Arterial oxygenation and one-lung anesthesia Andrew Ian Levin, Johan Francois Coetzee and Andre Coetzee Department of Anesthesiology and Critical Care, University of Stellenbosch and Tygerberg Academic Hospital, South Africa Correspondence to Andrew Levin, Department of Anesthesiology and Critical Care, Faculty of Health Sciences, Stellenbosch University, PO Box 19063, Tygerberg, 7505, South Africa Tel: +27 21 9389230; fax: +27 21 9389144; e-mail:
[email protected]
Current Opinion in Anaesthesiology 2008, 21:28–36
Purpose of review In the presence of the obligatory shunt during one-lung ventilation, arterial oxygenation is determined by the magnitude of the shunt in addition to the oxygen content of the mixed venous blood coursing through that shunt. The present discussion aims to heighten awareness of factors determining arterial oxygenation during one-lung anesthesia, other than the magnitude of the shunt and dependent lung low-ventilation perfusion units. Recent findings A convenient way to increase mixed venous and thereby arterial oxygenation is to raise cardiac output. While this approach has achieved some success when increasing cardiac output from low levels, other studies have highlighted limitations of this approach when cardiac output attains very high levels. The effect of anesthesia techniques on the relationship between oxygen consumption and cardiac output could also explain unanswered questions regarding the pathophysiology of arterial oxygenation during one-lung anesthesia. Summary The effects of anesthesia techniques on oxygen consumption, cardiac output and therefore mixed venous oxygenation can significantly affect arterial oxygenation during one-lung anesthesia. While pursuing increases in cardiac output may, under limited circumstances, benefit arterial oxygenation during one-lung ventilation, this approach is not a panacea and does not obviate the necessity to optimize dependent lung volume. Keywords cardiac output, hypoxic pulmonary vasoconstriction, mixed venous oxygen content, one-lung anesthesia, shunt Curr Opin Anaesthesiol 21:28–36 ß 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins 0952-7907
Introduction During one-lung anesthesia (OLA), the adequacy of arterial oxygenation is threatened by the presence of a right-to-left transpulmonary shunt. Figure 1 illustrates that the ability of the shunt to influence arterial oxygenation depends on two variables: the magnitude of the shunt (i.e. volume of blood flowing via the shunt [Qs]) and the oxygen content of the mixed venous blood (CvO2) that flows through the shunt. Emphasis is usually placed on the role of hypoxic pulmonary vasoconstriction (HPV) in limiting the magnitude of the shunt [1,2], however, increasing CvO2 should also improve arterial oxygen content (CaO2).
reveals that if one or both of the determinants of oxygen delivery (i.e. CaO2 and/or Qt) are inadequate, or oxygen consumption is high, CvO2 will decrease. Expressed differently, the ratio of whole body oxygen extraction to oxygen delivery has been referred to as the oxygen extraction ratio (OER) (Equation 2): OER ¼ VO2 =ðQt:CaO2 Þ
(2)
Mixed venous oxygen content as an indicator of circulatory efficiency
A decrease in the OER implies improved circulatory efficiency, and vice versa. Inspection of Equations 1 and 2 reveals that a decrease in the VO2/Qt ratio results in a decrease in OER and concomitant increases in both circulatory efficiency and CvO2. The corollary, that CvO2 will decrease should circulatory efficiency decrease or OER increase, is also valid. CvO2 can therefore be regarded as a useful indicator of global circulatory efficiency.
The determinants of CvO2 are described by the Fick equation solved for CvO2 (Equation 1):
The interaction of shunt and CvO2
CvO2 ¼ CaO2 ðVO2 =QtÞ
(1)
where VO2 represents oxygen consumption and Qt represents cardiac output. Inspection of Equation 1
The underlying physiology is encapsulated by the shunt equation which can be derived from Fig. 1: Qs=Qt ¼ ðCcO2 CaO2 Þ=ðCcO2 CvO2 Þ
(3)
0952-7907 ß 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins
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Oxygenation and one-lung anesthesia Levin et al. 29 Figure 1 A cartoon representing oxygen flux in the pulmonary and systemic circulations
Figure 2 The relationship between arterial oxygen content (CaO2) and shunt fraction (Qs/Qt) given by Equation 4 is represented by a series of straight lines with a common intercept equal to the pulmonary end-capillary oxygen content (CcO2).
