Evaluation of Systemic and Splanchnic Visceral Oxygen Variables in Dogs With Surgically Induced Gastric Dilatation-Volvulus

J. Komtebedde, DVM
Department of Surge~

S.C. Haskins, DVM, MS J.R. Snyder, DVM, PhD

DepWment of Surgey School of Veterinary Medicine University of California, Davis

W.G. GuitiOrd, BVSC, BPhil

Department of Physiological Sciences

Gastric dilatatiomvoivulus (GD~ was surgically induced in ten dogs to evaluate changes in the viscera systemic 02 ~sPOff foiiowing variabies: sutface Wgen partibipmssure (I%@) ofsphmhnk (D@), systemic 02consumpti~ (l@), and02ubYization fetio (02UR). These variabieshavebeen shown to be closely correlated to tissue viabiiity and patient sundvai in a variety of ischemic disorders. Gastric dilatation-voivuius was corrected atler 2.5 houm and the dogs were given iactated Ringers soiution (90 milkg) over30 minutes (resuscitation). At6 hours, tie dogs were euthanized withoutrecovery from anesthesia. Gastric dilatation-voivuius resulted in a significant (p c 0.05) decrease of spianchnic tiscefal Ps02 and D02 and a significant (p < 0.01) increase in 02UR. Systemic 02 consumption did not change significantly during the experiment. Resuscitation resulted in a transient and significant (p < 0.05) increase in Ps02 to baseiine, except for hqxtic Ps02. Systemic 02 transpott and 02UR increased significantly (p < 0.001) compared to baseiine. Surface oxygen pattiai pressure and D02 were signifimnW (P c 0.05) beiow baseiine at the conchwon of the experiment, whereas 02UR remained significantly (p < 0.05) above baseiine. Surface oxygen partieipressure of aii spianchnic viscera, except iiver psOa correlated M D02 ~rougho~ we experiment (r: 0.69-0.78). Assessment of DO~ V02 and ONRmaybe used to evaluate efficacy of cardiovascuiarsupportduring corrective surgery for canine GDV. Introduction
Viability of cells, tissues, and organs depends upon maintaining an appropriate balance betvveen oxygen delivery and oxygen consumption. These oxygen variables are usually not assessed in veterinary medicine, although substantial clinical evidence in humans suggests that variations in these parameters are strongly related to survival and death.2 Doppler ultrasonography, pulse oximetty, electromyography, and recently, surface oximetry are currently under experimental and clinical investigation for the assessment of tissue viability= Wtih the exception of surface oximetty, none of these techniques directly assess tissue oxygenation. Surface oximetry reflects the balance between tissue oxygen delivety and oxygen consumption by measuring the partial pressure of oxygen (PsOJ on the surface of tissues.3 Sudace oximetry

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is being used extensively in humans for continuous transcutaneous/transconjunctival oxygen partiai pressure measurements to evaluate systemic oxygen delivery. The value of Ps02 in the assessment of visceral organ viability and function (intestine, iiver, and heart) has been documented experimentally.*14 The relationship between PsOZ of splanchnic viscera and systemic oxygen variables has not been reported in the dog. Knowledge about this reiation maybe important for the interpretation of iocal PSOZ data obtained in patients with cardiopulmonary derangements. Gastric diiatation-voivuius (GDV) is associated with a high degree of morbidity and mottaiity as the result of hypovolemic shock, splanchnic visceral, and myocardiai ischemia.l&la An accurate assessment of gastric and intestinal viability during surgical correction of GDV is important for patient surdval. Assessment of the adequacy of reperfusion of other visceral organs, such as the pancreas and iiver, may influence management and assist prognostication. The use of standard clinical criteria and intravenous fluorescein fluorescence to predict gastric and intestinal viability can be unreliable.ig Surface oximetry may be a useful objective technique to assess visceral organ viability in dogs with GDV intraoperativeiy.34 The objectives of this study were: q to estabiish reference vaiues for PsOZ of several spianchnic viscera in halothane-anesthetized dogs inspiring 100% 02; q to quantitatively assess oxygenation of spianchnic viscera with surface oximetry in an experimental modei of canine GDV q to determine the influence of GDV on systemic oxygen variabieq and q to investigate the strength of potential correlations between PSOZvalues of splanchnic viscera and hemodynamic and systemic oxygen variables.

