What Constitutes Adequate Oxygenation?

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PEDIATRICS Vol. 85 No. 1 January 1 990 39

What

Constitutes

Adequate

Oxygenation?

Golde

Dudell,

MD; J. Devn

Cornish,

MD; and

Robert

H. Bartlett,

MD

From the University of California, San Diego, Medical Center and Children’s Hospital and

Health Center, San Diego, and the UnWersity of Michigan Medical Center,. Ann Arbor

In an attempt to avoid the substantial risks of

pulmonary injury associated with the use of high

ventilator pressures and high oxygen

concentra-tions, physicians often ask such questions as “What is the optimal Pao2?” and “What treatment should

be used to achieve an optimal Pao2?” Although the

intent to minimize secondary, ventilator-induced

lung injury is laudable, any attempt to provide a fixed numeric response to this query is misguided

not only because the oxygen requirements and

din-ical circumstances of our patients vary, but because

the Pao2 is a particularly poor indicator of these

needs.

An example is the large full-term neonate admit-ted to a newborn intensive care unit from the delivery room with obvious tachypnea and an ar-terial P02 of 60 mm Hg in room air. Is this Pa02 acceptable? A more appropriate question may be whether the infant’s “oxygenation” is adequate. But what is “oxygenation”? If by this vaguely applied

term we mean the partial pressure of oxygen in the

arterial blood, and if we define the acceptable limits

for this parameter as being between 50 and 80 mm

Hg, as is often done, then the answer must clearly be in the affirmative. If, on the other hand, we take oxygenation to mean the balance between the rate of oxygen delivery to the tissues and their rate of oxygen consumption, then we must admit that we cannot know on the basis of the information pro-vided by the Pa02 alone.

Oxygen delivery is determined by the concentra-tion of hemoglobin in the blood, its oxygen satura-tion, the rate at which this blood is circulated to the tissues (generally, the cardiac output), and the

efficiency with which the oxygen is “unloaded” from

Received for publication Oct 18, 1988; accepted Feb 14, 1989.

Reprint requests to (J.D.C.) San Diego Regional ECMO

Pro-gram, 8001 Frost St, San Diego, CA 92123.

American Academy of Pediatrics.

hemoglobin to the tissues. The relationship among these factors (except the last) is generally expressed in the following standard equation1: Do2 =

CO[(Hb)(% sat)(1.36) + (Pa02)(0.0031)], where

Do2

5 the rate of oxygen delivery and (Hb) is the

measured hemoglobin concentration, % sat is the

percentage of saturation of hemoglobin with

oxy-gen, 1.36 represents the oxygen-carrying capacity of normal adult human hemoglobin (1.36 mL of oxygen per gram of hemoglobin), Pa02 is the meas-ured partial pressure of oxygen in the blood, 0.0031

is the solubility coefficient for oxygen in blood

(0.0031 mL of 02/100 mL of blood per mm Hg), and CO is the cardiac output. The only contribution to oxygen delivery attributable to the Pa02 is

rep-resented by the final expression in the equation

and is based on the relatively insignificant amount of oxygen dissolved in the fluid phase of the blood.

Thus, if in our example the patient is particularly anemic or hypovolemic, has an abnormal hemoglo-bin with increased affinity for oxygen, or has a small cardiac output, then his oxygen delivery may be inadequate even in the presence of a normal

Pao2.

We have moved from thinking only of the partial pressure of oxygen in the arteries to discussing the larger concept of oxygen delivery. More important

still is the concept of oxygen sufficiency, ie, whether

the rate of oxygen delivery achieved is adequate to meet tissue oxygen demands. If a neonate is in-fected, has increased muscle activity, or has been deprived of oxygen, then the neonate’s oxygen re-quirement may be markedly increased and the oxy-gen supply inadequate even in the presence of a “normal” rate of oxygen delivery.2

Viewing the matter from the other direction, let

us suppose that a neonatal patient actually has an

initial Pao2 of only 40 mm Hg and that to our

surprise this neonate appears neither tachypneic

nor distressed. Can the neonate’s “oxygenation” possibly be adequate? Ifwe later find that the infant in question has cyanotic congenital heart disease,

