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    Mean ± SD Do2I (squares) and Sto2 (diamonds) values at euvolemia (baseline), after hemorrhage (Hypovolemia T1), 20 minutes later (Hypovolemia T2), after transfusion (posttransfusion), and after hetastarch administration (Hypervolemia) in 14 dogs. *Significantly (P < 0.05) different from baseline. †Significantly (P < 0.05) different from hypovolemia T1. ‡Significantly (P < 0.05) different from hypovolemia T2.

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  • 17. Hutchison Technology Inc. Tissue oxygen monitor. Available at: www.htibiomeasurement.com. Accessed Mar 15: 2013.

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Evaluation of tissue oxygen saturation with near-infrared spectroscopy during experimental acute hemorrhagic shock and resuscitation in dogs

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  • 1 Department of Small Animal Clinical Science, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.
  • | 2 Department of Small Animal Clinical Science, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.
  • | 3 Department of Small Animal Clinical Science, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.
  • | 4 Department of Small Animal Clinical Science, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.
  • | 5 Departments of Large Animal Clinical Science, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610.
  • | 6 Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610.
  • | 7 Laboratory for Study Design and Statistical Analysis, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061.

Abstract

Objective—To evaluate tissue oxygen saturation (Sto2) by use of near-infrared spectroscopy in experimental acute hemorrhagic shock and resuscitation in dogs.

Animals—14 healthy adult purpose-bred Beagles.

Procedures—Dogs were anesthetized with isoflurane via facemask, anesthesia was maintained with propofol and rocuronium bromide, and dogs were mechanically ventilated to maintain normocapnia. Dogs were studied under normovolemia (baseline), hypovolemia with target mean arterial blood pressure < 40 mm Hg achieved and maintained steady for 10 minutes (hypovolemia T1), then 20 minutes later (hypovolemia T2), following resuscitation with shed blood (after transfusion), and after administration of 20 mL of hetastarch/kg (hypervolemia). Conditions were executed sequentially during a single anesthetic episode, allowing stabilization between states (10 minutes). Hemoglobin concentration, mean arterial blood pressure, arterial blood gas concentrations, cardiac index, oxygen delivery indexed to body surface area, and Sto2 were monitored.

Results—From baseline to hypovolemia T1, there was a significant reduction in mean ± SD oxygen delivery index (619 ± 257 mL/min/m2 to 205 ± 76 mL/min/m2) and StO2 (94 ± 4.4% to 78 ± 12.2%). Following resuscitation, Sto2 (80 ± 8.5% vs 92 ± 6.45%) and oxygen delivery index (211 ± 73 mL/min/m2 vs 717 ± 221 mL/min/m2) significantly increased, returning to baseline values. Hypervolemia had no effect on Sto2 or oxygen delivery index. A strong correlation (r = 0.97) was detected between mean oxygen delivery index and Sto2 across all time points.

Conclusions and Clinical Relevance—Under the conditions of this study, there was a strong correlation between Sto2 and oxygen delivery, suggesting that Sto2 may be used to estimate oxygen delivery.

Abstract

Objective—To evaluate tissue oxygen saturation (Sto2) by use of near-infrared spectroscopy in experimental acute hemorrhagic shock and resuscitation in dogs.

Animals—14 healthy adult purpose-bred Beagles.

Procedures—Dogs were anesthetized with isoflurane via facemask, anesthesia was maintained with propofol and rocuronium bromide, and dogs were mechanically ventilated to maintain normocapnia. Dogs were studied under normovolemia (baseline), hypovolemia with target mean arterial blood pressure < 40 mm Hg achieved and maintained steady for 10 minutes (hypovolemia T1), then 20 minutes later (hypovolemia T2), following resuscitation with shed blood (after transfusion), and after administration of 20 mL of hetastarch/kg (hypervolemia). Conditions were executed sequentially during a single anesthetic episode, allowing stabilization between states (10 minutes). Hemoglobin concentration, mean arterial blood pressure, arterial blood gas concentrations, cardiac index, oxygen delivery indexed to body surface area, and Sto2 were monitored.

