Pediatric Critical Care Study Guide || Fundamentals of Gas Exchange and the Assessment of Oxygenation and Ventilation

1

Fundamentals of Gas Exchange and the Assessment of Oxygenation and Ventilation

CHAPTER 1

LEARNING OBJECTIVES Present and explain the alveolar gas equation; describe ■

the changes in the partial pressure of oxygen from the atmosphere to the mitochondria Defi ne dead space (alveolar and anatomic) and describe ■

its quantifi cation; describe the compensatory mechanisms invoked with increased dead space Describe the distribution of ventilation and pulmonary ■

blood fl ow Describe how ventilation and perfusion are coupled; ■

detail common causes of their uncoupling Describe the alveolar/arterial oxygen gradient and ■

demonstrate its calculation Describe the transport of gases within the body; focus ■

especially on the hemoglobin/oxygen dissociation curve and carbon dioxide transport Describe the differences between oxygen and carbon ■

dioxide transport Describe the mechanics of, uses, and limitations of pulse ■

oximetry, end tidal carbon dioxide monitoring and transcutaneous oxygen and carbon dioxide measurement

CHAPTER OUTLINELearning ObjectivesIntroductionThe Process of Gas Exchange

Alveolar Ventilation and the Oxygen CascadeDistribution of Alveolar VentilationCarbon Dioxide EliminationAssessing Adequacy of Gas Exchange

Mechanisms of HypoxemiaHypoventilationVentilation Perfusion MismatchShunting of Pulmonary BloodDiffusion Limitation

Monitoring of Gas ExchangeArterial Blood Gas DeterminationPulse OximetryCapnometryTranscutaneous Oxygen and CO2 Monitoring

SummaryReview QuestionsAnswersSuggested Readings

INTRODUCTION

The basic function of the respiratory system is to supply oxygen (O 2 ) to, and remove carbon dioxide (CO 2 ) from, the body. The essential steps in this process include the exchange of gas between the atmosphere and the alveoli (ventilation), the diffusion of these gases across the alveolar capillary membrane, the transportation of gases in the blood, and the diffusion of the gases to and from the tissue capillaries.

JOHN S. SULLIVAN AND TOAH A. NKROMAH

2 J.S. S U LLIVAN AN D T.A. N KROMAH

THE PROCESS OF GAS EXCHANGE

Alveolar Ventilation and the Oxygen Cascade The cardiorespiratory system functions to extract oxygen from the atmosphere and deliver it to the tissues where it is required for aerobic metabolism. Alveolar ventilation is the volume of fresh gas each minute that reaches the alveoli and takes part in gas exchange. It is the fi rst step in the oxygen cascade and the most important factor determining the partial pressure of oxygen in the arterial blood (PaO 2 ). Alveolar ventilation is also responsible for the amount of CO 2 that is exhaled from the alveoli. In normal lungs, because carbon dioxide diffuses so readily across the alveolar capillary membrane, the alveolar CO 2 (P A CO 2 ) is essentially equal to the arterial carbon dioxide tension (PaCO 2 ).

The oxygen cascade begins as oxygen enters the alveoli on inspiration (Fig. 1-1 ). Oxygen diffuses across the alveolar capillary membrane into the pulmonary capillary blood down a pressure gradient created by a pressure difference across the membrane. Diffusion is a pas-sive process defi ned as the transfer of a gas from an area of higher pressure to an area of lower pressure. This diffusion of oxygen across the alveolar capillary membrane is accounted for by Fick’s fi rst law of diffusion, which asserts that the amount of gas diffusing through a membrane is directly proportional to the surface area available for diffusion, but inversely proportional to the distance it has to diffuse. The diffusion capacity for the pulmonary vas-cular bed is optimal for achieving gas exchange because the membrane is exceedingly thin, and the surface area is vast due to the structure and arrangement of approximately 400 mil-lion alveoli. In addition, in the setting of increased O 2 demand, additional capillaries may be recruited which help to maintain adequate O 2 supply by decreasing diffusion distances.

Distribution of Alveolar Ventilation Both alveolar ventilation and perfusion pressures increase progressively from the apex of the lung to its base due to the effects of gravity. However, blood fl ow increases more rapidly than does ventilation. Therefore, the ventilation perfusion (V/Q) ratio is highest at the apex of the lung and lower toward the base giving rise to what has come to be known as the West zones of perfusion and ventilation (Fig. 1-2 ). West described three theoretical zones of the lung from the apex to the base according to their relative distribution of ventilation and pulmonary blood fl ow. In Zone I, the least amount of blood fl ow occurs because alveolar pressure is greater than both pulmonary artery pressure and pulmonary venous pressure. In Zone II,

0

20

40

60

80

100

120

140

160

Atmosphere Alveolus Arterialblood

Tissue/capillary

Venousblood

pO2

(mm

Hg)

FIGURE 1-1

The oxygen cascade (Adapted from http://www.springerimages.com/Images/RSS/2-COPD0101-10-005 )

In normal lungs, because carbon dioxide diffuses so readily across the alveolar capillary membrane, the alveolar CO 2 (P A CO 2 ) is essentially equal to the arterial carbon dioxide (PaCO 2 ).

The diffusion capacity for the pulmonary vascular bed is optimal for achieving gas exchange because the membrane is exceedingly thin, and the surface area is vast due to the structure and arrangement of approximately 400 million alveoli.

http://www.springerimages.com/Images/RSS/2-COPD0101-10-005



3 C HAPTER 1 • FU N DAM ENTALS OF GAS EXC HANG E

pulmonary arterial pressure is greater than alveolar pressure and blood fl ow is determined by the difference between alveolar and arterial pressures independent of venous pressures. In Zone III, pulmonary arterial pressure exceeds pulmonary venous pressure which exceeds alveolar pressure. Consequently, fl ow is a function of both pulmonary arterial and venous pressures, and because pulmonary arterial pressure is higher, blood fl ow is down this gradient.

Carbon Dioxide Elimination Once oxygen reaches the bloodstream, it is delivered to the tissues where it is consumed in both the processes of cellular respiration as well as in a number of non-energy producing oxidative reactions. During cellular respiration, which occurs in the mitochondria, oxygen is consumed generating energy in the form of adenosine triphosphate (ATP), with CO 2 being produced as a by-product. Alveolar ventilation is necessary to ultimately eliminate the CO 2 that is produced. Carbon dioxide exists in equilibrium with carbonic acid, H 2 CO 3 , a weak acid. Thus, the accu-mulation of carbon dioxide produces acidosis. In general, blood holds more CO 2 than oxygen, in part, because CO 2 is carried in three forms. Five to 10% of CO 2 is dissolved in the blood-stream, 5–20% is bound in the form of carbamino compounds, and the remainder (the vast majority) exists in the form of H 2 CO 3 . Carbon dioxide freely and effi ciently diffuses from the tissues into the blood, and then across the capillary alveolar membrane into the alveolar gas so that it can be eliminated through exhalation.

When CO 2 is not effectively eliminated by the lungs, hypercapnea results. In the face of hypercapnea, CO 2 freely diffuses into the cell, decreasing the intracellular pH by combining with H 2 O to release H + as delineated in the following equation:

2 2 2 3 3CO H O H CO H HCO .+ −+ ↔ ↔ + The resulting acidemia initially triggers a sympathetic and adrenal response with endoge-nous catecholamine stimulation. Subsequently, the body has several compensatory mecha-nisms that are activated in order to surmount and counteract this acidosis.

