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
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).
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
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.)
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
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
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.)
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.)
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.
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
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
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
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
IV 1424 Anesthesia Management ¯ SvO2 Decreased by Increased by Figure 44-12 Causes of changes in mixed venous oxygen saturation. (From Nanchal R, Taylor RW. Hemodynamic monitoring. In Papadakos PJ, Lachmann B [eds]: Mechanical Ventilation: Clinical Applications and Oxygen Oxygen Oxygen Oxygen Pathophysiology. Philadelphia, Elsevier, 2008.) consumption delivery delivery consumption Stress PaO2 PaO2 Hypothermia Pain Hemoglobin Hemoglobin Thyrotoxicosis Cardiac Cardiac Fever output output Seizures Shivering than 1 mm Hg. Mitochondria from skeletal muscle appear to A number of new systems for measuring tissue oxygena maintain their function with a Po2 as low as 0.1 mm Hg.83 tion are under laboratory investigation and have yet to reach Unlike arterial Po2 measurements, which should be nearly commercial availability. Such systems include phosphorescence, equal regardless of the artery sampled, Po2 varies considerably fluorescence, electron paramagnetic resonance oximetry, and within a particular organ or tissue bed because blood flow and nuclear magnetic resonance spectroscopy. A number of reviews O2 consumption are not uniform but vary from point to point detailing all of these techniques have been compiled.87 within the tissue. Because O2 diffuses down a gradient from arte rioles to mitochondria, measurements may also vary depending on where along this pathway a reading is obtained. Thus, it is generally thought that a distribution of Po2 measurements across Expired Gas Analysis the tissue must be obtained to best describe its oxygenation status. Because of variable O2 supply and demand, normal Po2 levels and The ability to rapidly measure concentrations of inspired and distributions differ from organ to organ. expired gas is of paramount importance in anesthetic practice. A variety of methods have been devised to directly measure Most anesthesia machines are equipped with oxygen sensors on oxygen tensions and concentrations within tissues, and it has the inspiratory limb of the circuit to help ensure that an adequate been an area of intense research for several decades. Most of the supply of oxygen is delivered to the patient at all times. Expired technologic advances have been made in the laboratory and have gas analysis is used to make inferences about blood concentra yet to be proved practical in the clinical setting. tions and depth of anesthesia. Several systems are available for the Polarography is the current standard modality for measur measurement of gas tensions in exhaled air. ing tissue oxygenation. It has the best resolution of all the avail able technology. Similar in principle to laboratory BGA, a Clark or needletype electrode is inserted into tissue (rather than a blood sample), and Po2 is proportional to the current generated Mass Spectrometry as oxygen is reduced. Oxygen tension as low as 0.1 mm Hg can be resolved quite accurately. Though too invasive for routine Mass spectrometry is a technique by which concentrations of gas clinical use, the technology is commercially available and has particles in a sample can be determined according to their mass found application in neurosurgery and oncology.84,85 charge ratio. A gas sample is passed through an ionizer and mol Near-infrared spectroscopy is a noninvasive system capable ecules become positively charged ions. Because all of the ions of measuring the oxygenation state of hemoglobin, myoglobin, generated carry the same positive charge, this allows separation and mitochondrial cytochromes.86 The ability to monitor the oxy of particles based solely on mass. A detector then counts the genation status of cytochromes along the electron transport chain number of ions of each mass, and the results are translated into will probably prove to be the best estimate of cellular oxygenation. concentrations. Measurements are quite reliable and can be Up to four wavelengths of light are applied to tissue, and the scat obtained in fractions of a second. tered light is returned via fiberoptic cables to the monitor for Clinical use of mass spectrometry for expired gas analysis analysis. The technology has been incorporated into devices began in respiratory care units in the mid1970s. They were intro capable of measuring blood O2 saturation in the brain, which have duced into operating rooms and anesthesia practice shortly been commercially available for some 20 years.87 Resolution is thereafter. Because of their size and complexity, hospitals often inferior to that of polarography, and problems with calibration connected many operating rooms to a single spectrometer and and interference have limited its widespread use. Images can be had the results relayed back to the anesthesiologist. The conven obtained depicting changes in Hb concentration, but the resolu ience plus low cost of infrared analyzers has largely phased mass tion is poor. spectrometry out of clinical use.
Respiratory Monitoring 1425 44 quantify inhaled and exhaled concentrations of both NO and Infrared Absorption NO2 have been sought. Continuous measurement of inhaled NO has traditionallyPresently, most expired gas analyzers used in anesthesia involve been accomplished with the use of electrochemical sensors. NOinfrared absorption. A gas sample is collected in a chamber is oxidized to nitric acid, and its concentration is proportional tothrough which infrared light is passed, and gas tensions are the current generated by the reaction. A number of electrochemiderived based on the intensity of the transmitted light. Today’s cal NO sensors have been independently evaluated and areinfrared gas analyzers are capable of measuring all anesthetic reported to be quite accurate in measuring inhaled NO and Section IV Anesthesia Managementagents currently in use, as well as CO2 and N2O. Oxygen does not NO2.91,92 The electrodes are sensitive to water vapor, and proabsorb infrared light and therefore must be measured by other longed exposure can shorten the life span of the sensor andmeans, such as electrochemical or paramagnetic analysis. promote inaccurate readings. Accuracy also begins to wane at concentrations below 1 part per million (ppm), thus making them inappropriate for measurement of exhaled concentrations, which Electrochemical Analysis are typically in the partsperbillion (ppb) range. Moreover, the slow response time of electrochemical sensors prevents their useThe same principles allowing electrochemical determination of for singlebreath and exhaled NO analysis.oxygen in blood or tissue can be used to measure Po2 in a mixture Because it is normally exhaled in very low concentrations,of gas. Polarographic (Clark type) electrodes, which require an NO in expired air can be measured only with mass spectrometryapplied voltage, or galvanic cells (most common) can be used for or a process known as chemiluminescence. These analyzers, curthis purpose. In either arrangement, the amount of current gener rently the most commonly used, have a shorter response time andated as oxygen is reduced is proportional to the amount of oxygen can detect less than 1 ppb NO and NO2. Wide variations inpresent in the gas mixture, thus providing reliable estimates exhaled NO readings have been reported with chemiluminesof Po2 electrochemically. These sensor types are often used to cence analyzers, and NO2 levels may be underestimated in themeasure inspired oxygen concentrations in anesthesia machines presence of high oxygen concentrations.93,94 Unstable instrumentand conventional ventilators. Response time is somewhat slow temperature, varying expiratory flow rate, and interference areand the method is rarely used for expired gas analysis. some of the factors that may explain these variations.95 Another study comparing four analyzers found that only the most rapid device provided accurate analysis in a continuous flow system and Paramagnetic Analysis that the other three overestimated low levels and underestimated high levels.96 A midinfrared laser spectroscopy system has beenBecause the oxygen molecule has magnetic properties, its developed that may eliminate some of the problems encounteredbehavior in a magnetic field can be used to determine the con with chemiluminescence analyzers by simultaneously measuringcentration of oxygen in a gaseous mixture. Some newer anesthesia CO2. It has shown promise in a small study comparing its resultsmachines (e.g., Datex Ohmeda S/5) have incorporated paramag with typical exhaled NO levels.95netic oxygen analyzers capable of measuring oxygen in both theinspired and expired limbs of the circuit. Paramagnetic devicesboast a longer life span and faster response time than electrochemical cells do. Waveform Analysis of Expired Measurement of Nitric Oxide Respiratory GasesNitric oxide (NO) is a potent pulmonary vasodilator and has been Capnographsused for a number of years to improve oxygenation in the face ofacute respiratory distress syndrome (ARDS) and severe pulmo Changes in the shape of the expired CO2 waveform in annary hypertension (see also Chapter 31). It is produced endog intubated patient can provide very useful monitoring informaenously and has multiple physiologic functions, including tion. Capnometry is the measurement of expired CO2 and hasneurotransmission, regulation of vascular tone, and mediation of become increasingly popular as a diagnostic tool in a number ofinflammation. Studies have identified NO as a marker of airway settings. It is now the confirmation method of choice in anestheeosinophil activation, and exhaled levels are elevated in a number sia for proper placement of an endotracheal tube. CO2 concentraof inflammatory airway diseases such as asthma and chronic tion is usually measured by infrared absorption with either aobstructive pulmonary disease (COPD).88 Elevation of exhaled mainstream or sidestream capnometer. Measurements can thenNO is greater than 90% specific for the diagnosis of asthma in be plotted against time or exhaled volume to generate a capno-both children and adults.89,90 NO2, the toxic oxidation product of graph. Capnography has found many useful clinical applications,NO, can accumulate with prolonged treatment or if stored NO is and in 1998 it was adopted by the American Society of Anesexposed to oxygen. Although accumulation of harmful levels is thesiologists as standard care for all general anestheticsrare, NO2 is known to cause pulmonary toxicity even at relatively administered.low concentrations. Thus, an ideal NO analyzer would also havethe ability to accurately measure NO2 levels to avoid delivery or Mainstream versus Sidestreamaccumulation of toxic levels of this byproduct. As the diagnostic The major difference between sidestream and mainstream capand therapeutic use of NO has increased, methods to accurately nometry is location of the sensor. However, this seemingly minor
IV 1426 Anesthesia Management sampling flow exceeds fresh gas flow. Particular attention should be paid to this factor in the pediatric setting, in which expired and fresh gas flow can be quite low. Oxygen masks or nasal can nulas can be adapted to allow CO2 monitoring (Fig. 4414). The respiratory rate can be monitored adequately, but Petco2 mea surements may be falsely low unless the sample tubing is placed close to the nostril. Cannulas specifically designed to allow Petco2 monitoring while administering O2 have been developed and are commercially available. There are several sources of potential error in sidestream capnometry. Water vapor condenses in the sample tubing and often accumulates in the measuring chamber. Liquids and par ticulate matter can also enter the measuring cell and produce erroneous readings. Most systems incorporate filters and water traps to help minimize these factors. Response time is delayed A B because gas samples must travel to the measuring cell through the sample tubing. Such delay can be minimized by using short tubing with a small lumen and high sample flow rates. The somewhat Figure 44-13 Sidestream sampling port placement. A, To minimize the effects of breathing circuit dead space, attachment of the sampling port complicated sampling system and tubing connections provide should be as close to the patient as possible (arrow). B, Placement of the multiple sites for damage or gas leakage. CO2 can diffuse out of port as shown (arrow) can cause artifactual lowering of the end-tidal sample tubing and cause falsely low readings. Longer tubing measurement. and slower sampling rates increase this error, and nylon appears to be less permeable to CO2 than other commonly used materials are. difference plays a major role in the complexity, accuracy, and MainstrEaM. Mainstream capnometers incorporate the response time of each system. infrared sensor into the circuit very close to the endotracheal sidEstrEaM. In sidestream capnometry, a fixed volume tube. Consequently, many of the problems with sidestream cap of gas is continuously sampled from the circuit. The sampled gas nometry have been eliminated. CO2 is measured directly in the is aspirated through nylon or Teflon tubing into the measuring circuit and no gas is subtracted, thus obviating the need for a cell and then released into the atmosphere or returned to the complicated sampling system. The effects of breathing circuit and circuit through a second tube (Fig. 4413). Sampling should take sample tubing dead space are minimized and the response time place as close to the patient as possible to minimize the effects is therefore faster with mainstream systems. They are often used of circuit dead space, and the rate is usually adjusted to between in the pediatric population, where circuit dead space can be more 50 and 500 mL/min. It is imperative that the sampling rate be significant and response time is more critical. The measuring adjusted properly. Erroneous measurements will be obtained if chamber must be warmed to about 40°C to prevent condensation the sampling rate exceeds the expiratory flow rate and causes of water vapor on the sensor window. Care must be taken to avoid inspired gas to be sampled. Hypoventilation may occur if the skin contact with the chamber. It is somewhat heavy, and the A B C Figure 44-14 Monitoring a spontaneously breathing patient with a sidestream capnometer. A, Attachment of the sampling line to a non-rebreathing mask usually provides waveforms adequate for monitoring the respiratory rate, but end-tidal CO2 tension (Petco2) is low because of mixing within the mask. B, Placement of a sample probe close to a nostril increases the accuracy of Petco2 measurement. C, A specially designed probe (Oridion, Needham, MA) samples exhaled gas from the nose and mouth for assessing exhaled gas from mouth breathers. A second port in the same device can be used to administer supplemental oxygen.
