Stephen M. Eskaros, Peter J. Papadakos, and Burkhard Lachmann   44                     Respiratory Monitoring      Key Poi...
IV   1412   Anesthesia Management     direct sampling, efforts to develop indirect methods of determin­                   ...
Respiratory Monitoring 1413       44 Box 44-1 Five Causes of Hypoxemia and the Associated                         tion­to­...
IV   1414    Anesthesia Management                                                                         PO2 (mm Hg)    ...
Respiratory Monitoring 1415       44with zero V Q ) but should be thought of as a total shunt because       lung. A host o...
IV   1416   Anesthesia Management                                                             Lung                        ...
Respiratory Monitoring 1417    44                                                               0.8                       ...
IV   1418     Anesthesia Management      Box 44-2 Algorithms for Correction to Body Temperature of                        ...
Respiratory Monitoring 1419     44of bias and precision.27 Bias is the difference between mean values                     ...
IV   1420                                    Anesthesia Management                                                        ...
Respiratory Monitoring 1421       44                              100                                                 Digi...
IV   1422    Anesthesia Management     Table 44-2 Artifacts in Pulse Oximetry      Factor                                 ...
Respiratory Monitoring 1423        44 Arterial pressure                                                                thi...
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
Oximetria valor
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  1. 1. Stephen M. Eskaros, Peter J. Papadakos, and Burkhard Lachmann 44 Respiratory Monitoring Key Points 1. Hypoxemia is caused by reduced Pio2, hypoventilation, and methemoglobin. Pulse oximetry may one day prove increased ventilation-perfusion ( V Q) heterogeneity, to be a reliable noninvasive monitor of volume status increased shunt, and diffusion nonequilibrium. and fluid responsiveness. Hypercapnia is almost always due to hypoventilation. 9. A sudden decrease in Petco2 usually results from a circuit 2. During mechanical ventilation in the operative and disconnection, airway obstruction, abrupt decrease in intensive care settings, hypoxemia is most often due to cardiac output, or pulmonary embolism. Petco2 is not increased V Q heterogeneity and shunt. always a reliable approximation of Paco2, particularly 3. A clinically useful approximation to the alveolar gas during general anesthesia or in the critically ill. equation for O2 is given by Pao2 = (Pb − 47) × Fio2 − 1.2 10. Mapping of pressure-volume curves in patients with × Pco2. Exchange of O2 and CO2 takes place acute respiratory distress syndrome (ARDS) and acute independently in the lung. lung injury (ALI) can provide valuable information about 4. The alveolar-arterial (a-a) gradient increases with age and lung mechanics and help guide positive end-expiratory supplemental O2. The Pao2/Fio2 and a/a ratios typically do pressure (PEEP) and tidal volume settings. Sustained not change with increased age or inspired O2. high airway pressure is needed to open collapsed alveoli, and PEEP stabilizes the recruited lung units. 5. When derangements in gas tensions are noted on arterial blood gas analysis, it is important to verify that 11. Computed tomography has greatly increased our the sample was obtained and analyzed in an appropriate understanding of the complicated interaction between and timely manner. PEEP and lung recruitment in ARDS. Electrical impedance tomography may in the future emerge as a useful 6. Refinements and further studies on continuous bedside monitor of lung recruitment, pulmonary edema, intravascular blood gas monitors may one day lead to and respiratory mechanics. widespread routine use of these devices. 12. Recruitment strategies and low–tidal volume ventilation 7. Pulse oximetry is a rapid, reliable indicator of have been shown to improve outcomes in ARDS and ALI. oxygenation status in surgical and critically ill patients. High-frequency ventilators are safe and effective in Newer oximeters feature reduced capability for errors refractory ARDS and may some day prove to be the ideal attributable to motion artifact and hypoperfusion. mode of lung protective ventilation. 8. Multiwavelength pulse oximeters are commercially available and allow measurement of carboxyhemoglobin Gas Exchange the respiratory system takes up oxygen and eliminates carbon dioxide are still being debated.The realization that gas exchange takes place in the lung was madeby the ancients. However, not until the 18th century, when Alveolar Gasesoxygen was discovered by Joseph Priestley, did Lavoisier ascertainthe true purpose of breathing: the biochemical combustion of A practicable method for directly sampling and analyzing alveo­carbon and oxygen to carbon dioxide, a process known as respira­ lar air was first described by Haldane and Priestly in 1905.2tion.1 More than 200 years later, the exact mechanisms by which Because of the inaccuracies and technical difficulty involved in 1411
  2. 2. IV 1412 Anesthesia Management direct sampling, efforts to develop indirect methods of determin­ PAO2 = PIO2 − PACO2 R (7) ing the composition of alveolar air ensued. Subsequently, many equations describing the concentration of alveolar gases have where R is the respiratory exchange ratio defined as VCO2 VO2 been derived, with a wide range of accuracy and complexity. All and relates CO2 output to O2 uptake. Normally, the ratio is rela­ are based simply on the law of conservation of mass and derive tively constant at 0.8 (i.e., 0.8 mol CO2 produced for every 1 mol from the universal alveolar air equation: O2 consumed), and the equation becomes Alveolar fraction of gas X = PAO2 = PIO2 − 1.25 × PACO2 (8) (Inspired fraction of X ± Output or uptake of X ) Note that the term Paco2/R in Equation 7 replaces the term Alveolar ventilation (PBdry × VO2 ) VA from Equation 4. Because Paco2 can be (i.e., output for CO2, uptake for O2 ) assumed to be equal to Paco2 based on the Enghoff modification and R relates O2 uptake to CO2 output, Paco2/R is essentially an (1) indirect measure of O2 uptake and is much easier to accurately The equation in this form is only approximate and requires cor­ calculate than VO2 VA .6 rections to account for differences in expired and inspired minute A common misconception from the appearance of Pco2 in volume, discussed later. Moreover, because of the inhomogeneous Equations 7 and 8 is that Pao2 is directly influenced by changes nature of the lung, the partial pressures calculated should be in Paco2. Rather, exchange of O2 and CO2 takes place independ­ interpreted as averages of various alveolar concentrations present ently in the lung, and Pao2 is influenced by only the four afore­ in heterogeneous gas exchange units. Put simply, the gas con­ mentioned factors. The apparent influence of Paco2 on Pao2 centrations in each alveolus are probably different, and values is actually reflective of a change in minute ventilation or O2 obtained from the equation represent the mean of all alveoli. consumption, more obvious in Equation 4. For example, as alveo­ In the case of O2, solving the universal equation for uptake lar ventilation decreases, Paco2 rises and Pao2 will decrease (VO2 ) yields a general Fick equation that can be solved for alveo­ according to Equation 8 as a result of the reduced alveolar ven­ lar O2: tilation. There is no “displacement” or direct alteration of O2 by CO2.6,7 VO2 = VA (FIO2 − FAO2 ) (2) Despite being quite adequate for clinical use, the Riley equation does not