I. H. Gøthgen

Measured and derived quantities with modern pH and blood gas equipment: Calculation algorithms with 54 equations

Modern pH and blood gas equipment, combining electrochemical and optical methods, measures pH, Pco2, po2, hemoglobin concentration, oxygen saturation, carboxy-hemoglobin, and methemoglobin. Measurements in arterial and mixed venous blood and in expired air (including measurement of expiratory ventilation) allow calculation of a series of derived quantities: concentrations of bicarbonate, total carbon dioxide, base excess, standard bicarbonate, total oxygen, 2,3-diphosphoglycerate; p50, arteriovenous CO2 and O2 differences, pulmonary shunting, ventilation-perfusion ratio, dead space ventilation, CO2 production, O2 consumption, respiratory quotient, energy metabolism, and cardiac output. Accurate measurement of carboxyhemoglobin even gives an opportunity of measuring blood volume.Equations are reviewed for these calculations including the Henderson-Hasselbalch equation for plasma and whole blood, the Van Slyke equation, the ODC-equation (hyperbolic tangent function), alveolar air equation, Bohr equation, an...

Classes of tissue hypoxia

We identify eight causes of tissue hypoxia, falling into three classes, A, B, and C, depending upon the effect on the critical mixed venous pO2 and the optimal oxygen consumption rate. The critical mixed venous pO2 is the value above which the oxygen consumption rate is optimal and independent of the mixed venous pO2 and below which the oxygen consumption rate decreases towards zero. Class A hypoxia: primary decrease in mixed venous pO2. Causes: 1) ischaemic hypoxia (decrease in cardiac output), 2) low‐extractivity hypoxia (decrease in oxygen extraction tension, p8). Class B hypoxia: primary increase in critical mixed venous pO2. Causes: 1) shunt hypoxia (increased a‐v shunting), 2) dysperfusion hypoxia (increased diffusion length from erythrocytes to mitochondria and/or decreased total capillary endothelial diffusion area, e. g., tissue oedema, microembolism), 3) histotoxic hypoxia (inhibition of the cytochrome chain). Class C hypoxia: primary increase in optimal oxygen consumption rate. Causes: 1) uncoupling hypoxia (uncoupling of the ATP formation associated with O2 reduction), 2) hypermetabolic hypoxia (increased energy metabolism, e. g., due to hyperthermia).

Evaluation of the Gas-STAT® fluorescence sensors for continuous measurement of pH, pCO2 and pO2 during cardiopulmonary bypass and hypothermia

Continuous measurement of pH, pCO2 and pO2 during extracorporeal circulation has become feasible using disposable fluorescence sensors (optodes). We have evaluated a commercial system: Gas-STAT (American Bentley) by reference to in-vitro measurements on discrete samples using conventional electrochemical sensors (BMS-3, Radiometer). The Gas-STAT measures at the actual temperature of the blood in the extracorporeal circuit. The reference measurements were performed at two fixed temperatures of 25 and 37 °C with interpolation of the values to the actual temperature of the Gas-STAT.10 patients undergoing coronary artery bypass grafting during hypothermic extracorporeal circulation with hemodilution were monitored in the venous as well as the arterial line with the Gas-STAT with 6–9 samplings of arterial and venous blood from each patient, a total of 136 samples.The comparisons revealed a large scatter which was due partly to inter-optode partly to intra-optode variation and partly to a memory effect which re...

Variability of the temperature coefficients for pH, pCO2, and pO2 in blood

Blood pH, pCO2 and pO2 were measured at 37 °C and 25 °C and the temperature coefficients were calculated as δpH/δT; δlg pCO2/δT, and δln pO2/δT. A total of 204 blood specimens were obtained from 10 patients undergoing coronary artery bypass grafting with extracorporeal circulation including hypothermia and hemodilution. Multivariate regression analysis gave the following equations:The constants in the parentheses are the mean values of the variables. There is a significant negative correlation between the two temperature coefficients. Unfortunately pH(37) and pCO2(37) were so closely correlated that it is impossible to separate the individual effects of the two, and the same applies to cHb and the plasma protein concentration. Therefore it may be fortuitous that the pH-temperature coefficient appears to vary with pCO2 (not pH) while the pCO2-temperature coefficient appears to vary more with pH than with pCO2.The pO2-temperature coefficient was found to vary with pO2 and cHb as previously predicted. At a v...