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40 Pao2 INCREASE AND DECREASE

we may be pleased that the Pa02 is so high. Again, we are reacting in a reflex manner to a relatively

meaningless number. The reason that a Pa02 of 40

mm Hg in such an infant may be totally acceptable

is not because babies with cyanotic heart disease are somehow metabolically different from other neonates (“babies with cyanotic hearts can tolerate

low Pa02 values”), nor is it because a Pa02 value

this low is probably high enough for most any

infant. Rather, neonates with cyanotic heart dis-ease often invoke a variety of mechanisms to com-pensate for their chronically inadequate oxygen

saturation, among which are an increased resting

cardiac output and a higher hemoglobin concentra-tion. The finding of a Pa02 of 40 mm Hg in and of

itself simply does not tell us whether tissue

oxygen-ation is adequate or not.

The measured Pao2 is a poor indicator of arterial oxygen content. It is only because of the nearly linear relationship between Pa02 and hemoglobin saturation in the usual physiologic range as mani-fested by the oxyhemoglobin dissociation curve that

the Pa02 is of any clinical use at all. Yet even the arterial hemoglobin saturation is an inadequate

clinical index of oxygen sufficiency at the tissue level, because it reflects only the oxygen content of arterial blood. It gives no information about the balance between oxygen delivery and oxygen

de-mand.

Ideally, rather than Pa02 or arterial hemoglobin saturation, we should measure systemic oxygen

de-livery and oxygen consumption simultaneously, but these measurements are difficult to make in infants.

The oxyhemoglobin saturation of mixed venous blood (SVo2) is directly related to the oxygen con-tent in blood returning from the tissues#{176}’4and can be measured in individual blood samples drawn from a pulmonary artery catheter or measured

con-tinuously using a fiber optic catheter. Continuous

SVo2 monitoring has become standard practice in many adult intensive care units.5’6 Small fiber optic catheters are available that can be placed in the right atrium of a neonate via an umbilical vein. In the neonate, right atrial saturation provides a rea-sonable estimate of mixed venous saturation. The time has come to bring this adult critical care technology to the neonatal intensive care unit.

Normally, oxygen delivery is four to five times the oxygen consumption. Therefore, 20% to 25% of the oxygen delivered is used, and the rest remains

in the venous blood. If the arterial blood is 100% saturated, normal venous blood will be 75% to 80%

saturated. An abrupt decrease in venous saturation

may be caused by a decrease in delivery or an increase in consumption and vice versa. The SVo2

is thus an excellent monitor of normal values,

al-though any abnormal values must be interpreted in

the light of other physiologic data.

Use of SVo2 as the critical indicator of oxygen sufficiency at the tissue level could allow us to

minimize unnecessary therapies while responding appropriately to clinically compromising events. Moreover, the true impact of various therapeutic

maneuvers might be more accurately assessed. If, for example, an increase in mean airway pressure

on the ventilator resulted in an increase in the Pa02 with an accompanying decrease in the SVo2, one might properly conclude that the improvement in arterial oxygenation was inadequate to compensate for the concomitant decrease in cardiac output

oc-casioned by the increase in intrathoracic pressure.

Therapeutic interventions directed toward main-taming SVo2 between 75% and 80% might allow more precise control of pulmonary vascular resist-ance and thus maintenance of greater

cardiorespi-ratory stability in infants with persistent pulmo-nary hypertension than does the physiologically less meaningful attempt to maintain arterial oxygen

tensions greater than 100 mm Hg, as is commonly recommended. This view is substantiated by data obtained from perigestational lambs7 maintained on partial arteriovenous extracorporeal membrane oxygenation. In this case, the therapeutic effects of delivering highly oxygenated blood to the pulmo-nary vasculature included a reduction in the size of the right to left shunt, an increase in pulmonary blood flow, and a decrease in pulmonary vascular resistance that were sustained despite borderline

arterial P02. Thus, SVo2 would provide a much

sounder basis for both the assessment and manage-ment of infants with pulmonary hypertension, par-ticularly because pulmonary arterial hypoxemia is a potent stimulus to pulmonary vasoconstriction.7

Saturation of mixed venous blood is presently in

wide use in neonatal extracorporeal membrane

ox-ygenation centers as an index of tissue oxygenation.