Materials and Methods

ANIMALS AND ANIMAL PREPARATION

Ten unconditioned mongrel dogs (mean body weight 23.8 & 3.6 kg) were attained from the Animal Resource Sewice, University of California at Davis. The experimental protocol was approved by the Animai Use and Care Committee. Food was withheld for 12 hours prior to the experiment. No anesthetic premeditation was given. Anesthesia was induced and maintained with haiothane (Halothane:Halocarbon Laboratories, Inc., Notth Augusta, N.C.). Ventilation was controlled throughout the experiment using a respirator (Mark 8 Respirato~Bird Corp., Palm Springs, Calif.) and adjusted to maintain

arterial partial COZ pressure between 38 and 42 mm Hg; inspired Oz was 100%. End tidal halothane concentration was maintained at an average of 1.3 MAC. A 7F flowdirected balioon-tipped thermodilution catheter (NOVA Medical Specialities, Indian Milis, N.J.) was inserted percutaneously via the right external jugular vein into the pulmonary artery for determination of cardiac output (CO) (IL 701 Cardiac Output System:lnstrumentation bboratories, inc., Lexington, Mass.); for determination of pulmonary artery, pulmonary wedge, and central venous pressure measurements (P23Db Statham Biood Pressure Transduce Gould, Inc., Oxnard, Caiif.); and for sampiing of mixed venous puimonary artery blood for pH and blood gas anaiysis.m A dorsal metatarsal attery was cannuiated (Teflon CathetecDeseret Pharmaceutical Co., Sandy, Utah) percutaneously for arterial pressure measurements (P23Db Statham Biood Pressure Transducer) and arterial biood sampiing. At the start of each experiment, the CO system was calibrated with a constant flow pump and the pressure transducers were calibrated with a Hg manomete~ Catheters placed for pressure measurements were mnnected to an eight channel electrostatic recorder (Gould ES1 000 RecorderGouid, inc.). A cephalic vein was cannulated (P23Db Statham Blood Pressure Tranducer) percutaneously for continuous administration of iactated Ringers soiution (5 ml/kg/hr). A lead it surface electrocardiogram (ECG) was monitored throughout the experiment. Body temperature was monitored via the thermodiiution catheter. A heating pad and heating lamp were used to maintain body temperature. Gastric dilatation-volvulus was created according to a previously described model.17 Briefly, a mylar balloon was inserted in the stomach with a stomach tube. The stomach was surgically rotated about 220 and the antrum secured to the ieft abdominal wali. The intragastric bailoon pressure was raised to and maintained at 28 to 32 mm Hg and the abdomen ciosed. Atter 2.5 hours of GDV the abdomen was reopened, GDV was corrected, and a bolus (90 mi/kg) of lactated Ringers soiution was given over 30 minutes (resuscitation). After resuscitation, anesthesia was maintained for another 3.0 hours, after which the dogs were euthanized with an overdose of pentobarbitai without recovery (Fig. 1).
DATA COLLECTION

The following hemodynamic variables were monitored: q heat rate, q mean arterial blood pressure (MAP), q puimonary artery pressure (PAP),

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120

30

90

150 180

240

300

360

FIG.1 Experimentaldesign. Phase 1 (PI.):

instrumentationperiod; Phase 2 (P2): GDV period; Phase 3 (Pa):resuscitationperiod; Phase4 (Pal): ostresusoitation p period. Single arrowsdepict blood sampling and hemodynamicvariable measurement time in minutes.

q q q

pulmonaty wedge pressure (PWP), central venous pressure (CVP), and

co.

Parameters were measured before GDV (baseline = O min.); duting GDV at 30, 90, and 150 minutes and after resuscitation at 160,240,300, and 360 minutes (see Fig. 1). Systemic vascular resistance (SVR = [MAP CVP]/CO), pulmonary vascular resistance (PVR = [PAP - PWP]/CO), and left ventricular minute work (LVMW = CO x MAP x 0.001) were caiculated?la Arterial and mixed venous blood samples for measurement of 02 and C02 partial pressures (IL1306 pH/ Bloodgas Analyser:lnstrumentation Laboratories, Inc., Lexington, Mass.) and hemoglobin concentration (Total Hemoglobin KK 525-A Cyanomethemoglobin Method:Sigma Chemical Co., St. Louis; DB SpectrofotometecBeckman Instruments, Inc., Schiller Park, Ill.) were collected at the same times as the hemodynamic variables (see Fig. 1). Oxygen and C02 partial pressures were corrected to body temperature. Oxyhemoglobin saturation, systemic arterial Oz delivety (DOZ) equal to CO x arterial 02 content x 0.01, systemc 02 consumption (VOz) equal to arteriovenous Oz content difference x CO x 0.01, and Oz utilization ratio (OJJR) equal to atieriovenous Oz content difference/arterial Oz content were calculated.21= At O, 30, 150, 160, and 360 minutes, PSOZ of stomach, duodenum, jejunum, pancreas, and liver (splanchnic viscera) was measured with an oxygen polarographic electrode (TOZM 2000: Biomedical Sensors, High Wycombe, England) at the same locations by the same investigator (see Fig. 1). Two recordings per site were obtained. Before each set of measure-