1. Chemoreceptors in the brainstem and in the carotid body rapidly detect changes in the PaCO 2 . In a spontaneously breathing, non-sedated patient with normal neuromuscular

Pulmonaryarterypressure

Pulmonaryvenouspressure

Blood flow

DistanceArterial Venous

Alveolarv

Zone 3Pa> Pv> PA

Zone 2Pa> PA> Pv

Zone1PA> Pa> Pv

PaPA

Pv

FIGURE 1-2

West zones of pulmonary perfusion and ventilation (Figure 4-8 in West ( 2005 ) ). Pa arterial pressure, PA alveolar pressure, Pv venous pressure

In general, blood holds more CO 2 than O 2 , in part, because CO 2 is carried in three forms. Five to 10% of CO 2 is dissolved in the bloodstream, 5–20% is bound in the form of carbamino com-pounds, and the remainder (the vast majority) exists in the form of H 2 CO 3 .


function, there is generally an initial increase in the minute ventilation in an attempt to increase carbon dioxide elimination and normalize the pH.

2. Deoxygenated hemoglobin molecules bind hydrogen ions as well as carbon dioxide to form carbaminohemoglobin in order to buffer the pH and prevent substantial changes in pH.

3. The kidneys increase the excretion of ammonium ion (NH 4 + ) (thereby eliminating hydro-

gen ions) and chloride while retaining HCO 3 − and sodium (Na + ) after being exposed to

hypercapnia for at least 6 h. The result is an increase in the plasma HCO 3 − concentration

by approximately 3.5–4 mEq/L for every 10 mm Hg increase in the PaCO 2 . The HCO 3 −

then serves as a buffer for the existing free hydrogen ions.

Assessing Adequacy of Gas Exchange Under normal conditions, the partial pressure of oxygen in the alveolus (P A O 2 ) is only slightly higher than that in the arterial blood (PaO 2 ), refl ecting a nearly balanced equilibrium between the alveolar gas and the pulmonary capillary blood. A signifi cant gradient between the alve-olar and arterial blood (A-a gradient) suggests a degree of lung injury causing a limitation of gas exchange. The composition of the alveolar gas depends on:

1. the oxygen content of both inspired air and the mixed venous blood; 2. the quantity of air and blood reaching the alveoli; 3. the ratio of alveolar ventilation to perfusion; and 4. the extent to which equilibrium is reached between the alveolar gas and the pulmonary

capillary blood.

While the arterial pO 2 is measured and reported in a blood gas analysis, it is more diffi cult to accurately measure the alveolar pO 2 . The P A O 2 , may be calculated from the following equation:

A 2 2 2P O PiO PaCO / RQ= −

where PiO 2 is the partial pressure of inspired oxygen and RQ is the respiratory quotient. The PiO 2 is determined by the atmospheric barometric pressure and the percent of oxygen being inspired. At sea level, where oxygen accounts for 21% of air, and atmospheric pressure is approximately 760 mm Hg, the partial pressure of inspired O 2 = 760 × 0.21. However, that equation does not account for the effect of water vapor, which humidifi es inspired air, and thereby, reduces the baro-metric pressure by 47 mm Hg. Therefore, the PiO 2 can be defi ned by the following equation:

2 B H2O 2PiO (P P ) FiO= − × At sea level, the PiO 2 will be approximately equal to 150 mm Hg (i.e. (760 mm Hg − 47 mm Hg) × 0.21 = 150 mm Hg). At altitude, i.e on the top of Mount Everest, where the barometric pressure is 380 mm Hg, the PiO 2 will be signifi cantly lower (i.e. (380 mm Hg − 47 mm Hg) × 0.21 = 70 mm Hg)). In hyperbaric oxygen chambers, where the barometric pressure is much higher than atmospheric, the PiO 2 will also be higher.

The sum of the partial pressures of alveolar gases must total to equal ambient pressure. Therefore, an increase in one gas must result in a decrease in another. As gas moves down the airway into the alveolus, the partial pressure of oxygen is progressively reduced by the presence of carbon dioxide in the alveolar gas. The partial pressure of arterial carbon dioxide is utilized in the equation in place of alveolar carbon dioxide because carbon dioxide is so readily diffusible that arterial and alveolar carbon dioxide quickly equilibrate. However, to account for the fact that more oxygen is usually consumed than carbon dioxide is eliminated, this value is divided by the respiratory quotient. The respiratory quotient (RQ) is the ratio of the amount of CO 2 being produced and excreted to the amount of oxygen being consumed and utilized. It also refl ects the oxidation of dietary carbohydrates relative to dietary fats.

Under ideal conditions, the partial pressure of oxygen in the alveolus (P A O 2 ) and in the arterial blood (PaO 2 ) should be nearly equal and no gradient should exist refl ecting a balanced equilibrium between the alveolar gas and the pulmonary capillary blood. A signifi cant gradient between the alveolar and arterial blood (A-a gradient) suggests a degree of lung injury causing a limitation of gas exchange.

The P A O 2 , may be calculated from the following equation:

A 2 2 2P O PiO PaCO / RQ= −

The PiO 2 can be defi ned by the following equation:

2 B H2O 2PiO (P P ) FiO= − ×


Under normal circumstances, the RQ approximates 0.8, but it can range between 0.67 and 1.3, depending on the clinical scenario. Consequently, assuming a PaCO 2 of 40 mm Hg, a normal diet, and sea level barometric pressure, the P A O 2 is approximately 100 mm Hg.

( )[ ][ ]

A 2 2 2

A 2

P O PiO PaCO / RQ P O 760 mm Hg – 47 mm Hg x 0.21 – 40 mm Hg / 0.8

~1 50 mm H g – 5 0 mm Hg ~ 10 0 mm Hg

–==

=

The P A O 2 is higher than the partial pressure of pulmonary artery and capillary blood, leading to the diffusion of oxygen from the alveoli into the bloodstream.

In the Bloodstream In the bloodstream, oxygen molecules combine with hemoglobin to form oxyhemoglobin, the primary form in which oxygen is delivered to the tissues. The affi nity that hemoglobin has for oxygen determines the degree of binding and the availability of oxygen for the tissues.

Several factors have been identifi ed that infl uence the degree of binding of oxygen to hemoglobin. The oxygen hemoglobin dissociation curve graphically depicts the relationship between the partial pressure of oxygen and the saturation of hemoglobin (Fig. 1-3 ). This graph depicts the affi nity of hemoglobin for oxygen, and therefore, can depict the relative avidity of oxygen at the tissue level. The P 50 is often used as a measure of this affi nity. The P 50 is defi ned as the PaO 2 at which hemoglobin is 50% saturated with oxygen. For normal adult hemoglobin (Hb A), the P 50 is 27 mm Hg.

