Table 38-1. Values for pH, PC02' Po2, and standard bicarbonate in cord blood and in arterial blood at different ages during the neonatal period

5.10 20 30 60 5 24 2 3 4 5 6 7uv VA minutes minutes minutes minutes hours hours days days days days days days.

pH n 45 27 44 28 62 43 36 72 53 49 38 40 35 42

fjmean 7.32 7.242 7.207 7.263 7.297 7.332 7.339 7.369 7.365 7.364 7.37 7.371 7.369 7.371SD 0.055 0.059 0.051 0.04 0.044 0.031 0.028 0.032 0.028 0.027 0.027 0.031 0.023 0.026Range 7.178 7.111 7.091 7.18 7.206 7.261 7.256 7.29 7.314 7.304 7.32 7.296 7.321 7.32

7.414 7.375 7.302 7.33 7.38 7.394 7.389 7.448 7.438 7.419 7.44 7.43 7.423 7.431

Pcoz n 44 27 43 28 62 43 36 71 53 49 39 40 35 42

I

mmHg mean 37.8 49.1 46.1 40.1 37.7 36.1 35.2 33.4 33.1 33.1 34.3 34.8 34.8 35.9SD 5.6 5.8 7 6 5.7 4.2 3.6 3.1 3.3 3.4 3.8 3.5 3.6 3.1Range 26 35 35 31 28 28 29 27 26 26 27 28 28 30

52 60 65 58 54 45 45 40 43 40 43 41 42 42St. ble. n 44 27 42 28 61 42 36 71 53 49 38 40 35 42meqlL mean 20 18.7 16.7 17.5 18.2 19.2 19.4 20.2 19.8 19.7 20.4 20.6 20.6 21.8

I,

SD 1.4 1.8 1.6 1.3 1.5 1.2 1.2 1.3 1.4 1.4 1.7 1.7 1.9 1.3Range 15.5 14 12.5 , 14 15 16 16 18 16.5 16 17.5 17.5 17 18.5

22.5 21 20.5 20 21 21.5 22 23.5 24.5 23.5 25 24.5 24.5 26

, POz n 45 29 42 24 54 31 30 62 47 42 33 32 30 38

r

mmHg mean 27.4 15.9 49.6 50.7 54.1 63.3 73.7 72.7 73.8 75.6 73.3 72.1 69.8 73.1 ::'SD 5.7 3.8 9.9 11.3 11.5 11.3 12 9.5 7.7 11.5 9.3 10.5 9.5 9.7 :;

';Range 15 7 33 31 31 38 55 54 62 56 60 56 55 57 '::'

40 23 75 85 85 83 106 95 (11 102 93 102 96 94'"

1MQC

Adapted from Kc..;h G, Wendel H: Adjustment of rterial blood gases and acid base balance in the normal newborn infant dur;r.g the first week of life. Bioi Neonate 12:136-161, 1968. With permissionfrom Karger S, Basel AG. Switzerland.St. bic., standard bicarbonate; UV. umbilical vein; VA, umbilical artery: results are reponed as mean and standard deviatiC' '.

-.'0c-o.::v.5'0'..."0...

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FromChatbum RL, Carlo WA: Assessment of neonatal gas exchange. In Carlo WA, Chatburn RL (eds): Neo1latal respiratory care, ed 2, Year Book,

Chicago,.1988.Arrows,elevated or depressed values; N, normal; lICO) -, bicarbonate; BE, base excess.

metabolicacid-base disorders are further classified asuncompensated, partly compensated, or completelycompensated. Primary respiratory acid-base disordersare compensated by metabolic adjustments, and viceversa. This compensatory effect is evident from theHenderson-Hasselba1ch equation, which shows that a

I relativelyconstant ratio of [HCO] -] to PC02 is necessaryto maintain pH in the normal range. By examining thepH, Peo2 and [HCO] -I (or base excess), a specific