ments, the sensor was allowed to calibrate in saline solution at ambient temperature and pressure (20-30 min.), and the monitors digital display was manually adjusted to the specific room air POZ.4 Special care was taken to avoid excessive pressure on the sensor and organ in question. No intestinal measurements were made during peristaltic movements. If the two recordings per site varied considerably, a second set of recordings was obtained. The average of two PsOZ readings was recorded.
DATA ANALYSIS All data were analyzed for temporal trends using a repeated measures analysis of variance. The presence or absence of a relationship between the Ps02 values of the different splanchnic viscera and certain hemodynamic and Oz transport variables was evaluated using a repeated measures analysis of invariance and by determining pooled regression (and correlation) coefficients, treating PS02 as a time-vatying covariate.=g4 In all of the previously mentioned analyses, significance is claimed whenever p < 0.05.

Resutts
GROSS OBSERVATIONS

Gastric dilatation-volvulus immediately resulted in cyanosis of the stomach, duodenum, and pancreas, intestinal hypermotility, and decreased meeenteric arterial pulsation. Edema and petechd hemorrhage of the pancreas, congestion of liver and spleen, and gastric serosal hemorrhage were additionally observed after 2.5 hours of GDV The cyanosis of stomach, duodenum, and
COmlwsd

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Oxygen Verieblee in

tlDV

Experimental Beeellne

Mirrutee Poetreeueoitetion 150 1s0 3s0

GDV 30

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p c 0.05.

pancreas rapidly resolved during resuscitation, mesenteric arterial circulation became hyperdynamic, and the wall of the stomach became edematous Mild to moderate amounts of abdominal transudation were observed. Fibrin was obsetved on the sutface of the liver and intestines after resuscitation, and mngestion of the Iiir appeared more severe. The amount of abdominal Wmdation increased after resusdtation.
OXYGEN VARIABLES

Results are reported as mean & standard deviation (SD) (Tables 1 and 2). The PSOZ equipment was easy to use. Sensor assembly and maintaining even sensortissue contact were the most difficult aspects of equipment use. Steady state recordings were obtained within 1 minute. If the two recordings per site varied considerably, uneven sensor-tissue contact was usually the cause. Difficulties with calibration indicated inaccurate sensor assembly or sensor defects. Baseline PsOZ values (mm Hg) were as follows: q stomach, 375 & 112; q duodenum, 339 & 125; q jejunum, 287 & 143; q pancreas, 43 * 11; and q live~ 68 * 56. Concurrent mean arterial partial oxygen pressure (Pa02) was 656 mm Hg; PaOz during the experiment ranged between 655 and 865 mm Hg. Gastric dilatation-volvulus caused a rapid and significant (p e 0.05) decline in the PsOZ levels of all measurwi splanchnic viscera at 30 minutes; the PSOZ levels after 2.5 hours

of GDV were similar to those at 30 minutes. Surface oxygen partial pressure values after 2.5 hours were significantly reduced from baseline by 95% for the stomach, 80% for the duodenum, 75% for the jejunum, and approximately 50% for the pancreas and liver. Resuscitation resulted in a rapid and significant (p e 0.05) increase of Ps02 levels to baseline levels for all measured splanchnic viscera except the liven liver PsOZ levels did not improve in the majority (7/1 O) of dogs. Liver PSOZ during resuscitation increased in three dogs but never returned to baseline. Three hours after resuscitation, PsO~ levels had declined significantly (p < 0.05) to between 38 and 64% of baseline levels. Hemoglobin mncentration at baseline was 11.8 & 1.8 @all.No significant dtierence was present after 2.5 hours of GDV. Resuscitation resulted in a rapid dedine to 7.6 & 1.7 g/all (p e 0.001). After resuscitatkm, hemoglobin mncentration gradually returned to baseline level. Arterial oxyhemoglobin saturation at baseline was 99% and did not change during the experiment. Venous oxyhemoglobin saturation at baseline was 84.1 & 5.6%. Venous oxyhemoglobin saturation dedined to 58 & 12.4% during GDV (p < 0.01). Resuscitation resulted in a rapid increase in venous oxyhemoglobin saturation to 90.8 & 8% (p -= 0.01). Venous oxyhemoglobin saturation gradually declined to 58.4 & 18.8% after resuscitation (p -= 0.01). Systemic arterial Oz delivery at baseline was 16.5 * 3.5 ml/kg per minute. Systemic arterial Oz delivety gradually dedined to 8.8 * 3.0 ml/kg per minute

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VOf&bkfS in GDV

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%luea ere expressed as k standcrd dm.tsfica, n = 10. b[Hbl . -bbin concentmtiq ~ . cptemic 02 transpo~ cardiac ouiput SVR = systemic vcccular resis+ancq LVMW CSignificcntiy dNMent fmm O minutee, p <0.001. dagn~at~ dfimti from O minutes, P <0.01. SignHbantty fs~nwy gslgnfi~y hSignMw~ iagn~w~y different fmm O minutes, p c 0.05 d~e~ h 1~ minti-, p < -ml. d~mnf dfimti d~~nt tim 150 minutes, p c 0.05. from I SO minutes, p < O.rnlfrom 1S0 minutes, P <0.01.

