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44 Respiratory Monitoring Stephen M. Eskaros, Peter J. Papadakos, and Burkhard Lachmann Key Points 1. Hypoxemia is caused by reduced PIO 2 , hypoventilation, increased ventilation-perfusion ( VQ ) heterogeneity, increased shunt, and diffusion nonequilibrium. Hypercapnia is almost always due to hypoventilation. 2. During mechanical ventilation in the operative and intensive care settings, hypoxemia is most often due to increased VQ heterogeneity and shunt. 3. A clinically useful approximation to the alveolar gas equation for O 2 is given by PAO 2 = (PB 47) × FIO 2 1.2 × PCO 2 . Exchange of O 2 and CO 2 takes place independently in the lung. 4. The alveolar-arterial (A-a) gradient increases with age and supplemental O 2 . The PaO 2 /FIO 2 and A/a ratios typically do not change with increased age or inspired O 2 . 5. When derangements in gas tensions are noted on arterial blood gas analysis, it is important to verify that the sample was obtained and analyzed in an appropriate and timely manner. 6. Refinements and further studies on continuous intravascular blood gas monitors may one day lead to widespread routine use of these devices. 7. Pulse oximetry is a rapid, reliable indicator of oxygenation status in surgical and critically ill patients. Newer oximeters feature reduced capability for errors attributable to motion artifact and hypoperfusion. 8. Multiwavelength pulse oximeters are commercially available and allow measurement of carboxyhemoglobin and methemoglobin. Pulse oximetry may one day prove to be a reliable noninvasive monitor of volume status and fluid responsiveness. 9. A sudden decrease in PETCO 2 usually results from a circuit disconnection, airway obstruction, abrupt decrease in cardiac output, or pulmonary embolism. PETCO 2 is not always a reliable approximation of PaCO 2 , particularly during general anesthesia or in the critically ill. 10. Mapping of pressure-volume curves in patients with acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) can provide valuable information about lung mechanics and help guide positive end-expiratory pressure (PEEP) and tidal volume settings. Sustained high airway pressure is needed to open collapsed alveoli, and PEEP stabilizes the recruited lung units. 11. Computed tomography has greatly increased our understanding of the complicated interaction between PEEP and lung recruitment in ARDS. Electrical impedance tomography may in the future emerge as a useful bedside monitor of lung recruitment, pulmonary edema, and respiratory mechanics. 12. Recruitment strategies and low–tidal volume ventilation have been shown to improve outcomes in ARDS and ALI. High-frequency ventilators are safe and effective in refractory ARDS and may some day prove to be the ideal mode of lung protective ventilation. Gas Exchange e realization that gas exchange takes place in the lung was made by the ancients. However, not until the 18th century, when oxygen was discovered by Joseph Priestley, did Lavoisier ascertain the true purpose of breathing: the biochemical combustion of carbon and oxygen to carbon dioxide, a process known as respira- tion. 1 More than 200 years later, the exact mechanisms by which the respiratory system takes up oxygen and eliminates carbon dioxide are still being debated. Alveolar Gases A practicable method for directly sampling and analyzing alveo- lar air was first described by Haldane and Priestly in 1905. 2 Because of the inaccuracies and technical difficulty involved in 1411
Transcript
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44 Respiratory Monitoring

Stephen M. Eskaros, Peter J. Papadakos, and Burkhard Lachmann

Key Points

1. Hypoxemia is caused by reduced Pio2, hypoventilation, increased ventilation-perfusion ( � �V Q ) heterogeneity, increased shunt, and diffusion nonequilibrium. Hypercapnia is almost always due to hypoventilation.

2. During mechanical ventilation in the operative and intensive care settings, hypoxemia is most often due to increased � �V Q heterogeneity and shunt.

3. A clinically useful approximation to the alveolar gas equation for O2 is given by Pao2 = (Pb − 47) × Fio2 − 1.2 × Pco2. Exchange of O2 and CO2 takes place independently in the lung.

4. The alveolar-arterial (a-a) gradient increases with age and supplemental O2. The Pao2/Fio2 and a/a ratios typically do not change with increased age or inspired O2.

5. When derangements in gas tensions are noted on arterial blood gas analysis, it is important to verify that the sample was obtained and analyzed in an appropriate and timely manner.

6. Refinements and further studies on continuous intravascular blood gas monitors may one day lead to widespread routine use of these devices.

7. Pulse oximetry is a rapid, reliable indicator of oxygenation status in surgical and critically ill patients. Newer oximeters feature reduced capability for errors attributable to motion artifact and hypoperfusion.

8. Multiwavelength pulse oximeters are commercially available and allow measurement of carboxyhemoglobin

and methemoglobin. Pulse oximetry may one day prove to be a reliable noninvasive monitor of volume status and fluid responsiveness.

9. A sudden decrease in Petco2 usually results from a circuit disconnection, airway obstruction, abrupt decrease in cardiac output, or pulmonary embolism. Petco2 is not always a reliable approximation of Paco2, particularly during general anesthesia or in the critically ill.

10. Mapping of pressure-volume curves in patients with acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) can provide valuable information about lung mechanics and help guide positive end-expiratory pressure (PEEP) and tidal volume settings. Sustained high airway pressure is needed to open collapsed alveoli, and PEEP stabilizes the recruited lung units.

11. Computed tomography has greatly increased our understanding of the complicated interaction between PEEP and lung recruitment in ARDS. Electrical impedance tomography may in the future emerge as a useful bedside monitor of lung recruitment, pulmonary edema, and respiratory mechanics.

12. Recruitment strategies and low–tidal volume ventilation have been shown to improve outcomes in ARDS and ALI. High-frequency ventilators are safe and effective in refractory ARDS and may some day prove to be the ideal mode of lung protective ventilation.

Gas Exchange

The realization that gas exchange takes place in the lung was made by the ancients. However, not until the 18th century, when oxygen was discovered by Joseph Priestley, did Lavoisier ascertain the true purpose of breathing: the biochemical combustion of carbon and oxygen to carbon dioxide, a process known as respira­tion.1 More than 200 years later, the exact mechanisms by which

the respiratory system takes up oxygen and eliminates carbon dioxide are still being debated.

Alveolar Gases

A practicable method for directly sampling and analyzing alveo­lar air was first described by Haldane and Priestly in 1905.2 Because of the inaccuracies and technical difficulty involved in

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direct sampling, efforts to develop indirect methods of determin­ing the composition of alveolar air ensued. Subsequently, many equations describing the concentration of alveolar gases have been derived, with a wide range of accuracy and complexity. All are based simply on the law of conservation of mass and derive from the universal alveolar air equation:

Alveolar fraction of gas XInspired fraction of X Output o

=± rr uptake of X

Alveolar ventilationi e output for CO

( )

( . ., ,2 uuptake for O2)

(1)

The equation in this form is only approximate and requires cor­rections to account for differences in expired and inspired minute volume, discussed later. Moreover, because of the inhomogeneous nature of the lung, the partial pressures calculated should be interpreted as averages of various alveolar concentrations present in heterogeneous gas exchange units. Put simply, the gas con­centrations in each alveolus are probably different, and values obtained from the equation represent the mean of all alveoli.

In the case of O2, solving the universal equation for uptake �VO2( ) yields a general Fick equation that can be solved for alveo­

lar O2:

� �V V F FO A IO AO2 2 2= −( ) (2)

F F V VAO IO O A2 2 2= −( )� � (3)

where Fao2 is the alveolar O2 fraction, Fio2 is the inspired frac­tion, and �VA is alveolar ventilation in volume per minute. In other words, the amount of O2 in alveoli is equal to the difference between the amount inspired and the amount taken up by pul­monary capillaries (conservation of mass). Multiplying through by dry barometric pressure (Pbdry) to obtain partial pressures, Equation 3 becomes

P P F V VAO B IO O Adry2 2 2= −( )� � (4)

where Pbdry = barometric pressure − saturated water vapor pressure.

It is most clear in this form of the equation that Pao2 is influenced only by four variables: barometric pressure, fraction of inspired O2, uptake of O2, and alveolar ventilation.3

The same manipulations of the universal equation yield a formula for determining alveolar CO2:

P P F V VACO B ICO CO Adry2 2 2= +( )� � (5)

Note that CO2 output must be added to the inspired concentra­tion to obtain Paco2. However, because Fico2 is usually zero and �VCO2 is relatively constant, it is clear that Paco2 is dependent

mainly on one factor, alveolar ventilation, to which it is inversely proportional:

P c VACO A2 1= ( )� (6)

where c is a constant. This approximation becomes less accurate in clinical situations in which CO2 output can be appreciably elevated, as with fever, sepsis, or shivering.4

Perhaps the simplest and most widely used approximation of the alveolar gas equation was derived by Riley and colleagues5 and relates Pao2 and Paco2 in the following way:

P P P RAO IO ACO2 2 2= − (7)

where R is the respiratory exchange ratio defined as � �V VCO O2 2 and relates CO2 output to O2 uptake. Normally, the ratio is rela­tively constant at 0.8 (i.e., 0.8 mol CO2 produced for every 1 mol O2 consumed), and the equation becomes

P P PAO IO ACO2 2 21 25= − ×. (8)

Note that the term Paco2/R in Equation 7 replaces the term P V VB O Adry ×( )� �2 from Equation 4. Because Paco2 can be

assumed to be equal to Paco2 based on the Enghoff modification and R relates O2 uptake to CO2 output, Paco2/R is essentially an indirect measure of O2 uptake and is much easier to accurately calculate than � �V VO A2 .6

A common misconception from the appearance of Pco2 in Equations 7 and 8 is that Pao2 is directly influenced by changes in Paco2. Rather, exchange of O2 and CO2 takes place independ­ently in the lung, and Pao2 is influenced by only the four afore­mentioned factors. The apparent influence of Paco2 on Pao2 is actually reflective of a change in minute ventilation or O2 consumption, more obvious in Equation 4. For example, as alveo­lar ventilation decreases, Paco2 rises and Pao2 will decrease according to Equation 8 as a result of the reduced alveolar ven­tilation. There is no “displacement” or direct alteration of O2 by CO2.6,7

Despite being quite adequate for clinical use, the Riley equation does not account for small differences in expired and 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 inert gases not being in equilibrium with blood (such as during nitrous oxide induction or washout). An equation proposed by Filley and coworkers8 corrects for this difference and does not entail calculation of R, which can be higher than the normal 0.8 in certain clinical settings, such as with metabolic acidosis or overfeeding:

P P P P P PAO IO ACO IO EO ECO2 2 2 2 2 2= − −( ) (9)

Though more accurate, it is more cumbersome than the Riley equation in that mixed expired gas concentrations must be measured. This equation should be used, for example, when calculating shunt fraction because precise Pao2 values are imperative.3

Arterial Gases

Exchange of gases between alveoli and blood occurs at the pul­monary capillaries. Arterial blood is formed by mixture of this pulmonary capillary blood with the mixed venous shunt fraction. Thus, three major factors influence the efficiency of this exchange and the resultant arterial gas tensions: � �V Q matching, alveolar diffusion capacity, and shunt fraction. Along with hypoventila­tion and low Pio2, derangements in any of these factors result in arterial hypoxemia (Box 44­1). Some determination of the cause of the hypoxemia can be made by evaluation of the a­a O2 gradi­ent; problems with gas exchange increase the gradient, whereas it is normal in hypoxemia because of low Pio2 or hypoventilation. The a­a gradient is usually elevated in a patient breathing sup­plemental oxygen. Two other indices of oxygenation that remain unchanged with fluctuating Fio2 are the Pao2/Fio2 and a/a ratios (normally 350 to 500 mm Hg and 0.8 to 0.85, respectively).

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The extent to which these factors affect the makeup of arte­rial blood differs for CO2 and O2 because they have different arteriovenous gradients and diffusing capacities. CO2 is estimated to have a diffusing capacity 20 to 30 times greater than that of O2,9 and its exchange is therefore minimally affected by derange­ments in alveolar membrane diffusion and � �V Q mismatching. The narrower arteriovenous gradient of CO2 (≈6 mm) versus O2 (∼60 mm) leads to less profound effects of venous shunt on arte­rial Pco2. Except in extreme circumstances there is little evidence that impaired diffusion of O2 or CO2 across the alveolar mem­brane occurs to any clinically significant extent, so this is not discussed further in this chapter.

� �V Q MismatchIn normal subjects, resting minute ventilation is roughly 4 L/m and pulmonary blood flow is 5 L/m, which results in a ventila­

tion­to­perfusion ratio of roughly 0.8 for the entire lung.10 This would represent the � �V Q ratio of each alveolus if ventilation and perfusion were uniformly distributed in the lung. In reality, dis­tribution is not uniform, and ratios range anywhere from zero (shunt) to infinity (dead space ventilation). For example, alveoli in dependent lung regions are better perfused than those in the apices and therefore have lower � �V Q ratios.11 Ventilation is usually more evenly distributed throughout the lung than blood flow is, so impaired oxygenation of arterial blood is most often due to derangements in perfusion.