100

80

60

40

20

20 40

DPG

T

pH 7.6

pH 7.2

H+

60 80 100

Oxy

hem

oglo

bin

satu

ratio

n (%

)

Po2 (mm Hg)

P50

PC02

DPG

T

H+

PC02

FIGURE 1-3

The oxygen hemoglobin dissociation curve; DPG signifi es 2,3-diphosphoglycerate, T signifi es temperature

RIGHTWARD SHIFTS OF THE DISSOCIATION CURVE (DECREASED OXYGEN AFFINITY, HIGHER P 50 )

LEFTWARD SHIFTS OF THE DISSOCIATION CURVE (INCREASED OXYGEN AFFINITY, LOWER P 50 )

Increased hydrogen ion (H + ) concentration Decreased hydrogen ion (H + ) concentration Increased RBC 2,3-diphosphoglycerate Decreased RBC 2,3-diphosphoglycerate Increased temperature Decreased temperature Increased partial pressure of carbon dioxide Decreased partial pressure of carbon dioxide Decreased pH Increased pH

Hemoglobin F (as compared to Hemoglobin A)

TABLE 1-1

CLINICAL FACTORS THAT INFLUENCE SHIFTS IN THE OXYGEN HEMOGLOBIN DISSOCIATION CURVE


Various clinical conditions alter the affi nity of hemoglobin for oxygen (Table 1-1 ). Conditions which cause a decrease in the affi nity of hemoglobin for oxygen result in a higher P 50 (a higher PaO 2 at which hemoglobin is 50% saturated with oxygen). These conditions cause a rightward shift of the oxygen hemoglobin dissociation curve; examples include aci-dosis and hyperthermia. Conversely, conditions that produce a leftward shift of the curve as the result of an increase in the affi nity of hemoglobin for oxygen, have a lower P 50 (a lower PaO 2 at which hemoglobin is 50% saturated with oxygen). Hemoglobin F, the predominant form of hemoglobin in fetuses and neonates, has a lower P 50 than hemoglobin A, and there-fore, the curve for hemoglobin F exists to the left of that of hemoglobin A.

The Bohr effect is a property of hemoglobin whereby its affi nity for oxygen changes depending on the concentration of H + and/or carbon dioxide. Increasing concentrations of H + and/or carbon dioxide will reduce the affi nity of hemoglobin for oxygen. The Bohr effect provides part of the rationale for the transfer of oxygen from the alveolus to the bloodstream, and subsequently, from the bloodstream to the tissues. In the lungs, the PCO 2 is low and the pH is high. Under these conditions, the affi nity of hemoglobin for oxygen is high enhancing the uptake of oxygen from the alveoli into the bloodstream and on to the hemoglobin mole-cule in the red blood cell. By contrast, in the tissues, the high tissue PCO 2 and low pH favor the release of oxygen (Fig. 1-4 ). Similarly, the Haldane effect describes a property of hemo-globin whereby deoxygenated blood has an increased ability to carry carbon dioxide, and oxygenated blood has a decreased affi nity for hydrogen ions and carbon dioxide. Therefore, in the lungs where oxygen is abundant, carbon dioxide is unloaded from the hemoglobin and made available to the alveolus for exhalation.

To the Tissues From the pulmonary capillary blood, oxygen returns to the heart via the pulmonary veins. From there, oxygen travels in the systemic arterial blood, into the systemic capillaries, and ultimately, into the mitochondria of the tissues. At each level of the oxygen cascade, the PO 2 progressively decreases until it reaches its clinically measurable nadir in the mixed venous blood returning to the heart. The PO 2 of mixed venous blood is determined by several fac-tors, including the amount of oxygen delivered to the tissues (the oxygen supply), the amount of oxygen required by the tissues (the oxygen demand), and the capacity of the tissues to extract oxygen. If there is any impedimant to oxygen, organs will become deprived of oxy-gen. The oxygen consumption is defi ned by the following equations:

2 2 2 2VO DO O extraction A VDO CO 10 dL / L= × = − × ×

H+ H+

OH−OH−

Red Blood Cell

Bohr Effect Haldane Effect

AlveoliTissues

O2

CO2CO2 CO2 CO2

O2

HCO3− HCO3

−

O2 O2HHb

HbO2

FIGURE 1-4

The Bohr effect and the Haldane effect on oxygen transfer

The Bohr effect is a property of hemoglobin whereby its affi nity for oxygen changes depending on the concentration of H + and/or carbon dioxide. Increasing the concentration of H + and/or carbon dioxide will reduce the affi nity of hemoglobin for oxygen. The Bohr effect provides the rationale for the transfer of oxygen from the alveolus to the bloodstream, and subsequently, from the bloodstream to the tissues.

The Haldane effect describes a property of hemoglobin whereby deoxygenated blood has an increased ability to carry carbon dioxide, and oxygenated blood has a decreased affi nity for hydrogen ions and carbon dioxide. Therefore, in the lungs where oxygen is abundant, carbon dioxide is unloaded from the hemoglobin and made available to the alveolus for exhalation.


where VO 2 is the oxygen consumption, DO 2 is the oxygen delivery (defi ned as the cardiac output times the arterial oxygen content [in mL O 2 /dL] × 10 dL/L), O 2 extraction is the frac-tional difference between arterial and venous O 2 content (1−CvO 2 /CaO 2 ), the A-VDO 2 is the arterio-venous difference in oxygen content (CaO 2 − CvO 2 ) and CO is the cardiac output.

MECHANISMS OF HYPOXEMIA

Hypoxemia is a decrease in the oxygen content in the arterial blood refl ecting a limitation of pulmonary gas exchange. The arterial oxygen content (CaO 2 ) is defi ned by the following equation:

2 2 2CaO 1.39 Hb SaO 0.003 PaO= × × + ×

where 1.39 represents the amount of oxygen in milliliters (mL) that a fully saturated gram of hemoglobin may carry (some sources use 1.36 mL per gram of hemoglobin rather than 1.39), Hb represents the hemoglobin concentration in grams per deciliter, SaO 2 represents the arte-rial oxygen saturation of hemoglobin, and 0.003 represents solubility coeffi cient of oxygen in milliliters of oxygen in a deciliter of blood for each mm Hg partial pressure. The units for the arterial content of oxygen are milliliters of oxygen per deciliter of blood as mathemati-cally illustrated below:

1.39 mL O 0.003 mL O mL Og Hb2 2

2CaO (mL O / dL) SaO PaO mm Hg2 2 2 2g Hb dL PaO mm Hg / dL dL2

= × × + × =

Hypoxemia may therefore be the result of anemia and/or abnormalities of oxygenation. There are four major abnormalities of pulmonary gas exchange that may contribute to arte-rial hypoxemia: hypoventilation, ventilation perfusion mismatch, shunted blood fl ow, and diffusion limitation.

Hypoventilation Hypoventilation is an inadequate minute ventilation to maintain a normal PaCO 2 resulting in respiratory acidosis. Hypoventilation is not an oxygenation diffusion abnormality, and there-fore, the A-a gradient usually does not increase. Rather, P A O 2 falls in accordance with the alveolar gas equation in response to increased P A CO 2 . The two main causes of hypoventila-tion are (1) abnormal respiratory mechanics causing increased airway resistance and/or decreased pulmonary compliance and (2) ventilatory control abnormalities such as ineffec-tive muscles of respiration as in the case of neuromuscular disorders, or damaged neural sensing and signaling as occurs in brain injury or deep sedation.

