Evaluate Oxygenation in Critically Ill Adult

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Accurate assessment and treatment ofdisturbances in oxygenation are crucial to

optimal outcomes in critically ill patients.

Oxygenation is dependent uponadequate pulmonary gas exchange,

oxygen delivery, and oxygen

consumption. Each of these physiologic

processes may vary independently in

response to pathophysiologic conditions

and therapeutic interventions.The author

reviews diagnostic measures available to

evaluate pulmonary gas exchange,

oxygen delivery, and oxygen

consumption in critically ill patients.

Currently available tools and theirpotential value as well as key

methodological limitations are addressed.

Failure on behalf of clinicians to fully

appreciate these limitations can lead to

misdiagnoses and inappropriate

treatment.The aim of this article is to

help advanced practice nurses more fully

understand the implications and

limitations of these diagnostic measures

to ensure accurate assessment andtreatment of disturbances in oxygenation.

(KEY WORDS: assessment of oxygen

consumption, assessment of oxygen

delivery, assessment of oxygenation,

assessment of pulmonary gas exchange)

506

AACN Clinical Issues

Volume 15, Number 4, pp. 506524

2004, AACN

Tissue Oxygenation

The outcome of critical illness depends onthe adequacy of oxygenation; therefore, ac-

curate assessment and treatment of oxygena-tion disturbances is critical to optimal patientoutcomes. A thorough evaluation of oxy-genation is one of the most important com-ponents of the advanced practice nurses as-sessment abilities.

Oxygenation is a physiologic process thatis dependent upon the integration and coor-dination of multiple body systems includingthe pulmonary, cardiovascular, neurologic,hematologic, and metabolic systems. Ade-

quacy of oxygenation depends on the inte-gration of three physiologic components:pulmonary gas exchange, oxygen delivery,and oxygen consumption (Figure 1). Pul-monary gas exchange physiology involvesthe physiologic processes of ventilation, dif-fusion, and perfusion as oxygen is broughtfrom the atmosphere to the pulmonary capil-lary bed. Delivery of oxygen via the blood-stream is dependent upon cardiac output and

the content of oxygen in arterial blood. Use

Diagnostic Measuresto Evaluate Oxygenationin Critically Ill Adults

Implications and Limitations

Karen L. Johnson, RN, PhD, CCRN

Assistant Professor, University of Maryland Schoolof Nursing, Baltimore.

Reprint requests to University of Maryland Schoolof Nursing, 655 W Lombard St, Baltimore, MD 21201([email protected]).


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of oxygen for energy metabolism requiresextraction and consumption of oxygenthrough aerobic metabolism. Each of thesethree physiologic processes must functionproperly to ensure adequate oxygenation.Each of these components may vary inde-

pendently in response to pathophysiologicconditions and therapeutic interventions.Therefore, an assessment of oxygenationmust include assessments of pulmonary gasexchange, oxygendelivery, and oxygen con-sumption. There are two goals in the assess-ment of oxygenation: (1) to determine over-all adequacy of oxygenation and (2) todetermine which element of oxygenationdysfunction should be manipulated to im-prove patient outcome.

Assessment of PulmonaryGas Exchange

Pulmonary gas exchange involves the inspi-ration and delivery of oxygen from the ex-

ternal environment to the alveoli, diffusionacross the alveolar-capillary membrane,and the combination of oxygen with hemo-globin (Hb) in the pulmonary capillaries.Pulmonary gas exchange is dependentupon the physiologic processes of alveolar

ventilation, diffusion of gases across thealveolar-capillary membrane, pulmonaryperfusion, and ventilation perfusion match-ing (V/Q) (see Figure 1). Therefore, an as-sessment of pulmonary gas exchangeshould ideally include an evaluation ofthese physiologic processes.

Assessment of Ventilation

Alveolar ventilation depends on respiratory

rate and tidal volume. An average tidal vol-ume of 600 mL results in an alveolar ventila-tion of 450 mL, with 150 mL required toovercome normal physiologic dead space ofthe conducting airways. At very low tidalvolumes, the dead space alone may be ven-tilated even though the minute volume (rate

507 JOHNSON AACN Clinical Issues

Figure 1. Johnsons conceptual model of oxygenation. CaO2, content of oxygen in arterial blood; CvO2, content

of oxygen in venous blood; O2, oxygen; ATP, adenosine triphosphate. Adapted with permission from Taylor CR,

Weibel ER. Design of the mammalian respiratory system. Respiration Physiology. 1981;41(p2). Copyright 1981by Elsevier Science.


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times tidal volume) is normal due to a highrespiratory rate.

Assessment of the adequacy of ventilationbegins with a focused physical examination

that can provide some of the most usefulclues about ventilation. Lethargy and somno-lence may indicate hypercapnea. Evaluationof rate, rhythm, and depth of respirationscan provide an insight into the work ofbreathing and adequacy of alveolar ventila-tion which are important factors to analyzewhen considering initiation of mechanicalventilation, alteration of ventilator settings,weaning a patient from the ventilator, or ad-vancing a patients activity level. A normal

respiratory rate and absence of the use of ac-cessory muscles may reflect a manageablework of breathing. Conversely, tachypneaand the use of accessory muscles of inspira-tion (sternocleomastoid or external inter-costals) or expiration (internal intercostals,abdominal muscles) may indicate the patienthas insufficient muscle strength to maintainthe work of breathing necessary to over-come increased resistance or decreased

compliance. Resistance and compliance canbe directly measured in patients receivingmechanical ventilation (See Assessment ofthe Patient Receiving Mechanical Ventila-tion in this issue).

Auscultation of the lungs can be used toevaluate the effectiveness of ventilation.Bronchial sounds may be indicative of ex-tensive consolidation, and bronchovesicularsounds may indicate early pulmonary dis-ease. Wheezing, produced by airflow

through narrow airways, may be heard onexpiration. Inspiratory wheezes may indicatebronchial constriction. Crackles may indicatefluid in the lung or weakened airway wallstrength. Cardiac disease is more likely toproduce excessive fluid type crackles that re-spond to fluid removal, while pulmonarydisease is more likely to produce cracklesthat are nonresponsive to fluid removal.