Respiratory Monitoring 1427 44circuit should be inspected frequently to avoid kinking of the mm Hg mm Hgendotracheal tube. Mainstream capnometers require frequent A 40 40 Bcalibration, usually daily, and are prone to soiling with saliva or CO2 CO2mucus because of their close proximity to the patient. C D mm Hg mm Hg 40 40 CO2 CO2Time versus Volume Capnographs E mm Hg mm Hg 40 F tiME. The most commonly used type of capnograph plots 40Pco2 versus time. The tracing is traditionally divided into an CO2 CO2 Section IV Anesthesia Management G Hinspiratory phase and three (sometimes four) expiratory phases mm Hg mm Hg 40 40(Fig. 4415): CO2 CO2 mm Hg I J mm Hg 40 40 Phase 0: inspiratory phase CO2 Phase I: dead space and little or no CO2 CO2 Phase II: mixture of alveolar and dead space gas mm Hg mm Hg K 40 40 L Phase III: alveolar plateau, with the peak representing end CO2 CO2 expiratory (endtidal) CO2 (Petco2). M mm Hg 40 mm Hg 40 N CO2 CO2 In patients with normal lung function, Petco2 generallyunderestimates Paco2 by 1 to 5 mm Hg because of the presence Figure 44-16 Examples of capnograph waves. A, Normal spontaneousof a small amount of alveolar dead space.7 Factors that increase breathing. B, Normal mechanical ventilation. C, Prolonged exhalation duringalveolar dead space will widen this gradient and increase the spontaneous breathing. As CO2 diffuses from mixed venous blood into alveoli,slope of phase III. During anesthesia there is often increased its concentration progressively rises (see Fig. 44-17). D, Increased slope of phase III in a mechanically ventilated patient with emphysema.alveolar dead space caused by reduced cardiac output and E, Added dead space during spontaneous ventilation. F, Dual plateau (i.e.,decreased perfusion of the lung apices.97 It is therefore not sur tails-up pattern) caused by a leak in the sample line. The alveolar plateau isprising that studies under anesthesia have found the Petco2 artifactually low because of dilution of exhaled gas with air leaking inward.Paco2 gradient to be slightly elevated at 5 to 10 mm Hg.98 An During each mechanical breath the leak is reduced because of higherextreme example of acutely increased alveolar dead space is pul pressure within the airway and tubing, thus explaining the rise in CO2 concentration at the end of the alveolar plateau. This pattern is not seenmonary embolism. Thus, an abruptly decreased Petco2 with ven during spontaneous ventilation because the required increase in airwaytilation held constant is often indicative of a sudden decrease in pressure is absent. G, Exhausted CO2 absorbent producing an inhaled CO2cardiac output or pulmonary embolism. Other common causes concentration greater than zero. H, Double peak in a patient with a singleof a widened gradient include obstructive lung disease, smoking, lung transplant. The first peak represents CO2 from the transplanted (normal) lung. Exhalation of CO2 from the remaining (obstructed) lung is delayed,and advanced age. Examples of commonly encountered capno thereby producing the second peak. I, Inspiratory valve stuck open duringgraphic waveforms are shown in Figure 4416. spontaneous breathing. Some backflow into the inspired limb of the circuit The slope of the alveolar plateau (phase III) can also be causes a rise in the level of inspired CO2. J, Inspiratory valve stuck openincreased in obstructive airway disease or during prolonged expi during mechanical ventilation. The “slurred” downslope during inspirationration. Two explanations for this phenomenon have generally represents a small amount of inspired CO2 in the inspired limb of the circuit. K and L, Expiratory valve stuck open during spontaneous breathing and mechanical ventilation, respectively. Inhalation of exhaled gas causes an increase in inspired CO2. M, Cardiogenic oscillations, when seen, usually occur on sidestream capnographs of spontaneously breathing patients at the end of each exhalation. Cardiac action causes to-and-fro movement of the interface between exhaled and fresh gas. The CO2 concentration in gas I II III IV (0) entering the sampling line therefore alternates between high and low values. N, Electrical noise resulting from a malfunctioning component. The seemingly PCO2 random nature of the signal perturbations (about three per second) implies a nonbiologic cause. End-tidal Exhaled PCO2 volume been forwarded. First, obstructed (slow) lung units with low V Q and high Pco2 empty slower and later than “fast” alveoli with normal V Q and low Pco2. This is manifested as a linear upslop Flow ing of phase III instead of the typical “plateau.” Second, as lung volume decreases during exhalation and CO2 excretion from cap Time illaries remains constant, Pco2 slowly rises throughout expiration and causes an upsloping plateau (Fig. 4417).99 Accordingly, evenFigure 44-15 Time and volume capnographs. A, Expired Pco2 versus time a person with completely normal lungs can have an upsloping(i.e., standard time capnogram). The waveform is conventionally subdividedinto phases. During phase I, exhaled gas from the large airways has a Pco2 of plateau during prolonged expiration. Endtidal CO2 therefore0. Phase II is the transition between airway and alveolar gas. Phase III (i.e., approximates peak alveolar CO2, whereas Paco2 can be thoughtalveolar plateau) is normally flat, but in the presence of VA Q mismatching, it of as average alveolar Pco2.has a positive slope. The downslope of the capnogram at the onset of At the terminal end of the phase III plateau, a sharp riseinspiration is usually referred to as phase 0, but sometimes there is a terminalincrease in the slope associated with the onset of airway closure (dashed line in Pco2 is sometimes observed and is referred to as phase IV.labeled IV). The Pco2 value at the end of exhalation is referred to as the end- Although its exact cause is unknown, this rise is thought to occurtidal Pco2 (Petco2). Also shown are the exhaled gas flow rate and volume. when closing capacity is reached and small airways close, usually
IV 1428 Anesthesia Management PCO2 PCO2 40 41 t t Normal 41 40 40 41 45 45 PCO2 PCO2 38 45 t t Airway 41 45 obstruction 37 43 45 45 Figure 44-17 Mechanisms of airway obstruction producing an upsloping phase III capnogram. In a normal, healthy person (upper panel), there is a narrow range of VA Q ratios with values close to 1. Gas exchange units therefore have similar Pco2 and tend to empty synchronously, and the expired Pco2 remains relatively constant. During the course of exhalation, alveolar Pco2 slowly rises as CO2 continuously diffuses from blood. This causes a slight increase in Pco2 toward the end of expiration, and this increase can be pronounced if the exhalation is prolonged (see Fig. 44-16C). In a patient with diffuse airway obstruction (lower panel), the airway pathology is heterogeneous, with gas exchange units having a wide range of VA Q ratios. Well-ventilated gas exchange units, with gas containing lower Pco2, empty first; poorly ventilated units, with higher Pco2, empty last. In addition to the continuous rise in Pco2 mentioned previously, there is a progressive increase caused by asynchronous exhalation. after prolonged expiration. These small airways may supply lung voluME. A volume capnograph is obtained by plotting units with little CO2 for various reasons, and their closure would expired Pco2 versus exhaled gas volume, usually obtained with a therefore allow CO2rich gas from other lung units to abruptly spirometer or pneumotachometer. There is no inspiratory phase reach the upper airway. BhavaniShankar and colleagues favor a in a volume capnograph, and the curve is divided into three different explanation and state that wellventilated, open lung expiratory phases. Several measurements that are not possible units have an upsloping increase in Pco2 whereas Pco2 in poorly with time capnography can be made, such as partitioning of dead ventilated, closureprone units increases linearly. When poorly space components. The area under the Pco2 curve is the total ventilated airways close, the pattern from wellventilated units volume of CO2 (Vco2) exhaled for that single breath. Dividing predominates and the slope of the plateau rises suddenly.99 This this value by the total exhaled tidal volume (Vt) gives the fraction concept is nicely cartooned at capnography.com in the phase IV of expired CO2 (Feco2), and the product of this fraction and section. barometric pressure yields a value for mixed expired Pco2 (Peco2). To summarize, any condition that increases alveolar dead The Enghoffmodified Bohr equation can then be used to deter space or V Q heterogeneity will increase the slope of phase III. mine total (physiologic) dead space (Vdsphys or Vdstot) (Figs. 4418 This includes acute and chronic airway obstruction, and pro and 4419): longed expiration in a normal subject can also generate this pattern. Sometimes this slope is so significant that the reported VDS tot = VT (PaCO2 − PECO2 ) PaCO2 (16) Petco2 actually exceeds Paco2. This has been observed during anesthesia in obese patients and in 50% of both normal infants Once Vdstot has been determined, subtracting the anatomic dead and pregnant women.100 It is probably secondary to reduced tho space (Vdsanat) derived from the capnograph (see Fig. 4418) racic compliance and functional residual capacity (FRC), increased yields the alveolar dead space component (Vdsalv): cardiac output, and increased CO2 production.101 High mixed venous CO2 tension and malignant hyperthermia have also been VDSalv = VD tot − VDSanat (17) reported to cause a negative Paco2Petco2 gradient.102 In such cases, Petco2 is clearly not an accurate estimate of Paco2, and the Alternatively, alveolar dead space can be calculated by replacing average alveolar Pco2 obtained from a volume capnograph may Peco2 in the Bohr equation with average alveolar Pco2 (Pa′co2), be more indicative of Paco2.103 which can be derived from the volume capnograph104:
Respiratory Monitoring 1429 44 End-tidal PCO2 require volume capnography to be detected reliably.105 The tech nique may also be better than time capnography for the diagnosis PCO2 (mm Hg) of pulmonary embolism.106 Additional Clinical Applications of Capnography II III In addition to those outlined in the preceding sections, capnog raphy has a host of clinical applications. Monitoring of Petco2 I can be invaluable during mechanical ventilation in the operating Section IV Anesthesia Management room and ICU to make inferences about cardiovascular status, Paco2 trends, and adequacy of ventilation. Disappearance of the capnograph waveform may warn of cardiovascular collapse or massive airway obstruction, but it is most often due to disconnec VDSanat Volume exhaled (mL) tion or a large leak in the circuit. Capnography has been used to assess the efficacy of chest compressions during cardiopulmonaryFigure 44-18 Volume capnograph: single-breath CO2 (SBCO2) curve. The resuscitation and even to verify proper placement of enterichorizontal axis of the graph represents expiratory/inspiratory tidal volume feeding tubes.107and is generally divided into three areas: I, the anatomic dead space volume(Vdsanat): II, the transitional phase II volume; and III, the phase III alveolarvolume. The sum of these values is the tidal volume. The vertical axisrepresents the concentration of CO2. Pco2, partial pressure of carbon dioxide. Errors(From Pilbeam SP, Cairo JM: Mechanical Ventilation: Physiological and ClinicalApplications, 4th ed. St. Louis, Elsevier, 2006.) Various disease states discussed previously may cause overestima tion or underestimation of Paco2 with use of Petco2. Condensa tion of water vapor in the sample tubing and measuring cell can elevate the reported Pco2 slightly. Warming these pieces of equip VDSalv = ( VT − VDSanat ) (PaCO2 − PA ′CO2 ) PaCO2 (18) ment plus avoiding the use of drying agents in the sample line reduces this error. Capnometers may underreport true Petco2 Capnography has been used to titrate positive end at higher respiratory rates. Exhausted CO2 absorbent increasesexpiratory pressure (PEEP) settings inasmuch as narrowing of the inspired CO2, and failure to recognize such depletion may lead toPaco2Petco2 gradient suggests reduced alveolar dead space and suspicion of rebreathing from other causes.shunt fraction as a result of alveolar recruitment and improved V Q matching. These changes are often subtle or absent on atime capnograph and may be detectable only with volume capnography.100 It has been suggested that an incompetent inspiratory valve and rebreathing during mechanical ventilation may Pulmonary and Chest Wall Monitoring Pressure-Volume Curve Analysis Percentage of CO2 in arterial blood Lung mechanics can be severely impaired in a number of respira Y tory disorders. Monitoring changes in mechanical function of the lung is vital in developing a safe and effective support strategy in Percentage of CO2 the face of respiratory failure. In a mechanically ventilated patient, Z construction of pressurevolume (PV) curves can provide impor X tant information about mechanics and help guide ventilator man agement. A dynamic PV curve is one that is constructed during gas flow, whereas static curves are derived when flow is absent. Techniques for constructing static curves were introduced in the Volume (mL) mid1970s and soon thereafter were shown to be useful in deter VDS VA mining the cause of acute respiratory distress (Fig. 4420). In recent years, the PV relationship has been studied extensively as Exhaled tidal volume a means of determining optimal PEEP and tidal volume in ARDS and ALI.Figure 44-19 Volume capnograph: graph of the percentage of carbondioxide (%CO2) (y axis) and volume (x axis). A horizontal line drawn at the topof the curve represents %CO2 in arterial blood. Three distinct regions are Static Curveestablished. Area X represents the actual CO2 exhaled in one breath A static curve is constructed by using the ventilator or a large(assuming that no CO2 is rebreathed), area Y is the amount of CO2 that is not syringe to deliver known tidal volumes, and patients must beeliminated because of alveolar dead space, and area Z is the amount of CO2 sedated and paralyzed for an optimal study. The resultant plateaunot eliminated because of anatomic dead space. The ratios of these areas arethe same as in the relationship seen in the Bohr equation: (Paco2 − Peco2)/ (Pplat) and peak inspiratory pressures (Ppk) are recorded after eachPaco2 = (Y + Z)/(X + Y + Z). Peco2, mixed expired Pco2; Va, alveolar volume; breath to allow determination of both static (Cstat) and dynamicVds, dead space volume. (Cdyn) compliance. Because Cstat is calculated by using plateau