Ventilation Perfusion Mismatch The most common cause of hypoxemia is ventilation perfusion mismatch. Gas exchange in the lung is best achieved when ventilation and perfusion are well matched. The degree to which ventilation matches perfusion determines how adequately gas exchange occurs. When alveolar ventilation matches pulmonary blood fl ow, carbon dioxide is appropriately elimi-nated and the blood becomes fully saturated with oxygen. The ventilation perfusion ratio can be determined using the following equation:

2 2 A 2V / Q [8.63 R(CaO CmvO )] / P CO= × −

Hypoxemia is a decrease in the oxygen content in the arterial blood refl ecting a limitation of pulmonary gas exchange. There are four major causes of arterial hypoxemia: hypoventilation, ventilation perfusion mismatch, shunted blood fl ow, and diffusion limitation.


where V/Q represents the ratio of ventilation to pulmonary perfusion, 8.63 is a constant that reconciles the units and conventional conditions of expression, R is the respiratory exchange ratio, CaO 2 is the arterial content of oxygen, CmvO 2 is the mixed venous content of oxygen, and P A CO 2 is the alveolar partial pressure of carbon dioxide.

When the V/Q ratio exceeds one, ventilation is wasted because it does not participate in gas exchange. This is referred to as dead space ventilation. The most extreme example is the patient in cardiac arrest who is being ventilated, but is no longer perfusing the lung. Anatomical dead space consists of the conducting airways (nasopharynx, trachea, subseg-mental bronchi, terminal bronchioles) within which approximately 25% of each tidal volume is lost. Alveolar dead space consists of the alveoli not participating in gas exchange due to inadequate perfusion. The PCO 2 in these alveoli is relatively low since CO 2 is not added from the circulation. Physiological dead space is defi ned as the combination of both anatomical and alveolar dead space. The causes of increased dead space ventilation include: tachypnea (anatomic dead space is fi xed, thus rapid shallow breathing increases relative dead space), obstructive lung disease, pulmonary emboli, and increases in the ventilator tubing length beyond the separation (“Y”) of the inspiratory and expiratory limbs in intubated patients.

The Bohr equation may be used to calculate the amount of physiological dead space:

2 2

2

[PaCO EtCO ]Vd / Vt

PaCO

−=

where Vd is the volume of dead space ventilation, Vt is the total ventilation volume, PaCO 2 is the arterial partial pressure of carbon dioxide, and EtCO 2 is the end tidal carbon dioxide.

As the V/Q ratio decreases below one, the PaO 2 decreases and the PaCO 2 increases. When ventilation ceases, the V/Q ratio reaches zero and mixed venous blood enters the arterial circulation unchanged. When the V/Q ratio is less than one throughout the lung, hypoxemia is responsive to supplemental O 2 . To compensate, a normal response would be to increase the minute ventilation producing either a low or normal PaCO 2 .

Shunting of Pulmonary Blood A shunt is another cause of arterial hypoxemia. It can be thought of as the most extreme form of ventilation perfusion mismatch where V/Q approaches zero. Shunts may occur at either the cardiac level with right to left intracardiac shunts or at the pulmonary level. The shunt fraction equation is:

s T 2 2 2 2Q / Q (CcO CaO ) / (CcO CvO )= − −

where Q s is the shunt blood fl ow, Q T is the total blood fl ow, and the Cc, Ca and Cv are the O 2 contents of the idealized alveolar capillary, measured arterial and measured mixed venous blood respectively. Under normal conditions, the percentage of intrapulmonary shunt is less than 10%. When the intrapulmonary shunt exceeds 30%, hypoxemia does not improve with supplemental oxygen because the shunted blood does not come in contact with enough of the high alveolar oxygen content. The PaO 2 levels fall proportionately to the degree of shunted blood fl ow.

Diffusion Limitation A fi nal cause of arterial hypoxemia is diffusion limitation. Diffusion limitation occurs when there is disequilibrium between the partial pressure of a gas in the alveoli and the pulmonary capillaries causing an increase in the A-a gradient. Hypoxemia can occur due to a diffusion limitation because of a decreased driving force to push oxygen across the alveolar capillary membrane. Hypoxemia usually results when the diffusion capacity of the lung decreases to less than 50%. Increasing the FiO 2 may be enough to improve the driving pressure and enhance the transfer of oxygen from the alveoli into the blood. Most causes of decreased oxygen diffusion are related to parenchymal lung diseases, which result in thickening of the

The Bohr equation may be used to calculate the amount of physiological dead space: Vd/Vt = [PaCO 2 − EtCO 2 ]/PaCO 2 where Vd is the volume of dead space ventilation, Vt is the total ventilation volume, PaCO 2 is the arterial partial pressure of carbon dioxide, and EtCO 2 is the end tidal carbon dioxide.


alveolar capillary membrane. However, diffusion limitation as a cause of arterial hypoxemia has been considered to be a rare event. It has been estimated that blood passing through the lungs remains in a pulmonary capillary for only 0.75 s. Despite this brief time period and a progressively decreasing alveolar capillary oxygen gradient (as the capillary blood becomes progressively more oxygenated), it has been estimated that pulmonary capillary blood approximates alveolar oxygen in only a third of this available time. This allows ample time for increased diffusion in clinical states of impaired perfusion.

MONITORING OF GAS EXCHANGE

Arterial Blood Gas Determination An arterial blood gas (ABG) provides valuable data to help determine the acid-base status of a patient, the cause of any imbalance, as well as the degree of lung injury. Taken together, it is quite useful in assessing the adequacy of oxygenation and ventilation. The following param-eters are provided in any ABG: pH, PaCO 2 , PaO 2 , HCO 3 , and the base excess or defi cit.

The pH describes whether acidemia or alkalemia are present. If the pH of the arterial blood is <7.35, then the patient is acidemic. If the pH of the arterial blood is >7.45, then the patient is alkalemic. The PaCO 2 is measured and may be used to determine the respiratory compo-nent of the pH. As a general rule, for every 10 mm Hg acute change in the PaCO 2 , there is an inverse change of 0.08 pH units. Thus, accepting a PaCO 2 of 40 mm Hg and a pH of 7.40 as “normal” baselines, a patient with a PaCO 2 of 50 mm Hg, should have a pH of 7.32 if all the acid base alteration is exclusively respiratory in origin. The PaCO 2 may also be used to deter-mine the extent of dead space ventilation by the Bohr equation (as previously described):

2 2

2

[PaCO EtCO ]Vd / Vt

P .aCO

−=

In addition to assessing the respiratory component, the arterial blood gas can be used to

assess the metabolic component of the acid base alteration. Most blood gases provide a mea-surement of the bicarbonate concentration (either by direct measurement or determined from the measured pH and PaCO 2 ) and a calculated base excess or defi cit. Because the carbon dioxide bicarbonate system only accounts for 75% of the buffering effect in the blood (the remainder being due to hemoglobin, phosphate and plasma proteins), the base excess (defi cit) is a calculation used to compare the buffering capacity of the patient to normal. It is deter-mined using the Siggaard-Anderson nomogram which relates pH, pCO 2 , and HCO 3 while factoring in the contributions of the other blood buffers. There are equations to approximate the base excess (defi cit) and its impact on pH that the pediatric critical care provider should understand. Specifi cally, the base excess can be approximated by the following equation:

Base Excess ( 1.2) (24 measured bicarbonate concentration).= − × − Moreover, for every change of 10 mEq/L in the base excess, there should be a 0.15 unit change in the pH. This equation can be used in the interpretation of a blood gas to assess the metabolic component of an acid base alteration. For example, a patient with a pH of 7.27, and a PCO 2 of 60 mm Hg should have a pH of 7.24 based solely on the respiratory compo-nent (carbon dioxide) of the overall pH. This is based on the principle described above that every 10 mm Hg acute change from 40 mm Hg in the carbon dioxide, should result in an inverse change of 0.08 in the pH. A PaCO 2 of 60 mm Hg is 20 mm Hg greater than 40 mm Hg, and consequently, the pH should be 0.016 less than 7.40, or 7.24. However, the pH in the example is 7.27. Remembering that for every change of 10 mEq/L in the base excess, there should be a 0.15 unit change in the pH, it can be stated that for every 0.01 change in pH from expected, there will be a corresponding 2/3 change in the base excess. In the example described above, the pH is 0.03 pH units higher than the expected pH based on the respira-tory component alone. Since there is a 2/3 change in the base excess for every 0.01 change

As a general rule, for every 10 mm Hg acute change in the PaCO 2 , there is an inverse change of 0.08 pH units.