The major route of elimination of carbondioxide (CO2) is through the lungs. There-

fore, a quantitative assessment of ventilationis made through CO2 evaluation. The higherthe serum CO2, the more significant the ven-tilatory failure. CO2 can be measuredthrough arterial blood gas analysis (PaCO2)or end-tidal CO2 monitoring (PetCO2).PetCO2 monitoring is a noninvasive mea-

surement of exhaled CO2. It ideally repre-sents an assessment of alveolar ventilation asPetCO2 should correlate with PaC02. Inhealthy individuals under normal conditions

of V/Q matching, the difference betweenPetCO2 and PaCO2 is minimal (5 mm Hg);as exhaled CO2 is always slightly lower thanPaCO2. In these situations, PetCO2 can beused as a substitute for PaCO2.1-4

Several patient conditions inhibit the useof PetCO2 to reflect PaCO2. PetCO2 does notaccurately reflect PaCO2 under conditions ofrespiratory failure, hemodynamic instability,or extremes in temperature.5 For example, ifperfusion to the lungs is decreased (cardiac

arrest, pulmonary embolism), then less CO2is carried to the lungs from the tissues andPetCO2 will be lower than PaCO2. Theremust be adequate perfusion to the lungs tobring CO2 to the alveolar capillary mem-brane so that gas exchange can occur andCO2 is exhaled. Increased peripheral CO2production, such as that which occurs in afebrile state, can increase PetCO2.

Isolated PetCO2values must be evaluated

cautiously in critically ill patients. Multiplemeasurements of PetCO2 or monitoring thePaCO2-PetCO2 gradient over time may pro-vide important clues related to either im-proved or worsening patient clinical status.5

A large PaCO2-PaC02 gradient (20 mm Hg)may reflect a large V/Q mismatch. A gradualimprovement in the gradient (a narrowing ofthe gradient) may represent improved V/Qmatching and ventilatory function.

Physiologic processes of the respiratory

system can be evaluated by different pul-monary function tests (PFTs). PFTs evaluatelung mechanics by measuring the volume ofair the patient is able to move in and outduring ventilation and estimating severallung capacities (Table 1). Potential uses ofPFTs in critically ill patients include: evalua-tion of known or suspected lung disease;evaluation of symptoms such as chroniccough, dyspnea, or chest tightness; monitor-ing the effects of exposure to pulmonary

toxic drugs; risk stratification prior tosurgery; and monitoring the effectiveness oftherapeutic interventions.6 Physiologic ab-normalities that may be measured by PFTsinclude obstruction to airflow, restriction oflung size, and a decrease in transfer of gasesacross the alveolar-capillary membrane.


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PFTs can detect these abnormalities early inthe course of a disease when the physicalexamination and radiographic studies stillappear normal.7

A major limitation of PFTs is that they re-quire considerable patient effort and cooper-ation which limits their use in the intensive

care unit (ICU) patient population. Inade-quate patient effort can lead to misdiagnosesand inappropriate treatment.8 However, incritically ill mechanically ventilated patients,it is important to monitor some of the com-ponents of PFTs including vital capacity,tidal volume, and minute ventilation (SeeAssessment of the Patient Receiving Me-chanical Ventilation elsewhere in this issue).These parameters can help measure the ef-fects of a disease process on ventilation. De-

creased tidal volume results in alveolar hy-poventilation and acute respiratory failure.Tidal volume and vital capacity monitor res-piratory muscle strength. Therefore, as thepatient experiences respiratory muscle fa-tigue, these values decrease. Increasedminute ventilation is associated with in-

creased work of breathing. Decreasedminute ventilation is associated with hy-poventilation.

Assessment of Intrapulmonary Shunt

Intrapulmonary shunt is the proportion of

blood that flows past alveoli without partici-pating in gas exchange. An elevated intra-pulmonary shunt indicates a large percent ofvenous blood has bypassed alveoli and en-tered arterial blood without being oxy-genated. Increased intrapulmonary shuntcan be attributed to: (1) diffusion impair-ment produced by a thickened alveolar cap-illary membrane, (2) ventilation to perfusion(V/Q) abnormalities, or (3) atelectasis, con-solidation, and pulmonary edema. Normal

intrapulmonary shunt is relatively low; 5%of the blood flow fails to make contact withfunctioning alveoli. A mild intrapulmonaryshunt is 5 to 15%, a major intrapulmonaryshunt is 15 to 30%, and a severe intrapul-monary shunt is greater than 30%. There areseveral methods to assess intrapulmonary

TABLE 1 Pulmonary Function Test Parameters

Measurement of Pulmonary Function Implications

Tidal volume: Amount of air inhaled or exhaled Decreases may indicate patient fatigue, alveolarduring normal tidal breathing (normal 3-7 mL/L). ventilation, or onset of parenchymal process.

Minute volume: Total amount of gas breathed per May indicate work of breathing onset of metabolicminute (normal 5-10 L/min). (Tidal volume rate changes, or changes in dead space.multiplied by respiratory rate.)

Forced Expiratory Reserve Volume (FEV): Measures Normal with restrictive airway disease. Reduced ratehow rapidly a person can forcefully exhale air of expiratory flow with obstructive airwayafter a maximal inhalation. Also expressed as the diseases. The ratio of FEV1/FEV is a specificamount of air exhaled in the first, second, and measure of airway obstruction with or withoutthird second of forced exhaled maneuver restrictive disorder. Normally the ratio is 75%;(FEV1, FEV2, FEV3). values 75% suggest obstruction.

Inspiratory capacity: Maximal volume of air that can Decreased value may indicate restrictive lung

be inhaled from the resting expiratory level. disease; one of the parameters used to determinepatients possibility of being weaned frommechanical ventilation.

Functional residual capacity: Volume of air in the Decreased value is the hallmark of Acutelungs at resting end expiration. Respiratory Distress Syndrome. Increased value

reflects overdistension of the lungs, which mayresult from obstructive disease or excessive use ofpositive end expiratory pressure.

Forced Vital Capacity: The total volume of air that Decreased value indicates resistance to expiratorycan be exhaled during a maximal forced ex- flow as in obstructive disease.piration effort.

Vol. 15, No. 4 Oct.-Dec. 2004 OXYGENATION 509


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shunt, each with advantages and limitations.The value of assessing intrapulmonary shuntis to identify alterations in pulmonary gas ex-change, determine the degree to which the

lung deviates from ideal as an oxygenator ofblood, and to evaluate patient response tointerventions.

PHYSIOLOGIC SHUNT. The physiologic shuntequation (Qs/Qt) is identified as the goldstandard for assessing impairment of pul-monary gas exchange in critically ill pa-tients.9 Qs/Qt can be measured by calculat-ing the difference between the content offully oxygenated pulmonary capillary (CcO2)

and arterial blood (CaO2) divided by a differ-ence between full CcO2 blood and mixed ve-nous blood (CvO2) according to the formulain Table 2. It is the most accurate indicator ofpulmonary gas exchange that is clinicallyavailable.9,10 However, it is time consumingto obtain, complex to calculate, and costly.

