EUROANESTHESIA 2005 Vienna, Austria 28-31 May 2005 MONITORING GAS EXCHANGE: FROM THEORY TO CLINICAL APPLICATION 5RC2 OLA STENQVIST Department of Anaesthesia and Intensive Care Sahlgrenska University Hospital Göteborg, Sweden Saturday May 28, 2005 14:00-14:45 Room K INTRODUCTION A three compartment model of the lung [1]; where one compartment is the ideal compartment with matched perfusion and ventilation, one compartment is a compartment with perfusion but no ventilation and one compartment is a compartment with ventilation but no perfusion, gives a very thorough picture of the performance of the lung. The perfusion/no-ventilation compartment reveals the oxygen exchange performance and the ventilation/no-perfusion compartment reveals the carbon dioxide exchange performance. The ratio between the three compartments gives a superior overview of the severity of the lung injury (Figure 1).To obtain this information we need to monitor oxygen consumption and carbon dioxide output. FIGURE 1. THE THREE COMPARTMENT LUNG MODEL Figure 1. Three compartment lung model, where half the ventilation reaches the ideal alveoli and half the alveolar dead space (ADS) which has no circulation. Half the CO passes through the non ventilated lung = shunt flow, which will have venous SaO 2 also after passage through the lung. The other half of the CO passes through ventilated lung and will be fully saturated. Arterial blood will have a SaO 2 of (100+48)/2 = 76 due to venous admixture. The alveolar dead space is diagnosed by the difference in arterial PCO 2 (kpa) and the end tidal CO 2 (%). The end tidal CO 2 will be (6+0)/2 = 3 % and the arterial PCO 2 is 6 kpa indicating that half of the ventilation is not in contact with circulation METABOLIC GAS EXCHANGE During normal resting conditions 250 ml/ min oxygen is consumed and 200 ml/min carbon dioxide is produced. The ratio of carbon dioxide production/oxygen consumption, the respiratory quotient (RQ), varies depending upon the energy substrate utilised. Thus, when fat is utilised RQ is 0.7 and when carbohydrates are used RQ is 1.0, but usually RQ is around 0.8 indicating that a mixture of substrates are used. Oxygen consumption increases by 7-10% per degree above 37 o C and is increased during sepsis, and by treatment with betaagonists. Sedation and beta-blockers decrease oxygen consumption. The carbon dioxide output changes in a similar way but the changes take longer than the changes in oxygen consumption due to the difference in the body s stores. The total oxygen store, which is mainly in very rapidly exchanged compartments, the lungs and the hemoglobin, is approximately 1 litre. The carbon dioxide stores are over 100 litres with only a small part as a rapid turn over store in the blood, with the majority in very slow turn over compartments like bone and fat. 71
The oxygen consumption (VO 2 ) and carbon dioxide production (VCO 2 ) can be measured by indirect calorimetry, where the VO 2 = F I O 2 x VI FEO 2 x VE and the VCO 2 = FECO 2 x VE (F I O 2 = inspiratory oxygen fraction, FEO 2 = mixed expiraty oxygen fraction, VI = inspiratory minute ventilation, VE = expiratory minute ventilation, FECO 2 = mixed expiratory carbon dioxide fraction) There is a small difference in inspiratory and expiratory minute ventilation which is as a result of the difference in oxygen consumption and carbon dioxide production. This difference cannot be measured adequately but the VI can be calculated from the VE (or vice versa), assuming no net exchange of nitrogen by Haldane transformation. This is taken care of automatically in devices for indirect calorimetry, but in a department where there is no access to such a device a good estimation of the metabolic gas exchange can be obtained by measurement of only the carbon dioxide production. This can be easily done by connecting a mixing box to the outlet of the ventilator. This mixing box can be made from an empty cardboard box of 5-6 litres volume and must not be tight to allow the expiratory gases to leak freely out into the atmosphere. The sample port of a capnometer is fitted with a three-way stop cock, so that gas either can be sampled, as usual, from the y-piece for breath by breath capnometry or switched to sample from the mixing box for mixed expiratory carbon dioxide concentration. Modern capnometers are digital and have software for detecting end-tidal and inspiratory gas concentrations. When gas is sampled from the mixing box the gas concentration is almost constant and it takes up to 30 seconds before the software