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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 7
uv 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
mean 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 7.371
SD 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 0.026 fj
Range 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
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 35.9
SD 5.6 5.8 7 6 5.7 4.2 3.6 3.1 3.3 3.4 3.8 3.5 3.6 3.1
Range 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 42
St. ble. n 44 27 42 28 61 42 36 71 53 49 38 40 35 42
I 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
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 1.3
Range 15.5 14 12.5 , 14 15 16 16 18 16.5 16 17.5 17.5 17 18.5
I, 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
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
r 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 permission

from Karger S, Basel AG. Switzerland. -.'

St. bic., standard bicarbonate; UV. umbilical vein; VA, umbilical artery: results are reponed as mean and standard deviatiC' '. 0

Chapter 38 Blood gas interpretation 453

Table 38.3. Blood gas classifications

Classification pH Pan)1 HCOJ- BE

Respiratory disorder
Uncompensated acidosis t N N
Partly compensated acidosis t 1-
I t
Compensated acidosis N t t t
Uncompensated alkalosis t N N
Partly compensated alkalosis t
Compensated alkalosis N
Metabolic disorder
Uncompensated acidosis N
Partly compensated acidosis
Compensated acidosis N
Uncompensated alkalosis t N t t
Partly compensated alkalosis t t t t
Compensated alkalosis N t t t
FromChatbum RL, Carlo WA: Assessment of neonatal gas exchange. In Carlo WA, Chatburn RL (eds): Neo1latal respiratory care, ed 2, Year Book,
Arrows,elevated or depressed values; N, normal; lICO) -, bicarbonate; BE, base excess.

metabolicacid-base disorders are further classified as . ratio between changes in PC02 to changes in [HC03 -]
uncompensated, partly compensated, or completely is about 10:1 when Peo2 increases greater than 40 mm
compensated. Primary respiratory acid-base disorders Hg, and is about 5: I when Peo2 falls below this value.51
are compensated by metabolic adjustments, and vice There needs to be significant hypercarbia or hypocarbia,
versa. This compensatory effect is evident from the therefore, for [HCO~ -1 to be substantially affected by
Henderson-Hasselba1ch equation, which shows that a changes in Peo2.
I relativelyconstant ratio of [HCO] -] to PC02 is necessary The measurement of standard bicarbonate is de-
to maintain pH in the normal range. By examining the signed to obviate the effect of Peo7 on [HCO~ -] and
pH, Peo2 and [HCO] -I (or base excess), a specific is included in the Iypical blood gas report. In this in
~. acid-basedisturbance can be properly assigned to one of vitro test, blood is equilibrated to a Peo2 of 40 mm
. theclassifications in Table 38-3. One problem that may Hg at 37°C, and Ihe rHCO] -] is determined. "his
k ariseis the determination of which abnormality is the method theoretically provides 'a more accurate index
primaryacid-base problem and which is the compensa- of metabolic acid-base balance than does actual bi-
torymechanism. For example, if a particular patient has carbonate. Standard bicarbonate rel1ects in vitro con-
a normal pH, but both the PC02 and [HCO] -] are ditions, however, and the results can differ somewhat
elevated,the blood gas disturbance may represent either from the "true" value for standard bicarbonate if the
a compensated respiratory acidosis or a compensated measurement could be performed in vivo.9 Under most
i. metabolicalkalosis. Usually, the clinical course of the circumstances, standard and actual bicarbonate values
;'.. patientand prior experience will claritYcompensatory will be similar, unless there is significant hypercarbia
~..mechanismsfrom the primary acid-base disorder. or hypocarbia.
~.. Asnoted, the indices indicating metabolic acid-base Base excess ([BE]) is another metabolic acid-base
~. balance are calculated values. These indices most index.17 [BE] is equal to the observed blood buffer base
minus the normal blood buffer base. It is a reflection of
commonlyinclude actual bicarbonate ([HCO] -]), stan-

~."dard bicarbonate, and base excess. rHCO] - ] is solved for the effect of all oluod buffers, not just bicarbonate;
~:[(usingthe Henderson-Hasselba1ch equation, once pH Under conditions of metabolic acidosis, buffering capac-
\ andPeo2 have been measured. The actual bicarbonate ity will be consumed, and the base excess will be
E canalsobe derived from the total CO2, which is a value negative; this condition is also referred to as a base
;: routinely reported with serum electrolyte measure- deficit. [BE] is calculated from a Siggaard-Anderson
~ ments.Total CO2 is a measure of the total amount of nomogram, which relates Peo2, pH, hemoglobin con-
g {:O2transported within the plasma. As mentioned, the centration, and base excess. This nomogram was devel-
~! majority of CO2 (80% to 85%) is transported as oped from data ootained in vitro.') As such, and like
~. bicarbonate.Theref?re, the total CO2 in serum electro- standard bicarbonate, the determination of [BE] may
~ lyte reports apprmumates the value for [HC03 -] ob- not exactly reflect the "true" [BE] in vivo.
' tained in blood gas measurements, and can be used to Primary respiratory disorders and compensatory
, verify the accuracy of the blood gas report. mechanisms. Respiratory acidosis is the most important
, [HC03-] is not an absolute indicator of metabolic disorder in this group because of its frequency and
I}'Ja&d-basestatus, because