VIZ

systemic 02 cawmpti.m

02UR

= 02 utilization ratio; MAP = meen atterial blood preaeurq

CO =

left ventricular minute work

during GDV (p e 0.001). Resuscitation resulted in a rapid increase of DOZ to 22.1 & 9.9 ml/kg per minute (p < 0.01); however, DOZ gradually returned to 11.3 & 5.4 ml/kg per minute after resuscitation (p < 0.01). Systemic arterial Oz delivery correlated with CO throughout the experiment (r > 0.85). Systemic 02 consumption at baseline was 3.7 * 0.7 ml/kg per minute and did not change significantly during GDV or following resuscitation. Systemic 02UR at baseline was 23 * 6%. Gastric dilatation-volvulus resulted in a gradual increase of 02UR to 46 & 11% (p < 0.01). During resuscitation, 02UR returned to baseline. Oxygen utilization ratio gradually increased to 47 & 17% after resuscitation (p < 0.05). In addition, 02UR correlated with D02 except for one time point (240 min.) (K 0.7-0.9).

HEMODYNAMIC VARIABLES Results are reported as mean * SD (see Table 2). Heart rate at baseline was 109 & 15 beats per minute. Gastric dilatation-volvulus resulted in a gradual increase of the heart rate to 164 & 29 beats per minute (p < 0.01). Resuscitation resulted in a decline of the heart rate to 143 & 32 beats per minute (p e 0.01). The heart rate increased graduaiiy to 166 & 36 beats per minute after resuscitation (p c 0.01). Mean arteriai pressure at baseiine was 82 & 20 mm Hg. Gastric diiatation-voivuius resulted in a graduai deciine of MAP to 53 & 19 mm Hg (p e 0.001). Mean arteriai pressure increased to 74 * 27 mm Hg during resusc.tition (p < 0.05). Also, MAP graduaiiy deciined to 58 & 25 mm Hg after resuscitation (p < 0.05).

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%lc.pe effect p value Indicaios UM degree of certalnlytih %he

which a change in FzQ? corwponds

with a change in eHher CO or ~.

regression coaffeclent indicates how large a change In CO or CQ

would be expected from a given change In P802.

Cardiac output at baseline was 94.7 & 13.9 ml/kg per minute. During GDVi CO dedined to 47.1 & 14.4 ml/kg per minute (p -= 0.001). Resuscitation resulted in a rapid Increase of CO to 177 & 52.2 ml/kg per minute (p < 0.001). Additionally, CO had decreased to 88.1 & 23.3 ml/kg per minute at 240 minutes (p < 0.001) and gradually decreased further to 65.7 & 20.7 ml/kg per minute (p < 0.01). Systemic vascular resistance at baseline was 0.88 ~ 0.25 mm Hg/(ml/kg/min). Systemic vascular resistance increased to 1.2 & 0.15 mm Hg/(ml/kg/min) during GDV. Resuscitation resulted in a rapid decline to 0.4 & 0.11 mm Hg/(ml/kg/min) (p e 0.001). Systemic vascular resistance gradually increased to baseline values after resuscitation (see Table 2). Left ventricular minute work at baseline was 7.81 & 2.28 (lJkg/min) x mm Hg. Gastric dilatation-volvulus resulted in a rapid decline to 2.5 & 1.9 (p e 0.01). Resuscitation resulted in a rapid increase to 14.1 & 7.9 (p < 0.05); howeve~ LVMW declined to 3.9 * 2.7 after resuscitation (p < 0.01). Central venous pressure at baseline was 0.6 & 3.3 cm of HZO. It dedined to -1.3 & 1.9 cm of HZO during GDV. Resuscitation resulted in a rapid increase to 4.6 z 4.0 cm of HZO (p < 0.01). Central venous pressure gradually declined to 0.1 & 3.0 cm of HzO after resuscitation.