IV 1430 Anesthesia Management Normal Pulmonary emboli Static compliance Volume Volume Figure 44-20 Pressure-volume curves reflecting changes Dynamic in static and dynamic compliance (Cstat and Cdyn) during compliance mechanical ventilation. Under normal conditions, the Cstat and Cdyn curves are similar. Because pulmonary emboli do Pressure Pressure not affect resistance or compliance, neither curve changes with this condition. With mucous plugging or Tension pneumothorax, atelectasis, bronchospasm, airway resistance (Raw) increases, the Cdyn Mucous plugging, pulmonary edema, pneumonia, curve shifts to the right and flattens (more pressure is bronchospasm bronchial intubation required), and the Cstat curve remains unchanged. With conditions that reduce lung compliance (Cl), both curves shift to the right and flatten. (From Bone RC: Monitoring ventilatory mechanics in acute respiratory failure. Respir Care 28:597-604, 1983.) Volume Volume Pressure Pressure pressure, it is mainly influenced by chest wall and alveolar elastic of the LIP and UIP. Thus, setting PEEP above the LIP is not always recoil: beneficial and may instead increase the risk for overdistention and barotrauma.114 Direct measures of appropriate response may C stat = VT (Pplat − PEEP ) (19) be more suitable in determining the best PEEP level (see Cdyn is derived by using Ppk and therefore takes airway and circuit “Analysis of the Level of PEEP”). resistance into account as well: Once the lung has been fully recruited, a deflation curve can be drawn by stepwise deflation of the lung, similar to mapping C dyn = VT (Ppk − PEEP ) (20) of the inspiratory limb. As lung volume decreases, critical closing In patients with normal lung function, the static PV curve is usually linear, and Cstat ranges from 50 to 100 mL/cm H2O (Fig. 4421). In disorders such as ARDS and ALI, where compliance 1.5 can be substantially decreased, the curve becomes sigmoidal or S Normal shaped.108,109 Upper (UIP) and lower (LIP) inflection points can often be identified. The LIP, sometimes called Pflex, signifies an Volume above FRC (L) abrupt increase in compliance and is thought to result from the sudden recruitment of a large number of alveoli. The plateau 1.0 ARDS pressure at which the LIP occurs is often referred to as the opening pressure of the lung. Overdistention of alveoli begins to occur once a critical volume (or pressure) is reached, marked by the UIP. Upper inflection point Maintaining airway pressures between the LIP and UIP is there 0.5 fore believed by many to prevent derecruitment and overdisten tion of alveoli, both of which contribute to ventilatorinduced lung injury.108,109 Using this reasoning, PEEP would be set slightly Lower inflection above the LIP to keep recruited alveoli open.110 Indeed, this point approach has been shown to result in earlier weaning from the 0 ventilator, less release of inflammatory cytokines, and a trend 0 10 20 30 40 toward reduced mortality in ARDS patients.108,111 Alveolar pressure (cm H2O) Despite positive results using the LIP and UIP to guide PEEP and Vt settings, recent evidence suggests that the LIP does Figure 44-21 Example of a static, inspiratory pressure-volume curve of the not correlate with the pressure at which recruited alveoli will respiratory system in a patient with acute respiratory distress syndrome (ARDS) versus a healthy subject. Upper (about 30 cm H2O) and lower (about begin to close, known as the critical closing pressure.112,113 A prob 10 cm H2O) inflection points are present in the patient with ARDS. FRC, able explanation is that contrary to previous thought, recruitment functional residual capacity. (From Hess DR, Kacmarek RM: Essentials of has been shown to occur along the entire PV curve, independent Mechanical Ventilation, 2nd ed. New York, McGraw-Hill, 2002.)
Respiratory Monitoring 1431 44 ventilators automatically display the curve with each tidal volume. Though useful in following general trends in compliance, identi Deflection fication of inflection points is more difficult on dynamic PV point curves. Several factors can alter the loop from breath to breath, Upper inflection and using dynamic curves for determination of optimal Vt and point PEEP is not generally recommended.122 Volume Section IV Anesthesia Management Analysis of the Level of PEEP Application of PEEP has long been known to improve lung mechanics and gas exchange in many forms of acute respiratory Lower inflection point failure. Appropriate PEEP increases FRC, decreases pulmonary edema, and maintains the patency of airways and recruited alveoli. Pressure It is important to note that PEEP does not recruit the lung; rather, it is sustained high pressure that reopens closed alveoli andFigure 44-22 Pressure-volume relationship of the lung showing the inflation airways, and PEEP stabilizes these recruited lung units. A host of(solid line) and the deflation limb (dashed line). Note the clear difference in tools and parameters described in this chapter have been used bylung volume between both limbs at identical pressure (hysteresis). (From van clinicians to evaluate PEEP settings, including capnography, titraKaam AHLC: Neonatal mechanical ventilation. In Papadakos PJ, Lachmann B[eds]: Mechanical Ventilation: Clinical Applications and Pathophysiology. tion to the best Pao2/Sao2 ratio, continuous SvO2 and shunt moniPhiladelphia, Elsevier, 2008.) toring, PV curve analysis, and others. None have unequivocally been shown to result in superior outcome. Consequently, there is no consensus on a single method of titrating and evaluatingpressure is reached, and a deflection point appears on the curve clinical response to PEEP. More than 30 years ago it was notedcorresponding to a rapid decrease in compliance and closure of that the PEEP level resulting in maximum O2 delivery also proa large number of lung units (Fig. 4422). Because compliance duced optimal compliance while minimizing dead space andimproves during inflation as lung units are recruited, higher shunt fraction.124 The authors coined the phrase “optimum” PEEPvolumes are observed at the same pressure during deflation than to refer to that producing the maximum improvement in pulmoduring inflation, a phenomenon referred to as hysteresis. Accord nary function with minimal hemodynamic compromise. Recentingly, critical closing pressure will be lower than opening pressure, trials have shown that during a derecruitment study, measuringand setting PEEP slightly above the deflection point rather than Cstat may be as useful and more costeffective than measuringthe LIP may provide superior alveolar stabilization with less risk Pao2 in determining closing pressure and guiding PEEP selecof overdistention and ventilatorinduced lung injury.115,116 A tion.115,116 Nowadays most clinicians use one of these two paramnumber of recent studies suggest that the LIP does not reliably eters to set PEEP after the recruitment maneuver. Inflectionindicate the pressure at which maximal alveolar derecruitment points on PV curves are not always easy to identify, and a decreaseoccurs.112,117 In addition, there is mounting evidence that using in Pao2 rather than Cstat should be used to identify closing presthe deflation limb rather than the inflation limb of PV curves to sure in such cases.guide ventilation may improve gas exchange and mechanics, Patients under GA are prone to compression atelectasis inoften at lower mPaw and PEEP levels.118,119 Therefore, although dependent lung regions (see Fig. 445).125 Thus, it is tempting tothe presence of an LIP on the PV curve indicates a need for lung apply PEEP to all patients undergoing surgery with mechanicalrecruitment, the deflection point may be more valuable in deter ventilation to prevent this atelectasis. It has been shown thatmining the amount of PEEP required to prevent alveolar collapse. application of PEEP during GA can attenuate and reverse dependEvaluating deflation Cstat in this manner to determine closing ent atelectasis but does not improve gas exchange.126 A studypressure is at least as effective as monitoring Pao2 for selection of comparing normal and obese subjects also found that applicationthe optimum PEEP level.115,116 Moreover, recruitment maneuvers of PEEP during GA did not alter gas exchange in normal patients,have been shown to be quite safe and are less injurious than allow but some improvement was noted in the obese population.127ing shear stress damage associated with derecruitment to proceed Thus, there is no evidence to support routine use of PEEP duringunchecked.120,121 GA. However, these studies did not use recruitment maneuvers, Static PV curves can also be obtained from a single breath and a trial by Tusman and colleagues showed that alveolar recruitdelivered slowly (2 to 3 L/m) until a predetermined pressure is ment can improve oxygenation during GA (see also Chapterreached and are referred to as slowflow or quasistatic PV loops. 15).128 In addition, PEEP combined with recruitment maneuversThe curves derived are comparable to those obtained with typical has been shown to provide a sustained increase in Pao2 and lungstatic techniques, but the deflation limb is often difficult to volume in mechanically ventilated postsurgical patients.128,129acquire.122,123 Several modern ventilators have incorporated thiscapability. The Hamilton Galileo ventilator allows selection of thedesired flow rate for the PV study, and an interactive curve is then Analysis of Lung Recruitmentdisplayed on the monitor, usually within 30 seconds. The importance of early lung recruitment in respiratory failureDynamic Curve and ARDS has been well documented.130 Lungprotective ventilaA number of ventilators are capable of mapping dynamic PV tion in ARDS via frequent recruitment maneuvers results incurves during tidal breaths delivered with normal gas flow. Newer improved 28day survival, earlier weaning from mechanical ven
IV 1432 Anesthesia Management tilation, and less barotrauma than with conventional ventilation dimensional image of the distribution of electrical impedance strategies.111 Effective recruitment is performed by applying sus within the thorax. The dynamic behavior and the qualitative tained high airway pressure, usually for 30 to 90 seconds. Many information extracted from EIT images look similar to that successful techniques, all using essentially these same principles, reported in dynamic studies (Fig. 4423).141,142 have been described.131,132 Recruitment maneuvers are typically This technology may be an excellent assessment tool for well tolerated, with no significant hemodynamic deterioration or easy bedside use to evaluate alveolar lung recruitment, pulmo inflammatory response.133,134 Although improvements in pulmo nary embolism, lung water, and other lung pathology. The impor nary compliance and oxygenation are indicative of successful tance of lung recruitment in both the operating room and the recruitment, direct methods of quantifying and monitoring lung ICU has clearly changed the practice of mechanical ventilation. recruitment are emerging. Amato’s group in Brazil recently completed a validation study of EIT.142 It is an easy bedside tool to evaluate mechanical Computed Tomography ventilation with immediate feedback. EIT devices may, in the Technologic advances in CT have made it a valuable tool for future, easily detect selective intubation, pneumothorax, and alve studying ARDS and lung recruitment. It has been used in numer olar atelectasis. Titration of PEEP may someday be evaluated in ous studies to evaluate the effects of a wide range of variables on real time, with EIT used instead of waiting for BGA, radiologic alveolar recruitment and stabilization.135 Recently, Gattinoni and studies, and CT scans. This technology may one day be integrated colleagues performed a trial to examine whether measuring the into the bedside monitor or into closedloop mechanical amount of recruitable lung by CT could help predict how the lung ventilators. would respond to PEEP after recruitment. They concluded that a higher amount of recruitable lung was correlated with a positive response to PEEP whereas PEEP was of little benefit and perhaps Inspiratory Pressure Monitoring detrimental in patients with less recruitable lung measured by CT.136 This conclusion was in line with previous studies showing Impaired respiratory muscle function from fatigue or neuromus that PEEP results in hyperinflation and increased stress in normal cular disorders can contribute to respiratory failure and difficulty lung regions when the amount of recruitable lung is low.137 Quan weaning from mechanical ventilation. Measurement of maximum titative CT analysis of potentially recruitable lung may therefore inspiratory pressure (MIP), also called negative inspiratory force, be useful in determining the best PEEP level, but further studies gives a useful bedside appraisal of respiratory muscle strength. It are needed on the practicality of routine use. CT was instrumental can be performed on intubated and nonintubated patients by in the discovery that lung recruitment occurs throughout inspira attaching a pressure manometer to the endotracheal tube or a tion and not solely around the LIP of the PV curve.138 noninvasive mouthpiece. Alternatively, use of a oneway valve that allows exhalation only has been described, although it is quite Electrical Impedance Tomography uncomfortable for the patient.143 Normal MIP is about −90 cm A new and exciting form of monitoring of pulmonary function H2O but can range between −50 and −120 cm H2O. To obtain may be electrical impedance tomography (EIT).139,149 It is a non accurate measurements, MIP should be measured after maximal invasive and radiationfree technique based on the measurement expiration because the diaphragm can generate the greatest pres of electric potentials at the chest wall surface. Within a particular sure at residual volume. Studies have demonstrated that inability crosssectional plane, harmless electrical currents are driven to generate MIP more negative than −20 cm results in tidal across the thorax in a rotating pattern to generate a potential volumes that are insufficient for generating a strong cough. More gradient at the surface, which is then transformed into a two over, this cutoff has been shown to result in weaning failure with CT EIT Figure 44-23 Comparison of a computed tomographic (CT) scan and an electrical impedance tomographic (EIT) image during mechanical ventilation of a patient with acute lung injury. The gray and white areas in the EIT image reflect areas with change in impedance (volume changes) and correlate with well- inflated areas on the CT scan. There is no impedance change on the EIT scan in the dorsal area, where atelectasis is present on the CT scan. (From Wolf GK, Arnold JH: High-frequency oscillatory ventilation for adult acute respiratory distress syndrome: A decade of progress. Crit Care Med 33(Suppl):S163-S169, 2005.)