For every change of 10 mEq/L in the base excess, there should be a 0.15 unit change in the pH.


in the pH, the base excess in this patient would be 3 × 2/3 = +2. This would suggest that the patient has some metabolic compensation for his respiratory acidosis.

The PaO 2 is also measured in the arterial blood gas and provides useful data refl ecting the degree of hypoxia. The PaO 2 is utilized in a number of equations assessing the degree of lung injury. For example, the PaO 2 is utilized in the A-a gradient equation:

A 2 2

2 2 2

Bar H2O 2 2 2(

A - a gradient P O PaO

[PiO PaCO / RQ] PaO

[( P - P ) FiO ) PaCO / RQ] PaO

= − = − − = × − −

In addition, the PaO 2 is also used in determining the oxygen index (OI):

2

2

(Mean airway pressure FiO ) 100

PaO

× ×

The OI has been used in a number of studies as a means to quantify and compare the

degree of lung injury. It can be thought of as the magnitude of potentially injurious therapeu-tic interventions to the alveoli (pressure and fraction of inspired oxygen) over the outcome (the partial pressure of arterial oxygen achieved from delivering such interventions). The higher the OI number, the more severe the lung injury. The PaO 2 can also be used to deter-mine the ratio of the partial pressure of oxygen and the fraction of inspired oxygen (P/F ratio). This P/F ratio has also been used extensively in both clinical and research work. In fact, the P/F ratio has been incorporated into the defi nition and distinction between acute lung injury and acute respiratory distress syndrome (ARDS). In addition to satisfying the other criteria, acute lung injury is defi ned as any P/F ratio <300 mm Hg while ARDS is defi ned as a P/F ratio <200. In contrast to the OI, the P/F ratio does not require a mean airway pressure, and therefore, can be utilized to assess the degree of lung injury in non-intubated patients. Although useful for that reason in the non-intubated patient, it may provide mis-leading assessments in patients receiving positive pressure ventilation. Since the P/F ratio often improves with increasing mean airway pressure, using it alone as an index of severity of lung disease will be misleading. An improved P/F ratio in response to the application of higher mean airway pressure does not mean that the patient has less lung injury. Using the oxygenation index, the increase in mean airway pressure contributes numerically to the OI balancing the improvement in PaO 2 which would itself decrease the calculated OI. The OI accounts for the effect of mean airway pressure on oxygenation.

Pulse Oximetry The use of pulse oximetry has become universally accepted for providing instantaneous information regarding the oxygen saturation of arterial blood. This technology is based on the light absorption characteristics of different forms of hemoglobin and utilizes two prin-ciples. First, the attenuation of light passing through tissues changes with the pulsation of arterial blood, and second, the degree of attenuation is based on the composition of the arte-rial blood. Present day pulse oximeters utilize two wavelengths of light, visible red (660 nm) and near-infrared (900–940 nm) to discriminate between oxyhemoglobin and deoxyhemo-globin. Oxygenated hemoglobin refl ects red light much better than other hemoglobin species resulting in the much “redder” appearance of oxygenated blood. As arterial blood is pumped through a tissue bed, the absorption of light changes in a pulsatile manner. Because the light absorption of the tissues, the venous blood, and the capillary blood is not changing, the degree of light absorption from these components can be subtracted from the total light absorption thereby leaving the amount of light absorption related to the arterial blood alone. Because the absorption of light in the near-infrared range is relatively constant over a wide range of oxygen saturations, changes in the absorption at the 660 nm wavelength of the

The oxygen index (OI) is a marker of lung injury and is determined by the equation [(Mean airway pressure * FiO 2 )*100] / PaO 2 .


arterial blood refl ect oxygenation and can be referenced to the near-infrared absorption. In this way, the arterial blood oxygen saturation may be determined using predetermined algo-rithms. Interestingly, the ratio of the oxygen saturation ascertained from pulse oximetery to the fraction of inspired oxygen (the S/F ratio) is now beginning to be used as a marker of lung injury for clinical and research purposes. Although there are limitations to this applica-tion, the S/F ratio is useful for those children with acute hypoxic lung injury who are not having routine arterial blood gas measurements performed.

Pulse oximetry has been found to be very accurate for oxygen saturations greater than 70% with confi dence limits of 2–4%. However, for saturations below 70%, the accuracy is substantially less. Moreover, there are clearly limitations to the use of pulse oximetry. Motion artifact is probably the most common example of erroneous data being generated by pulse oximetry. This is easily recognized and often results in frequent triggering of the oximeter alarms. Pulse oximeters have been developed that attempt to minimize the effect of motion artifact. In addition, environmental light may interfere with pulse oximetry accuracy. Although this has not been found to be applicable to all oximeters, shielding the pulse oxi-meter probe from external light may result in improved performance. Other limitations of pulse oximetry include any factor that might interfere with the ability to detect and monitor a pulse such as hypoperfusion, vasoconstriction and hypothermia. In these circumstances, the pulse oximeter will often not pick up at all, or display an inaccurate reading.

In addition to the potential for error described above, clinical situations in which hemo-globin binds to substances other than oxygen may also result in erroneous pulse oximetry values. For example, in the setting of carbon monoxide poisoning, hemoglobin binds with great affi nity to carbon monoxide to form carboxyhemoglobin. As can be seen in Fig. 1-5 , carboxyhemoglobin has a very similar light absorption as oxyhemoglobin at 660 nm. Consequently, the pulse oximeter will inappropriately interpret carboxyhemoglobin to be oxyhemoglobin, and thereby, overestimate the true oxygen saturation of the hemoglobin. The same may occur in the setting of signifi cant hemolysis where signifi cant amounts of carbon monoxide are formed and bind to hemoglobin to form carboxyhemoglobin. In the setting of carboxyhemoglobinemia, blood gas analysis with co-oximetric detection of the other forms of hemoglobin is necessary to truly ascertain the oxygen saturation of the blood.

The situation is different in the setting of methemoglobinemia. Initially, as methemoglo-bin levels increase, the pulse oximetry saturation will decrease to 80–85%. However, because methemoglobin adsorbs light equally well at 660 and 940 nm, the absorbance of light in pulsatile blood and baseline non-pulsatile reference tissue will increase at an equal pace. The ratio between the two points of light absorbance will be one resulting in a displayed

10

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.01

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hemoglobinCarboxyhemoglobin

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nt E

720 760 800 840 880 920 960 1000 FIGURE 1-5

Light absorbance characteristics of various forms of hemoglobin (Cordova and Marchetti 2002 )

The pulse oximeter inappropri-ately interprets carboxyhemoglo-bin to be oxyhemoglobin, and therefore, overestimates the true oxygen saturation of hemoglobin in the setting of carbon monoxide poisoning.


oxygen saturation of approximately 85%. Consequently, even with further increases in the methemoglobin, the pulse oximeter saturation reading will remain approximately 85%. As with carboxyhemoglobinemia, blood gas analysis with co-oximetry is necessary in the set-ting of methemoglobinemia to accurately determine the percentage of oxyhemoglobin.