alterations in respiratory acid- potentially life-threatening nature. Uncompensated, or

t basebalance (that is, changes in PC02) will also have a acute, respiratory acidosis is due to alveolar hypoventi-
. small effect on [HC03 - V This
effect is evident from lation, and is heralded by an elevation in Peo2 with a fall

i,;~mining the hydrolysis reaction, which shows that as in pH. For every increase in PC02of 10 mm Hg, the pH
will fall by about 0.07 units.4u Causes for hypoventilation

f Peo2 and [dissolved CO2] vary, so does [HCO]

~;, ]. The
Chapter 38 Blood gas interpretation 455 I'i'
1 "
100 I I I / A
Mixed 18 24 ; I
,; j:
90 -I I 'iij'" respiratory
0 and ["
-C metabolic t"
80-1 0 acidosis/ g;c.nirntn,.v / 1-7.1
Partly compensated . I.:
metabolicacidosis .B I'
70 -I .E
~ It!
I- 7.2
60 Partly compensated
respiratory acidosis f I
::;- I':
50 7.3 =a. f, .,
..s Compensated II
metabolic Compensated I
40-1 acidosis respiratory acidosis 7.4 !.

'" 7.5
30 -I _I_I_.;.
...:.1- 'iij
20-1 -,_w'k..\1,.,y ., , I "0 Metabolic alkalosis with 7.7
"0 respiratory acidosis 7,8

10-1 ///
Qj [ 76
"'<,; J/
9-1 ana meraOOIlCI I I- 8.5
o 10 20 30 40 50 60 70 80 90

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

,," an otherwise normal patient, metabolic acidosis neonatal sepsis is also a common cause for a mixed
--'lout respiratory compensation is unusual. A drop in respiratory and metabolic acidosis. In pulmonary hyper-
,- willalmostimmediatelystimulate hypelVentilation, tension, hYPclVentilation and bicarbonate administra-
.",VIthensuing hypocarbia and a shift in pH toward tion arc somctimes IIscd together therapeutically; this
r'QOnnaI.9 Adequate respiratory compensation for meta- leads to a mixed respiratory and metabolic alkalosis.
~lic acidosismay not occur, however, in the presence of Some mixed acid-base disturbances may initially
)uJmODary or CNS disease. 13 appear as compensated simple acid-base problems. An
i~~:Metabolicalkalosis is caused by either a loss of fixed example of this complexity can occur during the treat-
~d or a gain of blood base. Gastric fluid loss, as with \ ment of chronic lung disease with diuretics. The PC02
Oantingor continuous gastric suction, leads to a loss of and rHCo,l 1 will generally both be elevated in this
~oric acid and metabolic alkalosis. Hypokalemia, situation, thcrefore appearing as a metabolic alkalosis
.~bJoremia, diuretic therapy, excessive bicarbonate compensating for a respiratory acidosis. If the pH is
:'~ltdmiDistration,and adrenal hypersecretion are other overcompensated (pI I > 7.45), however, the mctabolic
:~uses of metabolic alkalosis.4u Compensation in meta- alkalosis would not just be a compensatory mechanism,
(.bonealkalosis is achieved through hypoventilation and but would represent an additional primary metabolic
i:hypercarbia.In adults, this compensatory mechanism is disorder induced by the use of diuretics.
!~re incomplete, because hypercarbia (and possibly To help in the assessment of simple and mixed
',=ncurrent hypoxia) will ultimately stimulate ventilatory acid-base disorders, a neonatal acid-hase map based on
~\fforts.46 the Henderson-Hasselbach equation has been devel- ,
Y' ine acid.base map. The classification of acid-base oped, and is shown in Fig. 3R-11.13Normalvalues in this I ~
: disordersshown in Table 38-3 will identify basic disor- system are pH = 7.30 to 7.45, PC02 = 35 to 45 mm Hg, ,
[;dcrsandtheircompensatorymechanisms,but it may not and rHCO,l- ] = 18 to 24 mEqlL. By plotting the pH, "
e helpful in properly identifying mixed acid-base PC02 and rHCO:. -1 on the map, simple as well as mixed
acid-base disturbances can be properly classified. , h
Mixeddisturbances are common,and can I
~'.:;r' iratory
in a distress
varietyof scenarios.For
syndrome can causeexample,severe
a mixed respi- I. Adam RD, Edwards LD, Becker ee, et al: Semiquantitative .~
~?)atoryand metabolic acidosis, due to coexisting hyper-
~.. .~ cultures and routine tip cultures on umbilical catheters. J Pediatr ,
!icarbia and lactic acidosis from hypoxia. Fulminating tOlI:t23, 19X2.

