1Royal Liverpool Childrens Hospital, Eaton Road, Liverpool L12 2AP, UK. 2St Lukes University Hospital, Gwardamangia, Malta. 3University of Liverpool, Liverpool, UK. 4Manchester Royal Infirmary, Manchester, UK 5Present address: Royal Hallamshire Hospital, Sheffield, UK*Corresponding author
Presented at the meeting of the Anaesthetic Research Society, Liverpool, March 2000.
Accepted for publication: October 17, 2000
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Abstract |
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Br J Anaesth 2001; 86: 34953
Keywords: carbon dioxide, elimination; heart, congenital defects; blood, haemoglobin
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Introduction |
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The theoretical relationship between the PaCO2PE'CO2 difference and the arterial saturation in patients with right-to-left shunting has been described by Fletcher.3 As saturation falls, the PaCO2PE'CO2 difference increases proportionately. The increase in the PaCO2PE'CO2 difference with decreasing saturation is greatest when the haemoglobin concentration is high. This relationship was confirmed in children with pulse oximeter saturations of 60100%.3
Thus, in the absence of pulmonary hypoperfusion, PaCO2 can be predicted accurately in cyanotic children with otherwise normal lung function from knowledge of the PE'CO2, haemoglobin concentration and saturation.4 However, should significant pulmonary hypoperfusion exist, then the PaCO2PE'CO2 difference will always be greater than its estimate from first principles. The difference increases as saturation decreases, unless there is a compensatory increase in cardiac output, as may occur in severely hypoxaemic children.4
We investigated whether the effect of pulmonary hypoperfusion could be detected by comparing observed and predicted values for PaCO2PE'CO2 in children with congenital heart disease.
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Theory |
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(PaCO2PE'CO2)=RxHbx0.0131x(100SaO2)/k
where R is the respiratory quotient, Hb is the haemoglobin concentration in grams per litre, 1.31 is the combining constant of haemoglobin in millilitres of oxygen per gram of haemoglobin, and k is the slope of the carbon dioxide dissociation curve for whole blood. It can be seen that PaCO2PE'CO2 will increase as saturation decreases and haemoglobin increases, reflecting the primary effect of the right-to-left shunt. This predicted difference takes no account of the effect of pulmonary hypoperfusion.
Calculation of predicted (obligatory) PaCO2PE'CO2 difference in patients with intracardiac shunting
A. Calculate total arterial carbon dioxide content
(i) Using measured PaCO2, determine bicarbonate carbon dioxide (ml litre1) from Fig. 1.
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B. Calculate pulmonary end-capillary carbamino content
Assume 100% saturation and standard carbamino content at haemoglobin concentration=15 g dl1 of 22 ml litre1 carbon dioxide. Correct for measured haemoglobin concentration.
C. Calculate arterial minus end-capillary oxygen difference
(i) End-capillary oxygen content=Hbx1.31+[((FIO2x (PBPH2O))(PE'CO2/R))x0.225] [using Hb in g litre1, PE'CO2 to estimate alveolar PCO2 (kPa) and assuming standard values for barometric pressure (PB), PH2O and R (0.8)].
(ii) Arterial oxygen content=(Hbx1.31xSaO2/100)+(PaO2x0.225) (using Hb in g litre1, PaO2 in kPa).
(iii) Subtract (i) from (ii) above for arterial minus end-capillary oxygen difference (ml litre1).
D. Calculate arterialend-capillary carbon dioxide difference
Multiply C (iii) above by R (assume standard value 0.8 for respiratory quotient).
E. Calculate pulmonary end-capillary bicarbonate carriage
End-capillary bicarbonate=total arterial carbon dioxide content [A (iii)] carbon dioxide difference (D) end-capillary carbamino content (B) (ml litre1).
F. Determine end-capillary PCO2
Using the derived bicarbonate value from E above, determine the end-capillary PCO2 from Fig. 1. This approximates to the predicted end-tidal PCO2 value and can be subtracted from the measured PaCO2 to determine the predicted PaCO2PE'CO2.
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Methods |
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Anaesthesia was induced with thiopentone 4 mg kg1 and neuromuscular block obtained with vecuronium 0.1 mg kg1 followed by 0.2 mg kg1 h1. Anaesthesia was maintained with 0.51% isoflurane in oxygen and/or air, supplemented with i.v. alfentanil 10 µg kg1, followed by an infusion at 2 µg kg1 min1. All patients were ventilated in a standardized fashion, using a Servo 900C ventilator (Siemens, Bracknell, UK), set to deliver 10 ml kg1 in volume control mode at a rate of 1525 bpm. The inspiratory time totalled 40% of the respiratory cycle, including a 10% end-inspiratory pause. An end-expiratory pressure of approximately 2 cm H2O was applied routinely. Intrinsic positive end-expiratory pressure was not measured. During chest opening by thoracotomy or sternotomy, we made simultaneous recordings of oesophageal temperature, haemoglobin concentration and oxygen saturation, oxygen and carbon dioxide tensions in arterial blood, and inspired oxygen and expired carbon dioxide concentrations.
