Acid–base disturbances, in particular metabolic acidosis, are frequently encountered in severely injured and critically ill patients.1 Several previous studies have shown admission base excess and lactate levels to be reliable variables in the triage of patients requiring ICU resources.2–7
Base excess was first introduced in 1960 by Siggard-Andersen to qualify the nonrespiratory component in acid–base imbalance.8 Base excess is defined as the amount (mmol l−1) of strong acid or strong base needed to restore arterial whole blood to a pH of 7.4, with the sample fully saturated with oxygen at 37°C and a partial pressure of carbon dioxide (pCO2) of 40 mmHg.9,10 This approach was later modified by introducing extracellular base excess or standard base excess (SBE), which proved to be independent of the respiratory pCO2.11–14 The availability of blood gas analysers for easy and rapid determination of base excess and lactate levels has led to the routine determination of both in the clinical evaluation of critically ill patients.2,3,6,7
Several previous investigations have established base excess as well as lactate levels as valuable indicators of both shock and the efficacy of resuscitation in trauma patients.15–21 Furthermore, both base excess and lactate levels have been shown to be predictive of transfusion requirements,22–24 oxygen debt,4,14,19,21,23,25–27 the increased risk of shock-related complications [i.e. multiple organ failure, acute respiratory distress syndrome (ARDS), renal failure, coagulopathy],14,18,21,27–29 the outcome of patients,6,14,19,23 survival after haemorrhage,4,5 as well as mortality after trauma.4,6,14,18,21,25,27,30,31 Thus, base excess and lactate levels, respectively, are recognized as important variables to evaluate the clinical condition of critically ill patients and serve as reliable indicators for prognosis.6,32,33 In addition, clinical decisions are often based on changes in both base excess and lactate levels over time.2,25,27,28
The determinations of base excess and lactate levels are usually performed by standard blood gas analysers. Most algorithms used today for calculating the base excess use measured pH, pCO2 and haemoglobin (Hb) values, and are based on the fundamental Van Slyke equation modified by Siggard-Andersen in 1977.9 However, arterial blood samples may be difficult to obtain owing to patient size, lack of patient cooperation and required technical skills. Furthermore, arterial puncture may cause complications, including pain, arterial damage, haemorrhage, aneurysm formation, thrombosis of the artery and infection.34 Therefore, the possibility of using venous blood for blood gas analysis and the calculation of base excess is being discussed and may be of clinical interest.
A modification of the Van Slyke equation for calculation of the whole blood base excess (BEz) has been proposed by Lang and Zander.35 This approach takes the known effect of oxygen saturation of Hb into account by including a correction term for oxygen saturation in the fundamental Van Slyke equation.36 Therefore, calculation of base excess from any blood sample (venous or arterial blood) based on measured pH, pCO2, Hb concentration (cHb) and O2 saturation (SO2) may be possible.35,36 At present, the accuracy of the Van Slyke equation modified according to Zander has been shown in vitro by using a wide-ranging triple-set of reference values for pH, pCO2 and base excess in normal oxygenated human blood.35 Over a wide range (−30 to +30 mmol l−1) of varying base excess, mean inaccuracy was less than 1 mmol l−1. In a further ex-vivo study, using venous blood from 50 healthy volunteers, the calculated base excess from venous blood according to Zander perfectly agreed with the normal base excess from arterial blood, even though pH, pCO2 and SO2 varied widely.37 The aim of the present study was to investigate in vivo whether both the base excess and the lactate level can be reliably determined in central venous blood under steady-state conditions and in haemorrhagic shock. In addition, we assessed the applicability of the Van Slyke equation modified according to Zander by comparing the calculated whole blood base excess according to Zander (BEz) with whole blood base excess values obtained from standard blood gas analysis according to the NCCLS (National Committee for Clinical Laboratory Standards) for all conditions.