Both ventilated areas of the lung and right-to-left transpulmonary shunt are illustrated. The shunt equation can be derived from the information presented in this diagram. VA, alveolar ventilation.
Rearranging gives: CaO2 ¼ CcO2 ðCcO2 CvO2 Þ:ðQs=QtÞ
(4)
where CcO2 represents the end-capillary oxygen content emanating from ventilated alveoli and Qs/Qt represents shunt fraction. Equation 4 indicates that, in the presence of a shunt, arterial oxygen content is determined by Qs/Qt, CvO2 and CcO2. Note also that, when administering high inspired fractional concentrations of oxygen (FiO2) in the presence of relatively normal lung parenchyma, pulmonary capillary blood exiting ventilated alveoli is 100% saturated with oxygen. Under these circumstances, CcO2 is primarily determined by hemoglobin concentration (Hb). CcO2 can therefore be regarded as being constant. Figure 2 is the graphic depiction of Equation 4 and illustrates the influence that CvO2 exerts on CaO2. The relationships between CaO2 and Qs/Qt are linear with the slopes of these relationships being determined by the CcO2CvO2 differences [3,4]. The common intercept at CcO2 indicates that CaO2 would equal CcO2 if there were no shunt.
The slopes of the plots are determined by the oxygen content differences between pulmonary end-capillary and the mixed-venous blood (CcO2 CvO2). Note that, for any shunt fraction (Qs/Qt), the CaO2 is less if CvO2 (represented in the presence of a constant Hb by venous saturation) is decreased. Values used to plot these relationships are hemoglobin concentration 15 g/dL, inspired oxygen fraction 0.5, and arterial carbon dioxide partial pressure 40 mmHg.
Inspection of Equation 5 reveals that four variables determine arterial oxygenation in the presence of a shunt. The relationships between these variables can be depicted graphically. In Fig. 3, plot A portrays the relationship described by Equation 5 when Hb is 15 g/dl and oxygen consumption is 150 ml/min in the presence of a shunt fraction of 0.2. Inspection of plot A reveals that the relationship is not linear, so that, at low cardiac output Figure 3 The influence of cardiac output on arterial oxygen content (CaO2) as predicted by Equation 5
Combining the Fick and shunt equations Equations 1 and 4 can be combined into a single expression for CaO2 [5]: CaO2 ¼ CcO2 ðVO2 =QtÞ
ðQs=QtÞ ð10½1 Qs=QtÞ
(5)
Note that the factor 10 in Equation 5 is inserted to compensate for the inconsistency of units as oxygen content is usually expressed in ml/100 ml, cardiac output in l/min and oxygen consumption in l/min.
The values used to plot these relationships are a FiO2 of 0.5 and PaCO2 40 mmHg. Plot A: Hb 15 g/dl, VO2 150 ml/min, Qs/Qt 0.2; Plot B: Hb 15 g/dl, VO2 150 ml/min, Qs/Qt 0.4; Plot C: Hb 15 g/dl, VO2 75 ml/min, Qs/Qt 0.4; Plot D: Hb 10 g/dl, VO2 150 ml/min, Qs/Qt 0.2.