Data needed to calculate oxygen con-tent in the Qs/Qt formula are availableonly from patients who have pulmonary

and peripheral artery catheters in place.These data are obtained by drawing simul-taneous mixed venous and arterial bloodgases from these catheters. It is a complexformula to calculate, although most bed-side monitoring systems in the ICU havethe capability to calculate Qs/Qt oncemixed venous and arterial blood gas dataare available (Hb, arterial oxygen satura-tion [SaO2], PaO2, partial pressure of ve-nous oxygen [PvO2], and venous oxygen

saturation [SvO2]) and are entered into thebedside monitoring system.

OXYGEN TENSION DERIVED INDICIES. Several in-

dices to estimate Qs/Qt were developed be-cause of the complexity of the classic shuntequation calculation, necessity for frequentsampling of arterial and mixed venousblood, and the need for a pulmonary arterycatheter.10-12 The indices are collectively re-ferred to as oxygen tension derived indicesof pulmonary gas exchange, and include:alveolar-arterial gradient, ratio of arterial-to-alveolar oxygen tension, and ratio of arterialoxygen tension to fraction of inspired oxy-

gen (Table 3). All relate the driving pressure(fraction of inspired oxygen [FiO2] or partialpressure of alveolar oxygen [PAO2]) for diffu-sion into the pulmonary capillary blood,which is the mean determinant of PaO2.There has been some debate on the use ofPAO2 versus FiO2 in a hypoxemia index.Some argue that PAO2 is more advantageousbecause it includes the effect of CO2.13 Oth-ers contend that this addition has little value,

adds further assumptions, and may varysomewhat with permissive hypercapnea.14

Alveolar-Arterial Gradient. The alveo-lar-arterial gradient (A-a) gradient was de-veloped based on the relationship be-tween alveolar and arterial oxygentension: PAO2 equals PaO2 when ventila-tion and perfusion are perfectly matched.The gradient describes the overall effi-ciency of oxygen uptake from alveolar gasto pulmonary capillary blood. In healthy

TABLE 2 Physiologic Shunt Equation

Qs/Qt CcO2 CaO2

CcO2 CvO2

where CcO2 (1.34 x ScO2 x Hb) (0.0031 PAO2);CaO2 (1.34 x SaO2 x Hb) (0.0031 PaO2); and CvO2 (1.34 x SvO2 Hb) + (0.0031 PvO2). Makingthese substitutions,

Qs/Qt =(1.34 ScO2 x Hb 0.0031 PAO2) (1.34 SaO2 Hb 0.0031 PaO2) x100

(1.34 x ScO2 Hb + 0.0031 PAO2) (1.34 SvO2 Hb + 0.0031 PvO2)

ScO2, pulmonary capillary oxygen saturation (100%); Hb, hemoglobin; PAO2, alveolar oxygen tension, calculated as: (FiO2 [Pb PH20] PaCO2/R), where FiO2 Fraction of inspired oxygen; Pb barometric pressure; PH20=Pressure of water vapor (47mm Hg); PaCO2 partial pressure of carbon dioxide; R respiratory quotient (CO2 production/O2 consumption in a steadystate 0.8); SaO2, saturation of oxygen in arterial blood; PaO2, partial pressure of oxygen in arterial blood; PvO2, partial pres-sure of oxygen in venous blood; SvO2, mixed venous oxygen saturation.


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conditions, there is generally a small differ-ence between PAO2 and PaO2 because PAO2is approximately 100 mmHg and PaO2 isabout 95 mmHg. As the gradient betweenPAO2 and PaO2 increases, intrapulmonaryshunt increases.

Table 4 illustrates the use of the A-a gradi-ent in different clinical situations. Patient Areflects a normal healthy person breathingroom air. The A-a gradient is 1.7, which rep-resents a near-perfect match between venti-lation and perfusion. Patient B reflects respi-ratory failure in a patient breathing room air.In this example, the A-a gradient is 31,which is a large gradient and, therefore, alarge ventilation perfusion disturbance.

Several studies have compared the A-agradient and Qs/Qt and have demonstratedthe two measures moderately correlate inevaluating ventilation perfusion imbalance in

critically ill patients (r= 0.58-0.68).15-18 How-

ever, one study reported that 51% of the A-agradients did not accurately reflect Qs/Qt 16;another found that in 25% of the measure-ments, Qs/Qt and A-a gradient varied in op-posite directions.15 Thus, while it appears A-agradient is useful in situations where the pa-tient is breathing room air, its use in criticallyill patients is limited because it cannot differ-entiate the severity of different clinical situa-tions.15-19 Patients C and D in Table 4 illus-trate this point. Patient C is receiving FiO2 1.0and is in respiratory failure; a large A-a gradi-ent is noted. Patient D is receiving FiO2 0.4,but has a normal PaCO2 and PaO2, yet the A-a gradient is still large. Another limitation ofthe A-a gradient is that varying FiO2 concen-trations affect the measurement.20,21 PatientsE and F in Table 4 reflect that with varyingFiO2, A-a gradient increases markedly. Pa-tient E is receiving FiO2 0.7 with a PaCO2 40

mmHg and a PaO2 of 70 mmHg that results

TABLE 3 Oxygen Tension Based Indices of Pulmonary Gas Exchange

Index Interpretation Normal Values

Alveolar-Arterial Gradient As the gradient between PAO2 and PaO2 increases, 10-15 mmHgPAO2-PaO2 intrapulmonary shunt increases

Ratio of arterial to alveolar As PaO2 decreases relative to PAO2, the ratio 0.75PaO2/PAO2 oxygen tension decreases, reflecting increasing intrapulmonary

shunt

Ratio of arterial oxygen tension As the ratio decreases, greater levels of FiO2 300-500to fraction of inspired oxygen are required to maintain a given PaO2,PaO2/FiO2 reflecting intrapulmonary shunt is increasing

PAO2, partial pressure of oxygen in alveoli; PaO2, partial pressure of oxygen in arterial blood; FiO2, fraction of inspired oxygen.