Blood gas and co-oximetry analysis was carried out using a Chiron Diagnostics 865 blood gas machine (Bayer, Newbury, UK). The anaesthetic gases were measured with a Capnomac Ultima gas monitor (Datex Engstrom, Sidcup, UK), which was calibrated against the blood gas machine each morning using a standard gas calibration mixture. The procedure involved initial analysis of the calibration gas by the blood gas machine, and noting the PCO2 measured by the machine. The capnograph was then calibrated using the calibration gas in the usual way, but entering the PCO2 concentration as measured by the blood gas machine rather than that printed on the gas canister.
For endotracheal tube sizes 3.04.5 mm, gas was sampled for inspired oxygen concentration and end-tidal carbon dioxide concentration using a special connector that allowed gas collection from the proximal endotracheal tube. This allowed greater accuracy of measurement in small subjects.2 In older children with larger endotracheal tube sizes, normal sidestream gas sampling was used. All blood gas samples were temperature-corrected at analysis.
The data collected were then used to calculate predicted values for PaCO2PE'CO2 as described previously. Carbon dioxide dissociation curves (Figs 1 and 2) were reproduced from Nunns Applied Respiratory Physiology5 6 and were enlarged and annotated with grid-lines to aid accuracy. The observed values recorded for arterial and end-tidal carbon dioxide tensions were compared with the predicted values by the use of paired t-tests and regression analysis.
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Results |
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The predicted PaCO2PE'CO2 value was calculated for each patient as described above. It was found that five patients within the first 10 had physiologically inconsistent data. One had a very negative PaCO2PE'CO2 and four had a normal PaCO2PE'CO2 with oxygen saturation less than 85%, a situation incompatible with the shunt equation. It was decided to remove these patients from the study, but, in order to reduce bias, data obtained from all of the first 10 patients were eliminated from further analysis.
The observed and predicted values for PaCO2PE'CO2 for the remaining 50 patients were plotted against arterial saturation (measured by the co-oximeter), as shown in Fig. 3. The mean observed PaCO2PE'CO2 difference was 1.07 (SD 0.58) kPa and the mean predicted value was 0.42 (0.29) kPa (P<0.0001). The figure shows that many of the observed values for PaCO2PE'CO2 were considerably greater than predicted. Furthermore, the observed PaCO2PE'CO2 exceeded zero in many of the well-oxygenated patients. In fact, the regression line indicated a difference of 0.7 kPa at 100% saturation. The expected negative correlation between PaCO2PE'CO2 and oxygen saturation was apparent for the predicted data; the correlation was less strong for the observed data.
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Discussion |
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To find a further explanation for the much increased alveolar deadspace in some apparently well-oxygenated children with congenital heart disease, oxygen saturation while breathing spontaneously in air was plotted against oxygen saturation obtained during controlled ventilation with an increased inspired oxygen concentration (Fig. 4). Most of the children showed an improvement in saturation, implying a degree of ventilationperfusion mismatch, other than a pure right-to-left shunt effect. In the well-oxygenated patients with significant left-to-right shunting, e.g. those with large ventricular septal defects, pulmonary congestion may have been responsible for the increased alveolar deadspace. Patients whose clinical history was suggestive of moderate to severe pulmonary congestion, typically those with a significant left-to-right shunt, are plotted separately in Fig. 3 to show their influence on the results of the group. Increased pulmonary blood flow causes loss of homeostasis at the alveolar/capillary level and a ventilation/perfusion mismatch.7 Increased slopes of phase III of the Single Breath Test for carbon dioxide, a sign of increased spread of ventilation/perfusion ratios, can be seen even in children with such relatively mild lesions as atrial septal defect.7 Very steep phase III slopes have been observed in children with congestive failure.7
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In the light of our findings, we suggest that the relationship between pulmonary congestion and PaCO2 PE'CO2 could be further investigated by performing a similar study on acyanotic children with congenital heart disease, who have been prospectively classified into normal and plethoric groups, by blinded reporting of chest radiographs, elements of the clinical history and the saturation response to increased FIO2.
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References |
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2 Rich GF, Sconzo JM. Continuous end-tidal CO2 sampling within the proximal endotracheal tube estimates arterial CO2 tension in infants. Can J Anaesth 1991; 38: 2013[Abstract]
3 Fletcher R. The relationship between the arterial to end-tidal PCO2 difference and haemoglobin saturation in patients with congenital heart disease. Anesthesiology 1991; 75: 2106[ISI][Medline]
4 Fletcher R. Gas exchange during anaesthesia and controlled ventilation in children with congenital heart disease. Paediatr Anaesth 1993; 3: 517
5 Nunn JF. Nunns Applied Respiratory Physiology, edn 4. Oxford: Butterworth-Heinemann, 1993; 225
6 Nunn JF. Nunns Applied Respiratory Physiology, edn 4. Oxford: Butterworth-Heinemann, 1993; 224
7 Fletcher R, Niklason L, Drefeldt B. Gas exchange during controlled ventilation in children with normal and abnormal pulmonary circulation: a study using the single breath test for carbon dioxide. Anesth Analg 1986; 65: 64552[Abstract]