Finally, pulse oximetry may not be completely accurate in the setting of high concentra-tions of sickle hemoglobin (hemoglobin S). In addition to the abnormal shape of sickled red blood cells that potentially alter the normal absorption of light, a rightward shift of the oxy-gen hemoglobin dissociation curve may result in lower pulse oximeter readings for any given partial pressure of arterial oxygen. In addition, signifi cant hemolysis associated with sickle cell disease may result in carboxyhemoglobinemia and erroneous pulse oximeter val-ues as described above.

Capnometry Capnometry is the measurement of carbon dioxide in expired gas. Capnometers measure carbon dioxide using one of two techniques, each with its own advantages and disadvan-tages. The more common form of capnometry in intubated patients is referred to as main-stream. The mainstream capnometer is placed in-line with the endotracheal tube circuit. It utilizes a light-emitting detector that is positioned on either side of an airway adaptor attached to the top of the endotracheal tube. It uses infrared light absorbance to detect carbon dioxide. Because of its in-line positioning, it allows for rapid breath-to-breath analysis of carbon dioxide. Although it does not depend on the aspiration of gas, it is susceptible to interference by secretions or humidity. Moreover, because of the need of an added adaptor, it may add to the dead space ventilation. This is usually not problematic except in the smallest of infants. Finally, the sensor used by most mainstream capnometers is large and heavy relative to the endotracheal tube, and therefore, may place undue tension on the tube.

Sidestream sampling is the other form of capnometry. It is less commonly used in intu-bated patients, but is increasingly being utilized in non-intubated circumstances. The side-stream technique continuously aspirates a small amount of gas as the patient ventilates either spontaneously or through a mechanical ventilator. The advantage of this method is that the apparatus adds no additional dead space or weight to an endotracheal tube. The disadvan-tage, particularly in smaller patients, is that it may decrease minute ventilation due to the aspiration of gas. Also, because of the method of sampling, mucous and water may be inad-vertently aspirated into the monitoring device obstructing optimal gas fl ow. Finally, because the gas has to be pulled out of the endotracheal tube/ventilator circuitry, there is a delay in the response time to changes in carbon dioxide. It should be noted, however, that some gas aspirating systems utilize an adapter positioned between the ventilator circuit and the endo-tracheal tube, adding to system dead space similar to mainstream capnometers.

Capnometry has become an important component of pediatric critical care monitoring. First, and perhaps foremost, it has become a standard of care to confi rm correct placement of an endotracheal tube after intubation. This may be accomplished in one of two ways. The fi rst, and perhaps the simplest, involves attaching the endotracheal tube to a colorimetric capnom-eter that will change colors when exposed to carbon dioxide usually from purple to yellow. The colorimetric capnometers contain a disc that when exposed to carbon dioxide produces hydrogen ions. The increase in hydrogen ions, and the resultant change in pH, results in the color change of the disc. If no carbon dioxide is detected, the colorimetric capnometer will remain purple. If carbon dioxide is detected, the disc will change color from purple to yellow. This method may only be used for short term confi rmation of exhaled carbon dioxide. The second method involves graphically displaying the detected level of carbon dioxide. The sec-ond method, capnography, may be used to quantify the amount of carbon dioxide detected and may refl ect the level of carbon dioxide at any given point in the respiratory cycle.

There are situations in which capnometry/capnography may provide misleading informa-tion regarding the appropriate positioning of an endotracheal tube. For example, the ingestion of carbonated beverages prior to intubation may result in the detection of carbon dioxide with esophageal placement of the tube. In addition, vigorous bag-valve mask ventilation prior to intubation may result in an air-fi lled stomach allowing for the detection of carbon dioxide

Capnometry has become a standard of care to confi rm appropriate endotracheal intubation.

Capnography may be used to estimate the percentage of dead space ventilation.


with an esophageal intubation. Furthermore, tube placement above the vocal cords in the hypopharynx may allow for suffi cient ventilation such that carbon dioxide may be detected despite the tube not being positioned in the trachea. In contrast, in the setting of cardiac arrest or extreme hypoperfusion, carbon dioxide may not be delivered to the lungs, and thus, there is little to no carbon dioxide in the exhaled breaths. Consequently, the capnometer/capno-graph will not detect carbon dioxide although the endotracheal tube is properly positioned in the trachea. Large air leaks around the endotracheal tube or obstructed tubes may also result in diminished amounts of carbon dioxide being detected despite appropriate positioning of the endotracheal tube. It is recommended that capnometry/capnography be assessed over at least the fi rst six breaths of ventilation to minimize the risk of misinterpretation.

In addition to confi rming endotracheal intubtion, capnometry may be used to non-inva-sively monitor arterial carbon dioxide content. Physiologically, carbon dioxide readily dif-fuses across the alveolar capillary membrane such that the concentrations of arterial and alveolar carbon dioxide quickly equilibrate. Consequently, the partial pressure of carbon dioxide in the alveolus closely approximates the partial pressure of carbon dioxide in the arterial blood. Once in the alveolus, the gas moves into a terminal bronchiole, a subsegmen-tal bronchus, a main bronchus, the trachea, the endotracheal tube, and out of the body. During that entire transit, very little additional gas exchange occurs. Consequently, under ideal cir-cumstances, by measuring the peak concentration of carbon dioxide (end tidal) as it exits the endotracheal tube or nasopharynx, it is possible to estimate the concentration of carbon dioxide in the alveolus, and therefore, the partial pressure of carbon dioxide in the arterial blood. This is the foundation upon which the development of capnometry was developed. In the patient without cardiopulmonary disease, the system works well and exhaled end tidal carbon dioxide approximates PaCO 2 . In fact, the end tidal carbon dioxide is usually 2–5 mm Hg lower than the PaCO 2 because of anatomic dead space ventilation and the expected, mild ventilation perfusion mismatch in the upper lung fi elds (West Zone I). In those upper lung fi elds, ventilation is slightly greater than perfusion because of the gravitational forces favor-ing blood fl ow to the lower, more dependent lung fi elds.

However, as might be anticipated, there are many clinical situations common to the pedi-atric intensive care unit where the premise of balanced ventilation and perfusion is invalid, and thus, capnometry provides erroneous estimates of arterial carbon dioxide. As the end tidal carbon dioxide (EtCO 2 ) represents the average partial pressure of ventilated alveoli and the PaCO 2 represents the same for perfused alveoli, any alteration in ventilation perfusion matching will result in an inaccurate EtCO 2 estimate of the PaCO 2 . For example, in any set-ting of an increased ventilation to perfusion ratio (e.g. increased dead space secondary to decreased cardiac output, pulmonary embolus, etc.), the EtCO 2 will underestimate the PaCO 2 (Fig. 1-6 ). For example, if the PaCO 2 is 40 mm Hg, and only half of the alveoli are being effectively perfused, the carbon dioxide coming out of the perfused alveoli will be 40 mm Hg. In contrast, if the other 50% of alveoli are not being perfused at all, the carbon dioxide coming out of these alveoli would be zero. When the gas from the two sets of alveoli meet and mix in the trachea, the resulting concentration of carbon dioxide detected at the capnom-eter would be 20 mm Hg (as opposed to the true arterial value of 40 mm Hg). In light of this, end tidal carbon dioxide monitoring is being utilized as a method to help assess adequacy of pulmonary blood during cardiopulmonary resuscitation. Similarly, in the setting of a decreased ventilation perfusion ratio, where alveoli are being perfused, but not ventilated, the carbon dioxide in these non-ventilated alveoli will never be detected by the capnometer. Therefore, the EtCO 2 detected by capnometry will refl ect only those alveoli that are actively participating in ventilation.