TABLE 4 Clinical Application of Oxygen Tension Derived Indices

PaO2 PaCO2 A-a a/APatient FiO 2 mmHg mmHg PAO 2 Gradient Ratio PaO 2/FiO2

A 0.21 98 40 99.7 1.7 0.98 467

B 0.21 50 55 80.9 30.9 0.61 238

C 1.00 50 55 644 594.3 0.08 50D 0.40 98 40 643 545 0.15 98

E 0.70 70 40 449 379 0.16 101

F 0.90 200 40 592 392 0.34 222

PAO2, partial pressure of oxygen in alveoli; PaO2, partial pressure of oxygen in arterial blood; FiO2, fraction of inspired oxygen;PaCO2, partial pressure of carbon dioxide in arterial blood; A-a gradient, PAO2-PaO2; a/A Ratio, PaO2/PAO2; mmHg, mmmercury.



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in an A-a gradient of 379. Patient F is receiv-ing an FiO2 0.9 with PaCO2 40 mmHg andPaO2 200 mmHg and the A-a gradient is stillhigh at 392. At increasing FiO2, A-a gradient

increases markedly, causing this index tolose clinical utility in critically ill patients.Its clinical usefulness is limited to patientswith a Qs/Qt 15% and FiO2 0.5.12

Arterial-Alveolar Oxygen Tension Ratio.The arterial alveolar oxygen tension ration(a/A ratio) was developed based on the rela-tionship between alveolar and arterial oxy-gen tension. This index uses the same vari-ables as the A-a gradient: PAO2 (PaCO2,FiO2) and PaO2. As PaO2 decreases relative

to PAO2, the ratio decreases and intrapul-monary shunt increases. A normal value is0.75 and a ratio 0.75 indicates pulmonarydysfunction due to ventilation perfusion ab-normality, shunt, or a diffusion limitation.22

Table 4 illustrates the clinical use of a-A ra-tio. Patient A reflects a normal healthy per-son breathing room air with an a-A ratio of0.98. This represents a near-perfect matchbetween ventilation and perfusion. Patient B

reflects respiratory failure in a patient breath-ing room air. Here, the a-A ratio is 0.61,which reflects a worsening intrapulmonaryshunt.

There are conflicting data on the accuracywith which this index reflects Qs/Qt. Caneand colleagues examined the relationship ofQs/Qt and a-A ratio in a heterogeneousgroup of 75 critically ill patients (50 medicaland 25 surgical ICU patients) and reported ahigh correlation between Qs/Qt and a-A ra-

tio (r= -0.78).18 Rasanen and colleagues ex-amined the relationship between Qs/Qt andthe a-A ratio in 17 critically ill patients withrespiratory failure, but reported a poor cor-relation (r = 0.47).12 Like A-a gradient, a-Aratio appears to be vulnerable to changes inperipheral circulation and oxygen therapy ascan be seen by analyzing the data in Table 4.Patient C in respiratory failure on FiO2 0.40has a low a-A ratio that reflects a significantintrapulmonary shunt. Patient D on FiO2 1.0

has a normal PaCO2 and PaO2, yet the a-Aratio is only 0.15. Again, as was noted withthe A-a gradient, the a-A ratio can also notdifferentiate the severity of two clinical situa-tions as noted in Patients E and F in Table 4.

PaO2/FiO2. The PaO2/FiO2 ratio was in-troduced in an attempt to overcome the limi-

tations of A-a gradient and a-A ratio and en-able the evaluation of PaO2 at varying FiO2.23

A normal ratio is 300 to 500 and a value250 reflects a clinically significant impair-

ment of pulmonary gas exchange.23

Table 4illustrates the clinical use of PaO2/FiO2. Pa-tient A reflects a normal healthy personbreathing room air with a normal PaO2/FiO2.Patient B, in respiratory failure, appears tohave an intrapulmonary shunt as reflectedby a PaO2/FiO2 of 238.

PaO2 /FiO2 and Qs/Qt are moderately tohighly correlated (r -0.51 to -0.90).10,17,18,24

Covelli and colleagues found that a PaO2/FiO2 200 correlated with a Qs/Qt 20% in

critically ill patients with acute respiratorydistress syndrome (ARDS).17 In a retrospec-tive analysis of previously published data of16 patients with ARDS, PaO2/FiO2 in patientswith moderate shunts (30%) varied consid-erably with alteration in FiO2.14 When theuse of the ratio was restricted to FiO2values0.5 and PaO2values 100, there was littlevariation in the ratio for a given patient. Withlow values of true shunt or with substantial

perfusion of alveolar units with low ventila-tion/perfusion ratios, PaO2 increased to100 and diminished the value of PaO2/FiO2as an index of hypoxemia.

The American-European consensus con-ference definition of acute lung injury andARDS is partially based on the PaO2/FiO2. APaO2/FiO2 of less than 300 defines acutelung injury and PaO2/FiO2 200 definesARDS.25 PaO2/FiO2 has been shown to behigher in patients with ARDS who survive26

and significantly lower in nonsurvivors.27However, several studies26,28 and a meta-analysis29 suggest that it is an inconsistentpredictor of outcome in patients with ARDS.Doyle and colleagues found no differencein mortality between patients with aPaO2/FiO2 ratio of 150 to 300 and thosewhose ratio was 150.28 The ProstaglandinE1 Study Group found that an improvementin the PaO2/FiO2 ratio after day 1 of conven-tional therapy predicted a favorable progno-

sis in their control patients.26 This improve-ment in oxygenation among survivors wasmaintained over a 7-day period. Thus, mon-itoring trends over time may provide moreuseful information than any single measure-ment. Despite these reports, PaO2/FiO2 remains the most important clinical


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physiologic variable used in the diagnosisand assessment of ARDS.30-32 In a survey of448 ICU medical directors in the UnitedStates, respondents considered the PaO2/

FiO2 ratio to be the physiologic variablemost important to determine the respiratorystatus of a patient with ARDS.31

Assessment of Oxygen Delivery

The second component in the assessment ofoxygenation is oxygen delivery (DO2) whichinvolves the process of transporting oxygento cells. The major function of the cardiovas-

cular system is to transport oxygen from thelungs to the tissues at a rate to meet cellularoxygen demands. The concept of a failure ofDO2 to meet metabolic demand require-ments commonly defines shock. Under nor-mal resting conditions, DO2 is more than ad-equate to meet tissue oxygen requirementsfor aerobic metabolism.

DO2 is dependent on cardiac output (CO)and the oxygen content in arterial blood(CaO2) as expressed in the Fick Formula

(Table 5). The overall transport of oxygen tocells is dependent on the quantityof bloodbeing pumped (CO) and the quality of theblood (CaO2). DO2 is approximately 1000mL/min and when indexed to body surfacearea, is approximately 600 mL/min/m2. DO2may be compromised by anemia, oxygendesaturation, and a low CO, either singu-larly, or in combination.