can identify and display the stable mixed expiratory concentration of carbon dioxide. The VCO 2 is calculated by multiplying the expiratory carbon dioxide concentration with the minute ventilation displayed on the ventilator. For example if the mixed expiratory carbon dioxide concentration is 2.2 % and the minute ventilation 11 litres/minute, the VCO 2 will be 2.2 x 11/100 =0.242 l/min. If we assume that the RQ is 0.8 the oxygen consumption will be 0.242/0.8 = 0.303 l/min. From this we can also calculate energy expenditure (EE) as we know that 1 litre of oxygen consumption equals 4.75 kcal at a RQ of 0.8. In this case the EE for a 24 hour period is 0.303 x 60 x 24 x 4.75 = 2513 kcal/24h. OXYGEN AND CARBON DIOXIDE CONTENT OF BLOOD The oxygen content of blood is a combination of the oxygen carried by hemoglobin (Hb), 1.34 ml/g Hb when fully saturated, plus the oxygen physically dissolved in plasma, 0.03 ml/mmhg (0.23 ml/kpa). With a normal hemoglobin level of 150 g/l the oxygen content of blood is 200 ml/l (Hb x 1.34 x SaO 2 + PaO 2 x 0.03, Hb g/l, SaO 2 %/100, PaO 2 mmhg). If cardiac output is 5 L/min then the oxygen delivery is 1000 ml/min. As the oxygen consumption is normally 250 ml/min the returning mixed venous blood will have a content of 150 ml/l and be saturated to a level of 75%. The total oxygen delivery is dependent on the hemoglobin level and in a typical intensive care patient this is around 100 and with 5 l/min of cardiac output the oxygen delivery will be only 667 ml/min, and with the same oxygen consumption the resulting mixed venous oxygen saturation will be as low as 63%. Whilst breathing air the arterial oxygen tension is ~ 100 mmhg and the mixed venous tension, PvO2 ~40 mmhg and the oxygen content difference 50 ml/l, resulting in a arterial-mixed venous content of ~1 ml/mmhg (Figure 2). 72
FIGURE 2. THE OXYGEN DISSOCIATION CURVE Figure 2. The oxygen dissociation curve Note the great arterio-mixed venous oxygen partial pressure difference, ~ 60 mmhg (9 kpa) as compared with carbon dioxide (Figure 3). The carbon dioxide content of blood is around 500 ml/l arterial blood and 520 ml/l mixed venous blood at the same partial pressure. However, the content is linearly decreasing with decreasing PCO 2 and the arterial content during normal conditions is 480 ml/l. The arterio-venous content difference is 40 ml CO 2 /L but the mixed venous-arterial tension difference is only 6 mmhg, resulting in an arterial mixed venous carbon dioxide content difference of ~7 ml/mmhg (Figure 3). FIGURE 3. THE CARBON DIOXIDE DISSOCIATION CURVES Figure 3. The carbon dioxide dissociation curves. Note that the partial pressure difference between mixed venous and arterial blood is very small, < 7.5 mmhg (1 kpa). 73
ALVEOLAR AND DEAD SPACE VENTILATION The alveolar ventilation (VA) can be calculated from the carbon dioxide production and the end tidal concentration, VA = VCO 2 /FETCO 2 The relationship between dead space ventilation and total ventilation is calculated using (PaCO 2 PECO 2 )/PaCO 2 and is normally around 0.3 but is increased in acute lung injury (ALI) and adult respiratory distress syndrome (ARDS). In the same way as the oxygen exchange function of the lung cannot be judged without knowledge of underlying factors such as hemoglobin, cardiac output and metabolism, the carbon dioxide exchange function of the lung, the dead-space cannot be judged from PaCO 2 alone but also requires knowledge of end-tidal carbon dioxide and carbon dioxide excretion. The dead space fraction has two components, the anatomical and the alveolar dead-space. The alveolar dead-space, alveoli without perfusion, increases when pulmonary capillary perfusion is insufficient and can also increase regionally, usually in the ventral part of the lung when ventilation pressures and end-expiratory pressure are increased. For the determination of the alveolar dead-space not only PaCO 2 and PECO 2 must be known but also end-tidal/alveolar PETCO 2, which is obtained my conventional capnography. The alveolar dead-space fraction is the difference between the total dead-space fraction (PaCO 2 -PECO 2 )PaCO 2 and the anatomical dead-space fraction (PETCO 2 -PECO 2 )/PETCO 2 (Figure 4). FIGURE 4. THE EFFECT UPON CARBON DIOXIDE OF THE VARIABLE DISTRIBUTION OF ALVEOLAR VENTIALTION SHUNT Figure 4. The effect on carbon dioxide from an alveolar dead space, ADS, receiving 50% of the alveolar ventilation (left graph). The PaCO 2 is ~ double the PACO 2. Increasing pulmonary circulation (right graph) by volume or/and inotropes