Results—From baseline to hypovolemia T1, there was a significant reduction in mean ± SD oxygen delivery index (619 ± 257 mL/min/m2 to 205 ± 76 mL/min/m2) and StO2 (94 ± 4.4% to 78 ± 12.2%). Following resuscitation, Sto2 (80 ± 8.5% vs 92 ± 6.45%) and oxygen delivery index (211 ± 73 mL/min/m2 vs 717 ± 221 mL/min/m2) significantly increased, returning to baseline values. Hypervolemia had no effect on Sto2 or oxygen delivery index. A strong correlation (r = 0.97) was detected between mean oxygen delivery index and Sto2 across all time points.

Conclusions and Clinical Relevance—Under the conditions of this study, there was a strong correlation between Sto2 and oxygen delivery, suggesting that Sto2 may be used to estimate oxygen delivery.

Oxygen is a key component in the oxidative reactions that drive cell metabolism and therefore is essential to survival. For multicellular organisms with physical boundaries that exceed the time-distance constraints of diffusion, circulatory systems have evolved to deliver oxygen to tissues remote to the gas exchange surface. Under normal physiologic conditions, Do2 greatly exceeds the 2 in these tissues. However, during hypovolemic shock, Do2 may become sufficiently diminished so that o2 becomes linearly dependent on Do2. As a linear relationship develops between o2 and Do2, Do2 becomes inadequate to maintain aerobic metabolism. Timely restoration of Do2 during hemorrhagic shock is associated with reduced morbidity and mortality rates in patients in hemorrhagic shock following traumatic injury.1 As a result, hemodynamic monitoring in the intensive care unit has become the cornerstone in the evaluation and treatment of critically ill patients.2

Traditional noninvasive methods for indirectly monitoring oxygen delivery have focused on indices of end organ function, such as blood pressure, urine output, and changes in mentation.3 Although these methods may be effective at identifying states of profound hypoperfusion, occult hypoperfusion may go undetected in some patients, leading to poor clinical outcomes.4,5 Lactate concentration and base deficit are commonly used in intensive care units to identify hypoperfusion in critically ill and injured patients. However, changes in lactate concentration and base deficit require time to develop and do not reflect instantaneous changes in perfusion status.6 Additionally, lactate concentration can be falsely increased in patients with insufficient hepatic clearance.7 Use of the pulmonary artery catheter (ie, the Swan-Ganz catheter) has allowed for continuous monitoring of PAP and right atrial pressure in addition to determination of CO, thereby allowing calculation of Do2 in critically ill patients. Nevertheless, this technology is highly invasive, associated with a range of complications, cost-prohibitive, and not easily used in an emergency.8

Near-infrared spectroscopy has been developed out of a need for a more precise, responsive, minimally invasive method to assess tissue perfusion. Near-infrared spectroscopy exploits the differential absorption properties of deoxygenated and oxygenated Hb to determine the ratio of oxygenated Hb to total Hb in muscle. On the basis of this ratio, Sto2 is calculated and reported as a percentage. In veterinary and human clinical studies, Sto2 in muscle has proved to be a good surrogate for global tissue perfusion.9,10 This is likely attributable to peripheral tissues being the first to develop hypoperfusion as blood is shunted toward the body's core and the last to reperfuse during resuscitation.11,12

The purpose of the study reported here was to evaluate Sto2 by use of NIRS in experimental acute hemorrhagic shock and resuscitation in dogs. We hypothesized that would correlate with whole organism Do2 during hemorrhagic shock and reperfusion.

Materials and Methods

Animals—Fourteen healthy purpose-bred university-owned adult Beagles were enrolled in the study. Dogs were determined to be healthy on the basis of results of physical examination, CBC, and serum biochemical profile. Food was withheld for 12 hours prior to each experiment, but dogs had unrestricted access to water. Dogs were housed and cared for according to the Association for Assessment and Accreditation of Laboratory Animal Care adopted guidelines. The Virginia Tech Animal Care and Use Committee approved this study.