In a setting such as extracorporeal membrane

oxy-genation in which arterial oxygenation and

sys-temic circulation are largely controlled by artificial means, it becomes obvious how imperfect the Pao2 value is as a predictor of the adequacy of oxygena-tion. Babies with elevated Pa02 values may have rapidly decreasing and then increasing SVo2 values associated with poor perfusion and ultimate tissue death. And infants with relatively poor Pao2 values may actually be oxygenating superbly at the tissue level because of the increased level of circulatory

support and thus of oxygen delivery.

Umbilical venous catheters can be introduced

into the right atrium of most neonates with relative

ease in the early postnatal period. Other practical means of monitoring this critical parameter are also

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SPECIAL ARTICLES 41

available. The clinical utility of the mixed venous oxygen saturation combined with its relative

acces-sibility in this setting should motivate clinicians to

monitor this parameter more routinely.

REFERENCES

1. Divertie MG, McMichan JC. Continuous monitoring of

mixed venous oxygen saturation. Chest. 1984;85:423-428 2. Finch CA, Lenfant C. Oxygen transport in man. N Engl J

Med. 1972;286:407-415

3. Miller MJ. Tissue oxygenation in clinical medicine: an

his-torical review. Anesth Analg. 1982;61:527-535

4. Kandel G, Aberman A. Mixed venous oxygen saturation: its

role in the assessment ofthe critically illpatient.Arch Intern Med. 1983;143:1400-1402

5. White KM. Completing the hemodynamic picture: SVo2.

Heart Lung. 1985;14:272’-280

6. Zwischenberger JB, Cilley RE, Kirsh MM, Dechert TE,

Bartlett RH. Does continuous monitoring of mixed venous

oxygen saturation accurately reflect oxygen delivery and

oxygen consumption following coronary artery bypass

graft-ing? Surg Forum. 1986;37:66-68

7. Griffith BP, Borovetz HS, Hardesty RL, Hung T-K,

Bahn-son HT. Arteriovenous ECMO for neonatal respiratory

sup-port. J Thorac Cardiovasc Surg. 1979;77:595-601

8. Bohr DF. The pulmonary hypoxic response. Chest. 1977;71:

244-246

PESTICIDE RISK FROM APPLES: WHO’S RIGHT?

No wonder there’s alarm-and confusion-over apples and pesticides.

An environmental group warns that preschoolers can face as much as 910

times the acceptable cancer risk from eating chemically treated apple prod-ucts. ...

Apple growers immediately protest. They say a person would have to eat

28,000 pounds of apples a day for 70 years to equal the dose of chemicals that causes cancer in laboratory rats. Makers of applesauce and apple juice say they

check for the specific cancer-causing agent, and hardly ever find it.

So how much of a threat is there from apples and the pesticide daminozide?

A consensus on the issue is unlikely. Scientific studies raise legitimate concern that a substance known as UDMH, which is produced as daminozide breaks down, can cause cancer. But the truth about the degree of risk probably lies somewhere between the numbers cited on both sides. ...

. . . the EPA says the Natural Resources Defense Council overstated the dangers to children tenfold or more. “We’re trying to say it’s not quite” the “basis for panic as people have assumed,” says. . .an extension horticulturist for

tree fruits. . .“All of us in the scientific industry feel that they [the council] are vastly overstating the problem.”.

The EPA’s biggest problem with the Natural Resources Defense Council

study is that the group’s cancer-potency figures for UDMH come from an EPA

study thrown out years ago as flawed. . .Still, preliminary results from the EPA’s new study have led it to conclude that Alar should be banned. .

From Rosewicz B. The Wall Street Journal. March 10, 1989.

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1990;85;39

Pediatrics

Golde Dudell, J. Devn Cornish and Robert H. Bartlett