� �V Q mismatching results in hypoxemia for two reasons. 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 dispropor­tionately large effect from the areas of low � �V Q and hence a reduction in Pao2. The second reason is due to the nature of oxy­hemoglobin (HbO2) dissociation. Alveoli with high � �V Q are on the plateau portion of the curve, where shifts in Pao2 have little effect on O2 content. These new areas of high (or higher) � �V Q introduced by scatter are unable to compensate for the new areas of low � �V Q, which are on the steep portion of the curve and therefore more profoundly affected by changes in Pao2 (Figs. 44­1 and 44­2).

ShuntOne extreme of � �V Q mismatch is a right­to­left shunt ( � �V Q = 0), the other extreme being dead space ventilation ( � �V Q = infin­ity). Normally, a small shunt fraction (<3% of cardiac output) exists because of drainage of bronchial and thebesian venous blood into the left heart.7 However, as a result of the steep arterio­

Figure 44-1 Alveolar-to-arterial Po2 difference caused by scatter of � �V Q ratios and its representation by an equivalent degree of venous admixture. A, Scatter of � �V Q ratios corresponding roughly to the three zones of the lung in a normal upright subject. Mixed alveolar gas Po2 is calculated with allowance for the contribution of gas volumes from the three zones. Arterial saturation is similarly determined and Po2 derived. There is an alveolar-arterial Po2 difference of 0.7 kPa (5 mm Hg). B, Theoretical situation that would account for the same alveolar-to-arterial Po2 difference caused solely by venous admixture. This is a useful method of quantifying the functional effect of scattered � �V Q ratios but should be carefully distinguished from the actual situation. (From Lumb AB: Nunn’s Applied Respiratory Physiology, 6th ed. Philadelphia, Elsevier/Butterworth Heinemann, 2005.)

Alveolar gas

Mixed venoussaturation 72.4%

Mixed venousblood

Arterial bloodsaturation 97.4%

PO2 = 12.9 kPa (97 mm Hg)PCO2 = 5.4 kPa (40.5 mm Hg)

PO2 = 13.6 kPa (102 mm Hg)PCO2 = 5.3 kPa (40 mm Hg)

End-capillary PO2 13.6 kPa (102 mm Hg)Saturation 97.6%

Arterial bloodsaturation 97.4%PO2 12.9 kPa (97 mm Hg)1% venous

mixture

Alveolar gasPO2 13.6 kPa

(102 mm Hg)

45 35 2012.4 (93) 13.6 (102) 16 (120)3.5 (41) 53 (40) 4.7 (35) V/Q ratios

1.7

0.9

0.7

% contribution

% contribution 57 33 1097.0 97.6 98.5O2 sat.

PO2PCO2

PCO2 5.5 (41) 5.3 (40) 4.7 (35)

A

B

..

Box 44-1 Five Causes of Hypoxemia and the Associated Alveolar-to-Arterial (a-a) O2 Gradient

Normal a-a O2 Gradient

Hypoventilation

Reduced Pio2

Increased a-a O2 Gradient

Increased � �V Q heterogeneity

Increased shunt

Diffusion limitation

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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 cir­culations 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 contri­butor to the baseline a­a gradient. The gradient increases with age, probably secondary to increased closing capacity and � �V Q scatter.7

Pathologic right­to­left shunting of blood occurs in areas of atelectasis or airway blockage, as in acute lung injury (ALI) or pneumonia. Alveoli are collapsed or unventilated but continue to be perfused. Venous drainage from lung tumors also constitutes a pathologic shunt. If hypoxic pulmonary vasoconstriction (HPV) fails to adequately limit blood flow to these regions, hypoxemia occurs. Indeed, inhaled anesthetics are known to cause attenua­tion of HPV, and induction of general anesthesia (GA) causes immediate development of atelectasis (see Chapter 15).12,13 Both

phenomena are probably contributors to the 5% to 10% shunt found in patients undergoing GA with mechanical ventilation.10

Calculating Shunt Fraction and Dead SpaceA simplified but useful three­compartment lung model aids in approximating what fraction of cardiac output �QT( ) constitutes shunt �QS( ) and what fraction of tidal volume (Vt) constitutes dead space ventilation �VDS( ) . Commonly known as the Riley approach, the lung is considered as though it were made up of three compartments at the three extremes of � �V Q matching: (1) a shunt compartment with perfused but unventilated alveoli, (2) a dead space compartment with ventilated but unperfused alveoli, (3) and an ideal compartment with normally distributed ventila­tion 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 as an oversimplified but clinically useful model.

The shunt fraction � �Q QS T( ) 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) blood:

� �Q Q Cc Ca Cc CvS T O O O O= ′ −( ) ′ −( )2 2 2 2 (10)

In a normal subject with capillary O2 saturation close to 100%, the following approximation can be made

� �Q Q Sa SvS T O O= −( ) −( )1 12 2 (11)

where SvO2 and Sao2 are mixed venous and arterial O2 saturation, respectively.

It is important to note that the fraction calculated in Equa­tion 10 is not a true shunt (intrapulmonary shunt through alveoli

Figure 44-2 Alveolar-arterial Po2 difference caused by scatter of � �V Q ratios resulting in oxygen tensions along the upper inflection of the oxygen 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 the effect of the different volumes of gas and blood contributed by the three 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 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.)

100

80

60

40

20

0

98.2%sat.

95.8%sat.

74%sat.

0 4 8 12 16

200 6040 80 120100

Oxy

gen

satu

ratio

n, %

Mean saturation89%

Mean arterial PO2

7.6 kPa (57 mm Hg)

Alveolar/arterial PO2

difference 3.1 kPa (23 mm Hg)

Mean alveolar PO2

10.7 kPa (80 mm Hg)

PO2 (kPa)

PO2 (mm Hg)

low V/Q mid V/Q high V/Q

Figure 44-3 Three-compartment (Riley) model of gas exchange. The lung is imagined to consist of three functional units consisting of alveolar dead space, “ideal” alveoli, and venous admixture (shunt). Gas exchange occurs only in the “ideal” alveoli. The measured alveolar dead space consists of true alveolar dead space together with a component caused by � �V Q scatter. The measured venous admixture consists of true venous admixture (shunt) 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 possible to sample “ideal” alveolar gas. (From Lumb AB: Nunn’s Applied Respiratory Physiology, 6th ed. Philadelphia, Elsevier/Butterworth Heinemann, 2005.)

Venous admixture(shunt)

Arterialblood

Mixed venousblood

Ideal alveolar gas

Alveolar dead space

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with zero � �V Q ) but should be thought of as a total shunt because it includes intracardiac and physiologic shunting and the contribution of areas with relatively low (shuntlike) but nonzero � �V Q. Thus, the model is unable to predict how much each of

these factors contributes to the calculated shunt because they all introduce undersaturated blood into the arterial circulation. It is though that breathing 100% O2 eliminates the shuntlike contribu­tion by fully saturating capillary blood in low­ � �V Q alveoli, but it appears instead that these regions may progress via resorption atelectasis into areas of true shunt.14 Making the distinction between true shunt and shuntlike regions caused by low � �V Q may be clinically important, particularly for anesthesiologists, in that reduced � �V Q has been shown to be more predictive of post­operative hypoxemia than increased shunt is.10 Techniques allowing more accurate distinction between the components of calculated shunt and dead space have been developed and are described later.

A method has been derived to estimate shunt fraction without sampling arterial or mixed venous blood.15 Arterial oxygen content is calculated from measured hemoglobin (Hb) and Spo2, and Po2 is obtained from the alveolar gas equation by using end­tidal Pco2 as an estimate of Paco2. Mixed venous O2 content is estimated by assuming a fixed arterial–to–mixed venous O2 gradient. Estimates of shunt fraction obtained by this method are expectedly somewhat imprecise (±16%) when compared with invasive measurements but are adequate for clinical use.

The dead space component in the three­compartment gas exchange model can be calculated with the Bohr equation:

V V Pa P PaDS T CO ECO O= −( )2 2 2 (12)

where Peo2 is the mixed expired Pco2

The fraction calculated includes anatomic, alveolar, and apparatus (i.e., breathing circuit) dead space, which together rep­resent physiologic dead space.

As with the shunt calculation described earlier, dead space determined by the equation is not true dead space because it includes an indeterminate contribution from relatively underper­fused or dead space–like alveoli with high � �V Q (see Fig. 44­3). Another limitation of the model is that alterations in cardiac output or Hb concentration can lead to different calculated values of shunt fraction, even when actual � �V Q ratios have not changed. A substantial rise in cardiac output will increase SvO2 and cause a subsequent rise in the O2 content of shunted blood and there­fore arterial blood (Fig. 44­4). The calculated shunt fraction would decrease without an actual decrease in percent shunt by volume.

Distinguishing between Shunt and Altered � �V Q as the Cause of Impaired OxygenationIn 1974, Wagner and coauthors described a technique known as multiple inert gas elimination (MIGET), which allows plotting of pulmonary ventilation and perfusion against the � �V Q ratio for a large number of lung compartments (rather than just three compartments as in the Riley approach), all with different � �V Q ratios.14 Six inert tracer gases with widely varying blood solubility are infused intravenously and allowed to reach steady state. Arte­rial and mixed expired gas concentrations are measured, and the mixed venous concentration is calculated via the Fick principle. Retention­solubility and excretion­solubility curves are created and then translated into a continuous plot of perfusion against � �V Q and ventilation against � �V Q, respectively, in relation to the

heterogeneous spectrum of � �V Q ratios present throughout the

lung. A host of other variables can be accurately measured, includ­ing intrapulmonary shunt and alveolar dead space. The technique is cumbersome and the numerical analyses rather complicated for routine use, but studies using the technique have been invaluable to our understanding of gas exchange in intensive care unit (ICU)16 and surgical17,18 settings. Figure 44­5 shows a typical plot in awake patients, with the development of shunt, increased dead space, and � �V Q scatter on induction of GA. Increasing shunt detected by multiple inert gas elimination (MIGET) has been correlated with increasing atelectasis noted on chest computed tomography (CT).19 Distinguishing between true shunt and low � �V Q can also be performed noninvasively by simultaneously

plotting Sao2 versus Pio2 (Fig. 44­6). Increasing shunt shifts the curve downward, whereas reducing � �V Q below the normal 0.8 shifts the curve rightward. The figure schematically shows the long­established observation that hypoxemia caused by true shunt is minimally responsive to increased Pio2, in contrast to hypoxemia caused by � �V Q mismatch. As mentioned, � �V Q reduction detected by a rightward shift of the curve intraopera­tively has been shown to correlate with hypoxemia up to 30 hours postoperatively. The technique may help identify patients at risk for postoperative hypoxemia and in need of supplemental O2 and closer monitoring. It can also be used in patients with chronic lung disease to determine whether additional O2 may be needed during air travel or at altitude.10

Blood Gas Analysis

Measurement of Blood Gas Tensions

The basic design that modern blood gas analyzers still use today was introduced by Severinghaus and Bradley in 1958.20 Designed by Leland Clark in 1953,21 the Po2 electrode is a platinum probe bathed in an electrolyte solution and separated from the sample (blood) by an O2 permeable membrane. Oxygen molecules pass from blood through the membrane and are reduced to hydroxyl ions. Po2 is proportional to the current generated by this reduc­tion reaction. Similarly, the Stow/Severinghaus Pco2 electrode is a pH­sensitive glass probe bathed in a bicarbonate solution and encased by a CO2 permeable membrane. Pco2 is proportional to the H+ generated as CO2 reacts with water to form H+ and HCO3

−. Severinghaus and Astrup have provided a detailed history of the development of blood gas analysis (BGA).22,23

Temperature Correction

Modern blood gas analyzers measure blood gas tensions at 37°C. Because patients rarely have a temperature of exactly 37°C, blood samples must be heated or cooled to 37°C for analysis. Heating a blood sample decreases pH, gas solubility, and Hb affinity for O2 and CO2. Thus, as the blood from a hypothermic patient (say 35°C) is heated and analyzed at 37°C, more gas becomes dissolved in solution and the measured Po2 and Pco2 will be higher than at 35°C. Raising the temperature also increases the H+ concentra­tion and would give a falsely low pH in a hypothermic patient. Modern analyzers use one of a number of algorithms to automati­cally correct pH and blood gas tensions for temperature, and Box 44­2 provides the formulas approved by the National Committee

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for Clinical Laboratory Standards (NCCLS). The corrections are all rather slight, and there is little evidence to suggest that tem­perature­corrected values are clinically more useful than 37°C values. Two approaches, pH­stat and alpha­stat, have been used to manage pH in hypothermic patients undergoing cardiopulmo­nary bypass. The alpha­stat approach lets pH rise naturally into the alkalotic range as the patient is cooled, and pH­stat maintains normal pH and presumably cerebral perfusion by adding CO2. Data favoring either approach are very limited.

Artifactual Changes in Arterial Blood Gas Values

Delay in analyzing a blood sample after it is drawn can artifactu­ally change the measured pH and gas tensions. Storing a sample longer than 20 minutes can cause a significant elevation in Pco2 and reduction in Po2 and pH, probably secondary to cellular metabolism. Leukocytosis and thrombocytosis accelerate these

Figure 44-4 Effect of cardiac output on Po2. A, Arterial and mixed venous O2 tension and content 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 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.

.

¯

.

¯

¯

.

..

.

.

.

¯

.

.

.

.