account for small differences in expired and FAO2 = (FIO2 − VO2 ) VA (3) inspired gas volume because of (1) the respiratory exchange ratio (less CO2 output than O2 uptake at a ratio of 4:5) and (2) respired where Fao2 is the alveolar O2 fraction, Fio2 is the inspired frac­ inert gases not being in equilibrium with blood (such as during tion, and VA is alveolar ventilation in volume per minute. In nitrous oxide induction or washout). An equation proposed by other words, the amount of O2 in alveoli is equal to the difference Filley and coworkers8 corrects for this difference and does not between the amount inspired and the amount taken up by pul­ entail calculation of R, which can be higher than the normal monary capillaries (conservation of mass). Multiplying through 0.8 in certain clinical settings, such as with metabolic acidosis or by dry barometric pressure (Pbdry) to obtain partial pressures, overfeeding: Equation 3 becomes PAO2 = PIO2 − PACO2 (PIO2 − PEO2 ) PECO2    (9) PAO2 = PB dry (FIO2 − VO2 VA ) (4) Though more accurate, it is more cumbersome than the where Pbdry = barometric pressure − saturated water vapor Riley equation in that mixed expired gas concentrations must pressure. be measured. This equation should be used, for example, when It is most clear in this form of the equation that Pao2 is calculating shunt fraction because precise Pao2 values are influenced only by four variables: barometric pressure, fraction imperative.3 of inspired O2, uptake of O2, and alveolar ventilation.3 The same manipulations of the universal equation yield a formula for determining alveolar CO2: Arterial Gases PACO2 = PB dry (FICO2 + VCO2 VA ) (5) Exchange of gases between alveoli and blood occurs at the pul­ monary capillaries. Arterial blood is formed by mixture of this Note that CO2 output must be added to the inspired concentra­ pulmonary capillary blood with the mixed venous shunt fraction. tion to obtain Paco2. However, because Fico2 is usually zero and Thus, three major factors influence the efficiency of this exchange VCO2 is relatively constant, it is clear that Paco2 is dependent and the resultant arterial gas tensions: V Q matching, alveolar mainly on one factor, alveolar ventilation, to which it is inversely diffusion capacity, and shunt fraction. Along with hypoventila­ proportional: tion and low Pio2, derangements in any of these factors result in arterial hypoxemia (Box 44­1). Some determination of the cause PACO2 = c (1 VA ) (6) of the hypoxemia can be made by evaluation of the a­a O2 gradi­ where c is a constant. This approximation becomes less accurate ent; problems with gas exchange increase the gradient, whereas it in clinical situations in which CO2 output can be appreciably is normal in hypoxemia because of low Pio2 or hypoventilation. elevated, as with fever, sepsis, or shivering.4 The a­a gradient is usually elevated in a patient breathing sup­ Perhaps the simplest and most widely used approximation plemental oxygen. Two other indices of oxygenation that remain of the alveolar gas equation was derived by Riley and colleagues5 unchanged with fluctuating Fio2 are the Pao2/Fio2 and a/a ratios and relates Pao2 and Paco2 in the following way: (normally 350 to 500 mm Hg and 0.8 to 0.85, respectively).
  3. 3. Respiratory Monitoring 1413 44 Box 44-1 Five Causes of Hypoxemia and the Associated tion­to­perfusion ratio of roughly 0.8 for the entire lung.10 This Alveolar-to-Arterial (a-a) O2 Gradient would represent the V Q ratio of each alveolus if ventilation and perfusion were uniformly distributed in the lung. In reality, dis­ Normal a-a O2 Gradient tribution is not uniform, and ratios range anywhere from zero Hypoventilation (shunt) to infinity (dead space ventilation). For example, alveoli in dependent lung regions are better perfused than those in Reduced Pio2 the apices and therefore have lower V Q ratios.11 Ventilation is Increased a-a O2 Gradient usually more evenly distributed throughout the lung than blood Section IV Anesthesia Management Increased V Q heterogeneity flow is, so impaired oxygenation of arterial blood is most often Increased shunt due to derangements in perfusion. V Q mismatching results in hypoxemia for two reasons. Diffusion limitation First, more blood tends to flow through alveoli with low V Q, such as dependent lung.9 Thus, when V Q scatter increases, flow through alveoli with low V Q (and therefore low Po2) is greater than flow through areas of high V Q, which causes a dispropor­ The extent to which these factors affect the makeup of arte­ tionately large effect from the areas of low V Q and hence arial blood differs for CO2 and O2 because they have different reduction in Pao2. The second reason is due to the nature of oxy­arteriovenous gradients and diffusing capacities. CO2 is estimated hemoglobin (HbO2) dissociation. Alveoli with high V Q are onto have a diffusing capacity 20 to 30 times greater than that of the plateau portion of the curve, where shifts in Pao2 have littleO2,9 and its exchange is therefore minimally affected by derange­ effect on O2 content. These new areas of high (or higher) V Qments in alveolar membrane diffusion and V Q mismatching. introduced by scatter are unable to compensate for the new areasThe narrower arteriovenous gradient of CO2 (≈6 mm) versus O2 of low V Q , which are on the steep portion of the curve and(∼60 mm) leads to less profound effects of venous shunt on arte­ therefore more profoundly affected by changes in Pao2 (Figs. 44­1rial Pco2. Except in extreme circumstances there is little evidence and 44­2).that impaired diffusion of O2 or CO2 across the alveolar mem­brane occurs to any clinically significant extent, so this is not Shuntdiscussed further in this chapter. One extreme of V Q mismatch is a right­to­left shunt ( V Q = 0), the other extreme being dead space ventilation ( V Q = infin­ V Q Mismatch ity). Normally, a small shunt fraction (<3% of cardiac output)In normal subjects, resting minute ventilation is roughly 4 L/m exists because of drainage of bronchial and thebesian venousand pulmonary blood flow is 5 L/m, which results in a ventila­ blood into the left heart.7 However, as a result of the steep arterio­ Alveolar gas PO2 = 13.6 kPa (102 mm Hg) PCO2 = 5.3 kPa (40 mm Hg) % contribution 45 35 20 PO2 12.4 (93) 13.6 (102) 16 (120) . . PCO2 3.5 (41) 53 (40) 4.7 (35) V/Q ratios 1.7Figure 44-1 Alveolar-to-arterial Po2 difference caused by Mixed venousscatter of V Q ratios and its representation by an equivalent blooddegree of venous admixture. A, Scatter of V Q ratioscorresponding roughly to the three zones of the lung in a 0.9normal upright subject. Mixed alveolar gas Po2 is calculatedwith allowance for the contribution of gas volumes from the 0.7three zones. Arterial saturation is similarly determined and % contribution 57 33 10Po2 derived. There is an alveolar-arterial Po2 difference of O2 sat. 97.0 97.6 98.50.7 kPa (5 mm Hg). B, Theoretical situation that would PCO2 5.5 (41) 5.3 (40) 4.7 (35)account for the same alveolar-to-arterial Po2 differencecaused solely by venous admixture. This is a useful methodof quantifying the functional effect of scattered V Q ratios Arterial bloodbut should be carefully distinguished from the actual saturation 97.4%situation. (From Lumb AB: Nunn’s Applied Respiratory PO2 = 12.9 kPa (97 mm Hg)Physiology, 6th ed. Philadelphia, Elsevier/Butterworth A PCO2 = 5.4 kPa (40.5 mm Hg)Heinemann, 2005.) Alveolar gas PO2 13.6 kPa (102 mm Hg) End-capillary PO2 13.6 kPa (102 mm Hg) Saturation 97.6% Mixed venous Arterial blood saturation 72.4% saturation 97.4% 1% venous PO2 12.9 kPa (97 mm Hg) B mixture