Materials and methods
In the framework of another study38 investigating anaemia tolerance, animals were randomized into two groups of 12 pigs each, receiving hydroxyethyl starch (HES) 130 (136 kD) or HES 650 (647 kD), blinded to the experimental investigator. Both HES solutions have identical molar substitution (0.42), C2/C6 ratio (5: 1) as well as concentration (6%). The study group consisted of 24 pigs with a mean body weight of 43 ± 4 kg. The pigs were fasted overnight but allowed free access to water. The study protocol was authorized by the Veterinary Office of the Canton de Vaud (Service Vétérinaire, Lausanne, Canton de Vaud, Switzerland). All experiments were performed according to the guidelines of the Swiss Federal Veterinary Office.38
Premedication and anaesthesia
Animals were premedicated with an intramuscular injection of 0.5 mg kg−1 xylazine (Rompun 2%, Bayer AG, Leverkusen, Germany), 20 mg kg−1 ketamine (Veterinaria AG, Zurich, Switzerland) and 1 mg atropine (Sintetica S.A., Mendrisio, Switzerland). After the animals were sedated, anaesthesia was induced by administration of 3% halothane (Dräger, Lübeck, Germany) by mask, followed by tracheal intubation. Volume controlled ventilation was performed using tidal volumes of 10 ml kg−1 with a ventilatory rate of 13–18 min−1 to maintain alveolar carbon dioxide pressure (pCO2) at 35–40 mmHg (Ventilator Dräger Sulla 900 V; Dräger). The inspired oxygen fraction (FiO2) was maintained at 1.0 during surgical instrumentation and then reduced to an FiO2 of 0.4 (air–oxygen mixture). Analgesia was ensured by continuous intravenous infusion of fentanyl (Sintetica S.A.) at a dosage of 4 μg kg−1 h−1 during the entire period of surgical instrumentation. Halothane was used to anaesthetize the animals at a mean of 0.8–2.0% according to heart rate and blood pressure response to surgical stimulation of each individual animal and left unchanged during the entire study. The ear vein was cannulated (18-gauge cannula).
The right internal jugular vein was catheterized for normovolaemic haemodilution, measurement of central venous pressure, venous blood withdrawal for laboratory measurements and venous blood gas analyses. The catheter tip was inserted into the superior vena cava. The right carotid artery was also catheterized allowing continuous measurement of mean arterial blood pressure and blood withdrawal for arterial blood gas analyses. Via the contralateral carotid artery, an arterial cannula (AAS10 V; Jostra AG, Hirrlingen, Germany) was inserted and connected to a cardioplegia pump (SIII Double Head Pump; Stöckert, Munich, Germany) for controlled withdrawal of blood for normovolaemic haemodilution. Vital monitoring of the pigs included continuous three-lead electrocardiogram, heart rate and temperature. Furthermore, a direct bladder catheterization was performed for urine sampling.
After all surgical preparations were completed, the animals were allowed to recover for 45 min before the investigational protocol was started and the first measurement was made. Progressive acute normovolaemic haemodilution was induced by steps of 10 ml kg−1 body weight with a 1: 1 exchange of blood with either HES 130 or HES 650 until a total exchange of 50 ml kg−1 body weight was reached. The HES solution was infused into the right internal jugular vein at the same time and the same rate that blood was removed from the left carotid artery. Subsequently, uncompensated progressive blood withdrawal, including haemorrhagic shock, was performed by withdrawing blood from the left carotid artery in steps of 10 ml kg−1 body weight until the death of the animal. Each period of haemodilution and blood withdrawal was conducted over exactly 30 min followed by a stabilization period of 15 min. At baseline and after each step of 10 ml kg−1 body weight blood exchange and blood withdrawal, serial blood gas analyses from arterial blood and central venous blood were obtained simultaneously.
Blood gas analysis
Arterial and central venous blood samples were collected using heparinized syringes (BD Present; BD Vacutainer Systems, Plymouth, UK). Blood gas analyses as well as determination of lactate levels were performed immediately after collection using the Rapidlab 865 (Bayer Vital GmbH, Fernwald, Germany). One major calibration of the Rapidlab 865 (Bayer Vital GmbH) was made before starting the first measurement in every pig. Afterwards, the blood gas analyser made automatic calibrations as programmed by the manufacturer. Whole blood base excess was calculated automatically by the blood gas analyser using the following standard (NCCLS) algorithm:
where BE denotes base excess, cHCO3 denotes bicarbonate concentration, cHb denotes haemoglobin concentration and pH denotes potential of hydrogen.
In addition, whole blood base excess from arterial and central venous blood samples was calculated using the Van Slyke equation modified according to Zander and Lang:37
where BE denotes base excess, cHb denotes haemoglobin concentration, pCO2 denotes partial pressure of carbon dioxide and pH denotes potential of hydrogen.
A trial database within Excel (Microsoft Office 2003; Microsoft Corporation Redmond, Washington, USA) was used to store study data. The statistical analyses were performed using SPSS (version 13; SPSS Inc., Chicago, Illinois, USA).