Respiratory Monitoring 1433 44a negative predictive value of 1.144 Though not yet a firmly established predictor of weaning outcome, MIP is useful in determin Work of Breathinging whether patient weakness or neuromuscular dysfunction isplaying a role in unsuccessful weaning trials. The work involved in normal respiration, often referred to as work of breathing (WOB), usually requires minimal energy expendi ture. Work is defined as the force needed to move a mass times Esophageal Monitoring the distance moved: W = F × d. In the respiratory system, it rep resents the pressure (or force) needed to inspire a certain volume Section IV Anesthesia ManagementTranspulmonary pressure, rather than peak or plateau pressure, of gas: WOB = P × V. With respiratory compromise, WOB can beis the most important determinant of alveolar distention and is quite high, as much as 40% of total oxygen consumption (nordefined as alveolar pressure (Pa) minus pleural pressure (Ppl).145 mally <5%). WOB can be estimated by measuring pressure andThus, true distending pressure of the lung cannot be measured volume changes from a PV curve. Total work is the area enclosedwithout determination of Ppl. Direct measurement of Ppl is clini by the curve (integral of pressure and volume). Thus, the largercally impractical, but it can be estimated quite reliably in upright the loop, the greater the WOB (Fig. 4425). However, studiespatients by measuring pressure in the distal third of the esopha indicate that mechanical work calculated in this manner maygus. The esophagus is a fairly passive structure and the third part underestimate true WOB and is weakly correlated with the VO2is very close to the pleural space, thus allowing transmission of respiratory muscles. Alternatively, many clinicians believe thatof pleural pressure to an intraesophageal pressure monitor.146 A the pressure-time product (PTP) is the most accurate measure ofballoontipped catheter is typically used, and this technique is work performed by the diaphragm during inspiration and betterconsidered the standard modality for evaluating inspiratory effort correlates with VO2 148 because the PTP takes isometric contracand work of breathing (WOB). In the supine position, this rela tion of the diaphragm into account, which consumes additionaltionship is less predictable because gravitational forces cause O2. Increases in PTP indicate stronger diaphragmatic contractioncompression of the esophagus and dependent lung, thereby and vice versa. Calculation of PTP requires measurement ofskewing the measurements. transdiaphragmatic pressure as outlined earlier and is not rou Placement of a second balloon catheter into the stomach tinely performed. Occlusion pressures (P100) measured with aallows simultaneous measurement of gastric pressure and pro dedicated valve system or conventional ventilator have also beenvides a means of obtaining a host of useful information about shown to correlate with WOB.148,149respiratory mechanics. For example, transdiaphragmatic pressuremonitoring can be performed to assess diaphragmatic contraction. As the diaphragm contracts and the domes descend, negative Closed-Loop AnalysisPpl (or Pes) should coincide with positive abdominal pressure (orPg) generating transdiaphragmatic pressure. Inability of the dia Closedloop ventilation involves computerbased realtime interphragm to contract properly results in loss of transdiaphragmatic pretation of respiratory mechanics with continuous adjustmentpressure and has been observed after uncomplicated upper of the level of support delivered to the patient.150 Any change inabdominal surgery (Fig. 4424). Diaphragmatic fatigue and mechanics or patient effort is detected and a new breathingphrenic nerve palsy elicit a similar pattern.147 This can also be pattern is initiated by the ventilator. Ventilator dyssynchrony andobserved clinically inasmuch as impaired diaphragmatic activity WOB are minimized. Moreover, erroneous or unsafe settingsis associated with paradoxical inward movement of the abdomen could potentially be minimized with a system that continuouslyduring inspiration. regulates ventilator support based on realtime assessment of the +10 +15 Pes 0 Pes (cm H2O) (cm H2O) 0 -20 -15 +30 +30 Pg Pg (cm H2O) (cm H2O) 0 0 A 4 sec B 4 secFigure 44-24 Examples of transdiaphragmatic pressure monitoring. A, Simultaneous esophageal (Pes) and gastric (Pg) pressure waveforms during tidalbreathing in a normal individual. Negative esophageal (and therefore pleural) pressure swings are accompanied by positive gastric pressure waves indicative ofthe development of transdiaphragmatic pressure during inspiration. B, The same waveforms in a patient with phrenic nerve palsy (and therefore absentdiaphragmatic contraction). Negative intrathoracic pressure swings (arrowheads) are accompanied by gastric pressure swings in the same direction.Intrathoracic pressure changes are directly transmitted through a passive diaphragm. These changes can also be observed in the early postoperative period inpatients who have undergone upper abdominal surgery. (From Brown KA, Hoffstein V, Byrick RJ: Bedside diagnosis of bilateral diaphragmatic paralysis in aventilator-dependent patient after open-heart surgery. Anesth Analg 64:1208, 1985.)
IV 1434 Anesthesia Management A B 500 500 Figure 44-25 Work of breathing (WOB) during continuous positive airway pressure (CPAP). WOB in this figure is the integral of airway pressure and tidal volume. Loop A is an example of a freestanding CPAP system. Spontaneous breaths occur clockwise, inspiration to Volume in mL Volume in mL expiration. Loop B is CPAP through a ventilator demand valve system. Breathing occurs clockwise. (Redrawn from Hirsch C, Kacmarek RM, Stanek K: Work of breathing during CPAP and PSV imposed by the new generation mechanical ventilators: A lung model study. Respir Care 36:815–828, 1991; and Kirby RR, Banner MJ, Downs JB: Clinical Applications of Ventilatory Support. New York, Churchill Livingstone, 1990.) 0 0 5 5 Pressure in cm H2O Pressure in cm H2O patient. Table 443 summarizes the four commercially available tent observation.152 A wide variety of continuous apnea monitor closedloop systems. A study was performed to compare ARDS ing systems have been developed. Most methods detect changes and COPD patients ventilated with a closedloop mode termed in chest wall movement, gas exchange, or gas flow to make infer adaptive support ventilation (ASV) available on the Hamilton ences about changes in respiratory pattern. Galileo ventilator. The authors found that on average, ARDS Movement of the chest wall is most commonly detected patients received lower tidal volumes with a higher respiratory by transthoracic impedance. The technology is usually incorpo rate than COPD patients did.151 This would be expected and rated into the electrocardiographic (ECG) monitoring system. A desired based on current knowledge of mechanics and the impor small current is passed between two ECG leads, and chest wall tance of low–tidal volume ventilation in ARDS. Moreover, the movement is detected by a change in impedance to the current results support the possibility that closedloop ventilation with induced by the motion. Respiratory inductive plethysmography ASV can appropriately tailor ventilation based on respiratory (RIP) is another method of apnea detection that monitors chest mechanics. It is highly conceivable that closedloop ventilator movement. The chest and abdomen are encircled by one or more modes may one day prove to be safer and more convenient than coils that measure changes in their crosssectional area occurring traditional mechanical ventilation. with respiration. Inductance of the bands depends on the area that they enclose and thereby allows detection of respiratory movements. A technique called photoplethysmography (PPG) also relies on detection of anatomic changes induced by breath Apnea Monitoring ing. Infrared PPG sensors placed near upper extremity veins can detect cyclic changes in venous blood flow occurring with respi The postoperative period is often characterized by episodes of ration.153 Respiratory muscle electromyography has also been apnea and hypoxemia. Paradoxical breathing and other ventila used as a means of monitoring respiration. A limitation common tory disturbances can also occur frequently. Though more to all these techniques is that respiratory efforts during episodes common with narcotic administration, residual effects of other of obstructive apnea may be interpreted as normal respirations anesthetic agents can play a role in the cause of these distur despite absent gas flow.154 Monitoring of gas flow and exchange bances. They are often subtle and are more likely to be noticed may therefore be a more reliable indicator of adequate with continuous respiratory monitoring as opposed to intermit respiration. Table 44-3 Main Characteristics of Proportional Assist Ventilation (PAV), Neurally Adjusted Ventilatory Assist (NAVA), Knowledge-Based System (KBS), and Adaptive Support Ventilation (ASV) PAV NAVA KBS ASV Principle Pinsp proportional to flowinsp Pinsp proportional to EMGdia Pinsp to maintain RR in comfort zone Pinsp and RR to minimize WOB Breath type Spontaneous Spontaneous PSV PSV, PCV, P-SIMV Sedated patients No No No Yes Active patients Yes Yes Yes Yes Automatic weaning No No Yes Yes EMGdia, diaphragmatic electromyographic activity; Flowinsp, inspiratory flow; PCV, pressure-controlled ventilation; P-SIMV, pressure-controlled intermittent mandatory venti- lation; PSV, pressure-support ventilation; RR, respiratory rate; WOB, work of breathing. From Wysocki M, Brunner JX: Closed-loop ventilation: An emerging standard of care? Crit Care Clin 23:223-240, 2007.