Pulmonary artery and pulmonaty wedge pressure at baseline were 7.4 & 2.0 and 3.1 & 2.2 mm Hg, respectively. Pressures declined to 5.2 & 2.5 and 0.3 & 1.9 mm Hg (p < 0.01), respectively, after resuscitation. Resuscitation resulted in a rapid but transient increase to 14.4 & 4.5 and 5.6 & 3.3 mm Hg (p < 0.001), respectively. Pulmonary artery pressure was 9.0 * 3.1 mm Hg and PWP was 1.3 & 2.2 mm Hg at 360 minutes (p < 0.05). Pulmonary vascular resistance at baseline was 0.05 & 0.02 mm Hg/(ml/kg/min). Gastric dilatation-volvulus resulted in a rapid increase to 0.11 * 0.045 mm Hg/(ml/kg/min) (p e 0.001). Pulmonary vascular resistance rapidly declined to baseline during resuscitation (p < 0.01); however, PVR gradually increased to 0.11 & 0.045 mm Hg/(ml/kg/min) after resuscitation (p < 0.001).
REIATION BETWEEN PSOZ AND HEMODYNAMIC AND

SYSTEMIC OXYGEN VARIABLES A significant relationship was present between PsC)Z (except the liver), CO, and DOZ as these variables changed over time for a given animal. The slope and intercept of this relation varied between organs but not significantly between animals. The pooled correlation coefficients and regression coefficients of this relation are presented (Table 3).

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Discussion
These studies indicate that surgically induced GDV reduces splanchnic visceral tissue oxygenation and that PsOZ can be used to indicate DOLJunless local factors account for a decrease in psQ. Surface oxygen partial pressure measured with surface oximetry estimates the mean tissue partial oxygen pressure of a surface area that contains a large number of capillary units. The mean tissue pattial oxygen pressure of a particular tissue area depends on several physiologic and pathologic factors. These include but are not limited to: q local 02 delivery (local flow and Oz content of capillary blood); q local 02 consumption; q tissue thickness (diffusion distance to the measurement electrode); and q POZ gradients. Some limitations of surface oximetry are evident, including: a relatively long time intend to obtain a steady state recording; variability resulting from operator experience; and intestinal peristaltic movements. These limitations, however, do not preclude its clinical use. The baseline PsOZ values for the stomach, duodenum, and jejunum in our study are higher than reported for the dog in previous experimental studies.3e The PaOz in these studies was < 100 mm Hg, and other anesthetic protocols were uwxf, both of which could have caused a difference in tissue oxygenation. If local 02 delivery exceeds local Oz consumption, mean tissue partial oxygen pressure and PSOZ will more nearly approximate PaOz. Conversely, the relationship between PaOz and PsOZ becomes more disparate when local Oz consumption is not met by local Oz delivery local Oz consumption becomes the limiting factor and PsOZ can be much lower than PaOz.l Baseline PS02 values for the liver in this experiment are in accordance with values previously repotied.11114 The reason(s) for the lower baseline PsOZ values of the pancreas and liver compared to other splanchnic viscera is unknown. We hypothesize that these organs have a relatively high Oz consumption. Additionally, the dual blood supply of the liver (arterial blood with high Oz content and portal venous blood with much lower Oz content) may have contributed to the lower PSOZ of this organ. The sharp dedine of PSOZ of all splanchnic viscera during GDV is attributed to decreased local blood flow caused by portal hypertension, hypovolemic shock, and in addition for the stomach, increased intramural pressure.-~ The observed hepatic congestion may be

due to contraction of hepatic vein sphincters= or the result of compression of hepatic veins at the junction of the caudal vena cava, liver, and diaphragm by the distended stomach. Considerable variation was seen in the PSOZ levels of the different splanchnic viscera during GDV indicating variation in degree of ischemia of each organ with this experimental model. The main cause for this individual variation is most likely the difference in gastric compliance between individuals. Stomach PsOZ during GDV is mainly dependent on intragastric pressure. In contrast, PsOZ of other splanchnic viscera depends more on individual variables such as gastric volume at a given pressure (compliance) and size of peritoneal cavity. The rapid return of PsOZ of stomach, duodenum, jejunum, and pancreas to baseline levels during resuscitation presumably reflects adequate reoxygenation and a return of mean tissue partial oxygen pressure to baseline levels. The increase in PsOZ was associated with clinical reperfusion, an increase in DOZ and a decrease in the O#R. Hepatic PsOZ increased minimally or not at all following resuscitation, in contrast to other splanchnic viscera. This implies that the liver was not adequately reoxygenated. The following factors muld have contributed to inadequate hepatic reoxygenation in this experiment: q persistent intrahepatic portal hypertension caused by hepatic vein sphincter contraction; q low portal venous Oz content due to postischemic Oz debt of other splanchnic viscerq and q increased hepatic metabolic activii as the result of the physiopathologic changes during GDV and resuscitation.w Because a close correlation between decreased liver bled flow (measured by indocyanine green clearance) and low hepatic PSOZ has been demonstrated, we favor the hepatic vein sphincter contraction hypothesis. 12 In a recent canine hemorrhagic hypotension experiment, hepatic PSOZ of shvors returned to baseline after blood transfusion while hepatic PsOZ of the nonsurvivors did not.ll It is unknown if the lack of improvement of PsOZ in the present study would have had similar prognostic value if this study had been a survival experiment. The decreasing Ps02 values and the increasing difference between PsOZ and PaOz at 360 minutes indicate an unfavorable local Oz delivery/consumption balance. The high OZUR of 47 & 17% suppofts a discrepancy between DOZ and VOZ. The decrease in hemoglobin concentration and arterial Oz content during resuscitation was caused by hemodilution. This could cause anemic tissue hypoxia unless a concomitant increase in CO could compen-