A

B

Lung

Tissue

Pc'O2=100O2 content=19.3

PsO2=40O2 content=13.9

PaO2=78O2 content=18.8

PvO2=40O2 content=13.9

SvO2=72%

PAO2=100 mm Hg

Hb = 14 g/dL

240 mL/min

QA = 90%

QS =10%

QT = 5 L/min Œ

O2

VO2

Lung

Tissue

PcO2=100O2 content=19.3

PsO2=48O2 content=15.9

PaO2=85O2 content=19.0

PvO2=48O2 content=15.9

SvO2=82%

PAO2=100 mm Hg

240 mL/min

= 90%

=10%

QT = 8 L/min Œ

O2

VO2

QA

QS

QT

QT

QT

QT

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Figure 44-5 Ventilation-perfusion ( � �V QA ) distribution and computed tomography in a supine subject. Left, � �V QA distribution in an awake (top) and anesthetized (bottom) subject. Note the appearance of a pulmonary shunt and an increase in � �V QA mismatch during general anesthesia with mechanical ventilation. Right, Computed tomography of the chest just above the top of the right diaphragm. Note the appearance of densities in the dependent lung regions during anesthesia. Vd, volume of distribution. (Redrawn from Gunnarsson L, Tokics L, Gustavsson H, et al: Influence of age on atelectasis formation and gas exchange impairment during general anesthesia. Br J Anaesth 66:423-432, 1991.)

0.6

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0.4

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0.00 0.01 0.1 1 10 100

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VD=35%

OS=0%

Anesthesia

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OS=5.9%

Anesthesia

Per

fusi

on o

r ve

ntila

tion

(L/m

in)

PerfusionVentilation

PerfusionVentilation

Figure 44-6 Hemoglobin-oxygen (HbO2) saturation versus inspired partial pressure of oxygen (Po2). The curves are plotted by changing inspired Po2 in stepwise fashion. A, Series of theoretical curves obtained by calculating the effect of different degrees of right-to-left shunt. Increasing shunt displaces the curves 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 of the shunt curve, but the fit is quite good when the 30% curve is shifted to the right. This implies a combination of shunt and � �V QA mismatch. (Adapted from Jones JG, Jones SE: Discriminating between the effect of shunt and reduced � �V QA on arterial oxygen saturation is particularly useful in clinical practice. J Clin Monit Comput 16:337, 2000.)

0 10 20 30 40 50 60 0 10 20

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arterial Po2 when skin is warmed, which causes blood flow to exceed the amount required for local O2 consumption. O2 from capillaries diffuses through the warmed skin, where it is analyzed by a Clark­type electrode adhered to it. Though useful in infants, transcutaneous gas monitoring has many limitations despite good agreement of Po2 values with traditional BGA.25 Peripheral vas­cular disease or vasoconstriction can generate erroneous values. Cutaneous hypoxia caused by reduced cardiac output will give falsely decreased Po2 readings. These devices must be calibrated frequently, have a relatively slow response time, and can cause skin burns with prolonged application.

In-Line Blood Gas Monitoring

Continuous intra­arterial pH measurement was accomplished as early as 1927 with antimony electrodes. Shortly after Clark devel­oped his Po2 electrode in 1956, the first continuous intravascular blood gas monitoring (CIBGM) devices were developed. Early devices consisted of electrochemical sensors and were essentially modified Clark electrodes. Problems with these devices included excessive drift, lack of reliability, large size, and interference from anesthetic gases. Later, Lubbers and Opitz, using a technology known as fluorescence quenching, created fiberoptic probes to continuously measure Po2 and Pco2, which they named optodes.26 Absorbance­based fiberoptic sensors were also developed. Only two single­parameter devices became commercially available: the Continucath 1000 electrochemical Po2 sensor for adults and the Neocath (Biomedical Sensors, High Wycomb, UK) O2 sensor for neonatal umbilical artery placement.

Advances in the design of single­parameter systems inevi­tably led to the development of multiparameter devices capable of measuring pH, Pco2, Po2, and temperature. Most are pure optode systems, with the Paratrend 7 being the only hybrid optode­electrode system. The upgraded Paratrend 7+ replaced the Clark Po2 electrode with an optode, thus making it a pure optode system (Fig. 44­7).

Agreement between sensor and traditional BGA measure­ments can be quantified by use of the Bland­Altman calculation

Figure 44-7 Cross section of the Paratrend 7 sensor tip. (Courtesy of Biomedical Sensors, High Wycombe, UK.)

pH sensor

Oxygen sensor

Void between sensorsfilled with acrylamide gel

containing phenol red

Microporous polyethylenetube (gas and ion permeable)

CO2 sensor

Thermocouple

Box 44-2 Algorithms for Correction to Body Temperature of Blood Gas Tensions Measured at 37°C

pH

ΔpH/ΔT = −0.0146 + 0.0065 (7.4 − pHm)

ΔpH/ΔT = −0.015

ΔpH/ΔT = −0.0147 + 0.0065 (7.4 − pHm)*

ΔpH/ΔT = −0.0146

Pco2

Δlog10 Pco2/ΔT = 0.019*

Δlog10 Pco2/ΔT = 0.021

Po2

∆ ∆

log.

..

log

.10 2

23 88

10

0 0252

0 234 100 10 00564P T

PCO

O=

( ) +

+

PP T

P T

CO

CO

SAO2

0 13 100

10 2

0 0052 0 27 1 10

5 49

2∆

∆ ∆

= + −[ ]= ×

− −( ). .

log.

.

110 0 071

9 72 10 2 3

0 012

1123 88

923 88

10 2

+× +

=

P

P

P T

P

O

O

CO

.

.

.

. .

log

.

∆ ∆

OO O

O

O O

m

m

SS Hb

P S S

2 2

2

2 2

714 1001 100 0 6 0 073

714 100 1

( ) + ( )−( )( ) +

+ −. .

OO Hb2 100 0 6( )( ).

So2 ≤ 95%: Δlog10 Pco2/ΔT = 0.31

S % P T eO COO

2 10 20 3 3095 0 032 0 0268 2> = − −( ): log . . .∆ ∆ S

*National Committee for Clinical Laboratory Standards (NCCLS)-approved standard.

Hb, blood hemoglobin concentration in g/dL; pHm and Po2m, pH and Po2 values measured at an electrode temperature of 37°C; Po2, partial pressure of oxygen in mm Hg; So2, percent hemoglobin-oxygen (HbO2) saturation; T, temperature in degrees centigrade (°C).

Data from Ashwood ER, Kost G, Kenny M: Temperature correction of blood-gas and pH measurements. Clin Chem 29:1877, 1983; and Siggaard-Andersen O, Wimberley PD, Gothgen I, Siggaard-Andersen M: A mathematical model of the hemoglobin-oxygen dissociation curve of human blood and of the oxygen partial pressure as a function of temperature. Clin Chem 30:1646, 1984.

*

changes.24 Because red cells do not contain mitochondria, this phenomenon is not observed in polycythemia. However, anaero­bic glycolysis can generate lactic acid and reduce pH. Placing the sample in ice immediately after it is obtained can maintain its stability, and addition of sodium fluoride or cyanide can inhibit cellular O2 consumption.24 The presence of air bubbles in the 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 incep­tion, the ability to assess a patient’s oxygenation status even more rapidly and easily has obvious advantages. One alternative is to measure gas tensions at the bedside transcutaneously. This tech­nology relies on the tendency of capillary Po2 to approximate

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of bias and precision.27 Bias is the difference between mean values obtained by standard methods (BGA) and those obtained with the new device being tested. Precision is the standard devia­tion of these differences and measures reproducibility of the results.

Like their predecessors, newer probes remain fragile and continue to exhibit motion artifact, wall effect (decreased Po2 readings because of contact with the arterial wall), and thrombo­genicity. Their accuracy diminishes with insufficient blood flow to the cannulated artery. Moreover, despite encouraging in vitro and animal studies, results from clinical trials have not consist­ently been as favorable. Data for Pco2 and pH measurements are impressive, but studies have found poor agreement of sensor Po2 measurements with those obtained by BGA in elevated Po2 ranges.28,29 Weiss and colleagues found accurate results with minimal drift in all parameters up to 10 days after insertion in pediatric patients, but the O2 sensor required frequent calibra­tion.30 Several published studies on the clinical performance of various CIABGM devices are summarized in Table 44­1.

Despite its limitations, CIABGM has many theoretical advantages over traditional BGA, although no outcome studies have proved these advantages (Box 44­3). Use of CIABGM in cardiac, thoracic, orthopedic, and transplant surgery may lead to earlier detection of severe blood gas and acid­base derange­ments.35,36 Detection of Po2 changes after cement implantation during hip replacement has been accomplished with this technology.33 It has been validated for use in anesthesia and intensive care in pediatric patients.32 Further technologic refine­ments, outcome studies, and data on cost­effectiveness are neces­sary for CIABGM to have widespread application in anesthesia and critical care.

Oxygen Saturation

Although traditional BGA remains the standard modality for determining oxygen content, an alternative is to measure oxygen saturation (So2). It can provide rapid and clinically useful infor­mation about oxygenation status.

Co-oximetry

The co­oximeter is a traditional blood gas analyzer that is also capable of measuring concentrations of HbO2, reduced hemo­

globin (HbR), carboxyhemoglobin (COHb), and methemoglobin (MetHb). Each of these species has unique absorption spectra, and corresponding wavelengths of light are used to analyze a small blood sample. It is currently the gold standard for measur­ing Sao2. Results are usually obtained in less than 2 minutes.

Transcutaneous Oximetry

The principle of transcutaneous oximetry is similar to that of transcutaneous gas tension monitoring, but Sao2 is measured instead of Po2. Two wavelengths of light are used to measure quantities of oxygenated and deoxygenated blood to give an esti­mate of Sao2, provided that the blood being analyzed is mostly arterial and other Hb species are absent. Two­wavelength ear oximeters were developed and used in practice more than 60 years ago.37 Robert Shaw patented an eight­wavelength ear oxi­meter in 1972, and a device using this technology was marketed in the late 1970s by Hewlett Packard. Problems with size and reli­ability of data prevented its widespread use.

Pulse Oximetry

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 routine use began. Pulse oximetry works by analyzing the pulsa­tile arterial component of blood flow, thereby ensuring that arte­rial saturation (Spo2) rather than venous saturation is being measured (Fig. 44­8). Two wavelengths of light are used, usually

Table 44-1 Results from Some Published Studies on Clinical Performance of Continuous Intra-arterial Blood Gas Monitoring

Investigator(s) DeviceNumber of Patients

Clinical Setting and Insertion Site

pH Bias ± Precision (pH Units)

Pco2 Bias ± Precision (mm Hg)

Po2 Bias ± Precision (mm Hg)

Ganter29 Paratrend 7+ 23 OR: thoracoscopic surgery (radial)

−0.01 ± 0.06 3 ± 9 −20 ± 86

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 ± 9

ICU, intensive care unit; OR, operating room; Ped, pediatric.

Box 44-3 Advantages of a Continuous Intra-arterial Blood Gas Monitoring System over Intermittent Blood Gas Analysis

Availability of continuous data

Earlier detection of deleterious events

Potential for trend analysis

Decreased blood loss

Decreased laboratory turnaround time

Decreased exposure of staff to potentially infected blood

From Venkatesh B: In-line blood gas monitoring. In Papadakos PJ, Lachmann B (eds): Mechanical Ventilation: Clinical Applications and Pathophysiology. Philadelphia, Elsevier, 2008.

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are calibrated against laboratory Sao2 down to 70% saturation, and lower saturations are determined by extrapolation of the curve. Thus, pulse oximeters cannot be calibrated by the user, and their reliability is dependent on the quality of signal processing and the stored calibration curve.

Accuracy of Pulse OximetryBecause of its impressive accuracy, reliability, and convenience, pulse oximetry has become one of the most important techno­logic developments in clinical monitoring. Several studies comparing co­oximetry and pulse oximetry report substantial agreement between Spo2 and Sao2 over a wide range of Sao2 values.38,39

Errors in Pulse OximetryBecause Spo2 measurements are averaged over a few seconds to provide readings, there is some degree of delay in response time. 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 (Fig. 44­10).41 Motion artifact and hypoperfusion are the most common causes of Spo2 inaccuracy,42,43 both of which are less problematic with newer oximeters. Caution is advised in using pulse oximetry to not make inferences about gas exchange. Spo2 should not be used to assess the adequacy of ventilation because Sao2 is only minimally affected by changes in Pco2 (via the Bohr effect). In addition, when Po2 is high, large decreases in oxygen tension produce only small changes (if any) in Sao2 and may not be detected with pulse oximetry (see Fig. 44­2).

Anemia, with an Hb concentration as low as 2.3 g/dL, has little or no effect on Spo2 readings when Sao2 is normal,44 but underestimation of Sao2 has been observed during hypoxemia.45 Because MetHb substantially absorbs both red and infrared light, falsely low Spo2 readings are generated when actual Sao2 is above 85%, and readings are falsely high when actual Sao2 is below 85%. Spo2 invariably reads 85% when very large amounts of MetHb are 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 elevated Spo2 readings. Erroneous Spo2 readings can be caused by structural hemoglobinopathies,47,48 as well as by a host of other factors, many of which are summarized in Table 44­2.