Respiratory Monitoring 1435 44 Apnea monitoring systems that rely on airflow detection allows semiquantitative measures of EVLW, as well as determinamay be a more sensitive alternative to monitors of patient move tion of its distribution and possible etiology. Even under suchment. In a study comparing transthoracic impedance and a nasal conditions, sensitivity is rather poor; a 30% to 35% increase inoral airflow system in the PACU, Wiklund and colleagues found EVLW is needed before radiographic changes consistent withthat impedance monitoring failed to detect apneic episodes more pulmonary edema can be detected on the chest film.161 In typicalfrequently than flow detection did.154 False alarm rates were critical care settings, where image quality and acquisition techsimilar between the two groups. Hök and associates studied an nique can vary greatly, it is estimated that a 100% increase inacoustic airflow monitoring system and reported that it was more EVLW may be needed to produce observable radiographic Section IV Anesthesia Managementsensitive in detecting episodes of apnea and hypoventilation than changes. Moreover, weak correlation of EVLW measurementspulse oximetry was.155 Another acoustic airflow sensor was com between chest radiography and other established methods haspared with a thoracic impedance system by Werthammer and been observed in the ICU environment.159colleagues.155a Of 26 apneic episodes observed by direct observa CT has been increasingly studied in recent years as a meanstion, the airflow sensor detected all 26, whereas only 7 episodes of quantification of EVLW. In animal experiments, CT densitomwere detected by the impedance monitor. Other airflow monitors etry could detect an increase in EVLW by as little as 50%.162 Usingdetect respiration by measuring changes in humidity. Tatara and thinsection CT, Scillia and colleagues found that significantTsuzaki studied a device called a rapidresponse hygrometer that hypoxemia secondary to pulmonary edema may not develop untilmonitors changes in humidity at the nostril and can measure the increase in EVLW approaches the 200% to 300% range.163respiratory rates of up to 60 breaths per minute.156 Respiratory Lack of portability and high radiation exposure limit the use ofphases could be identified almost 2 seconds faster than with cap CT for serial EVLW measurement. Research continues on anography. The development of fiberoptic humiditybased systems number of other imaging modalities, including ultrasonograhas also been described.157,158 phy,164 positron emission tomography,165 nuclear magnetic reso Because endtidal CO2 monitoring and pulse oximetry can nance,166 and EIT,167 but none have been incorporated into routinerapidly detect derangements in gas exchange, they may prove to clinical use.be the most dependable options for apnea monitoring. In a studyof more than 4000 apneic episodes from overnight polysomnograms, detection of apnea by pulse oximetry was compared with Indicator Dilution Methodsmanual detection, such as airflow or respiratory movement.158aOnly 1.32% of apneic episodes were reportedly missed by pulse Quantification of EVLW via double indicator dilution curves wasoximetry, whereas manual devices missed 7.9% of apnea events. first described more than 50 years ago. More recently, a transpulAlthough endtidal CO2 monitoring can be performed easily and monary thermodilution technique that uses cold saline as a singleaccurately on intubated patients, measurements from a mask or indicator has been described. Although controversy exists overnasal cannula are often unreliable. However, the respiratory rate the accuracy of dilution techniques, many studies report excellentis usually reported accurately, and trends in Petco2 can be moni reproducibility and correlation with gravimetric methods.159tored with these devices. As pulse oximetry and capnography One study using transpulmonary thermodilution reported thatsystems become more portable and inexpensive, their use for changes in EVLW of as little as 10% to 20% can be detectedapnea monitoring will probably continue to grow. Large outcome with high sensitivity.168 Both techniques are somewhat invasivestudies may be needed to demonstrate the possible superiority of and require placement of arterial and central venous catheters.one system over another. Although early devices were quite cumbersome, currently availa ble systems are relatively safe and easy to implement and allow bedside measurements to be obtained. Lung Water Analysis Despite recent improvements in a number of the aforemen tioned modalities, chest radiography remains the only tool widelyMany disease states can cause abnormal accumulation of extra integrated into clinical practice. A probable explanation is thatvascular lung water (EVLW), commonly known as pulmonary studies have suggested potential clinical utility in precise EVLWedema. Clinicians have long been aware of the severe cardiac and analysis, but none have shown that obtaining such measurementsrespiratory insufficiency that pulmonary edema can cause, yet it facilitates decisionmaking or improves patient outcome.remains unclear whether accurately quantifying it can guide management in a way that ultimately improves outcome. Nonetheless,investigators continue to seek simple and reliable methods fordetecting and quantifying EVLW, and many advances have beenmade in recent years. Research in this field is complicated by the Monitoring High-Frequencyfact that gravimetry, which requires analysis of postmortem lung Ventilationweight, remains the standard for EVLW measurement.159,160 As aresult, much of the data evaluating new techniques come from Recent data on the benefits of low–tidal volume, highPEEP venanimal studies. tilation in ARDS have prompted a search for the optimal lung protective mode of ventilation. First introduced in the late 1950s, highfrequency ventilation (HFV) offers an alternative to conven Radiographic Methods tional ventilation in patients with ARDS and ALI. HFV is char acterized by rapid delivery of small tidal volumes and maintenanceThe chest radiograph is the most widely used test to screen for of high mean airway pressure.169 Whereas routine use in adults ispulmonary edema. Under ideal conditions, obtaining a chest film a fairly recent trend, trials in preterm infants with neonatal res
IV 1436 Anesthesia Management piratory distress syndrome began almost 20 years ago.170 Clear Expiratory evidence of outcome benefit with HFV versus conventional ven limb tilation is lacking, but numerous studies have implied that HFV may reduce the risk for ventilatorinduced lung injury,171 improve HFV Zone of potential Pressure oxygenation,172 and be as safe as conventional ventilation in volutrauma ARDS.173 The FDA has defined HFV as any form of ventilation that delivers a respiratory rate greater than 150 breaths/min. Although several forms of HFV have evolved since its develop ment, the most widely used method in both adults and pediatric Zone of atelectrauma patients is highfrequency oscillatory ventilation (HFOV). Other modes include highfrequency jet ventilation (HFJV), high frequency flow interruption (HFFI), and highfrequency percus Volume sive ventilation (HFPV). Before the widespread availability of Figure 44-26 Pressure-volume curve depicting the “open lung” concept HFV modes, a conventional ventilator was used to deliver low using high-frequency ventilation (HFV). Potential lung injury is reduced when tidal volumes with high frequency, a technique that became ventilation of the lung is shifted onto the expiratory portion of the curve by known as highfrequency positivepressure ventilation aggressive lung recruitment. Lung volume is then maintained with high mean airway pressure and small tidal volumes. (From Singh JM, Stewart TE: (HFPPV). High-frequency ventilation. In Fink MP, Abraham E, Vincent JL, et al [eds]: Because mechanisms of gas exchange during HFV differ Textbook of Critical Care, 5th ed. Philadelphia, Elsevier, 2005.) from those regulating conventional ventilation, standard moni toring equipment may not provide accurate data. Fortunately, the reliability of pulse oximetry in assessing oxygenation status with other modes of ventilation seems to extend to HFV. Early studies assessing lung morphology in ARDS.179,180 CT has proved useful showed a correlation between airway pressure and gas exchange for such analyses but continues to be limited by portability issues. efficiency during HFJV, with higher peak and driving pressures Recently, some investigators have focused on EIT and RIP as resulting in lower Paco2 and higher Pao2. Monitoring Petco2 modalities that may be able to provide accurate lung volume conventionally during HFV produces unreliable measurements measurements at the bedside during HFV.181,182 RIP has been used for a number of reasons, but mainly because of difficulty obtain experimentally to construct PV curves during HFV and thereby ing undiluted, CO2rich gas samples.174,175 Though useful in moni determine optimal lung volume and pressure settings.183,184 In the toring conventional ventilation, the concept of “endtidal” CO2 is first infant study of this kind, Tingay and colleagues used the altogether misguided in HFV because no inspiratory or expira openlung concept to recruit lung and then map the deflation tory phases are identifiable on capnographic waveforms.176 More limb of the PV curve.185,186 The authors concluded that RIP could over, the likelihood that expired CO2 tensions accurately reflect be used during HFOV to construct satisfactory deflation curves. Paco2 is low in patients requiring HFV inasmuch as alveolar dead Ventilation along the deflation limb resulted in greater lung space and intrapulmonary shunting can be extensive.174 volume and oxygenation, often with lower distending pressure Despite its limitations, studies have demonstrated the requirements, than did ventilation on the inflation limb (Fig. ability of capnometry to provide accurate Paco2 estimates during 4426). This was in line with previous animal studies demonstrat HFV. A common technique is to interrupt or slow the ventilator ing improved mechanics and oxygenation with deflation limb down to deliver a normal breath. CO2 tensions measured with ventilation after recruitment.117 An earlier infant trial using single intermittent capnography have been shown to agree well with occlusion compliance measurements failed to demonstrate the simultaneously obtained Paco2 values.177 The accuracy of capno utility of PV curves in optimizing lung volume during HFV, but metric Pco2 readings may also depend on where the sample is neither recruitment maneuvers nor deflation limb ventilation had obtained. Gas sampled from the distal tip of the endotracheal tube been used.187 EIT has the advantage of providing information seems to provide more valid approximations of Paco2 than sam about global and regional changes in lung volume, as well as pling proximally does.176 However, these measurements must also continuous imaging of changes in impedance (and probably be obtained intermittently. In an effort to eliminate this problem volume) occurring throughout the respiratory cycle. Bedside and others associated with expired gas analysis during HFV, Berk availability would potentially allow clinicians to detect aeration enbosch and Tobias studied the accuracy of continuous transcu changes in real time and reverse them by adjusting ventilation taneous CO2 monitoring in this setting. When compared with parameters.182 Paco2 values from BGA obtained simultaneously, bias and preci Estimation of pulmonary mechanics during HFV has most sion were only 2.1 and 2.7 mm Hg, respectively.174 Studies by these often been accomplished by the conventional passive techniques authors and other investigators have also demonstrated that tran described earlier. This practice has raised concern among some scutaneous CO2 monitoring may approximate Paco2 better than authors, who argue that technical aspects of these strategies may Petco2 in both adults and children undergoing mechanical ven exacerbate derecruitment and provide inadequate information tilation.178,179 Although the technique has gained a footing in about lung parenchyma.187 In the study by Tingay and colleagues, pediatric critical care, transcutaneous O2 and CO2 monitoring in passive deflation was not used for PV analysis, and derecruitment adults will probably increase in popularity as refinements to this was further prevented by avoiding full deflation of the lung below technology continue to be made. closing pressure. Others suggest that the high frequencies and As the potential benefits of HFV continue to be elucidated, flow rates associated with HFV currently limit the feasibility of investigators have sought practical techniques for bedside moni obtaining accurate dynamic measurements. Thus, efforts have toring of lung mechanics, recruitment, and regional aeration. been undertaken to identify safe alternatives for reliably assessing Portable chest radiography has been shown to be a poor tool for lung compliance and determining optimal airway pressure during
Respiratory Monitoring 1437 44HFV. The oscillatory pressure ratio (OPR), defined as the ratio of widely variable heart rate and blood pressure during transportapressure swings at the distal and proximal ends of the endotra tion for diagnostic procedures.194 Thus, a continually displayedcheal tube, was shown to be inversely related to lung compliance electrocardiogram and blood pressure must be available duringin an animal model of ALI.188 The mPaw setting resulting in the transport of all critically ill patients. In addition, pulse oximetrylowest OPR also generated the best lung compliance and oxy should be used in light of its high reliability in forewarning ofgenation. Titrating mPaw to a minimal OPR may therefore prove hypoxemia and deterioration in gas exchange. A good rule ofto be a reliable, noninvasive means of optimizing lung mechanics thumb is to monitor critically ill patients at least as closely duringand oxygenation during HFV. The lowfrequency forced oscilla transport as deemed necessary within the ICU before transport. Section IV Anesthesia Managementtion technique is another experimental monitor that allows Complications are reduced when personnel trained to deal withpartitioning of lung mechanics into airway and parenchymal the intricacies of intrahospital transport are available.195 Emercomponents, as well as determination of chest wall impedance.189 gency cardiovascular drugs should be available for postoperativeMonitoring chest vibration can provide a crude indicator of transport of all hemodynamically unstable and critically ill subchanges in compliance during HFOV. Oscillator power is often jects. Preparation of equipment and medication checklists beforetitrated to generate vibrations from the clavicle down to the mid transport can help ensure readiness for any untoward events. Theportion of the thigh, and a change in pattern may signal the receiving location should confirm before transport that it has thedevelopment of an obstruction, pneumothorax, or worsening equipment and necessary staff in place to receive the patient.mechanics of any etiology. Transport of a mechanically ventilated patient presents the inherent risks of airway loss and further derangements in gas exchange. Equipment and medications needed to establish and maintain a secure airway must accompany such patients during any transfer. The presence of adequate oxygen supply with prop Monitoring the Respiratory erly functioning lowpressure alarms should be verified during System in Transport pretransport preparation. Many authors advocate the use of a mechanical ventilator rather than manual ventilation devices forIntrahospital transport of critically ill and mechanically venti intrahospital transport because more variability in pH and CO2lated patients becomes necessary in a number of situations (see tension has been observed with the use of manual devices.196 AChapter 79). The need for diagnostic or surgical procedures is higher incidence of significant Pao2/Fio2 deterioration may alsoamong the most frequent reasons for patient transport. A number be associated with manual versus mechanical ventilation (P =of studies have reported on the high number of transports that .056).196 In a blinded study using capnography, Tobias and associcritically ill patients require.190 Children and trauma victims seem ates noted a high incidence of unintentional hyperventilationto require more frequent transportation for diagnostic purposes when using manual devices during the intrahospital transfer ofthan other critically ill patients do. Not surprisingly, intrahospital intubated pediatric patients.197 Similar findings have been notedtransport of this tenuous patient population can be fraught with in adults, and tighter control of Paco2 can be achieved if Petco2198problems ranging from simple equipment malfunction to major or Vt is monitored during manual ventilation. These findingsdisasters such as anoxic brain injury and even death. Studies have led many experts to recommend Petco2 monitoring inreport a widely varying incidence of adverse events during trans addition to standard monitoring for highrisk patients requiringportation of critically ill patients. Complex and numerous pieces a more optimal level of ventilation.of equipment are often necessary to safely perform the transfer. Obvious contraindications to the transport of critically illOne study looking at 125 transports from the ICU found a 34% patients include an inability to provide adequate oxygenation andincidence of equipmentrelated adverse events, the most common ventilation during transport or at the receiving location. Unstablebeing ECG lead disconnection and monitor power failure.190 hemodynamics or an inability to adequately monitor cardiovas Lack of agreedupon monitoring techniques and defini cular status throughout the trip should prompt postponement ortions of “adverse events” partly explains the wide discrepancy in cancellation. The riskbenefit ratio should be considered beforereported incidence. Moreover, few outcome studies comparing all transports to help determine whether a trip is truly warranted;monitoring strategies during transport have been performed. It performing such analyses may be the most effective way of avoidhas long been observed, however, that transport of critically ill ing adverse events during transportation. Indeck and coworkerspatients may put them at increased risk for cardiovascular and found that 68% of patients transferred from a trauma unitrespiratory compromise, both during and after transport.191 A for diagnostic testing experienced serious physiologic changeshigher incidence of gas exchange deterioration and even pneu whereas only 24% of the transfers resulted in significant modificamonia has been reported after intrahospital transport.192,193 tion of patient management.199 The development of increasinglyArrhythmias, hypotensive episodes, and blood gas derangements sophisticated portable devices has provided a bedside alternativeare not uncommon. Studies in trauma patients have revealed for many diagnostic and therapeutic procedures.