  4. 4. IV 1414 Anesthesia Management PO2 (mm Hg) phenomena are probably contributors to the 5% to 10% shunt found in patients undergoing GA with mechanical ventilation.10 0 20 40 60 80 100 120 100 Calculating Shunt Fraction and Dead Space 80 A simplified but useful three­compartment lung model aids in 98.2% 95.8% 74% approximating what fraction of cardiac output (QT ) constitutes shunt (QS ) and what fraction of tidal volume (Vt) constitutes Oxygen saturation, % sat. sat. sat. 60 dead space ventilation ( VDS ) . Commonly known as the Riley 40 approach, the lung is considered as though it were made up of 20 three compartments at the three extremes of V Q matching: (1) a shunt compartment with perfused but unventilated alveoli, (2) 0 a dead space compartment with ventilated but unperfused alveoli, 0 4 8 12 16 (3) and an ideal compartment with normally distributed ventila­ Mean saturation PO2 (kPa) 89% tion and perfusion (Fig. 44­3). As discussed earlier, the lung is actually composed of many compartments with a wide distribution of V Q ratios, and this Mean arterial PO2 low V/Q mid V/Q high V/Q as an oversimplified but clinically useful model. 7.6 kPa (57 mm Hg) The shunt fraction (QS QT ) can be calculated by using the Berggren shunt equation to compare the O2 content of mixed venous (CvO2 ) , pulmonary capillary (Cc′o2), and arterial (Cao2) Alveolar/arterial PO2 blood: difference 3.1 kPa (23 mm Hg) QS QT = (Cc ′O2 − CaO2 ) (Cc ′O2 − CvO2 ) (10) In a normal subject with capillary O2 saturation close to Mean alveolar PO2 100%, the following approximation can be made 10.7 kPa (80 mm Hg) QS QT = (1 − SaO2 ) (1 − SvO2 ) (11) Figure 44-2 Alveolar-arterial Po2 difference caused by scatter of V Q ratios where SvO2 and Sao2 are mixed venous and arterial O2 saturation, resulting in oxygen tensions along the upper inflection of the oxygen respectively. dissociation curve. The diagram shows the effect of three groups of alveoli with Po2 values of 5.3, 10.7, and 16.0 kPa (40, 80, and 120 mm Hg). Ignoring It is important to note that the fraction calculated in Equa­ the effect of the different volumes of gas and blood contributed by the three tion 10 is not a true shunt (intrapulmonary shunt through alveoli groups, mean alveolar Po2 is 10.7 kPa. However, because of the shape of the dissociation curve, the saturation of blood leaving the three groups is not proportional to their Po2. The mean arterial saturation is in fact 89%, and Po2 is therefore 7.6 kPa. The alveolar-arterial Po2 difference is thus 3.1 kPa. The actual difference would be somewhat greater because gas with a high Po2 would make a relatively greater contribution to alveolar gas and blood with a Alveolar dead space low Po2 would make a relatively greater contribution to arterial blood. In this example, a calculated venous admixture of 27% would be required to account for the scatter of V Q ratios in terms of the measured alveolar-arterial Po2 difference at an alveolar Po2 of 10.7 kPa. (From Lumb AB: Nunn’s Applied Respiratory Physiology, 6th ed. Philadelphia, Elsevier/Butterworth Heinemann, 2005.) venous Po2 gradient, this shunt is partly responsible for the normal a­a O2 gradient of 5 to 10 mm Hg found in children and young adults breathing room air. Shunt introduced by these cir­ Ideal alveolar gas culations can increase to 10% of cardiac output in the presence of severe bronchial disease and aortic coarctation.9 The normal heterogeneity of V Q throughout the lung is the other contri­ butor to the baseline a­a gradient. The gradient increases with Mixed venous Venous admixture Arterial age, probably secondary to increased closing capacity and V Q blood (shunt) blood scatter.7 Pathologic right­to­left shunting of blood occurs in areas Figure 44-3 Three-compartment (Riley) model of gas exchange. The lung is of atelectasis or airway blockage, as in acute lung injury (ALI) or imagined to consist of three functional units consisting of alveolar dead space, “ideal” alveoli, and venous admixture (shunt). Gas exchange occurs pneumonia. Alveoli are collapsed or unventilated but continue to only in the “ideal” alveoli. The measured alveolar dead space consists of true be perfused. Venous drainage from lung tumors also constitutes alveolar dead space together with a component caused by V Q scatter. The a pathologic shunt. If hypoxic pulmonary vasoconstriction (HPV) measured venous admixture consists of true venous admixture (shunt) fails to adequately limit blood flow to these regions, hypoxemia together with a component caused by V Q scatter. Note that “ideal” alveolar gas is exhaled contaminated with alveolar dead space gas, so it is not occurs. Indeed, inhaled anesthetics are known to cause attenua­ possible to sample “ideal” alveolar gas. (From Lumb AB: Nunn’s Applied tion of HPV, and induction of general anesthesia (GA) causes Respiratory Physiology, 6th ed. Philadelphia, Elsevier/Butterworth immediate development of atelectasis (see Chapter 15).12,13 Both Heinemann, 2005.)
  5. 5. Respiratory Monitoring 1415 44with zero V Q ) but should be thought of as a total shunt because lung. A host of other variables can be accurately measured, includ­it includes intracardiac and physiologic shunting and the ing intrapulmonary shunt and alveolar dead space. The techniquecontribution of areas with relatively low (shuntlike) but nonzero is cumbersome and the numerical analyses rather complicated for V Q. Thus, the model is unable to predict how much each of routine use, but studies using the technique have been invaluablethese factors contributes to the calculated shunt because they all to our understanding of gas exchange in intensive care unitintroduce undersaturated blood into the arterial circulation. It is (ICU)16 and surgical17,18 settings. Figure 44­5 shows a typical plotthough that breathing 100% O2 eliminates the shuntlike contribu­ in awake patients, with the development of shunt, increased deadtion by fully saturating capillary blood in low­ V Q alveoli, but it space, and V Q scatter on induction of GA. Increasing shunt Section IV Anesthesia Managementappears instead that these regions may progress via resorption detected by multiple inert gas elimination (MIGET) has beenatelectasis into areas of true shunt.14 Making the distinction correlated with increasing atelectasis noted on chest computedbetween true shunt and shuntlike regions caused by low V Q tomography (CT).19 Distinguishing between true shunt and lowmay be clinically important, particularly for anesthesiologists, in V Q can also be performed noninvasively by simultaneouslythat reduced V Q has been shown to be more predictive of post­ plotting Sao2 versus Pio2 (Fig. 44­6). Increasing shunt shifts theoperative hypoxemia than increased shunt is.10 Techniques curve downward, whereas reducing V Q below the normal 0.8allowing more accurate distinction between the components of shifts the curve rightward. The figure schematically shows thecalculated shunt and dead space have been developed and are long­established observation that hypoxemia caused by truedescribed later. shunt is minimally responsive to increased Pio2, in contrast to A method has been derived to estimate shunt fraction hypoxemia caused by V Q mismatch. As mentioned, V Qwithout sampling arterial or mixed venous blood.15 Arterial reduction detected by a rightward shift of the curve intraopera­oxygen content is calculated from measured hemoglobin (Hb) tively has been shown to correlate with hypoxemia up to 30 hoursand Spo2, and Po2 is obtained from the alveolar gas equation by postoperatively. The technique may help identify patients at riskusing end­tidal Pco2 as an estimate of Paco2. Mixed venous O2 for postoperative hypoxemia and in need of supplemental O2 andcontent is estimated by assuming a fixed arterial–to–mixed venous closer monitoring. It can also be used in patients with chronicO2 gradient. Estimates of shunt fraction obtained by this method