The whole blood base excess calculated by the Van Slyke equation modified by Zander for venous blood and the whole blood base excess obtained from standard blood gas analysis (RapidLab 865, Bayer Vital GmbH) of venous and arterial blood according to the NCCLS were compared with each other. In addition, the central venous lactate levels were compared with the arterial lactate levels, both obtained by means of the RapidLab 865 (Bayer Vital GmbH). Continuous variables were summarized as mean ± SD. Differences between measurements were analysed using an analysis of variance (ANOVA) for repeated measures with the animal as the observational unit, period of time as the within factor and HES group as the between factor. The SD of the difference between parameters within animals in the two periods of time (haemodilution versus haemorrhage) is presented as median (range) and was compared using the Wilcoxon signed-rank test. Parameters are the difference between NCCLS arterial base excess versus central venous, arterial versus central venous lactate and NCCLS arterial base excess versus base excess calculated by the Van Slyke equation modified by Zander for central venous blood. Linear regressions were performed and the coefficients r2 of determination are reported; in all regressions, the equality line is also added. Corresponding P values were obtained in an ANOVA for repeated measures with covariates (ANCOVA). P values of 0.05 or less were considered significant.
Twenty-four pigs were analysed generating 195 values for each parameter over a time period of 390 min. The first 210 min was the period of haemodilution (six time points, generating 144 values for each parameter) and the next 180 min the period of haemorrhagic shock (four time points, generating 51 values for each parameter). Haemodynamic parameters at the beginning were as follows: heart rate was 95 ± 11 bpm, systolic arterial pressure 85 ± 9 mmHg, diastolic arterial pressure 55 ± 8 mmHg and mean arterial pressure 65 ± 9 mmHg. Shortly before the death of the animals, haemodynamic parameters were as follows: heart rate was 152 ± 39 bpm, systolic arterial pressure 42 ± 15 mmHg, diastolic arterial pressure 16 ± 7 mmHg and mean arterial pressure 24 ± 11 mmHg.
Whole blood base excess according to National Committee for Clinical Laboratory Standards: simultaneous measurements of central venous and arterial blood
Base excess in arterial blood measured according to the NCCLS was 2.27 ± 4.12 versus 2.48 ± 4.33 mmol l−1 (P = 0.099) for base excess in central venous blood measured according to the NCCLS. During haemodilution (first 210 min), the difference between central venous and arterial base excess was 0.33 ± 0.80 mmol l−1 and −0.13 ± 0.97 mmol l−1 during haemorrhage (for the last 180 min; P = 0.002). The median SDs within animals were 0.56 (0.22–1.79) mmol l−1 during haemodilution and 0.76 (0.06–1.88) mmol l−1 during haemorrhage (P = 0.355). The regression analysis showed a strong correlation between arterial and central venous base excess according to NCCLS (r2 = 0.960, P < 0.001; Fig. 1) and a significant effect (r2 = 0.083; P = 0.003) of time was found, indicating that there is some difference during late periods of haemodilution/severe acidosis (Fig. 2).
Arterial and central venous National Committee for Clinical Laboratory Standards lactate levels
Lactate measured according to the NCCLS in arterial blood was 2.66 ± 3.23 versus 2.71 ± 2.80 mmol l−1 in central venous blood (P = 0.330). During haemodilution (first 210 min), the difference between central venous and arterial lactate was 0.19 ± 0.29 mmol l−1 and −0.38 ± 0.91 mmol l−1 during haemorrhage (for the last 180 min; P < 0.001). The median SDs within animals were 0.11 (0.04–0.67) mmol l−1 during haemodilution and 0.67 (0.13–1.91) mmol l−1 during haemorrhage (P < 0.001). There was a strong correlation between central venous and arterial lactate (r2 = 0.983; P < 0.001; Fig. 3) and a significant effect (r2 = 0.193; P = 0.003) of time was found, indicating that there is some difference during late periods of haemodilution/severe acidosis (Fig. 4).
National Committee for Clinical Laboratory Standards base excess versus base excess calculated by the Van Slyke equation modified by Zander
The calculated base excess by the Van Slyke equation modified by Zander for central venous blood of 2.22 ± 4.62 mmol l−1 was significantly different (P < 0.001) from the measured arterial base excess according to the NCCLS (2.27 ± 4.12 mmol l−1). During haemodilution (first 210 min), the difference between arterial base excess according to the NCCLS and central venous base excess calculated by the Van Slyke equation modified by Zander was 0.20 ± 0.79 mmol l−1 and −0.76 ± 1.22 mmol l−1 during haemorrhage (for the last 180 min; P < 0.001). The median SDs within animals were 0.48 (0.12–1.88) mmol l−1 during haemodilution and 1.15 (0.12–2.32) mmol l−1 during haemorrhage (P = 0.024). The regression analysis of the arterial base excess according to the NCCLS and central venous base excess calculated by the Van Slyke equation modified by Zander shows a strong correlation (r2 = 0.942, P < 0.001; Fig. 5).
Central venous and arterial base excess determined according to the NCCLS showed an excellent correlation without a statistically significant difference between arterial and central venous measurements. The variation between values did not even increase during haemorrhage. Also central venous base excess determined by the Van Slyke equation modified by Zander overall correlated well with arterial base excess determined according to the NCCLS. However, during haemorrhage, the variation between these values increased significantly. Finally, also arterial and central venous lactate levels overall correlated well, but again, during haemorrhage, the variation between values increased significantly.