~. acid-basedisturbance can be properly assigned to one of. theclassifications in Table 38-3. One problem that mayk ariseis the determination of which abnormality is the

primaryacid-base problem and which is the compensa-torymechanism. For example, if a particular patient hasa normal pH, but both the PC02 and [HCO] -] areelevated,the blood gas disturbance may represent eithera compensated respiratory acidosis or a compensated

i. metabolicalkalosis. Usually, the clinical course of the;'.. patientand prior experience will claritYcompensatory~..mechanismsfrom the primary acid-base disorder.~.. Asnoted, the indices indicating metabolic acid-base~.balance are calculated values. These indices most~.'.' commonlyinclude actual bicarbonate ([HCO] -]), stan-~."dard bicarbonate, and base excess. rHCO] - ] is solved for~:[(usingthe Henderson-Hasselba1ch equation, once pH\ andPeo2 have been measured. The actual bicarbonateE canalsobe derived from the total CO2, which is a value;: routinely reported with serum electrolyte measure-

~ ments.Total CO2 is a measure of the total amount ofg {:O2transported within the plasma. As mentioned, the~! majority of CO2 (80% to 85%) is transported as

~. bicarbonate.Theref?re, the total CO2 in serum electro-~ lyte reports apprmumates the value for [HC03 -] ob-

I

' tained in blood gas measurements, and can be used to, verify the accuracy of the blood gas report.

. , [HC03-] is not an absolute indicator of metabolic}'Ja&d-basestatus, because alterations in respiratory acid-t basebalance (that is, changes in PC02) will also have a

i. small effect on [HC03 - V This effect is evident from

,;~mining the hydrolysis reaction, which shows that as

f Peo2and [dissolved CO2] vary, so does [HCO] ]. The~;,

. ratio between changes in PC02 to changes in [HC03 -]is about 10:1 when Peo2 increases greater than 40 mmHg, and is about 5: I when Peo2 falls below this value.51There needs to be significant hypercarbia or hypocarbia,therefore, for [HCO~ -1 to be substantially affected bychanges in Peo2.

The measurement of standard bicarbonate is de-signed to obviate the effect of Peo7 on [HCO~ -] andis included in the Iypical blood gas report. In this invitro test, blood is equilibrated to a Peo2 of 40 mmHg at 37°C, and Ihe rHCO] -] is determined. "hismethod theoretically provides 'a more accurate indexof metabolic acid-base balance than does actual bi-carbonate. Standard bicarbonate rel1ects in vitro con-ditions, however, and the results can differ somewhatfrom the "true" value for standard bicarbonate if themeasurement could be performed in vivo.9 Under mostcircumstances, standard and actual bicarbonate valueswill be similar, unless there is significant hypercarbiaor hypocarbia.

Base excess ([BE]) is another metabolic acid-baseindex.17 [BE] is equal to the observed blood buffer baseminus the normal blood buffer base. It is a reflection ofthe effect of all oluod buffers, not just bicarbonate;Under conditions of metabolic acidosis, buffering capac-ity will be consumed, and the base excess will benegative; this condition is also referred to as a basedeficit. [BE] is calculated from a Siggaard-Andersonnomogram, which relates Peo2, pH, hemoglobin con-centration, and base excess. This nomogram was devel-oped from data ootained in vitro.') As such, and likestandard bicarbonate, the determination of [BE] maynot exactly reflect the "true" [BE] in vivo.

Primary respiratory disorders and compensatorymechanisms. Respiratory acidosis is the most importantdisorder in this group because of its frequency andpotentially life-threatening nature. Uncompensated, oracute, respiratory acidosis is due to alveolar hypoventi-lation, and is heralded by an elevation in Peo2 with a fallin pH. For every increase in PC02of 10 mm Hg, the pHwill fall by about 0.07 units.4uCauses for hypoventilation

Chapter 38 Blood gas interpretation 453

Table 38.3. Blood gas classifications

Classification pH Pan)1 HCOJ- BE

Respiratory disorderUncompensated acidosis t N NPartly compensated acidosis t 1- tI

Compensated acidosis N t t tUncompensated alkalosis t N NPartly compensated alkalosis tCompensated alkalosis N

Metabolic disorder

Uncompensated acidosis N

Partly compensated acidosisCompensated acidosis NUncompensated alkalosis t N t tPartly compensated alkalosis t t t tCompensated alkalosis N t t t

o 10 30 9040 50

PC02(torr)

Fig. 38-11. A neonatal acid-base map. CRA, Compensated respiratory alkalosis; CMA,compensated metabolic alkalosis; RMA, mixed respiratory and metabolic acidosis. (FromChatburn RL, Carlo WA: Assessment of neonatal gas exchange. In Carlo WA, Chatburn RL[eds): Neonatal respiratory care, ed 2. Year Book, Chicago, 1988.)