Instrumentation—Following preoxygenation with 100% oxygen, anesthesia was induced with 5% isofluranea delivered by facemask. An endotracheal tube was placed and connected to a circle breathing system. Dogs were positioned in dorsal recumbency, and anesthesia was maintained with 1.3% to 2% isoflurane in 100% oxygen during the instrumentation period. The cephalic vein and the right dorsal pedal artery were catheterized with 20-gauge 32-mm-long over-the-needle catheters. A 7F 20-cm double lumen catheterb was placed in the left jugular vein, and a 5F 8.5-cm hemostatic introducerc was placed in the right jugular vein. Dogs were then positioned in left lateral recumbency, and a thermodilution balloon catheterd with heparin coating was advanced to the pulmonary artery. Placement was confirmed by observation of the characteristic waveform.

Dogs were instrumented for continuous monitoring of respiratory rate, Petco2, bispectral index, HR, SAP, MAP, diastolic arterial blood pressure, CVP, and PAP.e Pressure transducers were calibrated with a calibration device,f then placed and zeroed at the level of the sternum. Bispectral index was continuously acquired and displayed by use of a proprietary bispectral index module in the monitor.e Stainless steel subdermal needle electrodes with a 3-lead reference montage were connected to a proprietary sensorg and arranged as described.13 Briefly, the primary lead was placed on the midline over the frontal bone at the level of the zygomatic processes, the ground lead was placed rostral to the base of the left ear, and the secondary lead was placed over the temporal bone. Esophageal temperatures were continuously monitorede and maintained between 36° and 38°C by use of a forced-air patient warmer.h Arterial and mixed venous blood samples were obtained and immediately analyzedi for Hb, Pao2, pH, Po2, BE, and lactate concentration. Cardiac output measurements were obtained in triplicate by thermodilution by use of 3 mL of iced 5% dextrose injected into the proximal port of the Swan-Ganz catheter. Cardiac output was recorded as the mean of 3 measured values with < 10% variation. Pulmonary artery wedge pressure was measured after CO determination with the Swan-Ganz catheter. Cardiac index, SVI, SVRI, Cao2, Co2, o2, and Eo2 were calculated with standard formulas.14 Tissue oxygen saturation was determined with a Sto2 monitor.j The Sto2 probe was placed over the sartorius muscle of the left pelvic limb (dependent limb).j Prior to placement of the Sto2 probe, the site was shaved to minimize interference from the hair during signal acquisition. Adequate signal strength was determined by detection of a THI > 5. Tissue Hb index is a measure of Hb in the monitored tissue and an indicator of signal strength. In human patients, a THI > 5 indicates sufficient Hb to obtain an accurate Sto2 reading. The Sto2 was continuously monitored at 2-second intervals over 1 minute with the Sto2 monitor. The Sto2 recorded was the mean determined over a designated minute with a THI > 5.

Experimental protocol—Following instrumentation, anesthesia was transitioned from isoflurane to a constant rate infusion of propofol,a as part of an unrelated study, to facilitate mechanical ventilation with a specific ventilator. The constant rate infusion of propofol was adjusted to maintain anesthesia and a bispectral index < 65. Dogs were paralyzed with a loading dose of rocuronium bromidek (0.2 mg/kg, IV), followed by a constant rate infusion (0.8 mg/kg/h) to facilitate ventilation. Mechanical ventilationl with 100% oxygen was continued to maintain normocapnia (Petco2, 35 to 45 mm Hg). Before proceeding with the experimental protocol, complete washout of isoflurane was confirmed by use of the gas analyzer.e Dogs were evaluated at 3 volumetric states: euvolemia, hypovolemia, and hypervolemia. After a 30-minute stabilization period, euvolemic data were collected (baseline). Following this, a hypovolemic state was induced by removing blood through the double lumen catheter in the left jugular vein, until the MAP stabilized at 40 ± 5 mm Hg. The blood bag collection set, containing a citrate-phosphate-dextrose-adenine solution, was suspended from a hook on the top of a vacuum chamber placed on a scale to measure total blood drawn. In preparation for autotransfusion, blood was stored in an incubator at 37°C. Once the target MAP was achieved, dogs were maintained at a steady hemodynamic plane for a minimum of 10 minutes before data were collected (hypovolemia T1). If MAP increased to greater than the target value, additional blood was removed until the target MAP was restored. Following restoration of the target MAP, the 10-minute equilibration period was restarted prior to data collection. Dogs were maintained in a hypovolemic state for 20 minutes, and data were collected prior to resuscitation with the shed blood (hypovolemia T2). Shed blood was administered over 20 minutes, and data were collected immediately after to confirm restoration of euvolemia (after transfusion). Then hetastarcha was administered at 20 mL/kg over 20 minutes to achieve hypervolemia and immediately afterward data were collected (hypervolemia). Dogs were allowed to recover. A dose of buprenorphinem (0.02 mg/kg, IV) was administered during recovery. Dogs were monitored after surgery until they were walking without ataxia. If signs of hemorrhage were detected at the catheter sites, the dogs were transferred to the intensive care unit for 12 hours. The following day, a physical examination was performed, and PCV, total solids concentration, and BUN were checked. All dogs survived.