Individual cells and organs vary in theirsensitivity to impaired DO

2

. Cardiomyocytes,neurons, and renal tubular cells are particu-larly sensitive to an acute reduction in DO2.The kidneys and liver can tolerate 15 to 20minutes of hypoxia, skeletal muscle 60 to 90minutes; however, in contrast, hair and nailscan continue to grow for several days afterdeath.33 This variation in tissue tolerance toimpaired DO2 has important clinical implica-

tions. Maintenance of DO2 to the most hy-poxia-sensitive organs is crucial. Measure-ment of DO2 to individual organs is an im-portant goal for the future, but is not

currently possible in the clinical setting. Atpresent, only near infrared spectroscopy andgastric tonometry are used clinically to de-tect organ hypoxia.

Physical Assessment of DO2

Direct physical assessment of oxygen deliv-ery is difficult for a variety of reasons includ-ing that oxygen is a colorless, odorless gas.

Indirect assessments of DO2 can be madeusing parameters such as level of conscious-ness, skin color, capillary refill, and skintemperature. A diminished level of con-sciousness, confusion, or agitation may bemanifestations of hypoxemia. Capillary refillas a marker of DO2 is controversial. It maybe useful as a marker of hypovolemia andpoor myocardial function during early resus-citation in children34; however, in elderly pa-tients it does not correlate with objective

measures of hypovolemia.35 The poor sensi-tivity of capillary refill to blood loss (6% sen-sitivity and 93% specificity)36 leads to theconclusion that capillary refill has no provendiagnostic value in the adult.37 In a more re-cent investigation of the usefulness of thephysical examination of subjective extremityskin temperature in a population of criticallyill adult patients with a variety of diseaseprocesses, cool distal extremities correlatedwith other markers of hypoperfusion (basedeficit, high lactate levels, and low mixedvenous oxygen saturation).38

Other clinical indices used in the assess-ment of DO2 (such as heart rate, skin tem-perature, and urine output) are unreliableand slow to change, particularly in compen-satory shock states, and abnormal valuesmay only occur in the late stages of severe

TABLE 5 Fick Formula for Oxygen Delivery

DO2 CO CaO2 10where CaO2 (Hb 1.34 SaO2 ) (PaO2 0.003)

where CaO2 content of oxygen in arterial blood; 1.34 mL of O2/g of Hb; SaO2 hemoglobin saturationwith oxygen; PaO2 is the amount of O2 dissolved in blood; 0.003 is the solubility coefficient for O2 , and 10is a constant to express CaO2 in mL/min



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DO2 impairment.39 Even though urine outputis used as an index of kidney perfusion(based on the presumed sensitivity of thekidney to intravascular volume and pressure

changes), it is now widely accepted thateven in the face of adequate urine output,other crucial tissue beds may be underper-fused.40 In addition, polyuria may be ob-served in the course of some altered perfu-sion states including sepsis.41 Using thesetraditional clinical signs is more problematicin the aging patient population because ofchronic disease states and the use of concur-rent medications. Examples include the in-ability of some patients using cardioactive

medications to mount an appropriate tachy-cardia from volume loss, hypertensive pa-tients presenting with normal blood pressureas a manifestation of hypovolemia, and pa-tients with limited cardiac reserve in shockstates from relatively minor blood loss orwhose cardiac function deteriorates as theresult of pain and stress.42

The presence of peripheral edema shouldalert the clinician about the potential for im-

paired DO2 to individual cells. Tissue edemadue to increased vascular permeability or ex-cessive intravascular volume expansion mayresult in impaired oxygen diffusion fromcapillary blood to individual cells, particu-larly in clinical situations associated with ar-terial hypoxemia. In these situations, avoid-ing tissue edema may improve DO2 tocells.33

Assessment of Cardiac Output

Cardiac output (CO) is a product of strokevolume and heart rate. The role of hemody-namic monitoring is to evaluate the threecomponents of stroke volume (preload, af-terload, and contractibility) and optimizecomponents to ensure adequate CO (SeeHemodynamic Assessment elsewhere inthis issue).

The two most commonly used techniquesto measure CO are bolus thermodilution and

continuous CO. The choice of method de-pends on the patient and the clinical situa-tion. A detailed description of these andother techniques to measure CO is beyondthe scope of this article, but has been re-viewed elsewhere.43 ICU clinicians musthave a thorough understanding of the limita-

tions, bias, precision, and risks of themethod used to determine CO to avoid treat-ment decisions based on spurious data. Aneven greater challenge lies in understand-

ing the number once its generated. Tibbyand Murdock suggest an approach that mayassist clinicians in interpreting CO data.44

They recommend CO should ideally be in-terpreted from four aspects: (1) a quantita-tive element, (2) a qualitative element, (3) atemporal element, and (4) as part of a globalassessment of metabolic well-being. In otherwords, adequacy of CO should be deter-mined by answering the following question:Is the CO (x L/min.) adequate for thispa-

tient at this time? Integration of CO into aglobal metabolic assessment requires an ap-preciation of the contribution of CO to DO2and an understanding of the balance be-tween DO2 and oxygen consumption (VO2).This global assessment can be made by con-sidering the following questions: (1) Is theDO2 adequate to meet metabolic needs ofthe patient (both globally and regionally)?(2) Is DO2 occurring with adequate perfu-

sion pressure? (3) Is the patient able to useoxygen delivered? (4) If the answer is no toany of the above, why is this so?44

Measurement of Oxygen Contentin Arterial Blood

As Table 5 demonstrates, many measure-ments are required to calculate DO2. If allmeasurements had zero error, the Fickmethod would be accurate and repro-

ducible. However, all clinical measurements,particularly in critically ill patients, have as-sociated systematic measurement errors(bias) and random measurement errors (pre-cision). In the Fick equation these measure-ment errors are not simply added in theequation, but they are multiplied in the finalequation. Even with modest individual mea-surement errors, large overall errors occur inthe calculation of DO2.