IV 1438 Anesthesia Management References 1. deMicheli A: [Regarding respiration and the so 22. Severinghaus JW: First electrodes for blood Po2 and in saturation during low perfusion [abstract]. Crit called “animal heat.” A historical sketch.] Rev Invest Pco2 determination. J Appl Physiol 97:15991600, Care Med 29:A115, 2001. Clin 53:462467, 2001. 2004. 42. Welch JP, DeCesare R, Hess D: Pulse oximetry: 2. Haldane JS, Priestley JG: The regulation of the lung 23. Severinghaus JW, Astrup P, Murray JF: Blood gas Instrumentation and clinical application. Respir ventilation. J Physiol 32:225266, 1905. analysis and critical care medicine. Am J Respir Crit Care 35:584601, 1990. 3. Nunn JF: Alveolar air equations. Anesthesiology Care Med 157:S114S122, 1998. 43. Salyer JW: Neonatal and pediatric pulse oximetry. 85:946, 1996. 24. Schmidt C, MüllerPlathe O: Stability of Po2, Pco2 Respir Care 48:386396, 2003. 4. Frank SM, Fleisher LA, Olson KF, et al: Multivariate and pH in heparinized whole blood samples: Influ 44. Jay GD, Hughes L, Renzi FP: Pulse oximetry is determinants of early postoperative oxygen con ence of storage temperature with regard to leuko accurate in acute anemia from hemorrhage. Ann sumption in elderly patients. Effects of shivering, cyte count and syringe material. Eur J Clin Chem Emerg Med 24:3235, 1994. body temperature, and gender. Anesthesiology Clin Biochem 30:767773, 1992. 45. Severinghaus JW, Koh SO: Effect of anemia on pulse 83:241249, 1995. 25. Robertson PW, Hart BB: Assessment of tissue oximeter accuracy at low saturation. J Clin Monit 5. Riley RL, Lilienthal JL, Proemmel DO, Franke RE: oxygenation. Respir Care Clin N Am 5:221263, 6:8588, 1990. On the determination of the physiologically effec 1999. 46. Ralston AC, Webb RK, Runciman WB: Potential tive pressures of oxygen and carbon dioxide. Am J 26. Lubbers DW, Opitz N: The pco2/po2optode: A errors in pulse oximetry. III: Effects of interferences, Physiol 147:191198, 1946. new probe for measurement of pco2 or po2 in dyes, dyshaemoglobins and other pigments. Anaes 6. Story DA: Alveolar oxygen partial pressure, alveolar fluids and gases (authors’ transl). Z Naturforsch [C] thesia 46:291295, 1991. carbon dioxide partial pressure, and the alveolar gas 30:532533, 1975. 47. Craft JA, Alessandrini E, Kenney LB, et al: Com equation. Anesthesiology 84:1011, 1996. 27. Bland JM, Altman DG: Statistical methods for parison of oxygenation measurements in pediatric 7. Hlastala MP: Ventilation/perfusion: From the assessing agreement between two methods of clini patients during sickle cell crises. J Pediatr 124:93 bench to the patient. Cardiologia 41:405415, cal measurement. Lancet 1:307310, 1986. 95, 1994. 1996. 28. Ganter M, Zollinger A: Continuous intravascular 48. Katoh R, Miyake T, Arai T: Unexpectedly low pulse 8. Filley GF, MacIntosh DJ, Wright GW: Carbon mon blood gas monitoring: Development, current tech oximeter readings in a boy with unstable hemo oxide uptake and pulmonary diffusing capacity in niques, and clinical use of a commercial device. Br globin Köln. Anesthesiology 80:472474, 1994. normal subjects at rest and during exercise. J Clin J Anaesth 91:397407, 2003. 49. Nextgeneration pulse oximetry. Health Devices Invest 33:530539, 1954. 29. Ganter MT: Accuracy and performance of a modi 32:4787, 2003. 9. Lumb AB: Nunn’s Applied Respiratory Physiology, fied continuous intravascular blood gas monitoring 50. Bohnhorst B, Poets CF: Major reduction in alarm 6th ed. Elsevier, Butterworth Heinemann, 2005, pp device during thoracoscopic surgery. J Cardiotho frequency with a new pulse oximeter. Intensive 140, 125126, 128129. rac Vasc Anesth 18:587591, 2004. Care Med 24:277278, 1998. 10. Jones JG, Jones SE: Discriminating between 30. Weiss IK, Fink S, Harrison R, et al: Clinical use of 51. Irita K, Kai Y, Akiyoshi K, et al: Performance evalu the effect of shunt and reduced VA Q on arterial continuous arterial blood gas monitoring in the ation of a new pulse oximeter during mild hypo oxygen saturation is particularly useful in clinical pediatric intensive care unit. Pediatrics 103:440 thermic cardiopulmonary bypass. Anesth Analg practice. J Clin Monit Comput 16:337350, 2000. 445, 1999. 96:1114, 2003. 11. Hlastala MP, Glenny RW: Vascular structure deter 31. Coule LW, Truemper EJ, Steinhart CM, Lutin WA: 52. Durban CG, Rostow SK: Advantages of new tech mines pulmonary blood flow distribution. News Accuracy and utility of a continuous intraarterial nology pulse oximetry with adults in extremis. Physiol Science 14:182186, 1999. blood gas monitoring system in pediatric patients. Anesth Analg 94:S81S83, 2002. 12. Lundquist H, Hedenstierna G, Strandberg A, et al: Crit Care Med 29:420426, 2001. 53. O’Malley GF: Noninvasive carbon monoxide CTassessment of dependent lung densities in man 32. Hatherill M, Tibby SM, Durward A, et al: Continu measurement is not accurate. Ann Emerg Med during general anesthesia. Acta Radiol 36:626632, ous intraarterial bloodgas monitoring in infants 48:477478, 2006. 1995. and children with cyanotic heart disease. Br J 54. Suner S, Partridge R, Sucov A, et al: Noninvasive 13. Warner DO, Warner MA, Ritman EL: Atelectasis Anaesth 79:665667, 1997. screening for carbon monoxide toxicity in the and chest wall shape during halothane anesthesia. 33. Venkatesh B, Pigott DW, Fernandez A, Hendry SP: emergency department is valuable. Ann Emerg Anesthesiology 85:4959, 1996. Continuous measurement of arterial blood gas Med 49:718719, author reply 719, 2007. 14. Wagner PD, Laravuso RB, Uhl RR, West JB: Con status during total hip replacement: A prospective 55. Barker SJ, Curry J, Redford D, Morgan S: Measure tinuous distributions of ventilationperfusion ratios study. Anaesth Intensive Care 24:334341, 1996. ment of carboxyhemoglobin and methemoglobin in normal subjects breathing air and 100 per cent 34. Larson CP Jr, Vender J, Seiver A: Multisite evalua by pulse oximetry: A human volunteer study. O2. J Clin Invest 54:5468, 1974. tion of a continuous intraarterial blood gas moni Anesthesiology 107:892897, 2007. 15. Hope DA, Jenkins BJ, Willis N, et al: Noninvasive toring system. Anesthesiology 81:543552, 1994. 56. Dassel ACM, Graaff R, Sikkema M, et al: Reflect estimation of venous admixture: Validation of a 35. Aschkenasy SV, Hofer CK, Zalunardo MP, et al: ance pulse oximetry at the forehead improves by new formula. Br J Anaesth 74:538543, 1995. Patterns of changes in arterial Po2 during onelung pressure on the probe. J Clin Monit 11:237244, 16. Feihl F, Eckert P, Brimioulle S, et al: Permissive ventilation: A comparison between patients 1995. hypercapnia impairs pulmonary gas exchange in with severe pulmonary emphysema and patients 57. East CE, Brennecke SP, King JF, et al: The effect of the acute respiratory distress syndrome. Am J with preserved lung function. J Cardiothorac Vasc intrapartum fetal pulse oximetry, in the presence of Respir Crit Care Med 162:209215, 2000. Anesth 19:479484, 2005. a nonreassuring fetal heart rate pattern, on opera 17. Hachenberg T, Tenling A, Nyström SO, et al: Ven 36. Pavlidis T, Papaziogas B, Vretzakis G, et al: Con tive delivery rates: A multicenter, randomized, con tilationperfusion inequality in patients undergoing tinuous monitoring of arterial blood gases and pH trolled trial (the FOREMOST trial). Am J Obstet cardiac surgery. Anesthesiology 80:509529, 1994. during laparoscopic cholecystectomy using a Par Gynecol 194:606.e1606.e16, 2006. 18. Andersson L, Lagerstrand L, Thörne A, et al: Effect atrend sensor. Minerva Chir 57:1722, 2002. 58. Kyriacou PA, Powell SL, Jones DP, Langford RM: of CO2 pneumoperitoneum on ventilation 37. Severinghaus JW: Takuo Aoyagi: Discovery of Evaluation of oesophageal pulse oximetry in perfusion relationships during laparoscopic chole pulse oximetry. Anesth Analg 105(6 Suppl):S1S4, patients undergoing cardiothoracic surgery. Anaes cystectomy. Acta Anaesthesiol Scand 46:552560, 2007. thesia 58:422427, 2003. 2002. 38. Wouters PF, Gehring H, Meyfroid G, et al: Accuracy 59. Fournell A, Schwarte LA, Scheeren TW, et al: 19. Tokics L, Hedenstierna G, Svensson L, et al: V Q of pulse oximeters: The European multicenter trial. Assessment of microvascular oxygen saturation in distribution and correlation to atelectasis in anes Anesth Analg 94:S13S16, 2002. gastric mucosa in volunteers breathing continuous thetized paralyzed humans. J Appl Physiol 81:1822 39. Hannhart B, Haberer JP, Saunier C, Laxenaire MC: positive airway pressure. Crit Care Med 31:1705 1833, 1996. Accuracy and precision of fourteen pulse oxime 1710, 2003. 20. Severinghaus JW, Bradley AF: Electrodes of blood ters. Eur Respir J 4:115122, 1991. 60. Nijland R, Jongsma HW, van den Berg PP, et al: The Po2 and Pco2 determination. J Appl Physiol 13:515 40. Tobin RM, Pologe JA, Batchelder PB: A characteri effects of pulsating arteries on reflectance pulse oxi 520, 1958. zation of motion affecting pulse oximetry in 350 metry: Measurements in adults and neonates. J Clin 21. Clark LC Jr, Wolf R, Granger D, Taylor Z: Continu patients. Anesth Analg 94:S54S61, 2002. Monit 11:118122, 1995. ous recording of blood oxygen tension by polarog 41. Bebout DE, Mannheimer PD, Wun CC: Site 61. Moller JT, Pederson T, Rasmussen LS: Randomized raphy. J Appl Physiol 6:189193, 1953. dependent differences in the time t o detect changes evaluation of pulse oximetry in 20,802 patients: I.