Statistical analysis—Main outcomes of interest for this study were Sto2 and Do2. Other outcomes included respiratory rate, Petco2, HR, MAP, CVP, PAP, temperature (esophageal probe), Hb concentration, Pao2, Pao2, pH, Po2, BE, and lactate concentration. Normal probability plots revealed that all outcomes followed a normal distribution. Subsequently, data were summarized as mean ± SD values. Effects of time period (normovolemia [baseline], hypovolemia with target MAP < 40 mm Hg achieved and maintained steady for 10 minutes [hypovolemia T1], then 20 minutes later [hypovolemia T2], following resuscitation with shed blood [after transfusion] and after 20 mL of hetastarch/kg [hypervolemia]) on each outcome were assessed by use of mixed-model ANOVA followed by the Tukey procedure for multiple comparisons. The linear model specified time period as a fixed effect and dog as the random effect. To test the association between Do2 and Sto2, dog-level data for Do2 and Sto2 were initially summarized (by use of a mean value) at each time period before generating the Pearson correlation coefficient. Significance was set at P < 0.05. All analyses were performed with statistical software.n

Results

All 14 dogs (7 males and 7 females) used in the study recovered from anesthesia without complications. They were all 2 years of age and older, with a mean ± SD body weight of 10 ± 0.72 kg. Cardiopulmonary values were determined (Tables 1–3).

Table 1—

Mean ± SD values for cardiovascular variables measured in 14 dogs during euvolemia (baseline), after hemorrhage (hypovolemia T1), 20 minutes later (hypovolemia T2), after transfusion, and after hetastarch administration (hypervolemia).

VariableBaselineHypovolemia T1Hypovolemia T2After transfusionHypervolemia
HR (beats/min)89 ± 20.29125 ± 15.79*131 ± 16.66*127 ± 9.89*123 ± 12.21*
MAP (mm Hg)91 ± 15.0232 ± 5.11*41 ± 10.82*93 ± 16.9†‡109 ± 15.25*†‡§
CI (L/min/m2)3.79 ± 1.471.29 ± 0.35*1.57 ± 0.49*4.67 ± 1.34†‡5.63 ± 1.55*†‡
SVI (mL/beat/kg)1.94 ± 0.420.46 ± 0.14*0.56 ± 0.21*1.71 ± 0.502.08 ± 0.48
SVRI (dynes•s•cm−5/m2)2,276 ± 5822,290 ± 6821,707 ± 323*1,573 ± 361*1,561 ± 286*
CVP (mm Hg)4.69 ± 0.950.23 ± 0.95*1.07 ± 0.95*10.61 ± 0.95*†‡11.8 ± 0.95*†‡

Significantly (P < 0.05) different from baseline.

Significantly (P < 0.05) different from hypovolemia T1.

Significantly (P < 0.05) different from hypovolemia T2.

Significantly (P < 0.05) different from after transfusion.

Table 2—

Mean ± SD arterial and mixed venous blood gas values measured in the same dogs as in Table 1.