CaO2 is calculated according to the for-

mula in Table 5. Normal CaO2 is 20 mLO2/dL. PaO2 contributes minimally to overallDO2 and is frequently omitted from the cal-culation. Global DO2 depends more on SaO2than PaO2. Therefore, there is little extrabenefit from increasing PaO2 above 90mmHg due to the shape of the oxyhemoglo-


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bin dissociation curve when over 90% of Hbis already saturated with oxygen. IncreasingHb through blood transfusion may seem tobe an appropriate intervention to optimize

CaO2. However, blood viscosity increaseswith Hb 10 g/dL33 and can impair bloodflow. Recent evidence suggests that tradi-tionally accepted Hb concentrations for criti-cally ill patients of 10 g/dL may be too highsince an impaired outcome was observed ifHb was maintained between 7 to 9 g/dL(with the exception of patients with coro-nary artery disease in whom a level of 10g/dL may be appropriate).45

Pulse oximetry is used for continuous

measurement of SaO2 and when measuredthis way it is designated as SpO2. Becausedesaturation is detected earlier by pulseoximetry than by clinical observation, theuse of pulse oximetry is recommended forany patient at risk for hypoxemia.46 Pulseoximetry has become a standard monitoringdevice in the ICU upon which therapeuticinterventions are frequently made. Its usesinclude detection of hypoxemia,47 reductionin the frequency of arterial blood gases,48

titration of FiO2,49 and weaning from me-chanical ventilation.50 A full review of re-search related to pulse oximetry can befound in research-based clinical protocolson pulse oximetry.46,51

Comparison of pulse oximetry with directCO-oximeter measurements is reported interms of bias (mean difference between twotechniques) and precision (standard devia-tion between two techniques). In healthy

volunteers, oximeters have a bias of2%and a precision of 3% when Sa0290%.52,53 Comparable results have been re-ported in critically ill patients with good arte-rial perfusion.54,55 However, decreased biasand precision have been reported in hemo-dynamically compromised patients and pa-tients with hypoxemia, in whom accurateand reliable monitoring is of major impor-tance.

In low perfusion states with decreased

CO, the bias and precision reach unaccept-able limits of agreement (4%).56-58Accuracyof pulse oximeters appears to deterioratewhen SaO2 falls below 80%. In healthy indi-viduals under hypoxemic conditions, bias ofpulse oximetry ranges from 15% to 13%,while the precision ranges from 1 to 16%.52,59-

61 In a study of 54 mechanically ventilatedpatients with SaO2 90%, the bias and preci-sion of pulse oximetry was 1.7% and 1.2%,respectively, but when the SaO2was 90%,

the bias and precision of pulse oximetry was5.1 and 2.7%, respectively.49 Elevated car-boxyhemoglobin or methemoglobin levelscause inaccurate oximetry readings.62-64 Inpatients with sickle cell anemia in acute cri-sis, the mean bias of pulse oximetry was4.5%.65 More recently, Sequin andcolleagues66 found that SpO2 consistentlyoverestimated SaO2 and concluded that aminimum threshold SpO2 value of 96% ismore reliable to ensure an SaO2value90%.

Pulse oximeters have several technicallimitations that may lead to inaccurate read-ings. Accuracy decreases during states of di-minished blood flow through the point of at-tachment.67-69 as a result of vasoactive drugs,hypotension, or hypothermia. Accuracy offinger probes is generally found to be betterthan performance at other sites.70 Becausethe earlobe is the least vasoactive site and isleast susceptible to signal loss, it may showfaster response and greater accuracy duringperiods of vasoconstriction and hypoten-sion.46 Blue, green, or black nail polishcauses inaccurate SpO2 readings.71 Motion ofthe probe continues to be a significantsource of error and false alarms.72-74 Nearlyone-half of all false alarms in the ICU havebeen attributed to SpO2 signals.75

Many clinicians fail to appreciate the phys-ical and technical limitations of pulse oxime-try.76 The pulse oximeter remains a valuable

tool in the care of critically ill patients, but anawareness of its limitations is an importantcomponent of enhancing the quality of care.The major challenge facing pulse oximetry iswhether this technology can be incorporatedinto diagnostic and management algorithmsthat can improve the efficiency of clinicalmanagement in the ICU.77

Assessment of Oxygen

Consumption and OxygenExtraction

The third component of oxygenation is oxy-gen consumption (VO2); the process bywhich cells use oxygen to generate energy.Ingested substrates are converted in the



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Krebs Cycle to form adenosine triphosphate(ATP) through aerobic metabolism and re-sults in the creation of 38 molecules of ATP.As a back-up mechanism, cells can still

produce ATP with a limited oxygen supplythrough the process of anaerobic metabo-lism where carbohydrates are broken downto generate two ATP molecules. However, inaddition to ATP, the byproducts pyruvateand lactate are produced. The more timespent in anaerobic metabolism, the morelactate produced. Normal VO2 is approxi-mately 250 mL/min. When indexed to bodysurface area, VO2 is approximately 130mL/min/m2.

Direct measures of cellular VO2 are in var-ious developmental phases but are not yetavailable in the clinical setting. There are nophysical assessment parameters that can beused to evaluate VO2. Current clinical tech-niques for measuring VO2 focus on globalmeasurements that reflect the balance be-tween DO2 and VO2.

Assessment of Oxygen Consumption

Indirect calorimetry is the gold standard forthe determination of VO278 and is the recom-mended method to measure VO2 in criticallyill adults.79 It uses a direct measure of VO2and CO2 production. Although the use of in-direct calorimetry is considered to be themost accurate method, it is time consuming,involves the use of expensive and special-ized equipment, and requires trained per-sonnel to perform it.80 These limitations pre-

vent its widespread acceptance as a methodto measure VO2 in critically ill patients.

VO2 can also be measured using the Re-verse Fick equation according to the formulain Table 6. Data needed to calculate VO2 us-ing this equation are available from patientswho have pulmonary artery and peripheral

arterial catheters in place to allow for obtain-ing simultaneous mixed venous and arterialblood gases. Like the Qs/Qt, it is time con-suming to obtain, complex to calculate, and

costly. Most bedside monitoring systems inthe ICU have the capability to calculate itonce mixed venous and arterial blood gasdata are available (Hb, PaO2, SaO2, PvO2,SvO2) and entered into the bedside monitor-ing system.