lung disease to determine whether additional O2 may be neededare expectedly somewhat imprecise (±16%) when compared with during air travel or at altitude.10invasive measurements but are adequate for clinical use. The dead space component in the three­compartment gasexchange model can be calculated with the Bohr equation: Blood Gas Analysis VDS VT = (PaCO2 − PECO2 ) PaO2 (12)where Peo2 is the mixed expired Pco2 Measurement of Blood Gas Tensions The fraction calculated includes anatomic, alveolar, andapparatus (i.e., breathing circuit) dead space, which together rep­ The basic design that modern blood gas analyzers still use todayresent physiologic dead space. was introduced by Severinghaus and Bradley in 1958.20 Designed As with the shunt calculation described earlier, dead space by Leland Clark in 1953,21 the Po2 electrode is a platinum probedetermined by the equation is not true dead space because it bathed in an electrolyte solution and separated from the sampleincludes an indeterminate contribution from relatively underper­ (blood) by an O2 permeable membrane. Oxygen molecules passfused or dead space–like alveoli with high V Q (see Fig. 44­3). from blood through the membrane and are reduced to hydroxylAnother limitation of the model is that alterations in cardiac ions. Po2 is proportional to the current generated by this reduc­output or Hb concentration can lead to different calculated values tion reaction. Similarly, the Stow/Severinghaus Pco2 electrode isof shunt fraction, even when actual V Q ratios have not changed. a pH­sensitive glass probe bathed in a bicarbonate solution andA substantial rise in cardiac output will increase SvO2 and cause encased by a CO2 permeable membrane. Pco2 is proportional toa subsequent rise in the O2 content of shunted blood and there­ the H+ generated as CO2 reacts with water to form H+ and HCO3−.fore arterial blood (Fig. 44­4). The calculated shunt fraction would Severinghaus and Astrup have provided a detailed history of thedecrease without an actual decrease in percent shunt by volume. development of blood gas analysis (BGA).22,23Distinguishing between Shunt and Altered V Q as theCause of Impaired Oxygenation Temperature CorrectionIn 1974, Wagner and coauthors described a technique known asmultiple inert gas elimination (MIGET), which allows plotting of Modern blood gas analyzers measure blood gas tensions at 37°C.pulmonary ventilation and perfusion against the V Q ratio for a Because patients rarely have a temperature of exactly 37°C, bloodlarge number of lung compartments (rather than just three samples must be heated or cooled to 37°C for analysis. Heating acompartments as in the Riley approach), all with different V Q blood sample decreases pH, gas solubility, and Hb affinity for O2ratios.14 Six inert tracer gases with widely varying blood solubility and CO2. Thus, as the blood from a hypothermic patient (sayare infused intravenously and allowed to reach steady state. Arte­ 35°C) is heated and analyzed at 37°C, more gas becomes dissolvedrial and mixed expired gas concentrations are measured, and the in solution and the measured Po2 and Pco2 will be higher thanmixed venous concentration is calculated via the Fick principle. at 35°C. Raising the temperature also increases the H+ concentra­Retention­solubility and excretion­solubility curves are created tion and would give a falsely low pH in a hypothermic patient.and then translated into a continuous plot of perfusion against Modern analyzers use one of a number of algorithms to automati­ V Q and ventilation against V Q, respectively, in relation to the cally correct pH and blood gas tensions for temperature, and Boxheterogeneous spectrum of V Q ratios present throughout the 44­2 provides the formulas approved by the National Committee
  6. 6. IV 1416 Anesthesia Management Lung PAO2=100 mm Hg O2 PcO2=100 O2 content=19.3 . QA = 90% . QT . QS PsO2=40 ¯ PvO2=40 . =10% O2 content=13.9 O2 content=13.9 QT ¯ SvO2=72% PaO2=78 O2 content=18.8 . QT = 5 L/min Œ . 240 mL/min VO2 Figure 44-4 Effect of cardiac output on Po2. Hb = 14 g/dL A, Arterial and mixed venous O2 tension and content A Tissue are shown at a cardiac output of 5 L/min. B, Assuming constant VO2 , an increase in cardiac output to 8 L/min increases Pao2 from 78 to 85 mm Hg because SvO2 increases at higher cardiac output. The resulting increase in O2 content of the shunted blood (here Lung assumed to be 10% of cardiac output) then raises the arterial O2 content and Pao2. Po2 values are in mm Hg, and O2 content is in mL/dL. PAO2=100 mm Hg O2 PcO2=100 O2 content=19.3 . QA = 90% . QT . PsO2=48 ¯ PvO2=48 QS . =10% O2 content=15.9 O2 content=15.9 QT SvO2=82% ¯ PaO2=85 O2 content=19.0 . QT = 8 L/min Œ . 240 mL/min VO2 B Tissue for Clinical Laboratory Standards (NCCLS). The corrections are all rather slight, and there is little evidence to suggest that tem­ Artifactual Changes in Arterial Blood perature­corrected values are clinically more useful than 37°C Gas Values values. Two approaches, pH­stat and alpha­stat, have been used to manage pH in hypothermic patients undergoing cardiopulmo­ Delay in analyzing a blood sample after it is drawn can artifactu­ nary bypass. The alpha­stat approach lets pH rise naturally into ally change the measured pH and gas tensions. Storing a sample the alkalotic range as the patient is cooled, and pH­stat maintains longer than 20 minutes can cause a significant elevation in Pco2 normal pH and presumably cerebral perfusion by adding CO2. and reduction in Po2 and pH, probably secondary to cellular Data favoring either approach are very limited. metabolism. Leukocytosis and thrombocytosis accelerate these
  7. 7. Respiratory Monitoring 1417 44 0.8 Perfusion VD=35% Ventilation 0.6 0.4 Perfusion or ventilation (L/min) 0.2 O S =0% VA /Q Section IV Anesthesia Management 0.0 0 0.01 0.1 1 10 100 Anesthesia 0.8 Perfusion VD=41% Ventilation 0.6 0.4 O S =5.9% 0.2 VA /Q 0.0 0 0.01 0.1 1 10 100 AnesthesiaFigure 44-5 Ventilation-perfusion ( VA Q) distribution and computed tomography in a supine subject. Left, VA Q distribution in an awake (top) andanesthetized (bottom) subject. Note the appearance of a pulmonary shunt and an increase in VA Q mismatch during general anesthesia with mechanicalventilation. Right, Computed tomography of the chest just above the top of the right diaphragm. Note the appearance of densities in the dependent lungregions during anesthesia. Vd, volume of distribution. (Redrawn from Gunnarsson L, Tokics L, Gustavsson H, et al: Influence of age on atelectasis formation andgas exchange impairment during general anesthesia. Br J Anaesth 66:423-432, 1991.) 0% Shunt 100 10% 100 0% 20% HbO2 saturation (%) 30% 95 95 HbO2 saturation (%) 30% 90 90 40% 85 85 80 50% Shift 80 75 75 70 0 10 20 30 40 50 60 0 10 20 30 40 50 60 PO2 (kPa) PO2 (kPa) A BFigure 44-6 Hemoglobin-oxygen (HbO2) saturation versus inspired partial pressure of oxygen (Po2). The curves are plotted by changing inspired Po2 instepwise fashion. A, Series of theoretical curves obtained by calculating the effect of different degrees of right-to-left shunt. Increasing shunt displaces thecurves downward. B, The curve on the left of the graph (0%) is from a normal subject. The middle curve (30%) represented a 30% right-to-left shunt from the 30%curve seen in A. The curve on the right of this graph is from a patient undergoing thoracotomy for esophageal surgery. The points cannot be fitted by any ofthe shunt curve, but the fit is quite good when the 30% curve is shifted to the right. This implies a combination of shunt and VA Q mismatch. (Adapted fromJones JG, Jones SE: Discriminating between the effect of shunt and reduced VA Q on arterial oxygen saturation is particularly useful in clinical practice. J ClinMonit Comput 16:337, 2000.)