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Variable8

in QDV

sate, as it did in the present study. The graduai increase in hemoglobin concentration and arterial 02 content after resuscitation was most iikeiy caused by extravasation of intravascular fluid as the resuit of a iow plasma oncotic pressure and increased vascuiar permeability in spianchnic visceral organs. Venous oxyhemoglobin saturation during GDV and after resuscitation most iikeiy decreased as the resuit of decreased D@ since there were minimai changes in V02. An increase in DOZ and a decrease in the O#R were most likely responsible for the observed increase in venous oxyhemoglobin saturation during resuscitation. The deciine of DOZ during GDV and near the conclusion of the experiment was caused by a deciine in CO. The obsenmd changes in OJJR during GDV in this experiment are similar to those reported during experimental shock in dogs,31W and are attributed to a decrease in DOZ. The increase of OZUR during GDV and alter resuscitation is the expression of a physiologic compensatory mechanism to maintain oxidative metabolism during iow flow hypoxia (iow DO,). Systemic arteriai Oz deiivety has reached the anaerobic threshold when this compenstitory mechanism has reached its iimits. When DOZ faiis beiow the anaerotic threshoid, VOZ wiii decrease, an occurrence associated with death.131mThe reported anaerobic threshoid value of DOZ in the dog varies between 8 and 14 mi/kg per minute. 31~uMean D02 was 8.8 & 3.0 mi/kg per minute after 2.5 hours of GDV Systemic Oz consumption did not decrease during GDM suggesting that VOZ was stiii adequate; however, iocai Oz mnsumption could be inadequate in suppiydependent tissues in the face of adequate systemic oxygenation.2 The O$JR returned to baseiine during resuscitation, indicating adequate DOZ. Shortly after resuscitation, OAJR started to increase again as a reflection of the decreasing DOZ. The 02UR was higher at 240 minutes than at baseline and higher than the optimal OZUR of 31% in humans.w An 02UR above 31% in humans has beem shown to be strongly related to mortality and indh cates inadequate therapy.laa This relation has not been addressed in animals but it is noteworthy that at 240 and 300 minutes MAP was stiii within the iow nonnai mngefor tietized dogs(89ancj87 mm Hg, respectiveiy); while at the same the intends D02 and O#R, parameters that are superior predictors of survival in humans, were indicating inadequate therapy.lWm Hemodynamic changes observed in this study are simiiar to those previously repotted during experiment gastdc dilatation and GDV.IeI17~.W Hemodynamic function Improved rapidiy during resuscitation as the resuit of an increase in ve, M re-

turn after the obstruction had been reiieved, and circulatory voiume was being rapidiy expanded with crystalioids. The crystalloid resuscitation with 90 ml of iactated Ringers solution per kg over 30 minutes did not have a proionged circulatory stabilizing effect (see Tabie 2). The gradual deterioration of hemodynamic function after resusdation in this study has several potential causes, which inciude q third space extravasation of fluids (due to a decreased plasma oncotic pressure and capiiiary leakage); q cardio-inhib~ory substances;37 q poetischemic myocardiai hypocontractiiity= q endotoxins;15 q decreased sympathetic tone;37 and q inadequate fluid therapy. Additionaiiy, proionged haiothane anesthesia could be considered as a potentiai cause; howeve~ it has been associated with iess cardiovascular depression when compared to the cardiovascular depression during the first hour of haiothane anesthesia.= We fed that proionged haiothane anesthesia was not the cause of the deterioration of hemodynamic function toward the end of the experiment. Sham controls wouid be necessaty to definitiieiy evaluate the infiuence of haiothane. The presence of a significant correlation between PsO* of spianchnic viscera, CO, and DOZ was expected because CO and DOZ are both important determinants of tissue oxygenation. An imbaiance betwwn iocai Oz deiivery, Oz extraction, or iocai Oz mnsumption disturbs this reiation. We suspect this to be the cause of the absence of a reiation between iiver PsOZ, CO, and DOZ. Other iocai factors such as intraiuminai pressure, murai pressure, and edema also influence the relation between PsOZ, CO, and DOZ. Locai factors most iikeiy contribute to the observed variation in the slope of this reiation between the different spianchnic viscera and also are the reason why the correlation coefficients were iess than one. The results of thii study establish that spianchnic visceral tissue oxygenation assessed with sutface oximeby is significantly reduced during surgically induced GDV and that PsOZ is influenced by systemic and iocai oxygen variables. Based on the observed correlation be tween PsOZ and DOZ, a decrease in Ps02 indicates a simiiar change in the dogs hemodynamic and systemic oxygen transport status uniess iocai factors account for the decrease in PsOZ. Surface oximetty may, therefore, be used as an indicator of adequate reperfusion during corrective surgery for canine GDV. These resuits further estabiish that the liver exhibb a different response to resuscitation from surgically in-