Recent Advances in Pulse OximetryError corrEction. Motion sensitivity and signal loss

secondary to hypoperfusion are two of the more common errors 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 episodes more reliably than their predecessors can under these conditions.50,51 Indeed, one study reported that during hypoper­fusion or excessive motion, oximeters using this technology give accurate Sao2 readings in 92% of cases in which older monitors failed.52

MultiwavElEngth PulsE oxiMEtErs. Because only two wavelengths of light are used in traditional pulse oximeters, the presence of additional Hb species cannot be detected, which may result in erroneous readings. Using principles from both pulse

Figure 44-8 Principle of pulse oximetry. Light passing through tissue 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 nonpulsatile component (DC). Hemoglobin O2 saturation may be obtained by application of Equation 19. (Data from Tremper KK, Barker SJ: Pulse oximetry. Anesthesiology 70:98, 1989.)

Ligh

t abs

orpt

ion

Time

Absorption due topulsatile arterial blood

Absorption due tononpulsatile arterial blood

Absorption due to tissue

Absorption due to venous and capillary blood

AC

DC

100806040200

Mod

ulat

ion

ratio

(R

)

Observed R

Red

IR

SaO2 (%)

SpO2

Figure 44-9 Red/infrared modulation ratio (R) versus oxygen saturation (Sao2). At high Sao2 (right side of the graph), the pulse amplitude (or modulation) of the red signal is less than that of the infrared signal, whereas the reverse is true at low Sao2. Pulse oximeters measure R, the ratio of red to infrared pulse amplitudes (see Equation 13), and estimate Sao2 by applying the calibration curve (solid line) as depicted by the dashed line and arrow. (From Mannheimer PD: The light-tissue interaction of pulse oximetry. Anesth Analg 105(6 Suppl):S10-S17, 2007.)

660 nm (red) and 940 nm (infrared), because oxygenated and deoxygenated blood each absorb light quite differently at these wavelengths. At 660 nm, HbO2 absorbs less light than HbR does, whereas the opposite is observed with infrared light. Two diodes emitting light of each wavelength are placed on one side of the probe and a photo diode that senses the transmitted light on the opposite side. The amount of light absorbed at each wavelength by the pulsatile arterial component (AC) of blood flow can be distinguished from baseline absorbance of the nonpulsatile com­ponent and surrounding tissue (DC). The ratio R is calculated by the oximeter as follows and is empirically related to O2 saturation:

R AC DC AC DC= ( ) ( )660 660 660 660 (13)

A calibration curve (Fig. 44­9) is derived from R and labo­ratory measurements of arterial oxygen saturation in healthy vol­unteers and the algorithm stored in the oximeter. Modern devices

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Figure 44-10 Effect of pulse oximeter probe replacement on delay from onset of hypoxemia to a drop in measured Spo2. During cold-induced peripheral vasoconstriction in normal volunteers, the onset of hypoxemia was detected more quickly with an oximeter probe on the forehead than on the finger. Other studies have shown a similar advantage for pulse oximeter probes placed on the ear. (From Bebout DE, Mannheimer PD, Wun C-C: Site-dependent differences in the time to detect changes in saturation during low perfusion. Crit Care Med 29:A115, 2002.)

10:00

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oximetry and co­oximetry, the first eight­wavelength pulse oxi­meter capable of measuring several species of Hb has become commercially available and may prove to be a major advance in oxygen monitoring. The Massimo Rad­57 (Massimo Corp, Irvine, CA) gained Food and Drug Administration (FDA) clearance in 2006 and boasts the ability to accurately measure MetHb and COHb, in addition to all the features of conventional pulse oxi­metry. Two large studies comparing measurements from the unit with conventional co­oximetry in emergency department patients have produced equivocal results, with one reporting a significant number of false­positive readings.53,54 One smaller study in healthy volunteers reported good agreement between oximeter and laboratory measurements,55 and other investigations to deter­mine accuracy of the device are ongoing.

rEflEctancE PulsE oxiMEtry. The technology was developed to combat problems with signal transmission during hypoperfusion and for use when a transmission path is unavaila­ble. Probes are commonly placed on the forehead, where motion artifact and hypoperfusion tend to be less of a problem than with other sites.56 Forehead probes are commercially available and appear to detect hypoxemia more quickly than ear or finger probes do.41 The light­emitting and light­sensing diodes are on the same side of the probe instead of opposite sides as in tradi­tional pulse oximetry, and the reflected light from the tissue bed is analyzed. Indeed, reflectance oximetry has been used to monitor fetal oxygen saturation with scalp probes and been shown to decrease surgical intervention in the face of non­reassuring fetal status.57 Esophageal probes have been designed and have shown success in measuring Spo2 during cardiothoracic surgery when finger probes have failed.58 The investigators reported minimal bias and narrow limits of agreement when compared with finger probes used in the study. Monitoring of gastric Spo2 as an indica­tor of splanchnic perfusion has also shown promise.59 Excessive edema, poor skin contact, and motion artifact are the most common sources of error in reflectance oximetry. Artifacts have also been shown to occur with probe placement directly over a pulsating superficial artery.60

Clinical Applications of Pulse OximetryPulse oximetry is arguably most useful as an early warning sign of hypoxemia. Because this is of paramount importance in the

surgical setting, pulse oximetry became a standard of care in anesthesia practice in 1986. In a large study comparing intraop­erative pulse oximeter use with standard care, 80% of anesthesi­ologists felt more comfortable when using pulse oximetry.61 It is interesting to note that despite its widely accepted value, there is little evidence that pulse oximetry affects outcomes in anesthe­sia,62 and a study evaluating postsurgical patients did not demon­strate that routine Sao2 monitoring reduces mortality, cost of hospitalization, or ICU transfer.63

PErioPErativE. In a randomized, controlled study of 200 surgical patients, Moller and colleagues found a reduced inci­dence of hypoxemia intraoperatively and in the postanesthesia care unit (PACU) when pulse oximetry was used. In the recovery room, patients in the oximeter group on average received higher Fio2 and more naloxone, had a longer stay, and were discharged with supplemental O2 more frequently.64 The same group later conducted a study looking at postoperative complications with and without intraoperative pulse oximetry in 20,802 patients. No overall difference was found in complication rate, outcome, mean hospital stay, or in­hospital death between the groups, even though hypoxemia and hypoventilation were detected more fre­quently when pulse oximetry was used.64 However, post hoc analysis of this trial suggests that pulse oximetry may have decreased the incidence of myocardial ischemia.62 A number of studies report detection of hypoxemia several days postopera­tively with pulse oximetry.65,66 Intrapartum fetal pulse oximetry in the presence of a non­reassuring fetal heart rate is associated with a reduction in operative interventions.57 The peak effects of analgesia may correlate with hypoxemia, so monitoring of patients receiving narcotics may be important to prevent adverse cardiac events.67

critically ill. The complicated pathophysiologic milieu of critical illness is such that many monitoring devices can produce inaccurate data in this patient population. Pulse oxime­try, on the other hand, appears to maintain its reliability. Jubran and Tobin found that pulse oximeters accurately estimate Sao2 in critically ill patients when Sao2 is greater than 90% (bias, 1.7%; precision, ±1.2%) but are less accurate when Sao2 falls below 90%.68 An Spo2 of 92% was indicative of adequate oxygenation when titrating O2 in white patients. In black patients, however, significant hypoxemia was commonly present with an Spo2 of

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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 carrier-201)

No significant effect

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 oxygena­tion. After cardiac surgery, use of pulse oximetry has been shown to increase detection of hypoxemic episodes and decrease the number of arterial BGAs performed in the ICU.69

New and Future ApplicationsAnalysis of the plethysmographic waveform generated by pulse oximeters has been advocated as a means of assessing volume status, fluid responsiveness, and a number of other clinical varia­

bles.70,71 Respiratory variations in systolic pressure (dPs) and arte­rial pulse pressure (dPp) have been shown to be accurate indicators of volume status and fluid responsiveness in mechanically venti­lated patients (Fig. 44­11).72 Pulse pressure variation may predict fluid responsiveness more reliably than the use of dPs can. Such analyses require placement of an arterial catheter and are not always practical. Recently, variation in the pulse oximeter plethys­mograph (dPOP) amplitude was shown to be a reliable noninva­sive surrogate for dPp because both parameters are dependent on

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stroke volume.73 In a study of patients under GA, Cannesson and colleagues found that baseline dPOP was correlated with percent change in cardiac index induced by volume expansion.74 Similar results were obtained in a separate study on critically ill septic patients.75 The authors of these trials concluded that dPOP can predict response to fluid administration and quantifies the effect of volume expansion on a number of hemodynamic parameters. To elucidate where the oximeter probe should be placed to best detect these variations, Shelley and colleagues analyzed plethys­mographic waveforms from finger, ear, and forehead probes in patients undergoing positive­pressure ventilation during surgery, as well as in spontaneously breathing patients.76 Their results suggest that the ear and forehead may be better monitoring sites than the finger for detection of variation in respiratory waveform. Because error and artifact correction in most commercial pulse oximeters can obscure the often subtle respiratory variations, unaltered plethysmographic waveforms are needed for such analyses.

Many other novel applications of pulse oximetry in anes­thetic practice have been studied. Mowafi found that dPOP may be a better indicator of intravascular test dose injection during epidural placement than traditional hemodynamic markers are (i.e., heart rate and blood pressure).77 A 10% decrease in POP indicated intravascular injection with 100% sensitivity, specificity, positive predictive value, and negative predictive value. Sensitivi­ties using heart rate and blood pressure change as criteria were 85% to 95%. Changes in perfusion index (defined as AC940/DC940) have been used as confirmation of epidural placement and as an indicator of painful stimulus under anesthesia.78,79 Many modern oximeters are programmed to measure perfusion index.

Mixed Venous Monitoring

Shock represents an imbalance between oxygen demand, delivery, and utilization at the tissue level. Monitoring of mixed venous oxygen saturation SvO2( ) can give insight into the adequacy of

this balance. It can be calculated by rearranging the Fick equation for O2:

Sv Sa V Hb COO O O2 2 2 1 39= − × ×( )� . (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 oxygen delivery (Do2), or by increased O2 consumption �VO2( ). These variables are related in the following way:

�V D EROO O2 2 2= × (15)

where ERO2 is the extraction ratio (%) of O2.If oxygen delivery to tissue falls and consumption is to

remain constant, oxygen extraction by tissues must increase. Blood returning to the right heart will therefore have a reduced O2 content and SvO2 . Thus, a reduced SvO2 is suggestive of global tissue hypoxia, which often precedes multiorgan failure and death.80 Increased anaerobic metabolism as evidenced by increased lactate levels ensues and is associated with increased mortality.81 These processes are usually under way as SvO2 approaches 40%. A pulmonary artery catheter is required to measure mixed venous saturation, and continuous monitoring can be performed with a catheter that incorporates a fiberoptic bundle. A superior vena cava sample obtained from a central venous catheter is often used as a surrogate for mixed venous saturation when a pulmonary artery catheter is impractical or unavailable.82

Shock of any etiology can cause the aforementioned turn of events, and a low SvO2 sheds no light on the cause of the global hypoxia. As mentioned, low SvO2 may not always be secondary to impaired delivery but may be due to increased oxygen con­sumption in the face of fever, thyrotoxicosis, and other conditions (Fig. 44­12). Moreover, a normal SvO2 is not necessarily indicative of adequate tissue oxygenation. Although cardiogenic and hypo­volemic shock is very often associated with low SvO2 , it can be normal or elevated in shock secondary to severe sepsis or hepatic failure because these conditions are frequently associated with microvascular dysfunction and impaired oxygen extraction by tissues. Do2 is often elevated in these states.

In a novel application of continuous SvO2 measurement, pulse oximetry combined with SvO2 monitoring has been used in patients with acute respiratory failure to continuously monitor shunt fraction and adjust ventilator settings accordingly.82 The authors of this study adjusted continuous positive airway pressure (CPAP) levels to obtain the lowest shunt fraction and showed that use of this method results in CPAP settings similar to those obtained by conventional means. Though somewhat invasive, the technique was found to be cost­effective and accurate in titrating CPAP in this subset of patients.

Tissue Oxygenation

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 indices of tissue function (i.e., urine output, mental status) to make inferences about the state of affairs in cells. Oxygen is trans­ported from alveoli with a Po2 of around 100 mm Hg down a steep gradient, known as the oxygen cascade, to its final site of utilization, the mitochondrion, where Po2 is estimated to be less

Figure 44-11 Cyclic variation of vascular pressures during positive-pressure ventilation. Inspiratory reduction in preload leads to reduced left ventricular volume after a lag phase of a few heartbeats because of pulmonary vascular transit time. The inspiratory decrease in left ventricular volume results in decreased stroke volume and systolic blood pressure during expiration. Similar variations in amplitude can be noted in pulse oximeter waveforms. (From Nanchal R, Taylor RW. Hemodynamic monitoring. In Papadakos PJ, Lachmann B [eds]: Mechanical Ventilation: Clinical Applications and Pathophysiology. Philadelphia, Elsevier, 2008.)

