Effects of body temperature on blood gases

Andreas Bacher
Abstract Background:
Changes in body temperature have important impact on measurements of blood gases. In blood gas analyzers the samples are always kept constant at a temperature of exactly 37C during the measurements, and therefore results are not correct if body temperature differs from 37C. Objective: Lack of knowledge of the effects of body temperature on results of blood gas monitoring may lead to wrong and potentially harmful interpretations and decisions in the clinical setting. The following article elucidates alterations in monitoring of blood gases and oxyhemoglobin saturation (SO2) that occur during changes in body temperature.
Keywords Blood gas monitoring · Oxyhemoglobin saturation · Hypothermia ·Hyperthermia
Blood gas monitoring
Blood gases (oxygen and carbon dioxide) are usually reported as partial pressures (gas tensions) since according to Henry’s law the partial pressure of a gas is proportional to its concentration at a given temperature and pressure. However, as temperature decreases, the solubilityof oxygen and carbon dioxide in blood or any other fluid increases, which means that the relationship of partial pressure to the total content of oxygen or carbon dioxide in the fluid changes.
Carbon dioxide
If blood containing a given amount of carbon dioxide at a certain tension (PCO2) at 37C is cooled, with the possibility to equilibrate with air, the total content of CO2 in this blood sample remains constant, whereas PCO2 decreases due to the increased proportion of dissolved CO2 at lower temperature. Since the PCO2 of air or any inspired gas mixture is almost zero, no additional molecules of CO2 diffuse into the blood. If a blood sample is rewarmed to 37C in a blood gas analyzer under vacuumsealed conditions, the previously increased dissolved proportion of CO2 again contributes to PCO2. The measured PCO2 of this blood sample is the same as at 37C. Hypothermia reduces the metabolic rate and the rate of CO2 production. To hold the arterial CO2 content constant during cooling it is necessary to reduce CO2 elimination (i.e., by reducing minute ventilation in anesthetized patients) equivalently to the decrease in CO2 production. If this is performed, arterial carbon dioxide tension (PaCO2) measured in a blood gas analyzer at 37C remains at the same level as during normothermia. Blood gas analyzers are usually equipped with algorithms that enable the true PaCO2 to be calculated at the actual body temperature (Fig. 1) [1]. True PaCO2 corrected for current body temperature is of course lower during hypothermia than the PaCO2 value measured at 37C. The difference between these two values corresponds to the increase in CO2 solubility during cooling. The concept of CO2 management in which the PCO2 obtained by measurement at 37C is kept constant at 40 mmHg regardless of current body temperature is called alpha-stat. If the PCO2 value corrected for current body temperature is held constant during cooling at the same level as during normothermia (37C), the total amount of CO2 increases during hypothermia because of the constant PaCO2 and the increased proportion of CO2 that is soluble in blood. In this case CO2 elimination is not only reduced by the amount of decreased CO2 production but additionally by the increased amount of CO2 dissolved in blood during hypothermia. The latter concept of CO2 management is called pH-stat.
pH
pH varies with CO2 during variations in body temperature. If alpha-stat CO2management is applied, pH that is not corrected for current body temperature remains constant. True pH increases since true PaCO2 has decreased during hypothermia. If pH-stat CO2 management is applied, both true PaCO2 and true pH remain constant during cooling, and pH that is not corrected for current body temperature decreases. The amount of true pH change resulting from a change in body temperature may be calculated as follows: pHT=pH37 [0.0146+0.0065 (pH37 7.4)](T 37), where pHT is true pH at current body temperature, pH37 is pH at 37C, and T is current body
temperature (C).