,I , Causes for a low POz and a high Pcoz

, I
Inadequate respiratory effort Abnormal pulmonary interstitium
Central nervous system depression Interstitial edema
Asphyxia Interstitial emphysema
Trauma Interstitial fibrosis
Intracranial hemorrhage End tidal pressure too high
Maternal drugs Abnormal ventilationlpetj'usion ratio
Central nervous system immaturity Obstruction of small airways
Apnea of prematurity Meconium aspiration
Neuromuscular disease Atelectasis
II Myasthenia gravis Respiratory distress syndrome
Phrenic nerve palsy Pneumothorax
Myopathies Alveolar exudate
Mechanical ventilator settings Pneumonia
Rate and/or pressure too low Alveolar Ouid
Upper airway not patent Transient tachypnea
Choanal atresia Congenital heart disease

I Laryngeal web Fluid overload

Mucus, blood, or meconium blocking upper airway' Increased extrapulmonary right-to-left shunt
Mucus, blood, or meconium blocking endotracheal Pulmonary vasoconstriction
tube Respiratory distress syndrome
Displaced or kinked endotracheal tube Low pH
External compression of airway Severe infection ;,;
J ' Decreased lung tissue "Idiopathic" persistent pulmonary hypertension~:
Pl!lmonary hypoplasia Pulmonary hypoplasia with decreased pulmomu)'i
Thoracic dystrophy vasculature ' ,~~

Diaphragmatic hernia Thoracic dystrophy .

Potter's syndrome Diaphragmatic hernia
Decreased lung compliance Potter's syndrome
Atelectasis Cyanotic heart disease
Respir'~tory distress syndrome
, ,I
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, livery to the tissues (either decreased arterial
however. In adults, liver disease and certain drugs and content or decreased cardiac output) willcausethc- ','
toxins can elevate blood lactic acid levels.35.46.76Also, and Svo2 to fall; these decreases are evident from~
elevations in blood pyruvate will cause lactic acid levels examination of the Fick equation. Low Pvoz and
to rise. Lactic acidosis is therefore not a specific marker values are therefore felt to indicate tissue h)i
for hypoxia.22 Additionally, some studies have shown a Although some believe that Pv02 or Svoz are the.
poor correlation between decreased tissue oxygen de- overall inriicators of tissue hypoxia,26others have! .
livery and increased lactic acid levels, suggesting that a poor wrrelation between these indices and
lactic acidosis is not a sensitive marker for hypoxia.3 This indicators of tissue hypoxia. 54 There is also some'~ ..
~' lack of sensitivity may, in part, be due to the nonlinear as to which of these two indices is superior in
rise in lactic acid levels that occur during progressive tissue oxygenation.7.73Uthe oxyhemoglobindu
I hypoxia.36 Also, because lactic acid is normally metabo- curve shifts markedly to the left, Svoz may ~~~
,, ,
lized by the liver, elevated levels can be temporary.22 useful value, because venous blood will be mor~~
Therefore, the absence of lactic acidosis does not imply rated at any given, Pv02.73 It should be noted;
b, the absence of hypoxia. conditions causing cellular metabolic dysfunctiOn'
inability to utilize oxygen (such as cyanide poisODc<
V The measurement of mixed venous P02 and mixed
Jl venous oxygen saturation (SV02)is another method used venous oxygen indices will actually be high, in .
to assess for hypoxia. In adults, normal Pv02 is about 40 tissue hypoxia.
if I
mm Hg (range 35 to 45 mm Hg),46.73and normal SV02is Other biochemical markers have been use
about 75% (range 68% to 77%).53 The value of these research basis to assess for tissue hypoxia,though,'
L mixed venous oxygen indices is that they reflect the
equilibrium between oxygen delivery to the tissues and
are not part of the standard blood gas report. One~
is hypoxanthine. Hj
most studied of these markers
tissue oxygen consumption. If oxygen consumption anthine is a breakdown product of adenosine' .
., I
remains constant, conditions that decrease oxygen de- phate. Under aerobic conditions, hypoxanthinc.js,