Arterial pressure

Pulmonary arterial pressure

Central venous pressure

Systolic pulse variation

Inspiration Expiration

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than 1 mm Hg. Mitochondria from skeletal muscle appear to maintain their function with a Po2 as low as 0.1 mm Hg.83

Unlike arterial Po2 measurements, which should be nearly equal regardless of the artery sampled, Po2 varies considerably within a particular organ or tissue bed because blood flow and O2 consumption are not uniform but vary from point to point within the tissue. Because O2 diffuses down a gradient from arte­rioles 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 the tissue must be obtained to best describe its oxygenation status. Because of variable O2 supply and demand, normal Po2 levels and distributions differ from organ to organ.

A variety of methods have been devised to directly measure oxygen tensions and concentrations within tissues, and it has been an area of intense research for several decades. Most of the technologic advances have been made in the laboratory and have yet to be proved practical in the clinical setting.

Polarography is the current standard modality for measur­ing tissue oxygenation. It has the best resolution of all the avail­able 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 as oxygen is reduced. Oxygen tension as low as 0.1 mm Hg can be resolved quite accurately. Though too invasive for routine clinical use, the technology is commercially available and has found application in neurosurgery and oncology.84,85

Near-infrared spectroscopy is a noninvasive system capable of measuring the oxygenation state of hemoglobin, myoglobin, and mitochondrial cytochromes.86 The ability to monitor the oxy­genation status of cytochromes along the electron transport chain will probably prove to be the best estimate of cellular oxygenation. Up to four wavelengths of light are applied to tissue, and the scat­tered light is returned via fiberoptic cables to the monitor for analysis. The technology has been incorporated into devices capable of measuring blood O2 saturation in the brain, which have been commercially available for some 20 years.87 Resolution is inferior to that of polarography, and problems with calibration and interference have limited its widespread use. Images can be obtained depicting changes in Hb concentration, but the resolu­tion is poor.

A number of new systems for measuring tissue oxygena­tion are under laboratory investigation and have yet to reach commercial availability. Such systems include phosphorescence, fluorescence, electron paramagnetic resonance oximetry, and nuclear magnetic resonance spectroscopy. A number of reviews detailing all of these techniques have been compiled.87

Expired Gas Analysis

The ability to rapidly measure concentrations of inspired and expired gas is of paramount importance in anesthetic practice. Most anesthesia machines are equipped with oxygen sensors on the inspiratory limb of the circuit to help ensure that an adequate supply of oxygen is delivered to the patient at all times. Expired gas analysis is used to make inferences about blood concentra­tions and depth of anesthesia. Several systems are available for the measurement of gas tensions in exhaled air.

Mass Spectrometry

Mass spectrometry is a technique by which concentrations of gas particles in a sample can be determined according to their mass­charge ratio. A gas sample is passed through an ionizer and mol­ecules become positively charged ions. Because all of the ions generated carry the same positive charge, this allows separation of particles based solely on mass. A detector then counts the number of ions of each mass, and the results are translated into concentrations. Measurements are quite reliable and can be obtained in fractions of a second.

Clinical use of mass spectrometry for expired gas analysis began in respiratory care units in the mid­1970s. They were intro­duced into operating rooms and anesthesia practice shortly thereafter. Because of their size and complexity, hospitals often connected many operating rooms to a single spectrometer and had the results relayed back to the anesthesiologist. The conven­ience plus low cost of infrared analyzers has largely phased mass spectrometry out of clinical use.

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 Pathophysiology. Philadelphia, Elsevier, 2008.)

¯

Decreased by Increased by

Oxygen consumptionStressPainThyrotoxicosisFeverSeizuresShivering

Oxygen consumptionHypothermia

Oxygen deliveryPaO2 HemoglobinCardiac output

Oxygen deliveryPaO2 HemoglobinCardiac output

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Infrared Absorption

Presently, most expired gas analyzers used in anesthesia involve infrared absorption. A gas sample is collected in a chamber through which infrared light is passed, and gas tensions are derived based on the intensity of the transmitted light. Today’s infrared gas analyzers are capable of measuring all anesthetic agents currently in use, as well as CO2 and N2O. Oxygen does not absorb infrared light and therefore must be measured by other means, such as electrochemical or paramagnetic analysis.

Electrochemical Analysis

The same principles allowing electrochemical determination of oxygen in blood or tissue can be used to measure Po2 in a mixture of gas. Polarographic (Clark type) electrodes, which require an applied voltage, or galvanic cells (most common) can be used for this purpose. In either arrangement, the amount of current gener­ated as oxygen is reduced is proportional to the amount of oxygen present in the gas mixture, thus providing reliable estimates of Po2 electrochemically. These sensor types are often used to measure inspired oxygen concentrations in anesthesia machines and conventional ventilators. Response time is somewhat slow and the method is rarely used for expired gas analysis.

Paramagnetic Analysis

Because the oxygen molecule has magnetic properties, its behavior in a magnetic field can be used to determine the con­centration of oxygen in a gaseous mixture. Some newer anesthesia machines (e.g., Datex Ohmeda S/5) have incorporated paramag­netic oxygen analyzers capable of measuring oxygen in both the inspired and expired limbs of the circuit. Paramagnetic devices boast a longer life span and faster response time than electro­chemical cells do.

Measurement of Nitric Oxide

Nitric oxide (NO) is a potent pulmonary vasodilator and has been used for a number of years to improve oxygenation in the face of acute respiratory distress syndrome (ARDS) and severe pulmo­nary hypertension (see also Chapter 31). It is produced endog­enously and has multiple physiologic functions, including neurotransmission, regulation of vascular tone, and mediation of inflammation. Studies have identified NO as a marker of airway eosinophil activation, and exhaled levels are elevated in a number of inflammatory airway diseases such as asthma and chronic obstructive pulmonary disease (COPD).88 Elevation of exhaled NO is greater than 90% specific for the diagnosis of asthma in both children and adults.89,90 NO2, the toxic oxidation product of NO, can accumulate with prolonged treatment or if stored NO is exposed to oxygen. Although accumulation of harmful levels is rare, NO2 is known to cause pulmonary toxicity even at relatively low concentrations. Thus, an ideal NO analyzer would also have the ability to accurately measure NO2 levels to avoid delivery or accumulation of toxic levels of this by­product. As the diagnostic and therapeutic use of NO has increased, methods to accurately

quantify inhaled and exhaled concentrations of both NO and NO2 have been sought.

Continuous measurement of inhaled NO has traditionally been accomplished with the use of electrochemical sensors. NO is oxidized to nitric acid, and its concentration is proportional to the current generated by the reaction. A number of electrochemi­cal NO sensors have been independently evaluated and are reported to be quite accurate in measuring inhaled NO and NO2.91,92 The electrodes are sensitive to water vapor, and pro­longed exposure can shorten the life span of the sensor and 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 are typically in the parts­per­billion (ppb) range. Moreover, the slow response time of electrochemical sensors prevents their use for single­breath and exhaled NO analysis.

Because it is normally exhaled in very low concentrations, NO in expired air can be measured only with mass spectrometry or a process known as chemiluminescence. These analyzers, cur­rently the most commonly used, have a shorter response time and can detect less than 1 ppb NO and NO2. Wide variations in exhaled NO readings have been reported with chemilumines­cence analyzers, and NO2 levels may be underestimated in the presence of high oxygen concentrations.93,94 Unstable instrument temperature, varying expiratory flow rate, and interference are 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 that the other three overestimated low levels and underestimated high levels.96 A mid­infrared laser spectroscopy system has been developed that may eliminate some of the problems encountered with chemiluminescence analyzers by simultaneously measuring CO2. It has shown promise in a small study comparing its results with typical exhaled NO levels.95

Waveform Analysis of Expired Respiratory Gases

Capnographs

Changes in the shape of the expired CO2 waveform in an intubated patient can provide very useful monitoring informa­tion. Capnometry is the measurement of expired CO2 and has become increasingly popular as a diagnostic tool in a number of settings. It is now the confirmation method of choice in anesthe­sia for proper placement of an endotracheal tube. CO2 concentra­tion is usually measured by infrared absorption with either a mainstream or sidestream capnometer. Measurements can then be plotted against time or exhaled volume to generate a capno-graph. Capnography has found many useful clinical applications, and in 1998 it was adopted by the American Society of Anes­thesiologists as standard care for all general anesthetics administered.

Mainstream versus SidestreamThe major difference between sidestream and mainstream cap­nometry is location of the sensor. However, this seemingly minor

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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.

A B C

Figure 44-13 Sidestream sampling port placement. A, To minimize the effects of breathing circuit dead space, attachment of the sampling port should be as close to the patient as possible (arrow). B, Placement of the port as shown (arrow) can cause artifactual lowering of the end-tidal measurement.

A B

difference plays a major role in the complexity, accuracy, and response time of each system.

sidEstrEaM. In sidestream capnometry, a fixed volume of gas is continuously sampled from the circuit. The sampled gas is aspirated through nylon or Teflon tubing into the measuring cell and then released into the atmosphere or returned to the circuit through a second tube (Fig. 44­13). Sampling should take place as close to the patient as possible to minimize the effects of circuit dead space, and the rate is usually adjusted to between 50 and 500 mL/min. It is imperative that the sampling rate be adjusted properly. Erroneous measurements will be obtained if the sampling rate exceeds the expiratory flow rate and causes inspired gas to be sampled. Hypoventilation may occur if the

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 can­nulas can be adapted to allow CO2 monitoring (Fig. 44­14). The respiratory rate can be monitored adequately, but Petco2 mea­surements 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 par­ticulate 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 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 complicated sampling system and tubing connections provide multiple sites for damage or gas leakage. CO2 can diffuse out of sample tubing and cause falsely low readings. Longer tubing and slower sampling rates increase this error, and nylon appears to be less permeable to CO2 than other commonly used materials are.

MainstrEaM. Mainstream capnometers incorporate the infrared sensor into the circuit very close to the endotracheal tube. Consequently, many of the problems with sidestream cap­nometry have been eliminated. CO2 is measured directly in the circuit and no gas is subtracted, thus obviating the need for a complicated sampling system. The effects of breathing circuit and sample tubing dead space are minimized and the response time is therefore faster with mainstream systems. They are often used in the pediatric population, where circuit dead space can be more significant and response time is more critical. The measuring chamber must be warmed to about 40°C to prevent condensation of water vapor on the sensor window. Care must be taken to avoid skin contact with the chamber. It is somewhat heavy, and the

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circuit should be inspected frequently to avoid kinking of the endotracheal tube. Mainstream capnometers require frequent calibration, usually daily, and are prone to soiling with saliva or mucus because of their close proximity to the patient.

Time versus Volume CapnographstiME. The most commonly used type of capnograph plots

Pco2 versus time. The tracing is traditionally divided into an inspiratory phase and three (sometimes four) expiratory phases (Fig. 44­15):

Phase 0: inspiratory phasePhase I: dead space and little or no CO2

Phase II: mixture of alveolar and dead space gasPhase III: alveolar plateau, with the peak representing end­

expiratory (end­tidal) CO2 (Petco2).

In patients with normal lung function, Petco2 generally underestimates Paco2 by 1 to 5 mm Hg because of the presence of a small amount of alveolar dead space.7 Factors that increase alveolar dead space will widen this gradient and increase the slope of phase III. During anesthesia there is often increased alveolar dead space caused by reduced cardiac output and decreased perfusion of the lung apices.97 It is therefore not sur­prising that studies under anesthesia have found the Petco2­Paco2 gradient to be slightly elevated at 5 to 10 mm Hg.98 An extreme example of acutely increased alveolar dead space is pul­monary embolism. Thus, an abruptly decreased Petco2 with ven­tilation held constant is often indicative of a sudden decrease in cardiac output or pulmonary embolism. Other common causes of a widened gradient include obstructive lung disease, smoking, and advanced age. Examples of commonly encountered capno­graphic waveforms are shown in Figure 44­16.

The slope of the alveolar plateau (phase III) can also be increased in obstructive airway disease or during prolonged expi­ration. Two explanations for this phenomenon have generally

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 upslop­ing of phase III instead of the typical “plateau.” Second, as lung volume decreases during exhalation and CO2 excretion from cap­illaries remains constant, Pco2 slowly rises throughout expiration and causes an upsloping plateau (Fig. 44­17).99 Accordingly, even a person with completely normal lungs can have an upsloping plateau during prolonged expiration. End­tidal CO2 therefore approximates peak alveolar CO2, whereas Paco2 can be thought of as average alveolar Pco2.

At the terminal end of the phase III plateau, a sharp rise in Pco2 is sometimes observed and is referred to as phase IV. Although its exact cause is unknown, this rise is thought to occur when closing capacity is reached and small airways close, usually

Figure 44-15 Time and volume capnographs. A, Expired Pco2 versus time (i.e., standard time capnogram). The waveform is conventionally subdivided into phases. During phase I, exhaled gas from the large airways has a Pco2 of 0. Phase II is the transition between airway and alveolar gas. Phase III (i.e., alveolar plateau) is normally flat, but in the presence of � �V QA mismatching, it has a positive slope. The downslope of the capnogram at the onset of inspiration is usually referred to as phase 0, but sometimes there is a terminal increase in the slope associated with the onset of airway closure (dashed line labeled IV). The Pco2 value at the end of exhalation is referred to as the end-tidal Pco2 (Petco2). Also shown are the exhaled gas flow rate and volume.