At the present time, arterial blood gas analysis is the gold standard for assessing the acid–base status, though there are reports on the agreement of base excess and lactate levels determined in arterial and venous blood.39,40 However, the popularity of venous blood gas analysis is low and some studies have expressed reservations regarding the accuracy of venous blood gas analysis.41,42 The most obvious advantage of obtaining a venous blood gas analysis instead of an arterial blood gas analysis is that a venous blood sample can be drawn using the same intravenous line that is used to draw blood for other laboratory tests, thus necessitating only one puncture. This translates into decreased costs, labour and risk of needlestick injury to the healthcare provider. Furthermore, complications such as arterial laceration, haematoma and thrombosis are all but negated with venous blood sampling.
Central venous and arterial base excess determined according to the NCCLS showed an excellent correlation without a statistically significant difference between arterial and central venous measurements (Fig. 1). Interestingly, the variation between arterial and central venous base excess during haemodilution and haemorrhage was similar, and the difference between base excess determined in arterial blood versus central venous blood during haemodilution and haemorrhage, although statistically significant, was clinically irrelevant (0.33 ± 0.80 versus −0.13 ± 0.97 mmol l−1). Therefore, central venous blood can be used exchangeably with arterial blood to determine base excess.
In our study, we assessed the accuracy of the base excess calculation by the Van Slyke equation modified by Zander. Thereby, the most important comparison is the comparison between arterial base excess determined according to the NCCLS versus central venous base excess determined by the Van Slyke equation modified by Zander (Fig. 5) as the correction introduced by Zander and Lang37 aimed at correcting for the difference between the different oxygenation in arterial versus venous blood in order to allow venous blood to be used for the determination of the base excess. Overall, we found a close correlation between arterial base excess determined according to the NCCLS and central venous base excess determined by the Van Slyke equation modified by Zander (Fig. 5). However, during haemorrhage, the difference between the two base excess measures (−0.76 ± 1.22 mmol l−1) was greater than that during haemodilution (0.20 ± 0.79 mmol l−1) and, even more importantly, the variation during haemorrhage was significantly higher than that in the more steady-state condition during haemodilution. This is in contrast to the comparison between base excess determination according to NCCLS wherein, during haemorrhage, the variation between arterial and central venous base excess did not increase in comparison with haemodilution. The modification of the Van Slyke equation, proposed by Zander et al., thus did not improve the correlation between the determination of base excess in arterial and central venous blood according to the NCCLS; on the contrary, it even reduced it.
The good correlation between the arterial and central venous lactate levels we found (Fig. 3) is in line with previous studies.39,43–46 During haemorrhage, the difference between arterial and central venous lactate (−0.38 ± 0.91 mmol l−1) was statistically greater than that during haemodilution (0.19 ± 0.29 mmol l−1), although the magnitude is of potential clinical relevance. However, the variation between arterial and central venous lactate determination was significantly higher during haemorrhage than during haemodilution (Fig. 4). Central venous lactate levels, therefore, can be used to assess the acid–base status; however, during haemorrhage and in unsteady states, central venous lactate should be confirmed as soon as possible with an arterial lactate determination.
The limitation of this study is that we used a central venous line, with the tip of the catheter being placed in the superior vena cava. Therefore, central venous blood is a rather accurate substitute for arterial base excess and lactate under steady-state conditions, but remains to be compared with mixed venous blood and evaluated when global information about the behaviour of peripheral tissue is determined. As we do not have any information about peripheral venous blood, no recommendation for emergency situations in the clinical setting to use peripheral venous blood can be made. Furthermore, we can only suppose that the animals, even when being premedicated, had a certain level of stress, which induced these higher levels of lactate and base excess; this was shown in a study by Darrah et al.47 in which pigs also had elevated lactate levels.
Central venous blood gas analysis according to the NCCLS is a good predictor for base excess and lactate in arterial blood under steady-state conditions. However, the variation between arterial and central venous lactate increases significantly during haemorrhage. Central venous lactate levels, thus, can be used to assess the acid–base status; however, during haemorrhage and in unsteady states, central venous lactate should be confirmed as soon as possible with an arterial lactate determination. The modification of the Van Slyke equation by Zander did not improve the agreement between venous and arterial base excess and is, therefore, neither physiologically nor clinically useful.
The present study is supported by departmental funds and B. Braun Medical S.A., Crissier, Switzerland.
The department to which the work is attributed is the Institute of Anaesthesiology, University Hospital Zurich, Zurich, Switzerland.
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