Fiber-optic chemical sensors (Gas-Stat®) for blood gas monitoring during hypothermic extracorporeal circulation

Measurements of pO2, pCO2 and pH by optical fluorescence microsensing technology has recently become available for monitoring blood gases during extracorporeal circulation ECC). We have compared simultaneous measurements with fiber-optic sensors (Gas-Stat, Bentley) and electrochemical sensors (ABL-4, Radiometer) on discrete samples. In 10 patients undergoing coronary artery bypass grafting during hypothermic (25 degrees C) ECC and hemodilution (hemoglobin concentration 4 mmol.l-1) arterial and venous pO2, pCO2 and pH were measured in-line in the extracorporeal circuit at the actual blood temperature. Simultaneous and anaerobically collected blood samples in glass syringes were analyzed within five minutes at 37 degrees C in the ABL-4. Linear regression analysis of the values at actual temperature shows the following equations: Gas-Stat = Y, ABL-4 = X: pO2 (kPa): Y = 1.04 X + 0.5 r = 0.95 n = 136; pCO2 (kPa): Y = 0.71 X + 1.5 r = 0.79 n = 136; pH: Y = 0.788 X + 1.590 r = 0.76 n = 136. The advantage of the Gas-Stat is continuous monitoring of blood gas parameters during ECC. The present study shows that measurements of pO2, pCO2 and pH with fiber-optic chemical sensors may be reliable. The differences between the two principles of measurement may be due to unknown factors interfering with the in-line measurements or to variations in sensitivity and stability of the individual sensor.

Transcutaneous Oxygen Measurement During Thoracic Anaesthesia

The value of transcutaneous oxygen tension (tcPO2) as an oxygen parameter during uncomplicated thoracic anaesthesia was examined in ten patients anaesthetized with oxygen‐nitrous oxide and enflurane or flunitrazepam/fentanyl. tcPO2 was measured with the Radiometer TCM‐1® monitor at 45d̀C. Measuring interference due to the anaesthetic agents was not observed. tcPO2 was found to be lower than the arterial oxygen tension (PaO2) at any inspiratory oxygen fraction (FIO2). When the peroperative readings were related to the preoperative values, no statistically significant difference was found between PaO2 and tcPO2 at FIO2 = 0.5, 0.4 and 0.3 (P > 0.3). Linear regression between PaO2 and tcPO2 shows disparity in pre‐ and peroperative regression. tcPO2 (preoperative) = ‐2.2+ 1.03 X PaO2 (r = 0.89), tcPO2 (peroperative) = +3.1 +0.56 X PaO2 (r = 0.87). This disparity indicates a decrease in the tcPO2/PaO2 ratio with increasing PaO2. It is concluded that tcPO2 cannot substitute for PaO2, but tcPO2 and PaO2 proved to be equally useful as oxygen parameters in the examined patients. Interpretation of tcPO2 during anaesthesia, however, necessitates a preoperative measurement as reference.

Positive correlation between ‘the arterial oxygen extraction tension’ and mixed venous pO2 but lack of correlation between ‘the oxygen compensation factor’ and cardiac output in 38 patients

pH and blood gases were measured in simultaneous samples of arterial blood from the radial artery and mixed venous blood from the pulmonary artery using an ABL300 and OSM3 (Radiometer A/S, Denmark). Cardiac output was measured by thermodilution. The patients were suffering from chronic obstructive pulmonary disease or adult respiratory distress syndrome. The data indicate that patients respond to a decreased arterial oxygen availability by allowing the mixed venous pO2 to fall rather than by increasing the cardiac output to maintain a normal mixed venous pO2. In other words, the arterial oxygen extraction tension and the oxygen compensation factor were both highly correlated to the mixed venous pO2 but unrelated to the cardiac index. For this reason the arterial oxygen extraction tension appears to be a more relevant parameter of the overall arterial oxygen availability than the oxygen compensation factor. Comparison of the arterial and mixed venous data confirms the accuracy of the Oxygen Status Algorithm for calculating the various oxygen parameters, including the p50, the estimated 2,3-diphosphoglycerate concentration, and the estimated physiological shunt, on the basis of a single arterial blood sample.