  8. 8. IV 1418 Anesthesia Management Box 44-2 Algorithms for Correction to Body Temperature of arterial Po2 when skin is warmed, which causes blood flow to Blood Gas Tensions Measured at 37°C exceed the amount required for local O2 consumption. O2 from capillaries diffuses through the warmed skin, where it is analyzed pH by a Clark­type electrode adhered to it. Though useful in infants, transcutaneous gas monitoring has many limitations despite good ΔpH/ΔT = −0.0146 + 0.0065 (7.4 − pHm) agreement of Po2 values with traditional BGA.25 Peripheral vas­ ΔpH/ΔT = −0.015 cular disease or vasoconstriction can generate erroneous values. ΔpH/ΔT = −0.0147 + 0.0065 (7.4 − pHm)* Cutaneous hypoxia caused by reduced cardiac output will give ΔpH/ΔT = −0.0146 falsely decreased Po2 readings. These devices must be calibrated frequently, have a relatively slow response time, and can cause Pco2 skin burns with prolonged application. Δlog10 Pco2/ΔT = 0.019* Δlog10 Pco2/ΔT = 0.021 In-Line Blood Gas Monitoring Po2  0.0252  Continuous intra­arterial pH measurement was accomplished as ∆ log10 PCO2 ∆T =  + 0.00564 early as 1927 with antimony electrodes. Shortly after Clark devel­  0.234 (PO2 100 )3.88 + 1  oped his Po2 electrode in 1956, the first continuous intravascular ∆ log10 PCO2 ∆T = 0.0052 + 0.27[1− 10 −0.13(100 − SAO2 ) ] blood gas monitoring (CIBGM) devices were developed. Early 5.49 × 10 −11 PO2.88 + 0.071* 3 devices consisted of electrochemical sensors and were essentially ∆ log10 PCO2 ∆T = modified Clark electrodes. Problems with these devices included 9.72 × 10 PO2.88 + 2.3 −9 3 excessive drift, lack of reliability, large size, and interference from 0.012 (PO2m 714 ) + (SO2 100 ) anesthetic gases. Later, Lubbers and Opitz, using a technology (1− SO2 100)(Hb 0.6) + 0.073 known as fluorescence quenching, created fiberoptic probes to ∆ log10 PCO2 ∆T = PO2m 714 + SO2 100 (1− SO2 100 )(Hb 0.6) continuously measure Po2 and Pco2, which they named optodes.26 So2 ≤ 95%: Δlog10 Pco2/ΔT = 0.31 Absorbance­based fiberoptic sensors were also developed. Only two single­parameter devices became commercially available: the SO2 > 95%: ∆ log10 PCO2 ∆T = 0.032 − 0.0268e(0.3 SO2 − 30) Continucath 1000 electrochemical Po2 sensor for adults and the *National Committee for Clinical Laboratory Standards (NCCLS)- Neocath (Biomedical Sensors, High Wycomb, UK) O2 sensor for approved standard. Hb, blood hemoglobin concentration in g/dL; pHm and Po2m, pH and neonatal umbilical artery placement. Po2 values measured at an electrode temperature of 37°C; Po2, Advances in the design of single­parameter systems inevi­ partial pressure of oxygen in mm Hg; So2, percent hemoglobin- tably led to the development of multiparameter devices capable oxygen (HbO2) saturation; T, temperature in degrees centigrade of measuring pH, Pco2, Po2, and temperature. Most are pure (°C). optode systems, with the Paratrend 7 being the only hybrid Data from Ashwood ER, Kost G, Kenny M: Temperature correction of blood-gas and pH measurements. Clin Chem 29:1877, 1983; and optode­electrode system. The upgraded Paratrend 7+ replaced the Siggaard-Andersen O, Wimberley PD, Gothgen I, Siggaard- Clark Po2 electrode with an optode, thus making it a pure optode Andersen M: A mathematical model of the hemoglobin-oxygen system (Fig. 44­7). dissociation curve of human blood and of the oxygen partial Agreement between sensor and traditional BGA measure­ pressure as a function of temperature. Clin Chem 30:1646, 1984. ments can be quantified by use of the Bland­Altman calculation Microporous polyethylene changes.24 Because red cells do not contain mitochondria, this tube (gas and ion permeable) phenomenon is not observed in polycythemia. However, anaero­ bic glycolysis can generate lactic acid and reduce pH. Placing the Void between sensors filled with acrylamide gel sample in ice immediately after it is obtained can maintain its containing phenol red stability, and addition of sodium fluoride or cyanide can inhibit cellular O2 consumption.24 The presence of air bubbles in the pH sensor Thermocouple sample syringe can falsely elevate Po2 but has little effect on pH and Pco2. Syringes are usually heparinized to prevent coagulation. Transcutaneous Blood Gas Monitoring Although the turnaround time for obtaining Po2 with traditional blood gas analyzers has drastically decreased since their incep­ tion, the ability to assess a patient’s oxygenation status even more rapidly and easily has obvious advantages. One alternative is to CO2 sensor Oxygen sensor measure gas tensions at the bedside transcutaneously. This tech­ Figure 44-7 Cross section of the Paratrend 7 sensor tip. (Courtesy of nology relies on the tendency of capillary Po2 to approximate Biomedical Sensors, High Wycombe, UK.)