Time

I II III IV (0)

End-tidalPCO2

PCO2

Exhaled volume

Flow

Figure 44-16 Examples of capnograph waves. A, Normal spontaneous breathing. B, Normal mechanical ventilation. C, Prolonged exhalation during spontaneous breathing. As CO2 diffuses from mixed venous blood into alveoli, its concentration progressively rises (see Fig. 44-17). D, Increased slope of phase III in a mechanically ventilated patient with emphysema. E, Added dead space during spontaneous ventilation. F, Dual plateau (i.e., tails-up pattern) caused by a leak in the sample line. The alveolar plateau is artifactually low because of dilution of exhaled gas with air leaking inward. During each mechanical breath the leak is reduced because of higher pressure within the airway and tubing, thus explaining the rise in CO2 concentration at the end of the alveolar plateau. This pattern is not seen during spontaneous ventilation because the required increase in airway pressure is absent. G, Exhausted CO2 absorbent producing an inhaled CO2 concentration greater than zero. H, Double peak in a patient with a single lung transplant. The first peak represents CO2 from the transplanted (normal) lung. Exhalation of CO2 from the remaining (obstructed) lung is delayed, thereby producing the second peak. I, Inspiratory valve stuck open during spontaneous breathing. Some backflow into the inspired limb of the circuit causes a rise in the level of inspired CO2. J, Inspiratory valve stuck open during mechanical ventilation. The “slurred” downslope during inspiration 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 entering the sampling line therefore alternates between high and low values. N, Electrical noise resulting from a malfunctioning component. The seemingly random nature of the signal perturbations (about three per second) implies a nonbiologic cause.

A

C

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after prolonged expiration. These small airways may supply lung units with little CO2 for various reasons, and their closure would therefore allow CO2­rich gas from other lung units to abruptly reach the upper airway. Bhavani­Shankar and colleagues favor a different explanation and state that well­ventilated, open lung units have an upsloping increase in Pco2 whereas Pco2 in poorly ventilated, closure­prone units increases linearly. When poorly ventilated airways close, the pattern from well­ventilated units predominates and the slope of the plateau rises suddenly.99 This concept is nicely cartooned at capnography.com in the phase IV section.

To summarize, any condition that increases alveolar dead space or � �V Q heterogeneity will increase the slope of phase III. This includes acute and chronic airway obstruction, and pro­longed expiration in a normal subject can also generate this pattern. Sometimes this slope is so significant that the reported Petco2 actually exceeds Paco2. This has been observed during anesthesia in obese patients and in 50% of both normal infants and pregnant women.100 It is probably secondary to reduced tho­racic compliance and functional residual capacity (FRC), increased cardiac output, and increased CO2 production.101 High mixed venous CO2 tension and malignant hyperthermia have also been reported to cause a negative Paco2­Petco2 gradient.102 In such cases, Petco2 is clearly not an accurate estimate of Paco2, and the average alveolar Pco2 obtained from a volume capnograph may be more indicative of Paco2.103

voluME. A volume capnograph is obtained by plotting expired Pco2 versus exhaled gas volume, usually obtained with a spirometer or pneumotachometer. There is no inspiratory phase in a volume capnograph, and the curve is divided into three expiratory phases. Several measurements that are not possible with time capnography can be made, such as partitioning of dead space components. The area under the Pco2 curve is the total volume of CO2 (Vco2) exhaled for that single breath. Dividing this value by the total exhaled tidal volume (Vt) gives the fraction of expired CO2 (Feco2), and the product of this fraction and barometric pressure yields a value for mixed expired Pco2 (Peco2). The Enghoff­modified Bohr equation can then be used to deter­mine total (physiologic) dead space (Vdsphys or Vdstot) (Figs. 44­18 and 44­19):

V V Pa P PaDS T CO ECO COtot = −( ) 2 2 2 (16)

Once Vdstot has been determined, subtracting the anatomic dead space (Vdsanat) derived from the capnograph (see Fig. 44­18) yields the alveolar dead space component (Vdsalv):

V V V SDS D Dalv tot anat= − (17)

Alternatively, alveolar dead space can be calculated by replacing Peco2 in the Bohr equation with average alveolar Pco2 (Pa′co2), which can be derived from the volume capnograph104:

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 � �V QA 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 � �V QA 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.

Normal

Airwayobstruction

PCO2 PCO2

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t t

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40 40 41

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Capnography has been used to titrate positive end­ expiratory pressure (PEEP) settings inasmuch as narrowing of the Paco2­Petco2 gradient suggests reduced alveolar dead space and shunt fraction as a result of alveolar recruitment and improved � �V Q matching. These changes are often subtle or absent on a

time 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

require volume capnography to be detected reliably.105 The tech­nique may also be better than time capnography for the diagnosis of pulmonary embolism.106

Additional Clinical Applications of CapnographyIn addition to those outlined in the preceding sections, capnog­raphy has a host of clinical applications. Monitoring of Petco2 can be invaluable during mechanical ventilation in the operating 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 disconnec­tion or a large leak in the circuit. Capnography has been used to assess the efficacy of chest compressions during cardiopulmonary resuscitation and even to verify proper placement of enteric feeding tubes.107

Errors

Various disease states discussed previously may cause overestima­tion or underestimation of Paco2 with use of Petco2. Condensa­tion of water vapor in the sample tubing and measuring cell can elevate the reported Pco2 slightly. Warming these pieces of equip­ment plus avoiding the use of drying agents in the sample line reduces this error. Capnometers may underreport true Petco2 at higher respiratory rates. Exhausted CO2 absorbent increases inspired CO2, and failure to recognize such depletion may lead to suspicion of rebreathing from other causes.

Pulmonary and Chest Wall Monitoring

Pressure-Volume Curve Analysis

Lung mechanics can be severely impaired in a number of respira­tory disorders. Monitoring changes in mechanical function of the lung is vital in developing a safe and effective support strategy in the face of respiratory failure. In a mechanically ventilated patient, construction of pressure­volume (PV) curves can provide impor­tant information about mechanics and help guide ventilator man­agement. 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 mid­1970s and soon thereafter were shown to be useful in deter­mining the cause of acute respiratory distress (Fig. 44­20). In recent years, the PV relationship has been studied extensively as a means of determining optimal PEEP and tidal volume in ARDS and ALI.

Static CurveA static curve is constructed by using the ventilator or a large syringe to deliver known tidal volumes, and patients must be sedated and paralyzed for an optimal study. The resultant plateau (Pplat) and peak inspiratory pressures (Ppk) are recorded after each breath to allow determination of both static (Cstat) and dynamic (Cdyn) compliance. Because Cstat is calculated by using plateau

Figure 44-18 Volume capnograph: single-breath CO2 (SBCO2) curve. The horizontal axis of the graph represents expiratory/inspiratory tidal volume and is generally divided into three areas: I, the anatomic dead space volume (Vdsanat): II, the transitional phase II volume; and III, the phase III alveolar volume. The sum of these values is the tidal volume. The vertical axis represents the concentration of CO2. Pco2, partial pressure of carbon dioxide. (From Pilbeam SP, Cairo JM: Mechanical Ventilation: Physiological and Clinical Applications, 4th ed. St. Louis, Elsevier, 2006.)

PC

O2 (

mm

Hg)

Volume exhaled (mL)VDSanat

I

II III

End-tidal PCO2

Figure 44-19 Volume capnograph: graph of the percentage of carbon dioxide (%CO2) (y axis) and volume (x axis). A horizontal line drawn at the top of the curve represents %CO2 in arterial blood. Three distinct regions are established. Area X represents the actual CO2 exhaled in one breath (assuming that no CO2 is rebreathed), area Y is the amount of CO2 that is not eliminated because of alveolar dead space, and area Z is the amount of CO2 not eliminated because of anatomic dead space. The ratios of these areas are the same as in the relationship seen in the Bohr equation: (Paco2 − Peco2)/Paco2 = (Y + Z)/(X + Y + Z). Peco2, mixed expired Pco2; Va, alveolar volume; Vds, dead space volume.

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pressure, it is mainly influenced by chest wall and alveolar elastic recoil:

C V P PEEPstat platT= −( ) (19)

Cdyn is derived by using Ppk and therefore takes airway and circuit resistance into account as well:

C V P PEEPdyn pkT= −( ) (20)

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 can be substantially decreased, the curve becomes sigmoidal or S shaped.108,109 Upper (UIP) and lower (LIP) inflection points can often be identified. The LIP, sometimes called Pflex, signifies an abrupt increase in compliance and is thought to result from the sudden recruitment of a large number of alveoli. The plateau 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. Maintaining airway pressures between the LIP and UIP is there­fore believed by many to prevent derecruitment and overdisten­tion of alveoli, both of which contribute to ventilator­induced lung injury.108,109 Using this reasoning, PEEP would be set slightly above the LIP to keep recruited alveoli open.110 Indeed, this approach has been shown to result in earlier weaning from the ventilator, less release of inflammatory cytokines, and a trend toward reduced mortality in ARDS patients.108,111

Despite positive results using the LIP and UIP to guide PEEP and Vt settings, recent evidence suggests that the LIP does not correlate with the pressure at which recruited alveoli will begin to close, known as the critical closing pressure.112,113 A prob­able explanation is that contrary to previous thought, recruitment has been shown to occur along the entire PV curve, independent

of the LIP and UIP. Thus, setting PEEP above the LIP is not always beneficial and may instead increase the risk for overdistention and barotrauma.114 Direct measures of appropriate response may be more suitable in determining the best PEEP level (see “Analysis of the Level of PEEP”).

Once the lung has been fully recruited, a deflation curve can be drawn by stepwise deflation of the lung, similar to mapping of the inspiratory limb. As lung volume decreases, critical closing

Figure 44-20 Pressure-volume curves reflecting changes in static and dynamic compliance (Cstat and Cdyn) during mechanical ventilation. Under normal conditions, the Cstat and Cdyn curves are similar. Because pulmonary emboli do not affect resistance or compliance, neither curve changes with this condition. With mucous plugging or bronchospasm, airway resistance (Raw) increases, the Cdyn curve shifts to the right and flattens (more pressure is 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.)

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Figure 44-21 Example of a static, inspiratory pressure-volume curve of the respiratory system in a patient with acute respiratory distress syndrome (ARDS) versus a healthy subject. Upper (about 30 cm H2O) and lower (about 10 cm H2O) inflection points are present in the patient with ARDS. FRC, functional residual capacity. (From Hess DR, Kacmarek RM: Essentials of Mechanical Ventilation, 2nd ed. New York, McGraw-Hill, 2002.)

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pressure is reached, and a deflection point appears on the curve corresponding to a rapid decrease in compliance and closure of a large number of lung units (Fig. 44­22). Because compliance improves during inflation as lung units are recruited, higher volumes are observed at the same pressure during deflation than during inflation, a phenomenon referred to as hysteresis. Accord­ingly, critical closing pressure will be lower than opening pressure, and setting PEEP slightly above the deflection point rather than the LIP may provide superior alveolar stabilization with less risk of overdistention and ventilator­induced lung injury.115,116 A number of recent studies suggest that the LIP does not reliably indicate the pressure at which maximal alveolar derecruitment occurs.112,117 In addition, there is mounting evidence that using the deflation limb rather than the inflation limb of PV curves to guide ventilation may improve gas exchange and mechanics, often at lower mPaw and PEEP levels.118,119 Therefore, although the presence of an LIP on the PV curve indicates a need for lung recruitment, the deflection point may be more valuable in deter­mining the amount of PEEP required to prevent alveolar collapse. Evaluating deflation Cstat in this manner to determine closing pressure is at least as effective as monitoring Pao2 for selection of the optimum PEEP level.115,116 Moreover, recruitment maneuvers have been shown to be quite safe and are less injurious than allow­ing shear stress damage associated with derecruitment to proceed unchecked.120,121

Static PV curves can also be obtained from a single breath delivered slowly (2 to 3 L/m) until a predetermined pressure is reached and are referred to as slow­flow or quasi­static PV loops. The curves derived are comparable to those obtained with typical static techniques, but the deflation limb is often difficult to acquire.122,123 Several modern ventilators have incorporated this capability. The Hamilton Galileo ventilator allows selection of the desired flow rate for the PV study, and an interactive curve is then displayed on the monitor, usually within 30 seconds.

Dynamic CurveA number of ventilators are capable of mapping dynamic PV curves during tidal breaths delivered with normal gas flow. Newer

ventilators automatically display the curve with each tidal volume. Though useful in following general trends in compliance, identi­fication of inflection points is more difficult on dynamic PV curves. Several factors can alter the loop from breath to breath, and using dynamic curves for determination of optimal Vt and PEEP is not generally recommended.122

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 failure. Appropriate PEEP increases FRC, decreases pulmonary edema, and maintains the patency of airways and recruited alveoli. It is important to note that PEEP does not recruit the lung; rather, it is sustained high pressure that reopens closed alveoli and airways, and PEEP stabilizes these recruited lung units. A host of tools and parameters described in this chapter have been used by clinicians to evaluate PEEP settings, including capnography, titra­tion to the best Pao2/Sao2 ratio, continuous SvO2 and shunt moni­toring, 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 evaluating clinical response to PEEP. More than 30 years ago it was noted that the PEEP level resulting in maximum O2 delivery also pro­duced optimal compliance while minimizing dead space and shunt fraction.124 The authors coined the phrase “optimum” PEEP to refer to that producing the maximum improvement in pulmo­nary function with minimal hemodynamic compromise. Recent trials have shown that during a derecruitment study, measuring Cstat may be as useful and more cost­effective than measuring Pao2 in determining closing pressure and guiding PEEP selec­tion.115,116 Nowadays most clinicians use one of these two param­eters to set PEEP after the recruitment maneuver. Inflection points on PV curves are not always easy to identify, and a decrease in Pao2 rather than Cstat should be used to identify closing pres­sure in such cases.