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30 Thoracic anaesthesia Figure 4 Two views of a three-dimensional plot of the influence of changing both cardiac output and shunt fraction on arterial oxygen content (CaO2) at hemoglobin concentrations of 8 and 12 g/100 ml blood as predicted by Equation 5
The values used to plot these relationships are at FiO2 of 0.5 and PaCO2 40 mmHg.
values, CaO2 is reduced because high VO2/Qt ratios increase the value of the second term in Equation 5. With increasing cardiac output, this ratio decreases, causing CaO2 to increase steeply until the VO2/Qt ratio assumes such small values that the second term in Equation 5 becomes negligible. Theoretically, CaO2 approaches CcO2 asymptotically at high cardiac outputs. Plot B illustrates how the relationship shifts downwards if the shunt fraction doubles to 0.4. Plot C shows how plot B moves upwards and to the left if oxygen consumption is halved but the other criteria used to construct plot B are unchanged. Plot D demonstrates that, if Hb is reduced from 15 to 10 g/dl, curve A is shifted downwards.
such low values for oxygen content, tension and delivery that are incompatible with life. Furthermore, the model assumes that changes in cardiac output do not lead to changes in shunt fraction. This assumption is not always correct and the practical implications thereof will be addressed. Unfortunately, there have been few attempts to use a systematic approach to oxygenation during OLA, and this Figure 5 The influence of cardiac output on PaO2 as predicted by Equation 5
These complex relationships are depicted by the threedimensional graphs (Fig. 4) that show how, at two different hemoglobin concentrations, cardiac output and shunt fraction both determine CaO2. The curvilinear surfaces result from the shape of the oxygen dissociation curve. In view of the steep arterial–mitochondrial oxygen gradient, an adequate arterial oxygen tension (PaO2) is needed to maintain intra-mitochondrial oxygen tensions above the minimum required for aerobic metabolism. Figure 5 depicts the relationship between cardiac output and PaO2. Comparing Figs 4 and 5, it is interesting to note that decreasing Hb (plots A and D) does not (theoretically) have as great an influence on PaO2 as on CaO2. The graphs in Figs 2–5 serve the purpose of illustrating physiologic theory. In reality, there are combinations of shunt fraction and cardiac output that would result in
The values used to plot these relationships are at FiO2 of 0.5 and PaCO2 40 mmHg. The curves have similar conditions to those specified in Fig. 4. Construction of this relationship used a lookup table in Excel relating CaO2 to saturation for a particular Hb and then using an oxygen dissociation curve to relate saturation to PaO2.
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Oxygenation and one-lung anesthesia Levin et al. 31
has hampered interpretation of published research on the subject. For example, although differences in arterial oxygenation have been demonstrated when using different anesthetic regimens, the reasons for these differences are not always clear [6,7]. Propofol should theoretically have advantages over volatile anesthetics that cause dosedependent inhibition of HPV [1,8,9] because propofol potentiates [10] (or has at least been reported not to decrease) HPV [8]. While several human studies concur [11,12], others do not [6,13,14]. It is also noteworthy that, from 1970 to 2003, the reported incidence of arterial hypoxemia during OLA decreased from 25% [15] to less than 1% [16]. One may speculate that the effect of the (newer) inhalation anesthetic agents (IAAs) on hypoxic pulmonary vasoconstriction (HPV) are unimportant [9,17]. An alternative explanation may be that different anesthetic techniques variably affect the VO2/Qt ratio and circulatory efficiency, which will exert an important influence on arterial oxygenation during OLA. We will examine how evidence from the literature supports our view that all four variables in Equation 5 should be addressed to comprehend and optimize arterial oxygenation during OLA.
Shunt fraction The shunt fraction, as calculated using Equation 3, considers not only the magnitude of the true right to left shunt present in the nonventilated lung to hypoxia but also the contribution of low ventilation perfusion units in the ventilated (dependent) lung. Low ventilation perfusion units present in the ventilated dependent lung contribute (approximately 5–10% [18,19]) toward the calculated shunt fraction during OLA. Various factors are important in limiting shunt during OLA. These include HPV [20] that limits nonventilated lung shunt, administration of positive end-expiratory pressure (PEEP) to the dependent lung [21–23] and correct positioning of double lumen tubes [24]. A number of authors have demonstrated the benefit of dependent lung PEEP when titrated to restore functional residual capacity [21,22,25], whereas administration of predetermined [26] or excessive amounts of PEEP [22] does not always improve arterial oxygenation. Whereas the aforementioned are all important determinants of arterial oxygenation during OLA, this article will focus on the other, less frequently discussed, issues that appear in Equation 5.