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CRITICMCARE

duced GDV than other splanchnic viscera. The Wliure of hepatic PSOZ to improve afier resusc~tion ~Y ~ due to inadequate reperfusion and suggests a more important influence of this organ in the pathophysioiogy of GDV than previously appreciated. s

AmwwLmwENTs

Thsauthors thmkcrs.J.E Illdw, J.D.

for thslr awktsnw.

Pam, D.W. McNsd,

N.H. MAllits, snd B. Brusning

REFEREWES 1. Bhosmsksr WC Clrcukctory Mwhsnkms 04 Shock md llrelr Medktors. Crit Csm Msd 16787-7s4, 1ss7. 2. BryM-BmwI CW Blood Flew 10 Orgsrw Psmmeters for Funotbn snd Survival In CrWcal Illnsss. Crlt Cars Msd l&17G178, 1SSS. 3. LOckOtl Naussru, shOsmskOr WCkThs Ussof SutiOxlmWytOAswss BOwd visbiliiy. Amh Surg 11*1 Z52-125S, 1s34. 4. SnydorJR, Pwcos JR, Hdknd M, st d Sub Oximstry CMHsslthy snd kchemk Equine Intsstine. Am J Vst Rss 472520-2535, 1S2S. 5. KdkhsrJF PUkS Odmdty. J Clin Monit 5x3719S9. S. Msnn & Fszb VW, Lucss FW A @mpamtke Study of the Urn C4 Fluomzcein snd ths 00cmlsr Dsvics in ths DObrrninatkn ol Intestirrd Visbllhv. Sum Gvnacol Md 1!5453%5, 1ss2 7. Bmlin FE, Ssmmbw JL Buhonsnds ~ et ah Compsrkm of FhN Methcds of 12ss. ~ont of Inkdind Vlabillty. Bulg Gynscd ObstdlS&E12, 8. HaussrCJ. l.ockeRR. KaoHW. etskVkcersl SurbwDwcren Tension in EspsdmentdCdiUs lnmti. JLkb Ciintiwll12XW71, 1S2S. e. Wsm HB, ShomnsksrWC: Ms4hcdfor lntrq%sWbsAsswament of Orgsn Psrfuskm snd Vkbility Using a Minkturs Oxygsn Bsnwr. Am J Surg 14SM4-407, 1824. 10. *htin J,tin~, Gti&@*M~Wti ~-hltiMor of Mywsrdisl TksuO Ohygsnstkur. Cardiwasc Rw 22~, 1ss9. 11. Tmmper IfK+ Bsrkmr 2J, Hufskdkr GM, al at Tmnscutsnwus and Ltwr Surfsw P02 During Hsmorrhsgk hypotension snd Trsstment With Phsrrylephrine. Crlt Csrs Msd 1?537+41, 1ss2. 12 Ashsr EL Martin W, Rink MII, et W Corrdstbn of Hepstk Surfacs P02, Nutrtent Slwd Fkwsnd H.pstk Htdobgy After Hemodilutlon. Curr Surg 4M54+59, 1SS3. 13. Ssnksry EN, Rypins ES, Wssman V, et d Eflscts CMPortscaval Shunt snd Hepstk tk-kw Lbstlon on Lhw Surface Dxvaen Tsnsion and EffwWs l+s@G Blwd FIOVJ.J SUKI .Res k% 1837. 14. Cenzorr PF, Hobbhahn J, Gosk AE, et * Spknchnk Oxygen consumption snd Hspdk Suti oxygen Tension DurlnS Isoflursne Anssthssls. Anssthesbbgy 69@@ S51, 19s2.