Variations in the hemoglobin-oxygen dissociation curve in 10079 arterial blood samples

A multicenter study including 10079 arterial blood gas measurements were used to describe the clinical variation in the hemoglobin-oxygen dissociation curve i.e. the relationship between measured values of oxygen tension (pO2) versus oxygen saturation (sO2) and the concentration of total oxygen (ctO2). Very large variations in the actual in vivo hemoglobin-oxygen dissociation curve were found. At pO2 = 8 +/- 0.5 kPa the sO2 range was 69.7% to 99.4%, and at sO2 = 90 +/- 2% the pO2 extremes were 3.82 and 18.3 kPa. The actual p50 varied from 2.15 to 6.44 kPa. Arterial pO2 versus oxygen content i.e. at pO2 = 8 +/- 0.5 kPa the total oxygen concentration ranged from 2.04 to 10.76 mmol/L. The results indicate that it is essential to know the actual position of the hemoglobin-oxygen dissociation curve, as well as the hemoglobin concentration in the individual patient, for correct interpretation of pO2 or sO2 in arterial blood.

What is the lower limits of arterial pO2

I N this issue of the journal, Pytte et al. (1) report a case with successful outcome in spite of extreme acidosis and marked hypoxaemia (pH 1⁄4 6.66, pCO2 1⁄4 21.3 kPa, pO2 1⁄4 7.0 and sO2 1⁄4 0.45), and argue that the case illustrates the detrimental effects of grave acidosis on arterial blood oxygen content at subnormal pO2 values. Several other case reports has shown successful outcome despite extreme acidosis and hypoxaemia: Adnet et al. (2) report a similar case (pH1⁄4 6.73, pCO2 1⁄4 27.7 kPa, pO2 1⁄4 9.2 and sO2 1⁄4 0.72). Potkin and Swensson (3) reported a case with most extreme respiratory acidosis and hypoxaemia (pH 1⁄4 6.60, pCO2 1⁄4 50 kPa and pO2 1⁄4 5.3 kPa). Lund et al. (4) reported a case with severe hypoxaemia (pO2 1⁄4 3.9 kPa) without sign of tissue hypoxia. At the macro level, the circulation and oxyhaemoglobin dissociation may take part in the compensation. The oxygen dissociation curve (ODC) may be displaced to the right or to the left. The saturation sO2 is primarily an indirect measure of pO2 and is redundant information (5) instead the oxygen status algorithm by Siggaard-Andersen et al. (6) may be the method to evaluate the influence of pH on the ODC. The oxygen status algorithm calculates the actual oxygen extractivity of the blood, and expressed in one figure, named the oxygen extraction tension px. The oxygen status algorithm clearly demonstrated that right shift of ODC may increase oxygen extraction if pO2 is higher than the normal p50 and vice versa if pO2 is below the normal p50 a left shift may increase the oxygen extractivity. The circulation may compensate by increased cardiac output and capillary recruitment as well as marked changes in blood flow. This change has been named ‘Themaster switch of life’ by Scholander (7). In his article ‘The Master Switch of Life’ he describes studies, at the University of Oslo during the 1930s, of diving animals leading to the identification of the vertebrate animal’s ultimate defence against asphyxia: a gross redistribution of the circulation that concentrates oxygen in the brain and heart. This redistribution of the circulation was found in other critical situations, and Scholander suggests that selective ischaemia is an important asphyxial defence even in babies before, during and immediately after birth (7). At the micro level the oxygen diffusion and other mechanism may compensate. Hypoxaemia is pO2 below the normal range in arterial blood, but the critical arterial pO2 or critical oxygen delivery still has to be defined. Oxygen reduction in the mitochondria is normally a zero order reaction which depends on energy requirements rather than the amount of available oxygen (8). The cells are only able to extract enough oxygen if the end capillary pO2 remains above a critical value which ensures a sufficient diffusion gradient. The mixed venous oxygen tension is closely related to the average end capillary oxygen tension which determines the diffusion gradient for oxygen from erythrocytes to mitochondria. It is therefore more relevant to postulate the existence of a critical mixed venous oxygen tension than a critical oxygen delivery. Therapy should be directed towards maintaining the mixed venous pO2 above a critical value, usually about 3.5 kPa (5). Connett et al. (9) defining hypoxia as oxygen-limited energy flux with three dimensions of control: (i) the phophorylation state, (ii) the redox state and (iii) pO2. This may explain why hypoxaemic arterial pO2 may be tolerated as a result of the concept of adapted cell hypoxia, where intracellular pO2 is less than normal, perhaps as low as 0.1 kPa, but sufficient to maintain oxygen and adenosine triphosphate (ATP) flux because of adaptive change in the redox and phoshorylation drives on electron transport (9).