There are several methodological con-cerns about the accuracy and precision ofthe reverse Fick equation. It may underesti-mate whole body VO2 because it does notinclude the VO2 of the bronchial and thebe-

sian circulations.81,82 Pulmonary VO2 is aphysiologic variable of importance espe-cially in pulmonary inflammatory conditionssuch as acute lung injury and pneumonia be-cause it may be substantially increased.83

The Fick method is episodic and may not re-flect actual trends in VO2.84 Investigatorshave demonstrated there can be large, ap-parently spontaneous, changes in VO2 incritically ill patients.85,86

Studies that have compared simultaneousmeasurements using indirect calorimetryhave reported that indirect calorimetry mea-surements are 8 to 27% higher than mea-surements made using the Fick method.87-89

A more recent study reported a bias of 41mL/min/m2, precision of 3.95 mL/min/ m2,and a 95% confidence interval of 20 to 63mL/min/m2; which they considered to be fartoo wide and concluded that these two meth-ods should not be considered to be inter-

changeable.90

Assessment of Oxygen Extraction

With a normal resting DO2 of approximately1000 mL/min and VO2 of 250 mL/min, rest-

TABLE 6 Reverse Fick Equation to Measure VO2

VO2 (CaO2 - CvO2) CO 10where CaO2 (Hb 1.34 SaO2 ) (PaO2 0.003)

and CvO2 (Hb 1.34 SvO2) (PvO2 0.003)where CaO2 content of oxygen in arterial blood; CvO2 content of oxygen in venous blood; 1.34 mLof O2/g of hemoglobin (Hb); SaO2 saturation of oxygen in arterial blood; SvO2 saturation of oxygen inmixed venous blood; PaO2 is the partial pressure of oxygen in arterial blood; PvO2 is the partial pressure ofoxygen in venous blood; 0.003 is solubility coefficient for O2; 10 is a constant to express VO2 in mL/min.


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ing oxygen extraction is approximately 25%.The amount of oxygen consumed as a frac-tion of oxygen delivered defines the oxygenextraction ratio (O2ER). The O2ER estimates

the balance between oxygen delivery andoxygen consumption and is calculated asO2ER = VO2/DO2. As VO2 increases or DO2decreases the O2ER rises to maintain aerobicmetabolism. An O2ER greater than 0.35 im-plies an excessively high extraction of oxy-gen to meet metabolic demands and is oftenassociated with shock states.9 Tissue hy-poxia, either because DO2 is inadequate orcells do not extract and use oxygen nor-mally, may be a contributor to organ failure

in critical illness.83One of the most important clinical ques-

tions about oxygenation that clinicians mustevaluate is whether DO2 is adequate to meetthe metabolic needs of the patient. There areno direct methods currently clinically avail-able to assist clinicians in making this assess-ment. Instead, clinicians must rely on globaland regional parameters. These parametersindirectly assess the balance between DO2and VO

2.

Global Parameters of DO2/VO2 Balance

The relationship between whole body DO2and VO2 is illustrated in Figure 2. (It shouldbe noted that individual organ systems havetheir own DO2/VO2 relationship). As noted

in Figure 2, VO2 remains relatively constantover a wide range of DO2 because tissuescan extract more oxygen when needed.When this occurs, venous oxygen saturation

decreases. However, when DO2 reaches acritical threshold, tissue extraction of oxy-gen cannot be further increased to meetVO2. It is at this point that VO2 becomes di-rectly dependent on DO2 (DO2[Crit]) andcells convert to anaerobic metabolism. Thisis manifested by an increase in lactate, amore significant base deficit, a decrease inmixed venous oxygen saturation (SvO2),and an increase in the O2 ER. The DO2(Crit)in humans has not been widely determined,

but may be in the range of 180 to 330mL/min/m2.91,92

SERUM LACTATE. As noted in Figure 2, a criti-cal reduction in DO2 results in anaerobicmetabolism, which, in turn, produces a sig-nificant elevation in serum lactate levels.Serum lactate levels are considered to be theclinical gold standard as a marker of inade-quate cellular oxygenation.93-95 Normalserum lactate levels are 2 mMol/L. Themagnitude and duration of elevated lactatelevels maybe predictors of mortality andmorbidity in some critically ill patient popu-lations. In critically ill trauma, surgical, andburn patient populations, lactate normaliza-tion within 24 hours of admission is associ-ated with increased survival.96-100 Initial and

Figure 2. Global indices of DO2/VO2bal-

ance. L, lactate; SVO2, missed venous

oxygen saturation; O2ER, oxygen extrac-

tion ratio; VO2, oxygen consumption;

DO2, oxygen delivery; DO2(Crit), point at

which VO2 becomes directly dependent

on DO2.



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highest lactate levels appear to be higher innonsurvivors than survivors, and signifi-cantly higher in patients with multiple organfailure than without organ failure.101 How-

ever, in a recent study102

blood lactate levelswere not affected by worsening congestiveheart failure severity in status I cardiac trans-plant candidates.

Certain limitations and cautions must beconsidered when interpreting lactate levels.Serum lactate concentrations represent thebalance of many complex factors that influ-ence its production and clearance includingcancer, acute alcohol intoxication, cocaine,and grand mal seizure.103-105 Exogenous cate-

cholamine infusions can stimulate anaerobicmetabolism in skeletal muscle resulting inincreased production of lactate in the ab-sence of tissue hypoxia.106 Use of large-vol-ume lactated Ringers solution (28 mMol/L)may result in transiently elevated serum lac-tate levels because of the lag in lactate catab-olism, particularly if hepatic and renal perfu-sion remain poor.107 Because the kidneyscontribute to lactate removal, lactate can ac-

cumulate in the absence of tissue hypoxia insituations of impaired renal function.108 Evi-dence suggests that the lung can release lac-tate in the presence of acute lung injury.109

Despite these limitations, sequential use oflactate levels can establish and evaluatetrends in cellular oxygenation. Any increasein lactate is a cause for concern and the eti-ology should be aggressively pursued.

BASE DEFICIT. Base deficit is defined as the

amount of base (mMol) required to titrate 1L of arterial blood to a pH of 7.40 with thesample fully saturated with oxygen at 37Cand partial pressure of CO2 at 40 mmHg. It iscalculated from an arterial blood gas (ABG)analysis and is usually reported with theABG results. A normal base deficit is 3mMol to + 3mMol. Positive values reflectmetabolic alkalosis and negative values re-flect metabolic acidosis. Base deficit can re-sult from an accumulation of lactate associ-

ated with anaerobic metabolism and hasbeen classified in the trauma patient popula-tion as mild (-2 to -5 mMol), moderate (-6 to-14 mMol), or severe (> -15 mMol).110