VariableBaselineHypovolemia T1Hypovolemia T2After transfusionHypervolemia
Pao2 (mm Hg)475 ± 39452 ± 49450 ± 51482 ± 36471 ± 36
BE (mmol/L)−2.9 ± 2.18−6.6 ± 2.06*−8 ± 2.5*†−7.3 ± 1.73*−5.2 ± 1.72*†‡§
Po2 (mm Hg)75 ± 21.4237 ± 6.96*43 ± 6.78*84 ± 15.44†‡90 ± 21.10*†‡
Hb (g/dL)11 ± 0.9710.74 ± 1.599.08 ± 1.34*†10.32 ± 0.878.16 ± 1.29*†§
Lactate (mmol/L)0.77 ± 0.521.06 ± 0.691.24 ± 0.76*1.08 ± 0.560.51 ± 0.30†‡§

See Table 1 for key.

Table 3—

Mean ± SD values for cardiopulmonary variables calculated in the same dogs as in Table 1.

VariableBaselineHypovolemia T1Hypovolemia T2After transfusionHypervolemia
Cao2 (mL/dL)16.17 ± 1.3315.74 ± 2.1713.52 ± 1.84*15.23 ± 1.1412.35 ± 1.69*†§
Co2 (mL/dL)13.70 ± 1.488.29 ± 2.25*7.83 ± 1.95*12.97 ± 1.29†‡10.54 ± 1.62*†‡§
o2I (mL/min/m2)89.08 ± 29.7994.43 ± 41.4984.22 ± 17.30104.56 ± 21.6498.75 ± 21.59
Eo2 (%)0.15 ± 0.040.47 ± 0.12*0.42 ± 0.10*0.15 ± 0.03†‡0.15 ± 0.03†‡
THI16 ± 2.9114 ± 2.18*14 ± 2.40*16 ± 2.34†‡15 ± 2.90†‡

See Table 1 for key.

Mean ± SD duration for complete isoflurane washout was 50 ± 11 minutes. Dosage for the constant rate infusion of propofol ranged from 18 to 42 mg/kg/h. Mean time required to achieve the target MAP during hypovolemia was 26.7 ± 15.3 minutes. Blood volume removed from the dogs ranged from 297 to 519 mL, with a mean of 393.6 ± 62.3 mL. The 10-minute stabilization period had to be repeated in 6 dogs following the removal of additional blood. Following initiation of hypovolemia, there was a significant increase in HR, BE, and Eo2, compared with baseline values. These changes were accompanied by a significant decrease in MAP, CVP, CI, SVI, Po2, and Cmo2 (Tables 1–3). From baseline to hypovolemia T1, there was a 67% reduction in Do2I (619 ± 257 mL/min/m2 vs 205 ± 76 mL/min/m2; P < 0.001) and a 17% reduction in Sto2 (94 ± 4.4% vs 78 ± 12.2%; P < 0.001; Figure 1).

Figure 1—
Figure 1—

Mean ± SD Do2I (squares) and Sto2 (diamonds) values at euvolemia (baseline), after hemorrhage (Hypovolemia T1), 20 minutes later (Hypovolemia T2), after transfusion (posttransfusion), and after hetastarch administration (Hypervolemia) in 14 dogs. *Significantly (P < 0.05) different from baseline. †Significantly (P < 0.05) different from hypovolemia T1. ‡Significantly (P < 0.05) different from hypovolemia T2.

Citation: American Journal of Veterinary Research 75, 1; 10.2460/ajvr.75.1.48

Mean ± SD duration of the hypovolemic period, from hypovolemia T1 to hypovolemia T2, was 37.8 ± 10.9 minutes. During the hypovolemic period, there was a decrease in BE, SVRI, Hb, and Cao2 from hypovolemia T1 to T2 (Tables 1–3). There was no significant change in HR, MAP, CI, SVI, Po2, lactate concentration, and Co2. However, there was a significant increase in lactate concentration at hypovolemia T2, compared with the euvolemic value (Table 2).