  9. 9. Respiratory Monitoring 1419 44of bias and precision.27 Bias is the difference between mean values Box 44-3 Advantages of a Continuous Intra-arterial Bloodobtained by standard methods (BGA) and those obtained Gas Monitoring System over Intermittent Blood Gas Analysiswith the new device being tested. Precision is the standard devia­tion of these differences and measures reproducibility of the Availability of continuous dataresults. Earlier detection of deleterious events Like their predecessors, newer probes remain fragile andcontinue to exhibit motion artifact, wall effect (decreased Po2 Potential for trend analysisreadings because of contact with the arterial wall), and thrombo­ Decreased blood loss Section IV Anesthesia Managementgenicity. Their accuracy diminishes with insufficient blood flow Decreased laboratory turnaround timeto the cannulated artery. Moreover, despite encouraging in vitro Decreased exposure of staff to potentially infected bloodand animal studies, results from clinical trials have not consist­ently been as favorable. Data for Pco2 and pH measurements are From Venkatesh B: In-line blood gas monitoring. In Papadakos PJ,impressive, but studies have found poor agreement of sensor Lachmann B (eds): Mechanical Ventilation: Clinical Applications andPo2 measurements with those obtained by BGA in elevated Po2 Pathophysiology. Philadelphia, Elsevier, 2008.ranges.28,29 Weiss and colleagues found accurate results withminimal drift in all parameters up to 10 days after insertion in globin (HbR), carboxyhemoglobin (COHb), and methemoglobinpediatric patients, but the O2 sensor required frequent calibra­ (MetHb). Each of these species has unique absorption spectra,tion.30 Several published studies on the clinical performance of and corresponding wavelengths of light are used to analyze avarious CIABGM devices are summarized in Table 44­1. small blood sample. It is currently the gold standard for measur­ Despite its limitations, CIABGM has many theoretical ing Sao2. Results are usually obtained in less than 2 minutes.advantages over traditional BGA, although no outcome studieshave proved these advantages (Box 44­3). Use of CIABGM incardiac, thoracic, orthopedic, and transplant surgery may lead Transcutaneous Oximetryto earlier detection of severe blood gas and acid­base derange­ments.35,36 Detection of Po2 changes after cement implantation The principle of transcutaneous oximetry is similar to that ofduring hip replacement has been accomplished with this transcutaneous gas tension monitoring, but Sao2 is measuredtechnology.33 It has been validated for use in anesthesia and instead of Po2. Two wavelengths of light are used to measureintensive care in pediatric patients.32 Further technologic refine­ quantities of oxygenated and deoxygenated blood to give an esti­ments, outcome studies, and data on cost­effectiveness are neces­ mate of Sao2, provided that the blood being analyzed is mostlysary for CIABGM to have widespread application in anesthesia arterial and other Hb species are absent. Two­wavelength earand critical care. oximeters were developed and used in practice more than 60 years ago.37 Robert Shaw patented an eight­wavelength ear oxi­ meter in 1972, and a device using this technology was marketed in the late 1970s by Hewlett Packard. Problems with size and reli­ Oxygen Saturation ability of data prevented its widespread use.Although traditional BGA remains the standard modality fordetermining oxygen content, an alternative is to measure oxygen Pulse Oximetrysaturation (So2). It can provide rapid and clinically useful infor­mation about oxygenation status. Some of the problems with transcutaneous oximetry were solved with the invention of pulse oximetry. Though first developed in Japan in the early 1970s, it was not until a decade later that its Co-oximetry routine use began. Pulse oximetry works by analyzing the pulsa­ tile arterial component of blood flow, thereby ensuring that arte­The co­oximeter is a traditional blood gas analyzer that is also rial saturation (Spo2) rather than venous saturation is beingcapable of measuring concentrations of HbO2, reduced hemo­ measured (Fig. 44­8). Two wavelengths of light are used, usuallyTable 44-1 Results from Some Published Studies on Clinical Performance of Continuous Intra-arterial Blood Gas Monitoring Number of Clinical Setting and pH Bias ± Precision Pco2 Bias ± Po2 Bias ± Investigator(s) Device Patients Insertion Site (pH Units) Precision (mm Hg) Precision (mm Hg) Ganter29 Paratrend 7+ 23 OR: thoracoscopic surgery −0.01 ± 0.06 3±9 −20 ± 86 (radial) Coule et al.31 Paratrend 7+ 50 (Ped) ICU (radial/femoral) 0.00 ± 0.04 0.38 ± 4.8 0.75 ± 25 Weiss et al. 30 Paratrend 7 24 (Ped) ICU (radial/femoral) 0.005 ± 0.03 −1.8 ± 6.3 1.2 ± 24 Venkatesh et al. 33 Paratrend 7 10 OR: hip replacement (radial) 0.02 ± 0.03 0.53 ± 1.8 1.2 ± 20 Larson et al.34 PB 3300 29 OR/ICU (radial) 0.01 ± 0.04 1.2 ± 3.3 0.3 ± 9ICU, intensive care unit; OR, operating room; Ped, pediatric.
  10. 10. IV 1420 Anesthesia Management are calibrated against laboratory Sao2 down to 70% saturation, Absorption due to AC pulsatile arterial blood and lower saturations are determined by extrapolation of the curve. Thus, pulse oximeters cannot be calibrated by the user, and Absorption due to Light absorption nonpulsatile arterial blood their reliability is dependent on the quality of signal processing Absorption due to venous and the stored calibration curve. and capillary blood DC Accuracy of Pulse Oximetry Absorption due to tissue Because of its impressive accuracy, reliability, and convenience, pulse oximetry has become one of the most important techno­ logic developments in clinical monitoring. Several studies Time comparing co­oximetry and pulse oximetry report substantial agreement between Spo2 and Sao2 over a wide range of Sao2 Figure 44-8 Principle of pulse oximetry. Light passing through tissue values.38,39 containing blood is absorbed by tissue and by arterial, capillary, and venous blood. Usually, only the arterial blood is pulsatile. Light absorption may therefore be split into a pulsatile component (AC) and a constant or Errors in Pulse Oximetry nonpulsatile component (DC). Hemoglobin O2 saturation may be obtained by Because Spo2 measurements are averaged over a few seconds to application of Equation 19. (Data from Tremper KK, Barker SJ: Pulse oximetry. provide readings, there is some degree of delay in response time. Anesthesiology 70:98, 1989.) Hypothermia, low CO, and vasoconstriction secondary to drugs or peripheral hypoxia all increase bias, imprecision, and response time for hypoxic episodes (Table 44­2).40 This appears to be more common with finger probes than with ear or forehead monitoring 660 nm (red) and 940 nm (infrared), because oxygenated and (Fig. 44­10).41 Motion artifact and hypoperfusion are the most deoxygenated blood each absorb light quite differently at these common causes of Spo2 inaccuracy,42,43 both of which are less wavelengths. At 660 nm, HbO2 absorbs less light than HbR does, problematic with newer oximeters. Caution is advised in using whereas the opposite is observed with infrared light. Two diodes pulse oximetry to not make inferences about gas exchange. Spo2 emitting light of each wavelength are placed on one side of the should not be used to assess the adequacy of ventilation because probe and a photo diode that senses the transmitted light on the Sao2 is only minimally affected by changes in Pco2 (via the Bohr opposite side. The amount of light absorbed at each wavelength effect). In addition, when Po2 is high, large decreases in oxygen by the pulsatile arterial component (AC) of blood flow can be tension produce only small changes (if any) in Sao2 and may not distinguished from baseline absorbance of the nonpulsatile com­ be detected with pulse oximetry (see Fig. 44­2). ponent and surrounding tissue (DC). The ratio R is calculated Anemia, with an Hb concentration as low as 2.3 g/dL, has by the oximeter as follows and is empirically related to O2 little or no effect on Spo2 readings when Sao2 is normal,44 but saturation: underestimation of Sao2 has been observed during hypoxemia.45 Because MetHb substantially absorbs both red and infrared light, R = ( AC 660 DC 660 ) ( AC 660 DC 660 ) (13) falsely low Spo2 readings are generated when actual Sao2 is above A calibration curve (Fig. 44­9) is derived from R and labo­ 85%, and readings are falsely high when actual Sao2 is below 85%. ratory measurements of arterial oxygen saturation in healthy vol­ Spo2 invariably reads 85% when very large amounts of MetHb are unteers and the algorithm stored in the oximeter. Modern devices present.46 Conversely, COHb absorbs very little infrared light, but it is very similar to