~wnhGntrk 15. Wh@sld K B6tls CW, Rswllrrgs CA Psthophydobgy Diktstkm-Votwlus In the Dog. JAANA 12X3S-lQ 197S. 1s. MutdsyOF, Howsrd DR, E@wGf3etat Grpuimonksllylnduwd Gsstrk Dilststbn In th. ~ Csrdlopuhncmsry E!lwts. JAAHA 1Z143-14Q 1S7S. 17. Orton EC, Muir M Hemodynsmbs Outing Expatmsntd Gsstrtc DilstdkrWdWIUS In Dogs. Am J Vet Res 44151*1515, 19S3. la Bulldsy GB, Oshima G, Sslloy AW Pathophysk@ C4 Hspstk Isch8mis In Csrdkgenk Shock Am J Suq 151X7-97, 19SS. 19. Wheston LG, Thacker HL Caidwsll S Intmvsnous Fluomswin ssurlndkdord V Gsstrklsbilily in Gssbb Oiktskbn-Vc4vulus. JMHA 225 S7+04, 12SS. ZO. Sprung CL TIM PulrnonsryArtOry Cdhster. Sdtirnore, Uniusmity* Press, 1SS3. 21. Sodsl Bl, Hdcrdt JW Ussofths Pulmonary Arbry Csthdor lnths Critkdylll Pstient. H.srl & Lung 11:40S-409, 1SS2 22 Rulz SC, TuokerWK Wby RR Labomtory Rswort. AnssthsddosY 24SS-S1, 1Q75. 23. Wirier SJ (~ Btstkticd Prtndpks In G@wlmentsl Dss!gn. NW Yoriq McGmw Hill, 1971. 24. SAS Users Guido Ststkti% Versbn 5 EdMon. Cary, NC, SAS Indkuts Inc. 1S9S. 25. Boley W, AErsal GP, Wsursnmst skPsthqM@c4qk Effsctsof Sowsl Dktensbn on Intwtinsl Shod Ficw. Am J Surg 11722S-23% 1SSS. 2s. Chou GC, Qmssmick B Mdilily snd Blwd Flow Dbtributim within khs Wdi ofths Gsstminbstirml Trsct. Am J Physkl 235:H344i3s, lS7& 27. Cddwdl CS, Rkotts JJ Changss In Visoornl Blwd Fbw With Ebwtod lntr8-sbdomlnsl Pmssurs. J Surg Rss 4W4-ZQ 1SS7. 2S. Lsntz GC, Bsdykk SR R.psrfudon Injury in Gwrlmentd Csnins Gaskrlc DilststlOn-VOtwlus. Vet Surg 1S70, 1SSS. 2S. LsMl WW, Grwnwsy IX _PtUd Rdsw of the Hepstk Vsscukr sod. Hspstholqy 7S52+S2, 1SS7. W.~JLJdn-~~*hmbmd%ln_-~~ An Mgkgraphlc study. BrJ Rsdiol 42@13-SIS, 1W9. 31. Schwndz S, Fmntz R% Shownaksr WC: Ssquentbl Hemodynsmk and Osyg.n TrsnsForI Respcmsss in Hypmmkmi% Anemis snd Hypoxia Am J Phydd 241:HSS4H871, 1SS1. 32. Hssldns SC, Pstz JO: Katsrnins in Hypowkmic Do@ Crit Csm Msd @cepted). 33. Cilky RE, Polky TZ, Zwkchenbsrger JB, et 4 Indepsndsnt Measummsnt d Oxygen Consumption snd oxygen Odivsry. J Surg Res 47242-247, 1SSS. 34. ShosmskerWC, Blind RD, Appsl PLThsrspyofCritkdiy Ill P@opomtke Pstlents Bawd cm Outcome Prsdictbn md Pmspsctlvs Clinical Trkk. Surg CM North Am S&al 1-s34, 3S. Bland RD, Shoemsksr WC Common Physbiogk Pstbms in Gerrersl Surgical Owrstbn in Patients Hsmodvnarnic snd Oswen Trsnworl Chsnrass During sndAflsr PstisntsWith sr+wlthout Asscew Msd61 Pmblem~. Surg Clln NorW&n %793-S0S, 1S85. 3S. Home W4 Gilmors DR, Didzs % et SJ Effwts ot Gas4ric Distdbn-Volvulus on Ceronsrv ulood Fbw and Mvocsrdisd Dxmren ConsumrMon in tho Daa. Am J Vst Res -4s2s-164, 1ss5.

12s5.

37. Orton EC, MulrWW Isovolumdric Indices and Hurnsrd Csrdb Acttvs Substancs Biosssw Durirm Clinkd snd Gmsrimontsllv-lnduwd Gastric Dlktdion-Vduulus in Dorm AmJV& Res4%151S-15ZQ, 1S62. 3S. Btsffey EP, Gilkspk JR Ssrry JD, al * Circulatory Effwts of Hdothsns md Halothane-Nltmus Oxide Wmsthssk In tho Dq Contmikd Ventiktkm. Am J Vst Rss 3552se12S3, 1074.

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