In addition to the absolute numbers provided by the capnogram, the waveform may also be used to detect problems within the cardiopulmonary system. A normal capnogram consists of four stages (Fig. 1-7 ). First, there is an inspiratory baseline (I) where atmospheric air at the sensor has little to no carbon dioxide thereby providing a baseline value of zero. Once exhala-tion begins, and the air from the anatomic dead space is cleared (no or minimal carbon diox-ide present), the second stage is characterized by a rapid rise (steep) in the measured carbon dioxide as alveolar air rich with carbon dioxide rushes past the sensor (II). During exhalation, the concentration of carbon dioxide quickly stabilizes and the level of carbon dioxide roughly fl attens. The highest recorded value of carbon dioxide at the end of exhalation is recorded as


Normal

Deadspace Shunt

Arterialblood

V/Q = 1

V/Q = 0V/Q = ∝

Mixedvenousblood

PETCO2 = 40

PETCO2 = 21 PETCO2 = 36 PinCO2 = 0PinCO2 = 0

PinCO2 = 0

Alveolus 1 PACO2 = 40

PACO2 = 0 PACO2 = 42

PaCO2 = 42

Alveolus 2PACO2 = 40

PACO2 = 36

PACO2 = 44

PaCO2 = 40

PaCO2 = 40

Pv CO2 = 44 Pv CO2 = 44

Pv CO2 = 44

FIGURE 1-6

The relationship between end tidal carbon dioxide and arterial carbon dioxide at different ratios of ventilation and perfusion (Cordova and Marchetti ( 2002 ) )

the end tidal carbon dioxide. During the fi nal stage of the respiratory cycle, inspiration occurs. With the fresh rush of carbon dioxide free air across the sensor, the carbon dioxide level quickly plummets to zero (IV). The capnogram waveform may be used to detect conditions associated with increased airway resistance. For example, waveforms associated with a wider angle between the upslope and the plateau stages of exhalation suggest slower carbon dioxide removal and increased airway resistance. The same is true for an uprising stage III plateau.

Capnography is also being used for the monitoring of the non-intubated patient particu-larly in the setting of procedural sedation. Because the medications required for such seda-tion may be associated with respiratory compromise, close monitoring of the respiratory system is of paramount importance. Traditionally, oxygenation has been monitored with pulse oximetry and ventilation has been assessed with clinical observation alone. Sidestream capnography, by means of a nasal oral cannula which simultaneously monitors exhaled car-bon dioxide and delivers low fl ow oxygen, allows for a more precise and detailed assess-ment. Monitoring of the capnogram allows for the continuous monitoring of airway obstruction, apnea, and hypercarbia (Fig. 1-8 ). It also allows for a more exact measurement of the respiratory rate than traditional thoracic impedance devices. Capnography has also been used in non-intubated patients to monitor the respiratory status in the setting of sei-zures, altered mental status, and overdoses.


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FIGURE 1-7

A normal capnogram consists of four stages. First, there is an inspiratory baseline ( I ) where atmospheric air at the sensor has little to no carbon dioxide thereby providing a baseline value of zero. Once exhalation begins, and the air from the anatomic dead space is cleared (no or minimal carbon dioxide present), the second stage is character-ized by a rapid rise (steep) in the measured carbon dioxide as alveolar air rich with carbon dioxide rushes past the sensor ( II ). During exhalation, the concentration of carbon dioxide quickly stabilizes and the level of carbon dioxide roughly fl attens. The highest recorded value of carbon dioxide at the end of exhalation is recorded as the end tidal carbon dioxide. During the fi nal stage of the respiratory cycle, inspiration occurs and with the fresh rush of carbon dioxide free air across the sensor, the carbon dioxide level quickly plummets to zero ( IV ) (Cordova and Marchetti ( 2002 ) . Original reference Airway Management. Philadelphia: Lippincott-Raven, 1996)

a

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FIGURE 1-8

Capnograms during procedural sedation in non-intubated patients. ( a ) Normal waveform. ( b ) Patient with bradypneic hypoventilation, with normal tidal volume but slowed respira-tory rate. ( c ) Hypopneic hypoven-tilation with decreased tidal volume resulting in increased dead space ventilation. ( d ) Loss of a waveform consistent with either complete laryngospasm or apnea (From Krauss and Hess ( 2007 ) )


Finally, capnography is also being recommended in the setting of pediatric cardiopulmo-nary arrest to assess the adequacy of perfusion to the lungs. Although a specifi c value has not been uniformly defi ned, providing cardiopulmonary resuscitation to maintain the end tidal carbon dioxide level above a specifi ed value for each patient will help assure adequacy of pulmonary blood fl ow with compressions and minimize the chance of potentially deleterious hyperventilation.

Transcutaneous Oxygen and CO 2 Monitoring The monitoring and trending of oxygen and carbon dioxide can also be accomplished using transcutaneous technology. This technology has been used since the late 1970s and early 1980s and has largely been replaced by newer, more reliable technology (described above) which has overcome some of the limitations of transcutaneous monitoring. The use of the transcutaneous technology requires warming of the skin to promote hyperperfusion allowing the monitors to electrochemically detect O 2 and CO 2 levels. In this way, frequent blood draws are avoided and a mode of continuous monitoring is achieved. The limitations, however, pre-vent practical regular and reliable use. The electrodes frequently need to be recalibrated; the measurement is inaccurate when the skin is not optimally perfused, as in the case of edema, acidosis, shock or hypothermia. Furthermore, in order to achieve hyperperfusion, the skin is warmed and burns have been reported. Finally, the response time is much slower than the other non-invasive techniques described above. The clinical scenario in which transcutaneous CO 2 monitoring may be of particular benefi t is in the child on high frequency oscillatory ven-tilation in which end tidal CO 2 monitoring is not possible. Transcutaneous O 2 monitoring has been utilized to monitor the adequacy of tissue perfusion following vascular surgery.

SUMMARY

The effective transfer of oxygen from the atmosphere into the body and ultimately to the various tissues is essential to maintaining life. Conversely, the effi cient transfer of carbon dioxide from the body to the environment is also critical. The exchange of these gases occurs via a series of complicated physiological processes. Abnormalities in the effective transfer of oxygen from the atmosphere into the bloodstream have been categorized into four pathophysiological mechanisms: hypoventilation, ventilation perfusion mismatch, intrapul-monary shunt, and diffusion limitation. An understanding of each of these pathophysiologi-cal processes will facilitate therapeutic interventions to improve oxygenation. Moreover, close monitoring of the status of gas exchange is essential for the care of critically ill chil-dren. Both invasive and non-invasive methods exist to effectively monitor gas exchange in children. A clear understanding of these techniques will foster effective management of critically ill children with impaired gas exchange.