Oxygen
The effects of temperature changes on oxygen tension (PO2) differ markedly from those on PCO2. The principal effect that hypothermia leads to increased solubility of O2
in blood is the same as for CO2. Therefore during hypothermia one could expect a lower PO2 for a given amount of oxygen. However, in contrast to CO2, the oxygen
content of room air or any inspired gas mixture and of alveolar gas is never zero. The PO2 of room air at standard atmospheric pressure (patm) of 760 mmHg is approximately
159 mmHg. If an increased amount of O2 molecules dissolve in blood during cooling, PO2 does not decrease as does PCO2 because O2 from the environment and from alveolar gas diffuse into blood, and the PO2 values equilibrate between these two compartments. The O2 content in blood thus thereby increases. This schematic
model is in fact representative of that which occurs in the alveoli and capillaries of the lungs. If we take a blood sample at hypothermia and put it into a blood gas analyzer, this sample is rewarmed to 37C under vacuumsealed conditions. The previously increased proportion of dissolved O2 then contributes to PO2, which thereby increases. Thus PO2 values that are not corrected for current body temperature are higher than during normothermia (Fig. 1) [1]. Temperature-corrected PO2 is equal to the values obtained during normothermia. The clinical relevance of these effects is clear: Whenever
we measure arterial oxygen tension (PaO2) and do not correct these values for current (hypothermic) body temperature, true PaO2 does not increase during cooling,
but the observed increase in measured PaO2 is due only to the fact that body temperature and the temperature at which the sample is analyzed differ. Considering that the
gradient between PaO2 and cellular (mitochondrial) PO2 is the driving force that maintains normal O2 extraction by the tissue, it would be a mistake to adapt inspired
oxygen fraction (FIO2) to the uncorrected, apparently high values of PaO2 obtained during hypothermia. To maintain true PaO2 in the normal range the measured
PaO2 should always be corrected for current body temperature in hypothermic patients.
Apart from the effects of increased O2 solubility there is another effect that slightly affects PaO2 during hypothermia. Since PaO2 is related to the alveolar oxygen
tension (PAO2), true PaO2 might indeed increase a very
Fig. 1 Dashed line True (temperature corrected) PCO2 during changes in body temperature. PCO2 measured at 37C remains constant at 40 mmHg. Solid line PO2 measured at 37C during changes in body temperature. True (temperature corrected) PO2 remains constant
at 85 mmHg small amount during moderate hypothermia if pulmonary gas exchange conditions and the gradient between PaO2 and PAO2 (aADO2) remain constant. PAO2 depends on FIO2, patm, water vapor pressure (pH2O), PaCO2, and the respiratory quotient (RQ=CO2 production rate/O2 consumption rate). PAO2=FIO2(patm pH2O) PaCO2RQ 1. Water vapor pressure decreases exponentially with a decrease in temperature. At 37C pH2O is approx. 47 mmHg, at 30C approx. 31 mmHg, and at 15C approx. 12 mmHg. At FIO2 of 0.21, patm of 760 mmHg,
PaCO2 of 40 mmHg, and RQ of 0.8, PAO2 is 99.7 mmHg at 37C, 103.1 mmHg at 30C, and 107.1 mmHg at 15C. Table 1 illustrates changes in blood gases during alphastat and pH-stat regimens as body temperature decreases from 37C to 30C.Table 1 An example of changes in blood gases during alphastat and pH-stat regimens as
body temperature (BT) decreases from 37C to 30C BT 37C BT 30C Alpha-stat PCO2 (mmHg) 40 After rewarming to 37C in blood gas analyzer 40 True value (corrected): 29 PO2 (mmHg) 85 After rewarming to 37C in blood gas m analyzer 117 True value (corrected) 85 pH 7.40 After rewarming to 37C in blood gas analyzer 7.40 True value (corrected) 7.50 pH-stat PCO2 (mmHg) 40 After rewarming to 37C in blood gas analyzer 40 True value (corrected) 56 PO2 (mmHg) 85 After rewarming to 37C in blood gas analyzer 117 True value (corrected): 85 pH 7.40 After rewarming to 37C in blood gas analyzer 7.30 True value (corrected) 7.40 Fig. 2 Leftward shift of the oxyhemoglobin dissociation curve caused by hypothermia. Temperature (T) is 30C for the dotted curve. The true carbon dioxide tension (PCO2) of 27 mmHg and pH of 7.5 at 30C correspond to a PCO2 of 40 mmHg and pH of 7.4 at 37C. Oxyhemoglobin saturation(SO2)=100(a1PO2+a2PO22+a3PO23+PO24)/(a4+a5PO2+a6PO22+a7PO23+PO24). The seven coefficients (a1–a7) were determined by a least-squares fitting of