HbO2 in its red light absorbance. Oximeters using only two wavelengths therefore cannot distinguish between HbCO and HbO2, and the presence of HbCO produces falsely Red elevated Spo2 readings. Erroneous Spo2 readings can be caused IR by structural hemoglobinopathies,47,48 as well as by a host of other Modulation ratio (R) factors, many of which are summarized in Table 44­2. Observed R Recent Advances in Pulse Oximetry Error corrEction. Motion sensitivity and signal loss secondary to hypoperfusion are two of the more common errors SpO2 that occur with pulse oximetry. These inaccuracies have been reduced with the recent advances in signal analysis that have been incorporated into units from a number of manufacturers.49 Several studies suggest that newer units can detect hypoxemic 0 20 40 60 80 100 episodes more reliably than their predecessors can under these SaO2 (%) conditions.50,51 Indeed, one study reported that during hypoper­ Figure 44-9 Red/infrared modulation ratio (R) versus oxygen saturation fusion or excessive motion, oximeters using this technology give (Sao2). At high Sao2 (right side of the graph), the pulse amplitude (or accurate Sao2 readings in 92% of cases in which older monitors modulation) of the red signal is less than that of the infrared signal, whereas failed.52 the reverse is true at low Sao2. Pulse oximeters measure R, the ratio of red to MultiwavElEngth PulsE oxiMEtErs. Because only two infrared pulse amplitudes (see Equation 13), and estimate Sao2 by applying the calibration curve (solid line) as depicted by the dashed line and arrow. wavelengths of light are used in traditional pulse oximeters, the (From Mannheimer PD: The light-tissue interaction of pulse oximetry. Anesth presence of additional Hb species cannot be detected, which may Analg 105(6 Suppl):S10-S17, 2007.) result in erroneous readings. Using principles from both pulse
  11. 11. Respiratory Monitoring 1421 44 100 Digit 90 sec 90 sec 90 sensors SpO2 (%) 80 Section IV Anesthesia Management Forehead 70 sensors Reduced FlO2 Reduced FlO2 60 00:00 02:00 04:00 06:00 08:00 10:00 12:00 Elapsed time (mm:ss)Figure 44-10 Effect of pulse oximeter probe replacement on delay from onset of hypoxemia to a drop in measured Spo2. During cold-induced peripheralvasoconstriction in normal volunteers, the onset of hypoxemia was detected more quickly with an oximeter probe on the forehead than on the finger. Otherstudies have shown a similar advantage for pulse oximeter probes placed on the ear. (From Bebout DE, Mannheimer PD, Wun C-C: Site-dependent differencesin the time to detect changes in saturation during low perfusion. Crit Care Med 29:A115, 2002.)oximetry and co­oximetry, the first eight­wavelength pulse oxi­ surgical setting, pulse oximetry became a standard of care inmeter capable of measuring several species of Hb has become anesthesia practice in 1986. In a large study comparing intraop­commercially available and may prove to be a major advance in erative pulse oximeter use with standard care, 80% of anesthesi­oxygen monitoring. The Massimo Rad­57 (Massimo Corp, Irvine, ologists felt more comfortable when using pulse oximetry.61 It isCA) gained Food and Drug Administration (FDA) clearance in interesting to note that despite its widely accepted value, there is2006 and boasts the ability to accurately measure MetHb and little evidence that pulse oximetry affects outcomes in anesthe­COHb, in addition to all the features of conventional pulse oxi­ sia,62 and a study evaluating postsurgical patients did not demon­metry. Two large studies comparing measurements from the unit strate that routine Sao2 monitoring reduces mortality, cost ofwith conventional co­oximetry in emergency department patients hospitalization, or ICU transfer.63have produced equivocal results, with one reporting a significant PErioPErativE. In a randomized, controlled study of 200number of false­positive readings.53,54 One smaller study in surgical patients, Moller and colleagues found a reduced inci­healthy volunteers reported good agreement between oximeter dence of hypoxemia intraoperatively and in the postanesthesiaand laboratory measurements,55 and other investigations to deter­ care unit (PACU) when pulse oximetry was used. In the recoverymine accuracy of the device are ongoing. room, patients in the oximeter group on average received higher rEflEctancE PulsE oxiMEtry. The technology was Fio2 and more naloxone, had a longer stay, and were dischargeddeveloped to combat problems with signal transmission during with supplemental O2 more frequently.64 The same group laterhypoperfusion and for use when a transmission path is unavaila­ conducted a study looking at postoperative complications withble. Probes are commonly placed on the forehead, where motion and without intraoperative pulse oximetry in 20,802 patients. Noartifact and hypoperfusion tend to be less of a problem than with overall difference was found in complication rate, outcome, meanother sites.56 Forehead probes are commercially available and hospital stay, or in­hospital death between the groups, evenappear to detect hypoxemia more quickly than ear or finger though hypoxemia and hypoventilation were detected more fre­probes do.41 The light­emitting and light­sensing diodes are on quently when pulse oximetry was used.64 However, post hocthe same side of the probe instead of opposite sides as in tradi­ analysis of this trial suggests that pulse oximetry may havetional pulse oximetry, and the reflected light from the tissue bed decreased the incidence of myocardial ischemia.62 A number ofis analyzed. Indeed, reflectance oximetry has been used to monitor studies report detection of hypoxemia several days postopera­fetal oxygen saturation with scalp probes and been shown to tively with pulse oximetry.65,66 Intrapartum fetal pulse oximetrydecrease surgical intervention in the face of non­reassuring fetal in the presence of a non­reassuring fetal heart rate is associatedstatus.57 Esophageal probes have been designed and have shown with a reduction in operative interventions.57 The peak effects ofsuccess in measuring Spo2 during cardiothoracic surgery when analgesia may correlate with hypoxemia, so monitoring of patientsfinger probes have failed.58 The investigators reported minimal receiving narcotics may be important to prevent adverse cardiacbias and narrow limits of agreement when compared with finger events.67probes used in the study. Monitoring of gastric Spo2 as an indica­ critically ill. The complicated pathophysiologic milieutor of splanchnic perfusion has also shown promise.59 Excessive of critical illness is such that many monitoring devices canedema, poor skin contact, and motion artifact are the most produce inaccurate data in this patient population. Pulse oxime­common sources of error in reflectance oximetry. Artifacts have try, on the other hand, appears to maintain its reliability. Jubranalso been shown to occur with probe placement directly over a and Tobin found that pulse oximeters accurately estimate Sao2 inpulsating superficial artery.60 critically ill patients when Sao2 is greater than 90% (bias, 1.7%; precision, ±1.2%) but are less accurate when Sao2 falls belowClinical Applications of Pulse Oximetry 90%.68 An Spo2 of 92% was indicative of adequate oxygenationPulse oximetry is arguably most useful as an early warning sign when titrating O2 in white patients. In black patients, however,of hypoxemia. Because this is of paramount importance in the significant hypoxemia was commonly present with an Spo2 of