Dogs received a transfusion during a mean of 20 ± 11 minutes. Upon completion of autotransfusion of shed blood, MAP, CVP, CI, SVI, Pvo2, Hb, lactate concentration, Co2, and Eo2 returned to euvolemic values (Tables 1–3). Heart rate, BE, and SVRI failed to return to euvolemic values. In comparison to hypovolemia T2 values, Sto2 (80 ± 8.5% vs 92 ± 6.45%; P < 0.001) and Do2I (211 ± 73 mL/min/m2 vs 717 ± 221 mL/min/m2; P < 0.001) significantly increased, returning to euvolemic values (Figure 1).

Subsequent to the administration of hetastarch and induction of hypervolemia, MAP, CVP, HR, CI, and Po2 were significantly increased, compared with euvolemic values (Tables 1 and 2). There was a significant decrease in SVRI, Hb, BE, Cao2, and Co2, compared with euvolemic values. No significant differences were observed with respect to SVI, lactate concentration, Do2I, Sto2, or the Eo2, compared with euvolemic values. Across all time points in the study, there was no significant change in Pao2 or o2. Comparison of mean Do2I and Sto2 across all time points yielded a strong relationship, with a correlation coefficient of 0.97 (P = 0.005).

Discussion

The present study was performed to evaluate Sto2 by use of NIRS in experimental acute hemorrhagic shock and resuscitation in dogs. We sought to test the hypothesis that tissue-specific oxygenation as measured by Sto2 would correlate with whole organism Do2 during hemorrhagic shock and reperfusion.

Following induction of hemorrhagic shock, there was a significant decrease in Do2I and Sto2. Although the decrease in Do2I was greater than the decrease in Sto2, the data revealed a strong correlation between St and Do2I during the period between baseline and hypovolemia T1. As dogs received the autotransfusion, leading to the restoration of euvolemia, Sto2 and Do2I significantly increased toward baseline values and a strong correlation was again observed between Sto2 and Do2I. These results were similar to those obtained in previous studies in other species. McKinley et al10 monitored Sto2 during resuscitation and for the first 24 hours following admission of human patients who had sustained severe abdominal trauma; Sto2 correlated with changes in Do2 and was useful in guiding restoration of euvolemia. In a study15 of the relationship between Do2 and Sto2 during experimental acute hemorrhagic shock in splenectomized pigs, a target blood volume of 28% was removed. Similar to the present study, changes in Sto2 induced by hemorrhage were not as profound as those observed in Do2 and a strong correlation was evident between changes in Sto2 and Do2 during hemorrhage and reperfusion. The larger fluctuation in Do2, compared with that in Sto2, may be attributable to a buffering effect in the Do2. There may be a critical point beyond which changes in Do2 have little effect on St and before which changes in Do2 significantly affect Sto2, similar to the oxygen-Hb dissociation curve.

Changes in BE and lactate concentration, the traditional markers of perfusion, lagged behind changes in Do2I and Sto2 following induction of hemorrhagic shock and were slower to return to baseline following fluid resuscitation. This finding was in accordance with clinical and laboratory studies,6,15 in which changes in Sto2 precede changes in lactate concentration and base deficit. Following induction of hemorrhagic shock, statistical analysis indicated that the increase in lactate concentration was significant, but the increase was not of sufficient magnitude to be considered clinically important. This can be explained by the fact that Eo2 was increased in an attempt to maintain aerobic metabolism and the body reserves were not exhausted; therefore, critical Do2 was not achieved. Additionally, o2 did not change linearly with Do2, as would be expected after an anaerobic threshold is reached. Conversely, the Sto2 monitor detected changes in regional tissue perfusion before changes in lactate concentration and BE occurred, suggesting that Sto2 may be a valuable tool in identifying patients in the initial stage of shock before critical changes in cellular metabolism occur.