results in more of the lung being circulated and the ADS decreases, in this example to 25% of the alveolar ventilation. PaCO 2 falls with 25% but the end-tidal CO 2 concentration remains unchanged. The ventilation/perfusion ratio is a function of hemoglobin level, cardiac output and metabolism in this context oxygen consumption and carbon dioxide excretion. Thus, a patient with a PaO 2 /F I O 2 ratio of 199, which correlates with ARDS by the NAECC definition, has a shunt of 0.28 if he has a hemoglobin of 150 g/l, an oxygen consumption of 300 ml/min and a cardiac output of 6 L/min and a F I O 2 of 1.0. In another patient with the same PaO 2 /F I O 2 ratio the shunt is only 0.15 because the Hb was 100 g/l, the oxygen consumption 240 ml/min and the cardiac output 4 L/min and a F I O 2 of 0.5. Thus, despite these patients having the same PaO 2 /F I O 2 ratio, which classifies them both as having ARDS, their level of pulmonary dysfunction is totally different. Both of the patients have respiratory failure, but the severity of their pulmonary conditions is totally misjudged by the P/F ratio, and shunt is a much better measure of the severity of ventilation/perfusion mismatching. 74
FIGURE 5. THE EFFECT OF INCREASING F I O 2 FROM 0.5 TO 1.0 ON A CASE WITH 50% SHUNT FLOW Figure 5. The effect of increasing FIO 2 from o.5 to 1.0 on a case with 50% shunt flow. The small increase in arterial oxygen saturation is a result of an increase in physically dissolved oxygen in the blood passing the ventilated lung compartment. Shunt is calculated by the standard shunt formula (CcapO2 CaO2)/(CcapO2 CvO2) where CcapO2 is the content of oxygen in lung capillary blood and CaO2 is the arterial oxygen content and CvO 2 is the oxygen content of mixed venous blood. The CcapO 2 can be accurately calculated assuming fully saturated hemoglobin plus oxygen dissolved in plasma as PAO 2 (kpa) times 0.23 ml (PAO 2 (mmhg) times 0.03 ml. (kpa = mmhg/7.5). The PAO 2 (kpa) can for clinical purposes be regarded as equivalent to end-tidal oxygen concentration (%). The PAO 2 can be calculated as the inspired oxygen concentration (%) minus the endtidal carbon dioxide concentration (%). In the absence of a pulmonary artery catheter the central venous oxygen content can be used as a reasonable surrogate for SvO 2 [2,3] but the shunt can also be estimated using a default value for the arterial mixed-venous oxygen content difference. A value of 50ml has been proposed and shown to give good correlation between true shunt and estimated shunt [4,5], but in patients with a hyperdynamic circulation a value of 40ml may be more adequate (Figure 5,6,7,8,9 and 10). FIGURE 6. THE EFFECT OF INCREASING CARDIAC OUTPUT ON IN A PATIENT WITH 50% SHUNT FLOW Figure 6. The effect of increasing cardiac output on in a patient with 50% shunt flow. Arterial oxygen saturation increases substantially from 74 to 86% as the increase in cardiac output results in a lower a-v oxygen content difference, which results in an increase in mixed venous oxygen saturation from 48 to 72 %. 75
FIGURE 7. THE EFFECT OF AN INCREASE IN HEMOGLOBIN CONCENTRATION IN A PATIENT WITH 50% SHUNT FLOW Figure 7. The effect of an increase in hemoglobin concentration in a patient with 50% shunt flow. The increase in arterial oxygen saturation is a result of the decrease in a-v oxygen content difference following the increase in hemoglobin. FIGURE 8. THE EFFECT OF NITRIC OXIDE INHALATION IN A PATIENT WITH 50% SHUNT FLOW Figure 8. The effect of nitric oxide inhalation in a patient with 50% shunt flow. The marked increase in arterial oxygen saturation is a result of a selective dilatation of the pulmonary vasculature in the ventilated part of the lung, which will divert blood from the shunt to ventilated lung. 76
FIGURE 9. THE EFFECT OF A DECREASE IN METABOLISM/OXYGEN CONSUMPTION IN A PATIENT WITH 50 % SHUNT FLOW Figure 9. The effect of a decrease in metabolism/oxygen consumption in a patient with 50 % shunt flow. The marked increase in arterial oxygen saturation is a result of the decrease in a-v oxygen content difference when the oxygen uptake decreases. FIGURE 10. THE EFFECT OF A RECRUIT MANOEUVRE AND INCREASED PEEP AFTERWARDS IN A PATIENT WITH 50 % SHUNT FLOW Figure 10. The effect of a recruit manoeuvre and increased PEEP afterwards in a patient with 50 % shunt flow. The recruitment manoeuvre opens up collapsed lung and the non-ventilated lung compartment with shunt flow decreases. Arterial oxygen saturation increases markedly. 77
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