  12. 12. IV 1422 Anesthesia Management Table 44-2 Artifacts in Pulse Oximetry Factor Effect Toxic Alterations in Hemoglobin Carboxyhemoglobin (COHb) Slight reduction of the assessment of oxygen saturation (Sao2) by pulse oximetry (Spo2) (i.e., overestimates the fraction of hemoglobin available for O2 transport) Cyanmethemoglobin Not reported Methemoglobin (MetHb) At high levels of MetHb, Spo2 approaches 85%, independent of actual Sao2 Sulfhemoglobin Not reported (affects CO oximetry by producing a falsely high reading of MetHb) Structural Hemoglobinopathies Hemoglobin F No significant effect Hemoglobin H No significant effect (i.e., overestimates the fraction of hemoglobin available for O2 transport) Hemoglobin Köln Artifactual reduction in Spo2 of 8% to 10% Hemoglobin S No significant effect Hemoglobin Replacement Solutions Diaspirin cross-linked hemoglobin No significant effect Bovine polymerized hemoglobin (oxygen No significant effect carrier-201) Dyes Fluorescein No significant effect Indigo carmine Transient decrease Indocyanine green Transient decrease Isosulfan blue (patent blue V) No significant effect at low dose; prolonged reduction in Spo2 at high dose Methylene blue Transient, marked decrease in Spo2 lasting up to several minutes; possible secondary effects as a result of effects on hemodynamics Hemoglobin Concentration Anemia If Sao2 is normal, no effect; during hypoxemia with Hb values less than 14.5 g/dL, progressive underestimation of actual Sao2 Polycythemia No significant effect Other Factors Acrylic fingernails No significant effect Ambient light interference Bright light, particularly if flicker frequency is close to a harmonic of the light-emitting diode switching frequency, can falsely elevate the Spo2 reading Arterial O2 saturation Depends on manufacturer; during hypoxemia, Spo2 tends to be artifactually low Blood flow Reduced amplitude of pulsations can hinder obtaining a reading or cause a falsely low reading Henna Red henna, no effect; black henna, may block light sufficiently to preclude measurement Jaundice No effect; multiwavelength laboratory oximeters may register a falsely low Sao2 and falsely high COHb and MetHb Motion Movement, especially shivering, may depress the Spo2 reading Nail polish Slight decrease in Spo2 reading, with greatest effect using blue nail polish, or no change Sensor contact “Optical shunting” of light from source to detector directly or by reflection from skin results in falsely low Spo2 reading Skin pigmentation Small errors or no significant effect reported; deep pigmentation can result in reduced signal Tape Transparent tape between sensor and skin has little effect; falsely low Spo2 has been reported when smeared adhesive is in the optical path Vasodilatation Slight decrease Venous pulsation (e.g., tricuspid insufficiency) Artifactual decrease in Spo2 92%, and an Spo2 of 95% was needed to ensure adequate oxygena­ bles.70,71 Respiratory variations in systolic pressure (dPs) and arte­ tion. After cardiac surgery, use of pulse oximetry has been shown rial pulse pressure (dPp) have been shown to be accurate indicators to increase detection of hypoxemic episodes and decrease the of volume status and fluid responsiveness in mechanically venti­ number of arterial BGAs performed in the ICU.69 lated patients (Fig. 44­11).72 Pulse pressure variation may predict fluid responsiveness more reliably than the use of dPs can. Such New and Future Applications analyses require placement of an arterial catheter and are not Analysis of the plethysmographic waveform generated by pulse always practical. Recently, variation in the pulse oximeter plethys­ oximeters has been advocated as a means of assessing volume mograph (dPOP) amplitude was shown to be a reliable noninva­ status, fluid responsiveness, and a number of other clinical varia­ sive surrogate for dPp because both parameters are dependent on
  13. 13. Respiratory Monitoring 1423 44 Arterial pressure this balance. It can be calculated by rearranging the Fick equation for O2: Systolic pulse variation SvO2 = SaO2 − VO2 (Hb × 1.39 × CO) (14) From this equation, it is clear that decreased SvO2 can be caused by low Sao2, low Hb, or low cardiac output, all of which decrease Pulmonary arterial pressure oxygen delivery (Do2), or by increased O2 consumption ( VO2 ). These variables are related in the following way: Section IV Anesthesia Management VO2 = DO2 × ERO2 (15) where ERO2 is the extraction ratio (%) of O2. Inspiration Expiration If oxygen delivery to tissue falls and consumption is to Central venous pressure remain constant, oxygen extraction by tissues must increase. Blood returning to the right heart will therefore have a reducedFigure 44-11 Cyclic variation of vascular pressures during positive-pressure O2 content and SvO2 . Thus, a reduced SvO2 is suggestive ofventilation. Inspiratory reduction in preload leads to reduced left ventricular global tissue hypoxia, which often precedes multiorgan failurevolume after a lag phase of a few heartbeats because of pulmonary vasculartransit time. The inspiratory decrease in left ventricular volume results in and death.80 Increased anaerobic metabolism as evidenced bydecreased stroke volume and systolic blood pressure during expiration. increased lactate levels ensues and is associated with increasedSimilar variations in amplitude can be noted in pulse oximeter waveforms. mortality.81 These processes are usually under way as SvO2(From Nanchal R, Taylor RW. Hemodynamic monitoring. In Papadakos PJ, approaches 40%. A pulmonary artery catheter is required toLachmann B [eds]: Mechanical Ventilation: Clinical Applications and measure mixed venous saturation, and continuous monitoringPathophysiology. Philadelphia, Elsevier, 2008.) can be performed with a catheter that incorporates a fiberoptic bundle. A superior vena cava sample obtained from a centralstroke volume.73 In a study of patients under GA, Cannesson and venous catheter is often used as a surrogate for mixed venouscolleagues found that baseline dPOP was correlated with percent saturation when a pulmonary artery catheter is impractical orchange in cardiac index induced by volume expansion.74 Similar unavailable.82results were obtained in a separate study on critically ill septic Shock of any etiology can cause the aforementioned turnpatients.75 The authors of these trials concluded that dPOP can of events, and a low SvO2 sheds no light on the cause of the globalpredict response to fluid administration and quantifies the effect hypoxia. As mentioned, low SvO2 may not always be secondaryof volume expansion on a number of hemodynamic parameters. to impaired delivery but may be due to increased oxygen con­To elucidate where the oximeter probe should be placed to best sumption in the face of fever, thyrotoxicosis, and other conditionsdetect these variations, Shelley and colleagues analyzed plethys­ (Fig. 44­12). Moreover, a normal SvO2 is not necessarily indicativemographic waveforms from finger, ear, and forehead probes in of adequate tissue oxygenation. Although cardiogenic and hypo­patients undergoing positive­pressure ventilation during surgery, volemic shock is very often associated with low SvO2 , it can beas well as in spontaneously breathing patients.76 Their results normal or elevated in shock secondary to severe sepsis or hepaticsuggest that the ear and forehead may be better monitoring sites failure because these conditions are frequently associated withthan the finger for detection of variation in respiratory waveform. microvascular dysfunction and impaired oxygen extraction byBecause error and artifact correction in most commercial pulse tissues. Do2 is often elevated in these states.oximeters can obscure the often subtle respiratory variations, In a novel application of continuous SvO2 measurement,unaltered plethysmographic waveforms are needed for such pulse oximetry combined with SvO2 monitoring has been usedanalyses. in patients with acute respiratory failure to continuously monitor Many other novel applications of pulse oximetry in anes­ shunt fraction and adjust ventilator settings accordingly.82 Thethetic practice have been studied. Mowafi found that dPOP may authors of this study adjusted continuous positive airway pressurebe a better indicator of intravascular test dose injection during (CPAP) levels to obtain the lowest shunt fraction and showed thatepidural placement than traditional hemodynamic markers are use of this method results in CPAP settings similar to those(i.e., heart rate and blood pressure).77 A 10% decrease in POP obtained by conventional means. Though somewhat invasive, theindicated intravascular injection with 100% sensitivity, specificity, technique was found to be cost­effective and accurate in titratingpositive predictive value, and negative predictive value. Sensitivi­ CPAP in this subset of patients.ties using heart rate and blood pressure change as criteria were85% to 95%. Changes in perfusion index (defined as AC940/DC940)have been used as confirmation of epidural placement and as anindicator of painful stimulus under anesthesia.78,79 Many modern Tissue Oxygenationoximeters are programmed to measure perfusion index. The goal of optimizing pulmonary gas exchange is to ultimately optimize oxygenation at the cellular level. Analysis of alveolar, arterial, and venous gases is used in conjunction with clinical Mixed Venous Monitoring indices of tissue function (i.e., urine output, mental status) to make inferences about the state of affairs in cells. Oxygen is trans­Shock represents an imbalance between oxygen demand, delivery, ported from alveoli with a Po2 of around 100 mm Hg down aand utilization at the tissue level. Monitoring of mixed venous steep gradient, known as the oxygen cascade, to its final site ofoxygen saturation (SvO2 ) can give insight into the adequacy of utilization, the mitochondrion, where Po2 is estimated to be less

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