Presently, the effects of volume overload on NIRS-acquired Sto2 are unknown. It has been speculated that volume overload may alter the reflectance by creating scatter, leading to falsely decreased measurements of Sto2.16 In the present study, hypervolemia had no effect on Sto2 or Do2. However, the dogs in this study were not subject to extreme fluid overload and time was not allowed for fluid shift to occur. As fluid moves into the interstitial space, altering tissue density, the potential exists to affect the reflectance by creating scatter or decreasing tissue penetration by the near-infrared light. The data obtained in the present study indicated that Sto2 would not be an effective tool for assessing fluid overload. Additional studies are indicated to determine how fluid overload affects Sto2 over time.

Tissue hemoglobin index is an indicator of signal strength reported by the Sto2 monitor and is reported as a number in the range of 1 to 99. The THI corresponds to the amount of Hb present in the monitored tissue. A THI > 5.0 indicates sufficient Hb for the monitor to reliably measure Sto2 in human patients under most circumstances.17 The relationship between THI and signal accuracy has not been verified in dogs, and on the basis of clinical experience, we believe THI needs to be > 5.0 to indicate a reliable signal. Tissue hemoglobin indices in this study were all > 5.0. The usefulness of THI is still under investigation, but in the present study, changes in THI were similar to those in Do2 and Sto2 across all volemic states. These changes were probably caused by extravascular and vascular Hb concentrations resulting from changes in the volume of the underlying vascular bed, as occur during hemorrhage and reperfusion.

It is important to distinguish the difference between Sto2 and another commonly used oxygen measurement, Spo2. Whereas pulse oximetry, measures oxygen saturation in arterial blood, Sto2 is a measure of oxygen saturation in the vascular bed of the muscle. The Sto2 signal is composed of not only the arterial oxygen but also the oxygen in the capillaries and venous network. Unlike Spo2 which reflects changes in oxygenation, Sto2 reflects changes in oxygen extraction at the tissue level.17 Therefore, when local tissue conditions of supply and consumption change, Sto2 will change but Spo2 will not. This would be a typical finding in a patient with adequate ventilation but poor oxygen delivery from causes such as poor CO, anemia, or hypovolemia. In the present study, there were no changes in Spo2 with changes in volemic states (data not shown).

Problems associated with placement of the NIRS Sto2 probe and signal acquisition have been reported in human patients. Darker skin pigmentation, areas with large amounts of fat deposition, and interstitial edema have all been implicated in poor signal acquisition.18–20 In humans, the NIRS Sto2 probe is placed over the deltoid muscle or more commonly the thenar eminence (the group of muscles on the palm at the base of the thumb). Use of these regions yields a reliable measurement of St as determined by use of the THI. The decision to place the NIRS Sto2 probe on the medial aspect of the thigh over the sartorius muscle in the present study was based on previous work by Hall et al.21 In that study,21 probe placement was evaluated at 4 areas (lower region of the back, forearm, lateral aspect of the thigh, and medial aspect of the thigh) and it was determined that the medial aspect of the thigh provided the most reliable data. In the present study, the dogs did not have a pigmented area in the thigh and had minimal fat deposition. However, the authors have had difficulty with signal acquisition in the clinical setting in patients with dark hair and pigmented skin, suggesting that melanin may interfere. In the present study, the major challenge was to secure the probe to the skin and still allow good contact. We found that using surgical skin staples around the body of the probe worked well for this purpose.

The present study had several limitations. Blood was removed through an intravascular catheter instead of creating a surgical lesion. Although this methodology allows for standardization among animals, it does not completely reflect the clinical situation and this factor has to be considered when interpreting the results. Furthermore, the study was conducted while dogs received general anesthesia with a fraction of inspired oxygen of 0.95, and resuscitation of trauma patients in the emergency room may occur at lower oxygen concentrations, leading to an inability of Do2 to meet oxygen demands and therefore a faster onset of a state of shock.

Additionally, these dogs were not splenectomized, which accounted for the variability in the time to achieve target MAP and total blood volume removed. Six of the dogs required removal of additional blood after compensation, which was characterized by tachycardia and an increase in MAP. Despite the variability attributed to the splenic contraction in these dogs, this condition more closely resembled a clinical scenario and allowed for better extrapolation of the data.