Respiratory Monitoring 1439 44 Design, demography, pulse oximetry failure rate, 79. Hager H, Church S, Mandadi G, et al: The perfusion tion of arterial Pco2 from endtidal Pco2? Br J and overall complication rate. Anesthesiology index measured by a pulse oximeter indicates pain Anaesth 78:536540, 1997. 78:436444, 1993. stimuli in anesthetized volunteers. Anesthesiology 99. BhavaniShankar K, Kumar AY, Moseley HS,62. Young D, Griffiths J: Clinical trials of monitoring in 101:A514, 2004. AhyeeHallsworth R: Terminology and the current anaesthesia, critical care and acute ward care: A 80. Beal AL, Cerra FB: Multiple organ failure syndrome limitations of time capnography: A brief review. J review. Br J Anaesth 97:3945, 2006. in the 1990s: Systemic inflammatory response and Clin Monit 11:175182, 1995.63. Ochroch EA, Russell MW, Hanson WC 3rd et al: organ dysfunction. JAMA 271:226233, 1994. 100. Rich GF, Sconzo JM: Continuous endtidal CO2 The impact of continuous pulse oximetry monitor 81. Rivers E, Nguyen B, Havstad S, et al, for the Early sampling within the proximal endotracheal tube ing on intensive care unit admissions from a GoalDirected Therapy Collaborative Group: Early estimates arterial CO2 tension in infants. Can J postsurgical care floor. Anesth Analg 102:868875, goaldirected therapy in the treatment of severe Anaesth 38:201203, 1991. Section IV Anesthesia Management 2006. sepsis and septic shock. N Engl J Med 345:1368 101. BhavaniShankar K: Negative arterial to endtidal64. Moller JT, Johannessen NN, Espersen K, et al: 1377, 2001. CO2 gradients in children. Can J Anaesth 41:1125 Randomized evaluation of pulse oximetry in 82. Räsänen J, Downs JB, DeHaven B: Titration of con 1126, 1994. 20,802 patients: II. Perioperative events and postop tinuous positive airway pressure by realtime dual 102. Kwetny I, Finucane BT: Negative arterial to end erative complications. Anesthesiology 78:445453, oximetry. Chest 92:853856, 1987. tidal carbon dioxide gradient: An additional sign of 1993. 83. Connett RJ, Honig CR, Gayeski TE, Brooks GA: malignant hyperthermia during desflurane anesthe65. Wheatley RG, Shepherd D, Jackson IJ, et al: Hypox Defining hypoxia: A systems view of Vo2, glycolysis, sia. Anesth Analg 102:815817, 2006. aemia and pain relief after upper abdominal energetics, and intracellular Po2. J Appl Physiol 103. Breen PH, Mazumdar B, Skinner SC: Comparison surgery: Comparison of i.m. and patientcontrolled 68:833842, 1990. of endtidal Pco2 and average alveolar expired Pco2 analgesia. Br J Anaesth 69:558561, 1992. 84. Dings J, Meixensberger J, Jager A, Roosen K: Clini during positive endexpiratory pressure. Anesth66. Rosenberg J, Oturai P, Erichsen CJ, et al: Effect of cal experience with 118 brain tissue oxygen partial Analg 82:368373, 1996. general anesthesia and major versus minor surgery pressure catheter probes. Neurosurgery 43:1082 104. Fletcher R: Relationship between alveolar dead on late postoperative episodic and constant hypox 1095, 1998. space and arterial oxygenation in children with emia. J Clin Anesth 6:212216, 1994. 85. Hockel M, Knoop C, Schlenger K, et al: Intratu congenital cardiac disease. Br J Anaesth 62:168176,67. Gill NP, Wright B, Reilly CS: Relationship between moral po2 predicts survival in advanced cancer of 1989. hypoxaemic and cardiac ischaemic events in the uterine cervix. Radiother Oncol 26:4550, 105. Breen PH, Bradley PJ: Carbon dioxide spirogram the perioperative period. Br J Anaesth 68:471473, 1993. (but not capnogram) detects leaking inspiratory 1992. 86. McCormick PW, Stewart M, Goetting MG, et al: valve in a circle circuit. Anesth Analg 85:13721376,68. Jubran A, Tobin MJ: Reliability of pulse oximetry in Noninvasive cerebral optical spectroscopy for mon 1997. titrating supplemental oxygen therapy in ventilator itoring cerebral oxygen delivery and hemodynam 106. Verschuren F, Heinonen E, Clause D, et al: Volu dependent patients. Chest 97:14201425, 1990. ics. Crit Care Med 19:8997, 1991. metric capnography as a bedside monitoring of69. Bierman MI, Stein KL, Snyder JV: Pulse oximetry 87. Kavanagh MC, Tsang V, Chow S, et al: A compari thrombolysis in major pulmonary embolism. Inten in the postoperative care of cardiac surgical son in individual murine tumors of techniques for sive Care Med 30:21292132, 2004. patients: A randomized controlled trial. Chest measuring oxygen levels. Int J Radiat Oncol Biol 107. Sanders AB: Capnometry in emergency 102:13671370, 1992. Phys 44:11371146, 1999. medicine. Ann Emerg Med 18:12871290,70. Shamir M, Eidelman LA, Floman Y, et al: Pulse 88. Barnes PJ, Liew FY: Nitric oxide and 1989. oximetry plethysmographic waveform during asthmatic inflammation. Immunol Today 16:128 108. Ranieri VM, Suter PM, Tortorella C, et al: Effect of changes in blood volume. Br J Anaesth 82:178181, 130, 1995. mechanical ventilation on inflammatory mediators 1999. 89. Gabriele C, Nieuwhof EM, Van Der Wiel EC, et al: in patients with acute respiratory distress syndrome:71. Monnet X, Lamia B, Teboul JL: Pulse oximeter as a Exhaled nitric oxide differentiates airway diseases A randomized controlled trial. JAMA 282:5461, sensor of fluid responsiveness: Do we have our in the first two years of life. Pediatr Res 60:461465, 1999. finger on the best solution? Crit Care 9:429430, 2006. 109. Ventilation with lower tidal volumes as compared 2005. 90. Dupont LJ, Demedts MG, Verleden GM: Prospec with traditional tidal volumes for acute lung injury72. Michard F, Boussat S, Chemla D, et al: Relation tive evaluation of the validity of exhaled nitric oxide and the acute respiratory distress syndrome. The between respiratory changes in arterial pulse pres for the diagnosis of asthma. Chest 123:751756, Acute Respiratory Distress Syndrome Network. N sure and fluid responsiveness in septic patients with 2003. Engl J Med 342:13011308, 2000. acute circulatory failure. Am J Respir Crit Care Med 91. Purtz EP, Hess D, Kacmarek RM: Evaluation of elec 110. Muscedere JG, Mullen JB, Gan K, Slutsky AS: Tidal 162:134138, 2000. trochemical nitric oxide and nitrogen dioxide ana ventilation at low airway pressures can augment73. Cannesson M, Besnard C, Durand PG, et al: Rela lyzers suitable for use during mechanical ventilation. lung injury. Am J Respir Crit Care Med 149:1327 tion between respiratory variations in pulse oxime J Clin Monit 13:2534, 1997. 1334, 1994. try plethysmographic waveform amplitude and 92. Strauss JM, Krohn S, Sümpelmann R, et al: Evalua 111. Amato MB, Barbas CS, Medeiros DM, et al: Effect arterial pulse pressure in ventilated patients. Crit tion of two electrochemical monitors for measure of a protectiveventilation strategy on mortality in Care 9:R562R568, 2005. ment of inhaled nitric oxide. Anaesthesia 51:151154, the acute respiratory distress syndrome. N Engl J74. Cannesson M, Attof Y, Rosamel P, et al: Respiratory 1996. Med 338:347354, 1998. variations in pulse oximetry plethysmographic 93. Bernareggi M, Cremona G: Measurement of 112. Maggiore SM, Jonson B, Richard JC, et al: Alveolar waveform amplitude to predict fluid responsiveness exhaled nitric oxide in humans and animals. Pulm derecruitment at decremental positive end in the operating room. Anesthesiology 106:1105 Pharmacol Ther 12:331352, 1999. expiratory pressure levels in acute lung injury: 1111, 2007. 94. Etches PC, Harris ML, McKinley R, Finer NN: Comparison with the lower inflection point, oxy75. Feissel M, Teboul JL, Merlani P, et al: Plethysmo Clinical monitoring of inhaled nitric oxide: Com genation, and compliance. Am J Respir Crit Care graphic dynamic indices predict fluid responsive parison of chemiluminescent and electrochemical Med 164:795801, 2001. ness in septic ventilated patients. Intensive Care sensors. Biomed Instrum Technol 29:134140, 113. Rimmensberger PC, Pristine G, Mullen BM, et al: Med 33:993999, 2007. 1995. Lung recruitment during small tidal volume venti76. Shelley KH, Jablonka DH, Awad AA, et al: What is 95. Roller C, Namjou K, Jeffers J, et al: Simultaneous lation allows minimal positive endexpiratory pres the best site for measuring the effect of ventilation NO and CO2 measurement in human breath with a sure without augmenting lung injury. Crit Care Med on the pulse oximeter waveform? Anesth Analg single IVVI midinfrared laser. Opt Lett 27:107 27:19401945, 1999. 103:372377, 2006. 109, 2002. 114. Roupie E, Dambrosio M, Servillao G, et al: Titration77. Mowafi HA: The efficacy of plethysmographic pulse 96. Nishimura M, Imanaka H, Uchiyama A, et al: Nitric of tidal volume and induced hypercapnia in acute wave amplitude as an indicator for intravascular oxide (NO) measurement accuracy. J Clin Monit respiratory distress syndrome. Am J Respir Crit injection of epinephrinecontaining epidural test 13:241248, 1997. Care Med 152:121128, 1995. dose in anesthetized adults. Anesth Analg 101:1506 97. Shibutani K, Muraoka M, Shirasaki S, et al: Do 115. Hickling KG: Best compliance during a decremen 1511, 2005. changes in endtidal Pco2 quantitatively reflect tal, but not incremental, positive endexpiratory78. Uemura A, Yagihara M, Miyabe M: Pulse oximeter changes in cardiac output? Anesth Analg 79:829 pressure trial is related to openlung positive end perfusion index as a predictor for the effect of pedi 833, 1994. expiratory pressure: A mathematical model of acute atric epidural block. Anesthesiology 105:A1354, 98. Tavernier B, Rey D, Thevenin D, et al: Can pro respiratory distress syndrome lungs. Am J Respir 2006. longed expiration manoeuvres improve the predic Crit Care Med 163:6978, 2001.
IV 1440 Anesthesia Management 116. Marini JJ, Gattinoni L: Ventilatory management of lung aeration in patients with severe chest trauma. 152. Catley DM, Thornton C, Jordan C, et al: Pro acute respiratory distress syndrome: A consensus of Crit Care Med 32:968975, 2004. nounced, episodic oxygen desaturation in the post two. Crit Care Med 32:250255, 2004. 133. Talmor D, Sarge T, Legedza A, et al: Cytokine operative period: Its association with ventilatory 117. Mergoni M, Volpi A, Bricchi C, Rossi A: Lower release following recruitment maneuvers. Chest pattern and analgesic regimen. Anesthesiology inflection point and recruitment with PEEP in ven 132:14341439, 2007. 63:2028, 1985. tilated patients with acute respiratory failure. J Appl 134. Reis Miranda D, Klompe L, Mekel J, et al: Open 153. Nilsson L, Johansson A, Kalman S: Monitoring of Physiol 91:441450, 2001. lung ventilation does not increase right ventricular respiratory rate in postoperative care using a new 118. van Genderingen HR, van Vught AJ, Duval EL, et outflow impedance: An echoDoppler study. Crit photoplethysmographic technique. J Clin Monit al: Attenuation of pressure swings along the Care Med 34:25552560, 2006. Comput 16:309315, 2000. endotracheal tube is indicative of optimal distend 135. Gattinoni L, Caironi P, Valenza F, Carlesso E: The 154. Wiklund L, Hök B, Ståhl K, JordebyJönsson A: ing pressure during highfrequency oscillatory ven role of CTscan studies for the diagnosis and Postanesthesia monitoring revisited: Frequency of tilation in a model of acute lung injury. Pediatr therapy of acute respiratory distress syndrome. Clin true and false alarms from different monitoring Pulmonol 33:429436, 2002. Chest Med 27:559570, 2006. devices. J Clin Anesth 6:182188, 1994. 119. Tingay DG, Mills JF, Morley CJ, et al: The deflation 136. Gattinoni L, Caironi P, Cressoni M, et al: Lung 155. Hök B, Wiklund L, Henneberg S: A new respiratory limb of the pressurevolume relationship in infants recruitment in patients with the acute respiratory rate monitor: Development and initial clinical during highfrequency ventilation. Am J Respir Crit distress syndrome. N Engl J Med 354:17751786, experience. Int J Clin Monit Comput 10:101107, Care Med 173:414420, 2006. 2006. 1993. 120. Suh GY, Koh Y, Chung MP, et al: Repeated dere 137. Levy MM: PEEP in ARDS—how much is enough? 155a. Werthammer J, Krasner J, DiBenedetto J, Stark A: cruitments accentuate lung injury during mechani N Engl J Med 351:389391, 2004. Apnea monitoring by acoustic detection of airflow. cal ventilation. Crit Care Med 30:18481853, 2002. 138. Gattinoni L, Caironi P, Pelosi P, Goodman LR: Pediatrics 71:5355, 1983. 