Base deficit appears to be a sensitivemeasure of the degree and duration of inad-equate DO2 in the critically ill trauma patient

population. Rutherford and colleagues111

conducted a retrospective study of 3791trauma patients and reported that a basedeficit of -15 mMol within 24 hours postin-

jury was a significant marker of mortality inpatients 55 years of age. However, in pa-tients ages 55 and older, a base deficit of -8mMol was a significant marker of mortality.The use of a lower threshold of base deficitin elderly trauma patients is recommendedbecause elderly patients with significant in-juries and mortality risk may not manifest abase deficit out of the normal range.112 Amore recent study found that trauma patientswho had persistently high base deficit also

had lower VO2 (126 40 mL/min/m2versus156 30 mL/min/m2) than with patientswith a low base deficit.113 The investigatorsconcluded that a persistently high arterialbase deficit is associated with altered oxygenextraction and an increased risk of multipleorgan failure and mortality. For these rea-sons, many trauma centers support the useof a normal base deficit as an appropriateendpoint of adequate DO2.94

The use of base deficit in other patientpopulations is unclear. In samples of criti-cally ill surgical patients98 and burn pa-tients,100 initial base deficit was a poor pre-dictor of mortality and did not correlate withlactate levels. However, in a mixed sampleof medical and surgical ICU patients, Smithand colleagues114 found that a base deficitmore negative than -4 mMol/L and a lactate1.5 mMol/L led to a sensitivity of 80.3%and a specificity of 58.7% for mortality.

Limitations of base deficit exist and clini-cians should consider this in the interpreta-tion of these data. Administration of sodiumbicarbonate, hypothermia, and hypocapneacan affect base deficit. Certain conditionsthat result in a metabolic acidosis, unrelatedto lactic acidosis, can produce a base deficitthat does not reflect DO2/VO2 balance.These include hyperchloremic acidosis as aresult of infusions of large volumes of nor-mal saline,115 preexisting renal failure, acute

ingestion of certain substances (ie, alcohol,cocaine, aspirin), conditions associated withchronic CO2 retention (emphysema), and di-abetic ketoacidosis.95,116

MIXED VENOUS OXYGEN SATURATION. Mixed ve-nous oxygen saturation (SvO2) represents a


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global balance between DO2 and VO2. Nor-mal SvO2 is 60 to 75%. If SvO2 decreases,one of two problems exist: (1) DO2 has de-creased, or (2) VO2 has increased. To deter-

mine which of these situations is occurring,an assessment of DO2 must be made. If thecomponents of DO2 have not changed, thenthe source for an increase in VO2 must be in-vestigated.

In order to circumvent the need for apulmonary artery catheter, oxygen saturationof central venous blood (ScvO2) obtainedfrom the lower superior vena cava or rightatrium has been advocated as a surrogate.Studies evaluating the impact of this mea-

sure on the management of critically illtrauma patients have varied and its use is thesubject of ongoing debate.122A prospectivestudy of 40 critically ill trauma patients foundthat ScvO2 did not correlate with base deficitor lactate concentration.123 Others havedemonstrated that ScvO2 parallels elevationsin lactate and that it can be of value in de-tecting tissue hypoxia not confirmed by vitalsigns in patients who are critically ill.124,125

Very few studies have examined theagreement between ScvO2 and SvO2 and theresults are conflicting. Ladakis and col-leagues126 examined the mean ScvO2 andSvO2 values in 61 mechanically ventilatedpatients and reported the mean values weresimilar (mean SvO2 68.2% and ScvO269.4%); however, comparing mean valuesbetween methods does not answer if themethods agree. They did report similar pre-cision between the two methods (SvO2

1.2%; ScvO2 1.1%). In a more recent study in32 critically ill medical surgical patients,ScvO2 averaged 7 4% higher than SvO2.127

More studies are needed to more fully un-derstand the implications and limitations ofthe use of ScvO2 in the management of criti-cally ill patients.

MIXED VENOUS OXYGEN SATURATION: LACTATE RA-

TIO. Preliminary data are available to indi-cate that using SvO2 (or ScvO2) lactate ratio

may be valuable in recognizing DO2/VO2imbalances.128 For example, when a highSvO2 or ScvO2 is coupled with an elevatedlactate level, then inadequate cellular DO2may be present. More information is neededto determine if this ratio is clinically relevantand meaningful.

Organ Specific Monitoring of DO2/VO2

Global indices of DO2/VO2 balance lack thesensitivity necessary to be early warning sig-nals, particularly in shock states when mald-

istribution of circulating volume occurs andnot all organs become hypoxic all at once.The optimal tissue bed to monitor for DO2impairment is unclear. Access to various tis-sues to make monitoring useful is an obvi-ous consideration.

GASTRIC TONOMETRY. Splanchnic DO2 hasbeen quantified using gastric tonometrywhich is based on the knowledge that whenDO2 to the stomach decreases, anaerobicmetabolism in gastric cells produces thebyproducts of excess hydrogen ions, lactate,and CO2. As gastric CO2 levels increase, hy-poperfusion may be present. Currently avail-able methods of monitoring regional CO2 in-clude gastric tonometry and sublingualcapnography. An extensive review of thesemethods is beyond the scope of this article,but can be found elsewhere.129,130 Gastrictonometry is useful, particularly when used

to monitor the difference between gastricand arterial CO2. In normal physiologicstates, this difference is usually10 mmHg.A widening gap indicates compromisedblood flow to the splanchnic bed and a gapexceeding 20 mmHg requires aggressivetreatment.129,131 Carbon dioxide is measur-able in other tissue beds and using gastrictonometry principles, it has been extrapo-lated to other parts of the gastrointestinalsystem. Sublingual capnography was devel-

oped to overcome some of the limitations ingastric tonometry. Sublingual capnographyis noninvasive and portable, and data areavailable within minutes. It correlates wellwith gastric PCO2.132 A full review of thistechnology can be found elsewhere.130

Summary

Oxygenation is dependent upon three physi-ologic processes: pulmonary gas exchange,oxygen delivery, and oxygen consumption.An accurate and thorough assessment ofoxygenation must include an evaluation ofeach of these three processes. Diagnostictools available to ICU clinicians to monitorpulmonary gas exchange, oxygen delivery,



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and oxygen consumption presented in thisreview are summarized in Figure 3. It is im-perative that ICU clinicians recognize and

appreciate the implications and limitations ofthese diagnostic tools to avoid making treat-ment decisions based on spurious inaccuratedata. Accurate assessment and treatment ofdisturbances in oxygenation are crucial tooptimize patient outcomes.

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CO2, carbon dioxide; PaCO2, partial pressure of carbon dioxide in arterial blood; PetCO2, end-tidal carbon

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Evaluate Oxygenation in Critically Ill Adult

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