1. A four year old male with severe status asthmaticus has required intubation secondary to fatigue and progressive dyspnea. He is adequately oxygenated, but he is severely hypercarbic because the restricted airfl ow and prolonged expiratory phase has limited the ventilator rate to only eight breaths per minute to prevent further air trapping. Which of the following statements MOST accurately describes the response of the body to the hypercarbia? A. Cerebral blood fl ow will decrease in response to the

hypercarbia. B. Chemoreceptors in the brainstem and in the carotid body will

not respond to the elevated PaCO 2 because he is well oxygenated.

C. Deoxygenated hemoglobin molecules will bind hydrogen ions and carbon dioxide to form carbaminohemoglobin and buffer the pH.

D. The kidneys will decrease the excretion of ammonium ion and chloride while retaining HCO 3

− and sodium to buffer the pH. E. There will be increased responsiveness of the adrenergic

receptors to circulating catecholamines.

2. A twelve year old male with acute respiratory distress syndrome has required intubation for progressive hypoxemia. His initial ventilator settings are as follows:

Fraction of inspired oxygen: 1.0 Peak inspiratory pressure: 35 cm H 2 O Peak end expiratory pressure: 12 cm H 2 O

Mean airway pressure: 22 cm H 2 O Ventilator rate: 14 breaths per minute

His most recent arterial blood gas result revealed a pH 7.37, PaCO 2 40 mm Hg, PaO 2 100 mm Hg, and SaO 2 96%. The barometric pressure is 760 mm Hg, the partial pressure of water vapor is 47 mm Hg, and the respiratory quotient is assumed to be normal (0.8). Which of the following values most closely approximates the alveolar oxygen gradient? A. 538 mm Hg B. 563 mm Hg C. 573 mm Hg D. 610 mm Hg E. 663 mm Hg

3. A two month old infant with hypoplastic left heart syndrome status post Stage I Norwood Procedure is developing pulse oximetry evidence of increasing hypoxemia. Point of care arterial blood sampling reveals pH 7.38, PaCO 2 44 mm Hg, PaO 2 35 mm Hg, SaO 2 75%, and a hemoglobin 12.0 g/dL. Which of the following values best estimates the arterial oxygen content of this infant? A. 10.5 mL O 2 /dL. B. 11.2 mL O 2 /dL. C. 12.2 mL O 2 /dL. D. 14.2 mL O 2 /dL. E. 16.8 mL O 2 /dL.

4. A two year old male presents with profuse watery diarrhea and tachypnea. He is tachycardic and tachypneic on clinic exam with pulse oximetry readings of 85% and a good waveform which correlates with the heart rate. He is placed on increas-

ing concentrations of oxygen, but he appears dusky and his pulse oximetry readings and clinical exam remain essentially unchanged. Consequently, an arterial blood gas is performed which reveals pH 7.28, PaCO 2 34 mm Hg, PaO 2 189 mm Hg, and base defi cit (–7). Which of the following diagnoses is most likely? A. Carboxyhemoglobinemia B. Malfunctioning pulse oximeter C. Methemoglobinemia D. Sickle cell disease E. Ventilation perfusion mismatch

5. A sixteen year old trauma victim with a pulmonary contusion has developed evidence of acute respiratory distress syndrome. He currently is receiving mechanical ventilator support in the pressure regulated volume control mode with the following settings:

Fraction of inspired oxygen: 0.80 Inhaled tidal volume: 500 mL / exhaled tidal volume: 475 mL Peak end expiratory pressure: 10 cm H 2 O Mean airway pressure: 16 cm H 2 O Ventilator rate: 16 breaths per minute His pulse oximeter reading is 92% and his end tidal carbon

dioxide is 30 mm Hg. An arterial blood gas reveals a pH 7.35, PaCO 2 45 mm Hg, PaO 2 65 mm Hg, and oxygen saturation 90%. The best estimate of the percent dead space ventilation is which of the following? A. 2% B. 5% C. 15% D. 20% E. 33%

6. A fi ve year old male is found unresponsive in a smoke-fi lled room at the scene of a house fi re. He is intubated at the scene and transported to the Emergency Department being ventilated with 100% oxygen. Upon arrival to the Emergency Department, he is found to have a pulse oximeter reading of 100%. Which of the following statements provides the best interpretation of the pulse oximetry reading? A. Although the pulse oximetry reading accurately refl ects a

well oxygenated patient, the 100% oxygen should be contin-ued to treat potential carboxyhemoglobinemia.

B. It is diffi cult to determine if the pulse oximetry value repre-sents effective oxygenation because the pulse oximeter will inappropriately interpret carboxyhemoglobin to be oxyhemoglobin.

C. The ability to effectively oxygenate the patient with supple-mental oxygen via conventional ventilation as refl ected by the pulse oximeter reading obviates the need for hyperbaric oxygen.

D. The patient is well oxygenated and should have his fraction of inspired oxygen weaned to maintain a pulse oximetry level of 94 – 99% to minimize potential oxygen toxicity.

E. The pulse oximetry value likely overestimates the degree of oxygenation because the methemoglobin formed as a result of smoke inhalation has a very similar light absorption as oxyhemoglobin at 660 nm.

REVIEW QUESTIONS


Cheifetz IM , Venkataraman ST, Hamel DS. Chapter 42. Respiratory physiology. Respiratory monitoring. In: Nichols DG, editor. Rogers’ textbook of pediatric intensive care. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 662–85.

Cordova FC, Marchetti N. Chapter 9. Noninvasive monitoring in the intensive care unit. In: Criner GJ, D’Alonzo GE, editors. Critical care study guide: text and review. New York: Springer; 2002. p. 128–47.

Crocetti J, Krachman S. Chapter 22. Oxygen content, delivery and uptake. In: Criner GJ, D’Alonzo GE, editors. Critical care study guide: text and review. New York: Springer; 2002. p. 355–68.

Krauss B, Hess DR. Capnography for procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2007;50:176–7.

Powell FL, Heldt GP, Haddad GG. Chapter 41. Respiratory physiol-ogy. In: Nichols DG, editor. Rogers’ textbook of pediatric inten-

sive care. Philadelphia: Lippincott Williams & Wilkins; 2008. p. 631–61.

Rice TW, Wheeler AP, Bernard GR, Hayden DL, Schoenfeld DA, Ware LB. Comparison of the SpO2/FIO2 ratio and the PaO2/FIO2 ratio in patients with acute lung injury or ARDS. Chest. 2007;132:410–17.

Siggaard-Andersen O, Fogh-Andersen N, Gøthgen IH, Larsen VH. Oxygen status of arterial and mixed venous blood. Crit Care Med. 1995;23:1284–93.

Tatevossian RG, Charles CJ, Velmahos GC, Demetriades D, Shoemaker WC. Transcutaneous oxygen and CO2 as early warning of tissue hypoxia and hemodynamic shock in critically ill emergency patients. Crit Care Med. 2000;28:2248–53.

West JB. Respiratory physiology: the essentials, vol. 7. Philadelphia: Lippincott Williams & Wilkins; 2005.

SUGGESTED READINGS

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7. The capnogram depicted in the fi gure most likely represents which of the following clinical conditions? A. Acute respiratory distress syndrome B. Asthma

C. Compromised cardiac output D. Pneumothorax E. Pulmonary edema

1. C 2. B 3. C 4. C

5. E 6. B 7. B

ANSWERS

Documents

Pediatric Critical Care Study Guide || Fundamentals of Gas Exchange and the Assessment of Oxygenation and Ventilation