Cardiac output during OLA Slinger [6,7] has suggested that the newer anesthetics and drug combinations cause smaller decreases in cardiac output and possibly greater decreases in oxygen consumption (thereby favorably affecting the VO2/Qt ratio,
circulatory efficiency and CvO2). In human studies, higher cardiac outputs have been associated with improved arterial oxygenation [27–29] and a linear relationship between cardiac output and PaO2 has been demonstrated [27]. In a porcine OLA model, total intravenous anesthesia (TIVA) was associated with a greater cardiac output as well as greater mixed venous oxygenation and PaO2 compared with anesthesia using IAAs [30]. Two human studies demonstrated that deliberately increasing cardiac output by approximately 25% using dobutamine 5 mg/kg/min led to significant improvements in arterial oxygenation during OLA [28,29]. In one study, the increase in cardiac output was accompanied by an increase in mean mixed venous saturation from 60.0% to 74.6% [29]; mixed venous saturation was not reported in the other human study [28]. Figure 3 demonstrates that the most significant increases in CaO2 occur when cardiac output is increased from low values. The curve eventually flattens, demonstrating that limited improvement in CaO2 can be gained by increasing cardiac output. This was confirmed in a study [31] in which progressively greater dobutamine infusion rates (3, 5 and 7 mg/kg/min) increased cardiac output by approximately 25% from relatively high baseline levels of 4.4 l/min/m2, but this did not produce a change in either CaO2 or PaO2 during OLA in the lateral decubitus position with Qs/Qt between 0.36 and 0.4. Russell and James [32,33] reported that increasing cardiac output to very high values can actually cause deterioration in arterial oxygenation. They demonstrated that arterial oxygenation was compromised in a porcine OLA model, when sufficient inotrope was administered to double and even triple baseline cardiac output. Actively increasing cardiac output can inhibit HPV and increase nonventilated lung shunt via a number of mechanisms. (1) In spite of the low resistance offered by the pulmonary vasculature, very large increases in cardiac output increase pulmonary artery pressure (PAP). Even small increases in PAP oppose the weak forces affecting HPV [34,35] and will also increase nonventilated lung blood flow, thereby aggravating the shunt [34,35,36,37]. These increases in PAP will be greater in the presence of greater pulmonary vascular resistances associated with parenchymal disease and decreased lung volume. (2) The aggravation of the shunt in the supine position has been attributed to small increases in nonventilated lung PAP compared with OLA in the lateral decubitus or even semi-lateral positions [38]. We speculate that this mechanism will aggravate hypoxia further if cardiac output is actively increased in the supine position. (3) Inotropes directly inhibit HPV [39–42]. (4) Mixed venous oxygen tension affects the stimulus oxygen tension responsible for initiation of HPV. An inefficient circulation with a low mixed venous
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32 Thoracic anaesthesia
oxygen tension will promote HPV [43,44], especially in ventilated areas of the lung with low ventilation perfusion units [17,30,43]. Conversely, increasing cardiac output and circulatory efficiency will increase mixed venous oxygen tension: an increased mixed venous oxygen tension has been shown to inhibit HPV [43]. The consequence of increasing cardiac output on arterial oxygenation during OLA probably represents a balance of two opposing factors. We speculate that, as cardiac output is increased from low values, mixed venous and therefore arterial oxygenation will improve. However, when very high cardiac outputs are attained using high dosages of inotrope, transpulmonary shunting is increased, leading to decreases in arterial oxygenation.
hemodilution, patients who had COPD exhibited decreases in PaO2, whereas there were no changes in subjects with normal lungs, or in the control group with COPD who did not undergo hemodilution. The reasons for the difference between the groups is unclear, nevertheless we speculate that the shunt fraction was greater in the diseased lungs of the COPD group [31]. Guenoun and colleagues [52] reported that a preoperative hematocrit greater than 45% predicted lower PaO2 during one-lung ventilation. This is counterintuitive and does not fit with the theory discussed above. One possible explanation is that a high hematocrit increases viscosity [53]. Another is that patients with more severe lung disease are polycythemic preoperatively and have higher shunt fractions and lower PaO2 during OLA.