Patients under GA are prone to compression atelectasis in dependent lung regions (see Fig. 44­5).125 Thus, it is tempting to apply PEEP to all patients undergoing surgery with mechanical ventilation to prevent this atelectasis. It has been shown that application of PEEP during GA can attenuate and reverse depend­ent atelectasis but does not improve gas exchange.126 A study comparing normal and obese subjects also found that application of PEEP during GA did not alter gas exchange in normal patients, but some improvement was noted in the obese population.127 Thus, there is no evidence to support routine use of PEEP during GA. However, these studies did not use recruitment maneuvers, and a trial by Tusman and colleagues showed that alveolar recruit­ment can improve oxygenation during GA (see also Chapter 15).128 In addition, PEEP combined with recruitment maneuvers has been shown to provide a sustained increase in Pao2 and lung volume in mechanically ventilated postsurgical patients.128,129

Analysis of Lung Recruitment

The importance of early lung recruitment in respiratory failure and ARDS has been well documented.130 Lung­protective ventila­tion in ARDS via frequent recruitment maneuvers results in improved 28­day survival, earlier weaning from mechanical ven­

Figure 44-22 Pressure-volume relationship of the lung showing the inflation (solid line) and the deflation limb (dashed line). Note the clear difference in lung volume between both limbs at identical pressure (hysteresis). (From van Kaam AHLC: Neonatal mechanical ventilation. In Papadakos PJ, Lachmann B [eds]: Mechanical Ventilation: Clinical Applications and Pathophysiology. Philadelphia, Elsevier, 2008.)

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tilation, and less barotrauma than with conventional ventilation strategies.111 Effective recruitment is performed by applying sus­tained high airway pressure, usually for 30 to 90 seconds. Many successful techniques, all using essentially these same principles, have been described.131,132 Recruitment maneuvers are typically well tolerated, with no significant hemodynamic deterioration or inflammatory response.133,134 Although improvements in pulmo­nary compliance and oxygenation are indicative of successful recruitment, direct methods of quantifying and monitoring lung recruitment are emerging.

Computed TomographyTechnologic advances in CT have made it a valuable tool for studying ARDS and lung recruitment. It has been used in numer­ous studies to evaluate the effects of a wide range of variables on alveolar recruitment and stabilization.135 Recently, Gattinoni and colleagues performed a trial to examine whether measuring the amount of recruitable lung by CT could help predict how the lung 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 detrimental in patients with less recruitable lung measured by CT.136 This conclusion was in line with previous studies showing that PEEP results in hyperinflation and increased stress in normal lung regions when the amount of recruitable lung is low.137 Quan­titative CT analysis of potentially recruitable lung may therefore be useful in determining the best PEEP level, but further studies are needed on the practicality of routine use. CT was instrumental in the discovery that lung recruitment occurs throughout inspira­tion and not solely around the LIP of the PV curve.138

Electrical Impedance TomographyA new and exciting form of monitoring of pulmonary function may be electrical impedance tomography (EIT).139,149 It is a non­invasive and radiation­free technique based on the measurement of electric potentials at the chest wall surface. Within a particular cross­sectional plane, harmless electrical currents are driven across the thorax in a rotating pattern to generate a potential gradient at the surface, which is then transformed into a two­

dimensional image of the distribution of electrical impedance within the thorax. The dynamic behavior and the qualitative information extracted from EIT images look similar to that reported in dynamic studies (Fig. 44­23).141,142

This technology may be an excellent assessment tool for easy bedside use to evaluate alveolar lung recruitment, pulmo­nary embolism, lung water, and other lung pathology. The impor­tance of lung recruitment in both the operating room and the ICU has clearly changed the practice of mechanical ventilation.

Amato’s group in Brazil recently completed a validation study of EIT.142 It is an easy bedside tool to evaluate mechanical ventilation with immediate feedback. EIT devices may, in the future, easily detect selective intubation, pneumothorax, and alve­olar atelectasis. Titration of PEEP may someday be evaluated in real time, with EIT used instead of waiting for BGA, radiologic studies, and CT scans. This technology may one day be integrated into the bedside monitor or into closed­loop mechanical ventilators.

Inspiratory Pressure Monitoring

Impaired respiratory muscle function from fatigue or neuromus­cular disorders can contribute to respiratory failure and difficulty weaning from mechanical ventilation. Measurement of maximum inspiratory pressure (MIP), also called negative inspiratory force, gives a useful bedside appraisal of respiratory muscle strength. It can be performed on intubated and nonintubated patients by attaching a pressure manometer to the endotracheal tube or a noninvasive mouthpiece. Alternatively, use of a one­way valve that allows exhalation only has been described, although it is quite uncomfortable for the patient.143 Normal MIP is about −90 cm H2O but can range between −50 and −120 cm H2O. To obtain accurate measurements, MIP should be measured after maximal expiration because the diaphragm can generate the greatest pres­sure at residual volume. Studies have demonstrated that inability to generate MIP more negative than −20 cm results in tidal volumes that are insufficient for generating a strong cough. More­over, this cutoff has been shown to result in weaning failure with

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.)

CT EIT

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a negative predictive value of 1.144 Though not yet a firmly estab­lished predictor of weaning outcome, MIP is useful in determin­ing whether patient weakness or neuromuscular dysfunction is playing a role in unsuccessful weaning trials.

Esophageal Monitoring

Transpulmonary pressure, rather than peak or plateau pressure, is the most important determinant of alveolar distention and is defined as alveolar pressure (Pa) minus pleural pressure (Ppl).145 Thus, true distending pressure of the lung cannot be measured without determination of Ppl. Direct measurement of Ppl is clini­cally impractical, but it can be estimated quite reliably in upright patients by measuring pressure in the distal third of the esopha­gus. The esophagus is a fairly passive structure and the third part is very close to the pleural space, thus allowing transmission of pleural pressure to an intraesophageal pressure monitor.146 A balloon­tipped catheter is typically used, and this technique is considered the standard modality for evaluating inspiratory effort and work of breathing (WOB). In the supine position, this rela­tionship is less predictable because gravitational forces cause compression of the esophagus and dependent lung, thereby skewing the measurements.

Placement of a second balloon catheter into the stomach allows simultaneous measurement of gastric pressure and pro­vides a means of obtaining a host of useful information about respiratory mechanics. For example, transdiaphragmatic pressure monitoring can be performed to assess diaphragmatic contrac­tion. As the diaphragm contracts and the domes descend, negative Ppl (or Pes) should coincide with positive abdominal pressure (or Pg) generating transdiaphragmatic pressure. Inability of the dia­phragm to contract properly results in loss of transdiaphragmatic pressure and has been observed after uncomplicated upper abdominal surgery (Fig. 44­24). Diaphragmatic fatigue and phrenic nerve palsy elicit a similar pattern.147 This can also be observed clinically inasmuch as impaired diaphragmatic activity is associated with paradoxical inward movement of the abdomen during inspiration.

Work of Breathing

The work involved in normal respiration, often referred to as work of breathing (WOB), usually requires minimal energy expendi­ture. Work is defined as the force needed to move a mass times the distance moved: W = F × d. In the respiratory system, it rep­resents the pressure (or force) needed to inspire a certain volume of gas: WOB = P × V. With respiratory compromise, WOB can be quite high, as much as 40% of total oxygen consumption (nor­mally <5%). WOB can be estimated by measuring pressure and volume changes from a PV curve. Total work is the area enclosed by the curve (integral of pressure and volume). Thus, the larger the loop, the greater the WOB (Fig. 44­25). However, studies indicate that mechanical work calculated in this manner may underestimate true WOB and is weakly correlated with the �VO2 of respiratory muscles. Alternatively, many clinicians believe that the pressure-time product (PTP) is the most accurate measure of work performed by the diaphragm during inspiration and better correlates with �VO2

148 because the PTP takes isometric contrac­tion of the diaphragm into account, which consumes additional O2. Increases in PTP indicate stronger diaphragmatic contraction and vice versa. Calculation of PTP requires measurement of transdiaphragmatic pressure as outlined earlier and is not rou­tinely performed. Occlusion pressures (P100) measured with a dedicated valve system or conventional ventilator have also been shown to correlate with WOB.148,149

Closed-Loop Analysis

Closed­loop ventilation involves computer­based real­time inter­pretation of respiratory mechanics with continuous adjustment of the level of support delivered to the patient.150 Any change in mechanics or patient effort is detected and a new breathing pattern is initiated by the ventilator. Ventilator dyssynchrony and WOB are minimized. Moreover, erroneous or unsafe settings could potentially be minimized with a system that continuously regulates ventilator support based on real­time assessment of the

Figure 44-24 Examples of transdiaphragmatic pressure monitoring. A, Simultaneous esophageal (Pes) and gastric (Pg) pressure waveforms during tidal breathing in a normal individual. Negative esophageal (and therefore pleural) pressure swings are accompanied by positive gastric pressure waves indicative of the development of transdiaphragmatic pressure during inspiration. B, The same waveforms in a patient with phrenic nerve palsy (and therefore absent diaphragmatic 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 in patients who have undergone upper abdominal surgery. (From Brown KA, Hoffstein V, Byrick RJ: Bedside diagnosis of bilateral diaphragmatic paralysis in a ventilator-dependent patient after open-heart surgery. Anesth Analg 64:1208, 1985.)

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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 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.)

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patient. Table 44­3 summarizes the four commercially available closed­loop systems. A study was performed to compare ARDS and COPD patients ventilated with a closed­loop mode termed adaptive support ventilation (ASV) available on the Hamilton Galileo ventilator. The authors found that on average, ARDS patients received lower tidal volumes with a higher respiratory rate than COPD patients did.151 This would be expected and desired based on current knowledge of mechanics and the impor­tance of low–tidal volume ventilation in ARDS. Moreover, the results support the possibility that closed­loop ventilation with ASV can appropriately tailor ventilation based on respiratory mechanics. It is highly conceivable that closed­loop ventilator modes may one day prove to be safer and more convenient than traditional mechanical ventilation.

Apnea Monitoring

The postoperative period is often characterized by episodes of apnea and hypoxemia. Paradoxical breathing and other ventila­tory disturbances can also occur frequently. Though more common with narcotic administration, residual effects of other anesthetic agents can play a role in the cause of these distur­bances. They are often subtle and are more likely to be noticed with continuous respiratory monitoring as opposed to intermit­

tent observation.152 A wide variety of continuous apnea monitor­ing systems have been developed. Most methods detect changes in chest wall movement, gas exchange, or gas flow to make infer­ences about changes in respiratory pattern.

Movement of the chest wall is most commonly detected by transthoracic impedance. The technology is usually incorpo­rated into the electrocardiographic (ECG) monitoring system. A small current is passed between two ECG leads, and chest wall movement is detected by a change in impedance to the current induced by the motion. Respiratory inductive plethysmography (RIP) is another method of apnea detection that monitors chest movement. The chest and abdomen are encircled by one or more coils that measure changes in their cross­sectional area occurring 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 breath­ing. Infrared PPG sensors placed near upper extremity veins can detect cyclic changes in venous blood flow occurring with respi­ration.153 Respiratory muscle electromyography has also been used as a means of monitoring respiration. A limitation common to all these techniques is that respiratory efforts during episodes of obstructive apnea may be interpreted as normal respirations despite absent gas flow.154 Monitoring of gas flow and exchange may therefore be a more reliable indicator of adequate 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.

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Apnea monitoring systems that rely on airflow detection may be a more sensitive alternative to monitors of patient move­ment. In a study comparing transthoracic impedance and a nasal­oral airflow system in the PACU, Wiklund and colleagues found that impedance monitoring failed to detect apneic episodes more frequently than flow detection did.154 False alarm rates were similar between the two groups. Hök and associates studied an acoustic airflow monitoring system and reported that it was more sensitive in detecting episodes of apnea and hypoventilation than pulse oximetry was.155 Another acoustic airflow sensor was com­pared with a thoracic impedance system by Werthammer and colleagues.155a Of 26 apneic episodes observed by direct observa­tion, the airflow sensor detected all 26, whereas only 7 episodes were detected by the impedance monitor. Other airflow monitors detect respiration by measuring changes in humidity. Tatara and Tsuzaki studied a device called a rapid­response hygrometer that monitors changes in humidity at the nostril and can measure respiratory rates of up to 60 breaths per minute.156 Respiratory phases could be identified almost 2 seconds faster than with cap­nography. The development of fiberoptic humidity­based systems has also been described.157,158

Because end­tidal CO2 monitoring and pulse oximetry can rapidly detect derangements in gas exchange, they may prove to be the most dependable options for apnea monitoring. In a study of more than 4000 apneic episodes from overnight polysomno­grams, detection of apnea by pulse oximetry was compared with manual detection, such as airflow or respiratory movement.158a Only 1.32% of apneic episodes were reportedly missed by pulse oximetry, whereas manual devices missed 7.9% of apnea events. Although end­tidal CO2 monitoring can be performed easily and accurately on intubated patients, measurements from a mask or nasal cannula are often unreliable. However, the respiratory rate is usually reported accurately, and trends in Petco2 can be moni­tored with these devices. As pulse oximetry and capnography systems become more portable and inexpensive, their use for apnea monitoring will probably continue to grow. Large outcome studies may be needed to demonstrate the possible superiority of one system over another.

