eldav(chnidx),save adi save, temp nov temp, @ch(chnidx) ine ca(etniax) ine ch(ehnias) ine etmidx ine anid sob ml, loop ec count eq Sone : wait for signals to change change: emp rtentil, iit, bel dene. tet @abflag(List) me done gee point dee int Bic #177740,poine next: tet tag beg next clr tflag mov cine, chnl cir amiax mov points save mov Hadflag nov adefin(einidx),@fadcose waitav: tse agflag ee wmitay 100 multiply dac value by 10 1 divide fine average by 16 + eum is result, rstop if buffers are full rreached tine Limit? rabort request? rupdate pointer Phas it been 1 meee? fine sample - channel 0 fwait for ade to sampleoopek: check: adeint rtcints ‘ub 0a sine or ‘cire(point) newav(chnidx) adcout ynewa(chnidx) adoout jcire(point) 4#40,point enniax, ehnids eh, Ieopav save,point, emnis,chnl emigre pow (chnid) , temp eldav(chnids) ; tem check, temp ine,tomp try sample caniax Gnide ‘etal loopeke change Gnumber (1ist) temp cont, tenp ‘temp, Gruner (List) re interrupt service routine fetsT2, Ohrtocer 4¥4000,r1 ret #170000,1 FLyadcout (spleen adéiag re Jnterrupt service routine bie She op eg re fovftag,rtecsr aL, flag, tent eonth, #5536. Snentil £ 60, take another sample HE 60, take another sample send ¢ of samples tnck 10 calling program tallow count of rte to ke latched push old value of rl move Gata to work register ieheck for negative result ;pop old value of ri relear overflow flag in cer teet mill isec. flag Sner low order clack court time to incr high count?PELLEEEELEEELEEZELE| apee Ree 102 reset low order comter Her high counter on rtc overflow163 ADMIT -FOR Written by STEPHEN BART Modifica by SB March 25, 1982 This program takes an output file generated by DIFSSP.FOR (version 4), calculates the admittance, and prepares the new file for OUT-POR. define storage integer lunun, output, y,otemp,adm, jy(3) nchan,chan byte prgnam(10), £i1¢(10), infil(12) ,emntl (64), e emnt2(64) ,cmnta(64) real ovolt,camp, time, volt ,amps, temp,a,b,¢ data outpat/1/,iunum/4/ 5 type 10 10 format (* Enter output file name (aaaaaa-ADM):",$) accept 20, file 20 format (10a1) iF (fite(1) .eq. ' 1) go to 999 25 open (unit=l;name= file,type ='NEW', © form ="UNFORMATTED" ,ert=1030) Input scaling paraneters type 30 30 format (* Enter volts/volt accept 31a 31 format (£52) If (2 sre. 0-0) vole type 40 40 format (' Enter volts/amp:',$) accept 41,b 41 format (15.2) I? (B -ne- 0.0) amps=b type 50 50 format (* Enter volts/degc:',§) accept 51,¢ 51 format (£5.2) If (© se. 0.0) tempee open DIFSSP output File 60 type 65 65 format (/x,'input file? (aaaaaa.DIP)",$) aecept 70, infil 70 format (1ba) If (infil(1) eq. *) go to 999 open (unit=Lunum,namesinfil, types OLD", © forme UNFORMATTED' } read data from DIPSSP file104 read (1unum) prgnan 80 read (Lunum) cmntt,cmnt2,cmnté decode (64, 82,cmnt4) chan 82 format (62%, i2) 4 format ("STEPHEN BART", volts/voat: 100 read (1unum, end=110) time, (Jy(i), achan = cha-I iF (nohan seq. 0) go to 1050 type *,"nchan is", nchan encode’ (64,82,cnn¢4) nchan encode (64,84,cmnt1) volt,amps, temp 13.2, 1£5.2,' wolte/deac:' , £512) e volts/amp: write output file weite (output) pranam weite (output) cmntl,emnt2,cnnt4 read, modify, and write the data chan) gvolt = volit float (3y(1))*0.001 iF (ovelt -eg. 0) go to 101 camp = amps* éioat(jy(2))*0.002 otemp = temp*float (3y(3))#0.001 aan = ((oamp/ovolt)*1000.0)+0.5 ge to 102 101 aim = 0 102 TF (chan -eq. 3) go to 104 weite(output) tine,aan ge to 100 104 write(output) time,adm,otemp 105 go to 100 110 Close (uniteoutput) close (unit=lunum) Repeat sequence 999 type 1000 1000 format (" Do you wish to run again ? (Yes=1)+",$) accept 1010,¥ 1010 format (11) IE (y seq: 1) go to $ 1020 stop: 1030 type 1040 1080 format (* open Error") 1085. stop 1050 type 1055 1055 format (" ERROR More than one. chamnel of © data ie neceseary!') stop end