Oxygen consumption and OLA There is scant evidence that changes in oxygen consumption indeed influence arterial oxygenation during OLA to a clinically significant degree. While administration of 1-MAC IAA leads to 20–30% decreases in oxygen consumption [45,46,47], concomitant decreases in cardiac output will probably negate the beneficial effect on arterial oxygenation. In this respect, we have shown that balanced anesthesia (opioid target-controlled infusion combined with low-dose IAA) strikingly reduces oxygen consumption by approximately 40%, while maintaining cardiac output during OLA [48]. This resulted in mixed venous oxygen saturations exceeding 85% [48]. Administration of positive inotropic drugs may possibly oppose the beneficial effects of increased cardiac output because approximately 10% increases in oxygen consumption have been reported during certain inotrope infusions [32,33,49,50]. The increases in cardiac output should, however, more than compensate for minor increases in oxygen consumption. This is exemplified in the Russell and James studies [32,33] by an increase in CvO2, in spite of the reported increases in oxygen consumption.
CcO2 and OLA: the effect of hemoglobin concentration Plots D in Figs 3 and 5 and the response surfaces of Fig. 4 depict how changes in Hb theoretically affect arterial oxygen content in the presence of a transpulmonary shunt. Little research has, however, been conducted as to how changes in Hb indeed affect arterial oxygenation during OLA. Szegedi and colleagues [51] assessed the effects of acute normovolemic hemodilution on arterial oxygen tensions during OLA in patients with and without chronic obstructive pulmonary disease (COPD). After
CcO2 and OLA: the effect of alveolar ventilation and FiO2 Provided alveolar partial pressure of oxygen is adequate, pulmonary capillary blood exiting ventilated alveoli is fully saturated with oxygen. The simplified alveolar gas equation (Equation 6) [54] predicts that the two methods whereby oxygen tension in ventilated alveoli can be improved are by increasing alveolar ventilation, or the inspired partial pressure of oxygen (PiO2), or both. PA O2 ¼ PiO2 ðPaCO2 =respiratory quotientÞ
(6)
(Note that PiO2 ¼ [Pb PH2O]FiO2.) Increasing alveolar ventilation using larger tidal volumes is theoretically attractive as it may also prevent small airway closure and the development of low ventilation perfusion units that result from the decrease in dependent lung volume during OLA [1]. The use of larger (15 ml/kg) [55] and smaller tidal volumes [56,57] during OLA have been linked with increases and decreases, respectively, in arterial oxygenation; however, utilizing larger tidal volumes has not universally resulted in statistically significant [4,58–60] or clinically important [21,55] increases in arterial oxygenation. The reasons for this conflicting evidence include firstly that increases in lung volume lead to increases in pulmonary vascular resistance and diversion of blood flow toward the nonventilated lung [4,21,25,58–60]. Secondly, large tidal volumes can result in decreased cardiac output [61]. Thirdly, the relationship between alveolar oxygen tension and alveolar ventilation is not linear [62]. Fourthly, a growing body of evidence [7,63,64,65,66,67,68–75,76] suggests that ventilatorassociated lung injury is an important cause of primary [77] acute lung injury. In other words, attempts to gain short-term intraoperative benefit using large tidal volumes (exceeding 6.7 ml/kg [65]) may incur the cost of ventilator-induced postthoracotomy acute lung injury.