the equation to paired values of PO2 and SO2 (a1= 8532.2289, a2=2121.4010, a3= 67.073989, a4=935960.87, a5= 31346.258, a6= 2396.1674, a7= 67.104406). Oxygen tension is measured at current conditions of pH, PCO2, and T. Then it must be converted into a PO2 that would be obtained at a pH of 7.40, a PCO2 of 40 mmHg, and T
of 37C. The equation to convert the actual PO2 to this virtual PO2 is: [PO2 virtual]=[PO2 actual]100.0024 (37 T)+0.40 (pH 7.40)+0.06[log10 (40) log10 (PCO2)]. Then the equation for the standard oxyhemoglobin dissociation curve is again applied to predict actual SO2
Effects of hypothermia on SO2
Arterial (SaO2), mixed venous (SvO2), and jugular bulb (SjvO2) oxyhemoglobin saturation are strongly affected by changes in body temperature. The curve of the relationship between SO2 and PO2, i.e., the oxyhemoglobin dissociation curve, is Sshaped. Hypothermia, a decrease in the intracellular concentration of 2,3diphosphoglycerate in erythrocytes, a decrease in PCO2, and an increase in pH cause a leftward shift of the oxyhemoglobin dissociation curve, which means that at a given PO2 the SO2 value is higher than under normal conditions. The corresponding
SO2 to a given PO2 may be calculated with sufficient accuracy (Fig. 2) [2]. Due to the S-shape of the oxyhemoglobin dissociation curve changes in SO2 caused by a leftward shift are more pronounced when PO2 is in the medium range. Therefore hypothermia leads to an
increase in SvO2 and SjvO2 rather than SaO2 because normal SaO2 is already close to 100%. Hypothermia inhibits oxygen release from hemoglobin in the capillaries (i.e., oxygen extraction) without providing any benefits with regard to increasing SaO2. In other words, a much lower tissue PO2 would be required to obtain the same degree of oxyhemoglobin desaturation in the capillary. The total amount of O2 flow from the capillary to the cells and mitochondria would then decrease because the driving force of O2 diffusion, i.e., the gradient between mitochondrial PO2 and capillary or tissue PO2 is reduced. Oxygen consumption (VO2) decreases during hypothermia. The relationship between cerebral VO2 and temperature has been well investigated [3, 4]. This isdetermined by the factor Q10: Q10=cerebral VO2 at Tx/ cerebral VO2 at Ty,whereTx Ty=10C. Q10 is not constant over the entire temperature range that is clinically possible [3, 4]. In dogs Q10 is approx. 2.2 when T=37 27C, approx. 4.5 when T=27 14C, and approx. 2.2 when T=13 7C [3, 4]. Cerebral VO2 at a given
temperature may be calculated as follows: VO2 at Ty= VO2 at TxQ10(Ty Tx)/10 Because hypothermia leads to a leftward shift of the oxyhemoglobin dissociation curve and to a decrease in VO2, SvO2 should significantly increase during cooling,
particularly if O2 delivery remains unchanged. This has in fact been found in hypothermic (32C) patients under endogenous circulation, i.e., without the use of extracorporeal In conclusion, variations in body temperature significantly affect the results of important and frequently used monitoring techniques in intensive care, anesthesia, and emergency medicine. The knowledge of physical and technical changes during hypothermia or hyperthermia is necessary to avoid pitfalls in monitoring of blood gases, SO2, and etCO2. Ignoring these effects may lead to harmful and incorrect conclusions derived from our measurements in the clinical setting as well as for scientific purposes
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