Lung Water Analysis

Many disease states can cause abnormal accumulation of extra­vascular lung water (EVLW), commonly known as pulmonary edema. Clinicians have long been aware of the severe cardiac and respiratory insufficiency that pulmonary edema can cause, yet it 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 for detecting and quantifying EVLW, and many advances have been made in recent years. Research in this field is complicated by the fact that gravimetry, which requires analysis of postmortem lung weight, remains the standard for EVLW measurement.159,160 As a result, much of the data evaluating new techniques come from animal studies.

Radiographic Methods

The chest radiograph is the most widely used test to screen for pulmonary edema. Under ideal conditions, obtaining a chest film

allows semiquantitative measures of EVLW, as well as determina­tion of its distribution and possible etiology. Even under such conditions, sensitivity is rather poor; a 30% to 35% increase in EVLW is needed before radiographic changes consistent with pulmonary edema can be detected on the chest film.161 In typical critical care settings, where image quality and acquisition tech­nique can vary greatly, it is estimated that a 100% increase in EVLW may be needed to produce observable radiographic changes. Moreover, weak correlation of EVLW measurements between chest radiography and other established methods has been observed in the ICU environment.159

CT has been increasingly studied in recent years as a means of quantification of EVLW. In animal experiments, CT densitom­etry could detect an increase in EVLW by as little as 50%.162 Using thin­section CT, Scillia and colleagues found that significant hypoxemia secondary to pulmonary edema may not develop until the increase in EVLW approaches the 200% to 300% range.163 Lack of portability and high radiation exposure limit the use of CT for serial EVLW measurement. Research continues on a number of other imaging modalities, including ultrasonogra­phy,164 positron emission tomography,165 nuclear magnetic reso­nance,166 and EIT,167 but none have been incorporated into routine clinical use.

Indicator Dilution Methods

Quantification of EVLW via double indicator dilution curves was first described more than 50 years ago. More recently, a transpul­monary thermodilution technique that uses cold saline as a single indicator has been described. Although controversy exists over the accuracy of dilution techniques, many studies report excellent reproducibility and correlation with gravimetric methods.159 One study using transpulmonary thermodilution reported that changes in EVLW of as little as 10% to 20% can be detected with high sensitivity.168 Both techniques are somewhat invasive and require placement of arterial and central venous catheters. Although early devices were quite cumbersome, currently availa­ble systems are relatively safe and easy to implement and allow bedside measurements to be obtained.

Despite recent improvements in a number of the aforemen­tioned modalities, chest radiography remains the only tool widely integrated into clinical practice. A probable explanation is that studies have suggested potential clinical utility in precise EVLW analysis, but none have shown that obtaining such measurements facilitates decision­making or improves patient outcome.

Monitoring High-Frequency Ventilation

Recent data on the benefits of low–tidal volume, high­PEEP ven­tilation 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 conven­tional ventilation in patients with ARDS and ALI. HFV is char­acterized by rapid delivery of small tidal volumes and maintenance of high mean airway pressure.169 Whereas routine use in adults is a fairly recent trend, trials in preterm infants with neonatal res­

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piratory distress syndrome began almost 20 years ago.170 Clear evidence of outcome benefit with HFV versus conventional ven­tilation is lacking, but numerous studies have implied that HFV may reduce the risk for ventilator­induced lung injury,171 improve oxygenation,172 and be as safe as conventional ventilation in 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 develop­ment, the most widely used method in both adults and pediatric patients is high­frequency oscillatory ventilation (HFOV). Other modes include high­frequency jet ventilation (HFJV), high­ frequency flow interruption (HFFI), and high­frequency percus­sive ventilation (HFPV). Before the widespread availability of HFV modes, a conventional ventilator was used to deliver low tidal volumes with high frequency, a technique that became known as high­frequency positive­pressure ventilation (HFPPV).

Because mechanisms of gas exchange during HFV differ from those regulating conventional ventilation, standard moni­toring 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 showed a correlation between airway pressure and gas exchange efficiency during HFJV, with higher peak and driving pressures resulting in lower Paco2 and higher Pao2. Monitoring Petco2 conventionally during HFV produces unreliable measurements for a number of reasons, but mainly because of difficulty obtain­ing undiluted, CO2­rich gas samples.174,175 Though useful in moni­toring conventional ventilation, the concept of “end­tidal” CO2 is altogether misguided in HFV because no inspiratory or expira­tory phases are identifiable on capnographic waveforms.176 More­over, the likelihood that expired CO2 tensions accurately reflect Paco2 is low in patients requiring HFV inasmuch as alveolar dead space and intrapulmonary shunting can be extensive.174

Despite its limitations, studies have demonstrated the ability of capnometry to provide accurate Paco2 estimates during HFV. A common technique is to interrupt or slow the ventilator down to deliver a normal breath. CO2 tensions measured with intermittent capnography have been shown to agree well with simultaneously obtained Paco2 values.177 The accuracy of capno­metric Pco2 readings may also depend on where the sample is obtained. Gas sampled from the distal tip of the endotracheal tube seems to provide more valid approximations of Paco2 than sam­pling proximally does.176 However, these measurements must also be obtained intermittently. In an effort to eliminate this problem and others associated with expired gas analysis during HFV, Berk­enbosch and Tobias studied the accuracy of continuous transcu­taneous CO2 monitoring in this setting. When compared with Paco2 values from BGA obtained simultaneously, bias and preci­sion were only 2.1 and 2.7 mm Hg, respectively.174 Studies by these authors and other investigators have also demonstrated that tran­scutaneous CO2 monitoring may approximate Paco2 better than Petco2 in both adults and children undergoing mechanical ven­tilation.178,179 Although the technique has gained a footing in pediatric critical care, transcutaneous O2 and CO2 monitoring in adults will probably increase in popularity as refinements to this technology continue to be made.

As the potential benefits of HFV continue to be elucidated, investigators have sought practical techniques for bedside moni­toring of lung mechanics, recruitment, and regional aeration. Portable chest radiography has been shown to be a poor tool for

assessing lung morphology in ARDS.179,180 CT has proved useful for such analyses but continues to be limited by portability issues. Recently, some investigators have focused on EIT and RIP as modalities that may be able to provide accurate lung volume measurements at the bedside during HFV.181,182 RIP has been used experimentally to construct PV curves during HFV and thereby determine optimal lung volume and pressure settings.183,184 In the first infant study of this kind, Tingay and colleagues used the open­lung concept to recruit lung and then map the deflation limb of the PV curve.185,186 The authors concluded that RIP could be used during HFOV to construct satisfactory deflation curves. Ventilation along the deflation limb resulted in greater lung volume and oxygenation, often with lower distending pressure requirements, than did ventilation on the inflation limb (Fig. 44­26). This was in line with previous animal studies demonstrat­ing improved mechanics and oxygenation with deflation limb ventilation after recruitment.117 An earlier infant trial using single­occlusion compliance measurements failed to demonstrate the utility of PV curves in optimizing lung volume during HFV, but neither recruitment maneuvers nor deflation limb ventilation had been used.187 EIT has the advantage of providing information about global and regional changes in lung volume, as well as continuous imaging of changes in impedance (and probably volume) occurring throughout the respiratory cycle. Bedside availability would potentially allow clinicians to detect aeration changes in real time and reverse them by adjusting ventilation parameters.182

Estimation of pulmonary mechanics during HFV has most often been accomplished by the conventional passive techniques described earlier. This practice has raised concern among some authors, who argue that technical aspects of these strategies may exacerbate derecruitment and provide inadequate information about lung parenchyma.187 In the study by Tingay and colleagues, passive deflation was not used for PV analysis, and derecruitment was further prevented by avoiding full deflation of the lung below closing pressure. Others suggest that the high frequencies and flow rates associated with HFV currently limit the feasibility of obtaining accurate dynamic measurements. Thus, efforts have been undertaken to identify safe alternatives for reliably assessing lung compliance and determining optimal airway pressure during

Figure 44-26 Pressure-volume curve depicting the “open lung” concept using high-frequency ventilation (HFV). Potential lung injury is reduced when ventilation of the lung is shifted onto the expiratory portion of the curve by aggressive lung recruitment. Lung volume is then maintained with high mean airway pressure and small tidal volumes. (From Singh JM, Stewart TE: High-frequency ventilation. In Fink MP, Abraham E, Vincent JL, et al [eds]: Textbook of Critical Care, 5th ed. Philadelphia, Elsevier, 2005.)

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HFV. The oscillatory pressure ratio (OPR), defined as the ratio of pressure swings at the distal and proximal ends of the endotra­cheal tube, was shown to be inversely related to lung compliance in an animal model of ALI.188 The mPaw setting resulting in the lowest OPR also generated the best lung compliance and oxy­genation. Titrating mPaw to a minimal OPR may therefore prove to be a reliable, noninvasive means of optimizing lung mechanics and oxygenation during HFV. The low­frequency forced oscilla­tion technique is another experimental monitor that allows partitioning of lung mechanics into airway and parenchymal components, as well as determination of chest wall impedance.189 Monitoring chest vibration can provide a crude indicator of changes in compliance during HFOV. Oscillator power is often titrated to generate vibrations from the clavicle down to the mid­portion of the thigh, and a change in pattern may signal the development of an obstruction, pneumothorax, or worsening mechanics of any etiology.

Monitoring the Respiratory System in Transport

Intrahospital transport of critically ill and mechanically venti­lated patients becomes necessary in a number of situations (see Chapter 79). The need for diagnostic or surgical procedures is among the most frequent reasons for patient transport. A number of studies have reported on the high number of transports that critically ill patients require.190 Children and trauma victims seem to require more frequent transportation for diagnostic purposes than other critically ill patients do. Not surprisingly, intrahospital transport of this tenuous patient population can be fraught with problems ranging from simple equipment malfunction to major disasters such as anoxic brain injury and even death. Studies report a widely varying incidence of adverse events during trans­portation of critically ill patients. Complex and numerous pieces of equipment are often necessary to safely perform the transfer. One study looking at 125 transports from the ICU found a 34% incidence of equipment­related adverse events, the most common being ECG lead disconnection and monitor power failure.190

Lack of agreed­upon monitoring techniques and defini­tions of “adverse events” partly explains the wide discrepancy in reported incidence. Moreover, few outcome studies comparing monitoring strategies during transport have been performed. It has long been observed, however, that transport of critically ill patients may put them at increased risk for cardiovascular and respiratory compromise, both during and after transport.191 A higher incidence of gas exchange deterioration and even pneu­monia has been reported after intrahospital transport.192,193 Arrhythmias, hypotensive episodes, and blood gas derangements are not uncommon. Studies in trauma patients have revealed

widely variable heart rate and blood pressure during transporta­tion for diagnostic procedures.194 Thus, a continually displayed electrocardiogram and blood pressure must be available during transport of all critically ill patients. In addition, pulse oximetry should be used in light of its high reliability in forewarning of hypoxemia and deterioration in gas exchange. A good rule of thumb is to monitor critically ill patients at least as closely during transport as deemed necessary within the ICU before transport. Complications are reduced when personnel trained to deal with the intricacies of intrahospital transport are available.195 Emer­gency cardiovascular drugs should be available for postoperative transport of all hemodynamically unstable and critically ill sub­jects. Preparation of equipment and medication checklists before transport can help ensure readiness for any untoward events. The receiving location should confirm before transport that it has the equipment and necessary staff in place to receive the patient.

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 prop­erly functioning low­pressure alarms should be verified during pretransport preparation. Many authors advocate the use of a mechanical ventilator rather than manual ventilation devices for intrahospital transport because more variability in pH and CO2 tension has been observed with the use of manual devices.196 A higher incidence of significant Pao2/Fio2 deterioration may also be associated with manual versus mechanical ventilation (P = .056).196 In a blinded study using capnography, Tobias and associ­ates noted a high incidence of unintentional hyperventilation when using manual devices during the intrahospital transfer of intubated pediatric patients.197 Similar findings have been noted in adults, and tighter control of Paco2 can be achieved if Petco2

198 or Vt is monitored during manual ventilation. These findings have led many experts to recommend Petco2 monitoring in addition to standard monitoring for high­risk patients requiring a more optimal level of ventilation.

Obvious contraindications to the transport of critically ill patients include an inability to provide adequate oxygenation and ventilation during transport or at the receiving location. Unstable hemodynamics or an inability to adequately monitor cardiovas­cular status throughout the trip should prompt postponement or cancellation. The risk­benefit ratio should be considered before all transports to help determine whether a trip is truly warranted; performing such analyses may be the most effective way of avoid­ing adverse events during transportation. Indeck and coworkers found that 68% of patients transferred from a trauma unit for diagnostic testing experienced serious physiologic changes whereas only 24% of the transfers resulted in significant modifica­tion of patient management.199 The development of increasingly sophisticated portable devices has provided a bedside alternative for many diagnostic and therapeutic procedures.

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