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Oxygenation and one-lung anesthesia Levin et al. 33
Rather than the use of large tidal volumes, restoration and maintenance of optimal dependent lung volume toward functional residual capacity [4,21,23] employing recruitment [78] and extrinsically applied PEEP [22,25] are more appropriate measures to address small airway patency and improve alveolar oxygen tension. An increase in respiratory rate with the aim of attaining normocarbia during OLA has been recommended [79], but will not necessarily improve alveolar ventilation. Faster respiratory rates decrease ventilatory efficiency by increasing dead space ventilation [62]. Furthermore, increased respiratory rates may lead to greater levels of intrinsic PEEP during OLA [80], which could contribute to ventilator-induced lung injury [7]. Avoidance of excessive intrinsic PEEP requires an adequate expiratory time (therefore slow respiratory rates) to permit the lung emptying, especially in the presence of low lung elastic recoil [80–84]. Adequate alveolar oxygen partial pressures can be achieved without employing potentially damaging pulmonary ventilation strategies if a high FiO2 is employed. Equation 6 shows that PAO2 and PiO2 increase in parallel [62] so that the use of a high FiO2 can compensate for moderate hypoventilation consequent to lung protective ventilation strategies, provided small airway and alveolar patency are maintained. Permissive hypercapnia is a common consequence of using protective lung strategies [60,85,86] and the concern is often expressed that it will threaten arterial oxygenation. For example, hypercarbia may lead to increased PAP [60] with subsequent diversion of blood away from the dependent, ventilated lung toward the nonventilated lung, thereby increasing the shunt. Nonetheless, hypercarbia associated with hypoventilation has not been shown to decrease arterial oxygenation during OLA [60]; firstly, because hypercarbia potentiates HPV [87] and, secondly, because lower airway pressures are associated with a higher cardiac output [61]. Akca and colleagues [88,89] have demonstrated that increased arterial carbon dioxide tensions up to 8– 9 kPa benefit tissue oxygenation. Probable explanations for this observation include sympathetic nervous system stimulation-driven [90] increases in cardiac output [89,91,92,93], rather than peripheral vasodilatation [60,94]. Whether the rightward shift of the oxygen dissociation curve plays a role in improving tissue oxygenation is uncertain [95]. Although only demonstrated in animals by one group of investigators, it may be relevant that hypercapnic acidosis has been shown to protect against lung injury after lung ischemia–reperfusion by attenuating pulmonary inflammation and reducing free radical production [96–98].
Monitoring circulatory efficiency Measurement of mixed venous oxygenation is a useful method to evaluate circulatory efficiency and it may indicate whether deliberately increasing cardiac output would lead to a benefit. Sampling central venous blood (as opposed to mixed venous blood utilizing a pulmonary artery catheter) would be straightforward and convenient, but whether central venous blood can be regarded as a surrogate for the latter during thoracic surgery is not known [46,99–101,102]. Different anesthetic techniques [103] and low flow states [99,104,105] increase the difference between central and mixed venous oxygenation. Furthermore, the oxygenation of blood sampled from a central venous catheter close to the right atrium may not truly represent mixed venous blood if a considerable proportion of the sample comprises desaturated coronary sinus blood [46]. Calculation of shunt fraction always requires sampling of mixed venous blood.
Areas for further research Areas for further research include the following questions. (1) What is the role of Hb on mixed venous and arterial oxygenation during OLA? (2) Does permissive hypercarbia benefit arterial oxygenation during OLA because of associated increases in cardiac output? (3) Is the lack of a difference in arterial oxygenation between propofol and IAAs secondary to different effects on the VO2/Qt relationship? (4) Are the differences [106], or the lack of a difference [107], in arterial oxygenation when comparing OLA ventilatory strategies due to the effects on cardiac output? (5) Do central and mixed venous oxygenation reflect each other adequately enough for clinical purposes?
Conclusion The relationship described by Equation 5 [5] indicates that nonventilated lung shunt and low ventilation perfusion units in the ventilated, dependent lung are not the only factors determining arterial oxygenation during OLA. This discussion is intended to raise awareness, for both the clinician and the researcher, of the number of factors and their interrelationships that potentially affect arterial oxygenation during OLA.
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