20

6;i';ID an otherwise normal patient, metabolic acidosis,,"--'lout respiratory compensation is unusual. A drop in,-willalmostimmediatelystimulate hypelVentilation,

.",VIthensuing hypocarbia and a shift in pH towardr'QOnnaI.9Adequate respiratory compensation for meta-~lic acidosismay not occur, however, in the presence of)uJmODaryor CNS disease. 13

i~~:Metabolicalkalosis is caused by either a loss of fixed~d or a gain of blood base. Gastric fluid loss, as with

Oantingor continuous gastric suction, leads to a loss of~oric acid and metabolic alkalosis. Hypokalemia,.~bJoremia, diuretic therapy, excessive bicarbonate:'~ltdmiDistration,and adrenal hypersecretion are other

:~uses of metabolic alkalosis.4u Compensation in meta-(.bonealkalosis is achieved through hypoventilation andi:hypercarbia.In adults, this compensatory mechanism is!~re incomplete, because hypercarbia (and possibly',=ncurrent hypoxia) will ultimately stimulate ventilatory~\fforts.46Y' ine acid.base map. The classification of acid-base: disordersshown in Table 38-3 will identify basic disor-[;dcrsandtheircompensatorymechanisms,but it maynot

e helpful in properly identifying mixed acid-base~~disturbances.Mixeddisturbancesare common,and can~

.:;r' in a varietyof scenarios.For example,severe~'. iratory distress syndrome can cause a mixed respi-~?)atoryand metabolic acidosis, due to coexisting hyper-~.. .~

!icarbia and lactic acidosis from hypoxia. Fulminating

60 8070

neonatal sepsis is also a common cause for a mixedrespiratory and metabolic acidosis. In pulmonary hyper-tension, hYPclVentilation and bicarbonate administra-tion arc somctimes IIscd together therapeutically; thisleads to a mixed respiratory and metabolic alkalosis.

Some mixed acid-base disturbances may initiallyappear as compensated simple acid-base problems. Anexample of this complexity can occur during the treat-

\ ment of chronic lung disease with diuretics. The PC02and rHCo,l 1 will generally both be elevated in thissituation, thcrefore appearing as a metabolic alkalosiscompensating for a respiratory acidosis. If the pH isovercompensated (pI I > 7.45), however, the mctabolicalkalosis would not just be a compensatory mechanism,but would represent an additional primary metabolicdisorder induced by the use of diuretics.

To help in the assessment of simple and mixedacid-base disorders, a neonatal acid-hase map based onthe Henderson-Hasselbach equation has been devel-oped, and is shown in Fig.3R-11.13Normalvalues in thissystem are pH = 7.30 to 7.45, PC02 = 35 to 45 mm Hg,and rHCO,l- ] = 18 to 24 mEqlL. By plotting the pH,PC02 and rHCO:. -1 on the map, simple as well as mixedacid-base disturbances can be properly classified.REFERENCES

I. Adam RD, Edwards LD, Becker ee, et al: Semiquantitativecultures and routine tip cultures on umbilical catheters. J PediatrtOlI:t23, 19X2.

I'i'Il.1 "

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Chapter 38 Blood gas interpretation 455

100 I I I / A 7.0

Mixed 18 24

90 -I I '" respiratory'iij and0

metabolic-C'u

acidosis/80-1 0 / 1-7.1Partly compensated .

g;c.nirntn,.v

metabolicacidosis .B70 -I .E

Q)

Partly compensatedI- 7.2

60respiratory acidosis

::;-7.3 =a.+ ........ 50J:

..s CompensatedCompensatedmetabolic

40-1 acidosis respiratory acidosis 7.4

-I ..--......atary '" 7.530 _I_I_.;....:.1- 'iij0

[ 76

"0...:.:

20-1 -,_w'k..\1,.,y ., , I "0 Metabolic alkalosis with 7.7.

respiratory acidosis 7,8"0..D

10-1 ///

ana meraOOIlCI

0 8.0alkalosis Qj("0

"'<,; J/9-1 I I- 8.5

I"