Despite NIRS becoming more commonly accepted in human medicine, several obstacles to the use of NIRS for the determination of Sto2 must be overcome before this technology can gain widespread clinical application in the veterinary field. The technology is cost-prohibitive for the veterinary profession, with the cost of a single-use, disposable NIRS Sto2 probe at approximately $200. There is considerable debate on how best to use this technology. Presently, we do not know what specific Sto2 would warrant interventions and what specific interventions should be performed when Sto2 is low. However, under the experimental conditions of hemorrhagic shock and resuscitation in the study reported here, there was a strong correlation between Sto2 and Do2I, suggesting that Sto2 may be used to estimate Do2. Additionally, changes in Sto2 preceded those in BE and lactate concentration, indicating that Sto2 might be used as an early indicator of hypoperfusion.

ABBREVIATIONS

BE

Base excess

Cao2

Arterial oxygen content

CI

Cardiac index

Co2

Mixed venous oxygen concentration

CO

Cardiac output

CVP

Central venous pressure

Do2

Oxygen delivery

Do2I

Oxygen delivery index

Eo2

Oxygen extraction ratio

Petco2

End-tidal partial pressure of CO2

Hb

Hemoglobin

HR

Heart rate

MAP

Mean arterial blood pressure

NIRS

Near-infrared spectroscopy

PAP

Pulmonary artery pressure

Po2

Mixed venous oxygen partial pressure

Spo2

Oxygen saturation as measured by pulse oximetry

Sto2

Tissue oxygen saturation

SVI

Stroke volume index

SVRI

Systemic vascular resistance index

THI

Tissue hemoglobin index

o2

Oxygen consumption

o2I

Oxygen consumption index

a.

Abbott Laboratories, North Chicago, Ill.

b.

MILA International Inc, Erlanger, Ky.

c.

St. Jude Medical Inc, Saint Paul, Minn.

d.

Arrow International Inc, Reading, Pa.

e.

S/5 Anesthesia monitor, GE Healthcare Datex-Ohmeda, Waukesha, Wis.

f.

Delta-Cal, Utah Medical Products Inc, Midvale, Utah.

g.

Pediatric BIS sensor (tree electrode sensor), Aspect Medical Systems Inc, Newton, Mass.

h.

Bair hugger, Arizant Inc, Eden Prairie, Minn.

i.

I-STAT, Abbott Point of Care Inc, East Windsor, NJ.

j.

Hutchinson Technology Inc, Hutchinson, Minn.

k.

APP Pharmaceuticals LLC, Schaumburg, Ill.

l.

Newport Medical, Costa Mesa, Calif.

m.

Reckitt Benckiser Healthcare Ltd, Hull, England.

n.

JMP Pro, version 10, SAS Institute Inc, Cary, NC.

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Appendix

Equations used in a study of Sto2 during experimental acute hemorrhagic shock and resuscitation in dogs.

BSA (in m2) = 0.0072 • (height [in cm])0.725 • (weight [in kg])0.425
CI = CO/BSA
SVI = (CO/Body weight)/HR
SVRI = (Arterial blood pressure – CVP) • 79.92/CI
Cao2 = (1.34 • Hb • Sao2) + (0.003 • Pao2)
Co2 = (1.34 • Hb • Sao2) + (0.003 • Po2)
Do2I = CaO2 • CI • 10 dL/L
o2I = (Cao2 – Cmo2) • CI • 10 dL/L
Eo2 = Vo2/Do2

BSA = Body surface area. Sao2 = Arterial oxygen saturation. Svo2 = Venous oxygen saturation.

Contributor Notes

This manuscript represents a portion of a thesis submitted by Dr. Pavlisko to the Virginia-Maryland Regional College of Veterinary Medicine as partial fulfillment of the requirements for a Master of Science degree.

Supported by a VMRCVM Internal Research Competition Intramural Grant.

Presented in abstract form at the annual American College of Veterinary Anesthesiologists Meeting, San Antonio, September 2012.

The authors thank Dana Calicott for technical assistance.

Address correspondence to Dr. Pavlisko (pavlisko@vt.edu).