121. Fujino Y, Goddon S, Dolhnikoff M, et al: Repetitive What has computed tomography taught us about 156. Tatara T, Tsuzaki K: An apnea monitor using a highpressure recruitment maneuvers required to the acute respiratory distress syndrome? Am J rapidresponse hygrometer. J Clin Monit 13:59, maximally recruit lung in a sheep model of acute Respir Crit Care Med 164:17011711, 2001. 1997. respiratory distress syndrome. Crit Care Med 139. van Genderingen HR, van Vught AJ, Jansen JR: 157. Folke M, Granstedt F, Hök B, Scheer H: Compara 29:15791586, 2001. Estimation of regional volume changes by electrical tive provocation test of respiratory monitoring 122. Ranieri VM, Giuliani R, Fiore T, et al: Volume impedance pressure tomography during a pressure methods. J Clin Monit Comput 17:97103, pressure curve of the respiratory system predicts volume maneuver. Intensive Care Med 29:233240, 2002. effects of PEEP in ARDS: “Occlusion” versus “con 2003. 158. Roback K, Nelson N, Johansson A, et al: A new stant flow” technique. Am J Respir Crit Care Med 140. Frerichs I, Dargaville PA, Dudykevych T, fiberoptical respiratory rate monitor for the neona 149:1927, 1994. Rimensberger PC: Electrical impedance tomogra tal intensive care unit. Pediatr Pulmonol 39:120 123. Albaiceta GM, Piacentini E, Villagrá A, et al: Appli phy: A method for monitoring regional lung aera 126, 2005. cation of continuous positive airway pressure to tion and tidal volume distribution. Intensive Care 158a. George CF, Millar TW, Kryger MH: Identification trace static pressurevolume curves of the respira Med 29:23122316, 2003. and quantification of apneas by computerbased tory system. Crit Care Med 31:25142519, 2003. 141. Gattinoni L, D’Andrea L, Pelosi P, et al: Regional analysis of oxygen saturation. Am Rev Respiratory 124. Suter PM, Fairley B, Isenberg MD: Optimum end effects and mechanism of positive endexpiratory Disease 137:1238, 1988. expiratory airway pressure in patients with acute pressure in early respiratory distress syndrome. 159. Lange NR, Schuster DP: The measurement of lung pulmonary failure. N Engl J Med 292:284289, JAMA 269:21222127, 1993. water. Crit Care 3:R19R24, 1999. 1975. 142. Victorino JA, Borges JB, Okamato VN, et al: Imbal 160. Katzenelson R, Perel A, Berkenstadt H, et al: Accu 125. Gunnarsson L, Tokics L, Gustavsson H, Heden ances in regional lung ventilation: A validation racy of transpulmonary thermodilution versus stierna G: Influence of age on atelectasis formation study on electrical impedance tomography. Am J gravimetric measurement of extravascular lung and gas exchange impairment during general Respir Crit Care Med 169:791800, 2004. water. Crit Care Med 32:15501554, 2004. anaesthesia. Br J Anaesth 66:423432, 1991. 143. Kacmarek RM, CycykChapman MC, YoungPal 161. FernándezMondéjar E, GuerreroLópez F, Col 126. Tokics L, Hedenstierna G, Strandberg A, et al: Lung azzo PJ, Romagnoli DM: Comparison of two tech menero M: How important is the measurement of collapse and gas exchange during general anesthe niques for the determination of maximal inspiratory extravascular lung water? Curr Opin Crit Care sia: Effects of spontaneous breathing, muscle pressure (MIP) in mechanically ventilated patients. 13:7983, 2007. paralysis, and positive endexpiratory pressure. Respir Care 39:868878, 1989. 162. Forster BB, Muller NL, Mayo JR, et al: High Anesthesiology 66:157167, 1987. 144. Yang KL, Tobin MJ: A prospective study of indexes resolution computed tomography of experimental 127. Pelosi P, Ravagnan I, Giurati G, et al: Positive end predicting the outcome of trials of weaning from hydrostatic pulmonary edema. Chest 101: expiratory pressure improves respiratory function mechanical ventilation. N Engl J Med 324:1445 14341437, 1992. in obese but not in normal subjects during anesthe 1450, 1991. 163. Scillia P, Delcroix M, Lejeune P, et al: Hydrostatic sia and paralysis. Anesthesiology 91:12211231, 145. Stewart TE: Establishing an approach to mechanical pulmonary edema: Evaluation with thinsection CT 1999. ventilation. Can Respir J 3:403408, 1996. in dogs. Radiology 211:161168, 1999. 128. Tusman G, Böhm SH, Vazquez de Anda GF, et al: 146. Benditt JO: Esophageal and gastric pressure meas 164. Agricola E, Bove T, Oppizzi M, et al: “Ultrasound Alveolar recruitment strategy improves arterial urements. Respir Care 50:6875, discussion 7577, comettail images”: A marker of pulmonary edema: oxygenation during general anaesthesia. Br J 2005. A comparative study with wedge pressure and Anaesth 82:813, 1999. 147. Roussos C, Zakynthinos S: Fatigue of the respira extravascular lung water. Chest 127:16901695, 129. Dyhr T, Laursen N, Larsson A: Effects of lung tory muscles. Intensive Care Med 22:134155, 2005. recruitment maneuver and positive endexpiratory 1996. 165. Serizawa S, Suzuki T, Niino H, et al: Using H215O pressure on lung volume, respiratory mechanics 148. Bellani G, Patroniti N, Weismann D, et al: Measure and C15O in noninvasive pulmonary measurements. and alveolar gas mixing in patients ventilated after ment of pressuretime product during spontaneous Chest 106:11451151, 1994. cardiac surgery. Acta Anaesthesiol Scand 46:717 assisted breathing by rapid interrupter technique. 166. Caruthers SD, Paschal CB, Pou NA, et al: Regional 725, 2002. Anesthesiology 106:484490, 2007. measurements of pulmonary edema by using mag 130. Papadakos PJ, Lachmann B: The open lung concept 149. Pesenti A, Pelosi P, Foti G, et al: An interrupter netic resonance imaging. J Appl Physiol 84:2143 of alveolar recruitment can improve outcome in technique for measuring respiratory mechanics and 2153, 1998. respiratory failure and ARDS. Mt Sinai J Med 69:73 the pressure generated by respiratory muscles 167. Freimark D, Arad M, Sokolover R, et al: Monitoring 77, 2002. during partial ventilatory support. Chest 102:918 lung fluid content in CHF patients under intrave 131. Grasso S, Mascia L, Del Turco M, et al: Effects of 923, 1992. nous diuretics treatment using bioimpedance recruiting maneuvers in patients with acute respira 150. Wysocki M, Brunner JX: Closedloop ventilation: measurements. Physiol Meas 28:S269S277, tory distress syndrome ventilated with protective An emerging standard of care? Crit Care Clin 2007. ventilatory strategy. Anesthesiology 96:795802, 23:223240, ix, 2007. 168. FernandezMondejar E, RiveraFerna’ndez R, 2002. 151. Arnal JM, Nafati C, Wysocki M, et al: Utilization of GarcíaDelgado M, et al: Small increases in extravas 132. Schreiter D, Reske A, Stichert B, et al: Alveolar adaptive support ventilation (ASV) in a polyvalent cular lung water are accurately detected by transpul recruitment in combination with sufficient positive intensive care unit [abstract]. Intensive Care Med monary thermodilution. J Trauma 59:14201424, endexpiratory pressure increases oxygenation and 30:S84, 2004. 2005.
Respiratory Monitoring 1441 44169. Chan KP, Stewart TE, Mehta S: Highfrequency definition of an ARDS Severity Score. CT Scan ventilation in the preterm lamb. Pediatr Crit Care oscillatory ventilation for adult patients with ARDS. ARDS Study Group. Intensive Care Med 26:1046 Med 5:172180, 2004. Chest 131:19071916, 2007. 1056, 2000. 190. Smith I, Fleming S, Cernaianu A: Mishaps during170. Highfrequency oscillatory ventilation compared 180. Puybasset L, Gusman P, Muller JC, et al: Regional transport from the intensive care unit. Crit Care with conventional mechanical ventilation in the distribution of gas and tissue in acute respiratory Med 18:278281, 1990. treatment of respiratory failure in preterm infants. distress syndrome. III. Consequences for the effects 191. Waydhas C, Schneck G, Duswald KH: Deteriora The HIFI Study Group. N Engl J Med 320:8893, of positive endexpiratory pressure. CT Scan ARDS tion of respiratory function after intrahospital 1989. Study Group. Intensive Care Med 26:12151227, transport of critically ill surgical patients. Intensive171. Bollen CW, Uiterwaal CS, van Vught AJ: Cumula 2000. Care Med 21:784789, 1995. tive metaanalysis of highfrequency versus conven 181. Brazelton TB III, Watson KF, Murphy M, et al: Iden 192. Kollef MH, Von Harz B, Prentice D, et al: Patient Section IV Anesthesia Management tional ventilation in premature neonates. Am J tification of optimal lung volume during high transport from intensive care increases the risk of Respir Crit Care Med 168:11501155, 2003. frequency oscillatory ventilation using respiratory developing ventilatorassociated pneumonia. Chest172. Mehta S, Lapinsky SE, Hallett DC, et al: Prospective inductive plethysmography. Crit Care Med 29:2349 112:765773, 1997. trial of highfrequency oscillation in adults with 2359, 2001. 193. Bercault N, Wolf M, Runge I, et al: Intrahospital acute respiratory distress syndrome. Crit Care Med 182. Wolf G, Arnold J: Noninvasive assessment of lung transport of critically ill ventilated patients: A risk 29:13601369, 2001. volume: Respiratory inductance plethysmography factor for ventilatorassociated pneumonia—a173. Derdak S, Mehta S, Stewart TE, et al: Multicenter and electrical impedance tomography. Crit Care matched cohort study. Crit Care Med 33:24712478, Oscillatory Ventilation for Acute Respiratory Dis Med 33(Suppl):S163S169, 2005. 2005. tress Syndrome Trial (MOAT) Study Investigators: 183. Gothberg S, Parker TA, Griebel J, et al: Lung 194. Hurst JM, Davis K Jr, Johnson DJ, et al: Cost and Highfrequency oscillatory ventilation for acute volume recruitment in lambs during high complications during inhospital transport of respiratory distress syndrome in adults: A rand frequency oscillatory ventilation using respiratory critically ill patients: A prospective cohort study. J omized, controlled trial. Am J Respir Crit Care Med inductive plethysmography. Pediatr Res 49:3844, Trauma 33:582585, 1992. 166:801808, 2002. 2001. 195. Szem JW, Hydo LJ, Fischer E, et al: Highrisk intra174. Berkenbosch JW, Tobias JD: Transcutaneous 184. Brazelton TB III, Watson KF, Murphy M, et al: Iden hospital transport of critically ill patients: Safety carbon dioxide monitoring during highfrequency tification of optimal lung volume during high fre and outcome of the necessary “road trip.” Crit Care oscillatory ventilation in infants and children. Crit quency oscillatory ventilation using respiratory Med 23:16601666, 1995. Care Med 30:10241027, 2002. inductive plethysmography. Crit Care Med 29:2349 196. Nakamura T, Fujino Y, Uchiyama A, et al: Intrahos175. Clark RH: Highfrequency ventilation. J Pediatr 2359, 2001. pital transport of critically ill patients using 124:661670, 1994. 185. Tingay DG, Mills JF, Morley CJ, et al: The deflation ventilator with patienttriggering function. Chest176. Nishimura M, Imanaka H, Tashiro C, et al: Cap limb of the pressurevolume relationship in infants 123:159164, 2003. nometry during highfrequency oscillatory ventila during highfrequency ventilation. Am J Respir 197. Tobias JD, Lynch A, Garrett J: Alterations of end tion. Chest 101:16811683, 1992. Crit Care Med 173:414420, 2006. tidal carbon dioxide during the intrahospital trans177. Frietsch T, Krafft P, Becker HD, et al: Intermittent 186. Lachmann B: Open up the lung and keep the lung port of children. Pediatr Emerg Care 12:249251, capnography during highfrequency jet ventilation open. Intensive Care Med 18:319321, 1992. 1996. for prolonged rigid bronchoscopy. Acta Anaesthe 187. Kalenga M, Battisti O, François A, et al: High 198. Palmon SC, Liu M, Moore LE, Kirsch JR: siol Scand 44:391397, 2000. frequency oscillatory ventilation in neonatal RDS: Capnography facilitates tight control of ventilation178. Berkenbosch JW, Lam J, Burd RS, Tobias JD: Non Initial volume optimization and respiratory during transport. Crit Care Med 24:608611, invasive monitoring of carbon dioxide during mechanics. J Appl Physiol 84:11741177, 1998. 1996. mechanical ventilation in older children: Endtidal 188. Pillow JJ: Highfrequency oscillatory ventilation: 199. Indeck M, Peterson S, Smith J, Brotman S: Risk, versus transcutaneous techniques. Anesth Analg Mechanisms of gas exchange and lung mechanics. cost, and benefit of transporting ICU patients 92:14271431, 2001. Crit Care Med 33(3 Suppl):S135S141, 2005. for special studies. J Trauma 28:10201025,179. Rouby JJ, Puybasset L, Cluzel P, et al: Regional dis 189. Pillow JJ, Sly PD, Hantos Z: Monitoring of lung 1988. tribution of gas and tissue in acute respiratory dis volume recruitment and derecruitment using oscil tress syndrome. II. Physiological correlations and latory mechanics during highfrequency oscillatory