448 PULMONARY DISEASE IN THE NEONATE

, ,I, I

Causes for a low POz and a high Pcoz

II

Hypoventilation

Inadequate respiratory effortCentral nervous system depression

AsphyxiaTraumaIntracranial hemorrhageMaternal drugs

Central nervous system immaturityApnea of prematurity

Neuromuscular diseaseMyasthenia gravisPhrenic nerve palsyMyopathies

Mechanical ventilator settingsRate and/or pressure too low

Upper airway not patentChoanal atresiaLaryngeal webMucus, blood, or meconium blocking upper airway'Mucus, blood, or meconium blocking endotracheal

tube

Displaced or kinked endotracheal tubeExternal compression of airway

Decreased lung tissuePl!lmonary hypoplasia

Thoracic dystrophyDiaphragmatic herniaPotter's syndrome

Decreased lung complianceAtelectasis

Respir'~tory distress syndromePneumothorax

'I

I

J '

, ,I

Abnormal pulmonary interstitiumInterstitial edema

Interstitial emphysemaInterstitial fibrosis

End tidal pressure too highAbnormal ventilationlpetj'usion ratio

Obstruction of small airwaysMeconium aspiration

AtelectasisRespiratory distress syndromePneumothorax

Alveolar exudatePneumonia

Alveolar OuidTransient tachypneaCongenital heart diseaseFluid overload

Increased extrapulmonary right-to-left shuntPulmonary vasoconstriction

Respiratory distress syndromeLow pHSevere infection ;,;"Idiopathic" persistent pulmonary hypertension~:

Pulmonary hypoplasia with decreased pulmomu)'ivasculature ' ,~~

Thoracic dystrophy .Diaphragmatic herniaPotter's syndrome

Cyanotic heart disease

From Phillips BL, McQuitty 1. Durand Dl: Blood gases: technical aspects and interpretation. In Goldsmith IP. Karotkin I:H, Barker S(eds):vell/ilalion of IIII'",'lIIlale, cd 2. WB Saunders. Philadelphia. I<J/!/!.

acid may accumulate in conditions other than hypoxia,however. In adults, liver disease and certain drugs andtoxins can elevate blood lactic acid levels.35.46.76Also,elevations in blood pyruvate will cause lactic acid levelsto rise. Lactic acidosis is therefore not a specific markerfor hypoxia.22 Additionally, some studies have shown apoor correlation between decreased tissue oxygen de-livery and increased lactic acid levels, suggesting thatlactic acidosis is not a sensitive marker for hypoxia.3 Thislack of sensitivity may, in part, be due to the nonlinearrise in lactic acid levels that occur during progressivehypoxia.36 Also, because lactic acid is normally metabo-lized by the liver, elevated levels can be temporary.22Therefore, the absence of lactic acidosis does not implythe absence of hypoxia.

The measurement of mixed venous P02 and mixedvenous oxygen saturation (SV02)is another method usedto assess for hypoxia. In adults, normal Pv02 is about 40mm Hg (range 35 to 45 mm Hg),46.73and normal SV02isabout 75% (range 68% to 77%).53 The value of thesemixed venous oxygen indices is that they reflect theequilibrium between oxygen delivery to the tissues andtissue oxygen consumption. If oxygen consumptionremains constant, conditions that decrease oxygen de-

~'

I, ,,

b,VJl

Iif I

!~.L

I,.

livery to the tissues (either decreased arterialcontent or decreased cardiac output) willcausethc- ','and Svo2 to fall; these decreases are evident from~examination of the Fick equation. Low Pvoz andvalues are therefore felt to indicate tissue h)iAlthough some believe that Pv02 or Svoz are the.overall inriicators of tissue hypoxia,26others have! .a poor wrrelation between these indices andindicators of tissue hypoxia.54 There is also some'~ ..as to which of these two indices is superior intissue oxygenation.7.73Uthe oxyhemoglobinducurve shifts markedly to the left, Svoz may ~~~useful value, because venous blood will be mor~~rated at any given, Pv02.73 It should be noted;conditions causing cellular metabolic dysfunctiOn'inability to utilize oxygen (such as cyanide poisODc<

venous oxygen indices will actually be high, in .tissue hypoxia.

Other biochemical markers have been use

research basis to assess for tissue hypoxia,though,'are not part of the standard blood gas report. One~most studied of these markers is hypoxanthine. Hjanthine is a breakdown product of adenosine' .phate. Under aerobic conditions, hypoxanthinc.js,