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
meqlL
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
1M
QC

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

t
...

Table 38.3. Blood gas classifications
Classification
Respiratory disorder
Uncompensated acidosis
Partly compensated acidosis
Compensated acidosis
Uncompensated alkalosis
Partly compensated alkalosis
Compensated alkalosis
Metabolic disorder
Uncompensated acidosis
Partly compensated acidosis
Compensated acidosis
Uncompensated alkalosis
Partly compensated alkalosis
Compensated alkalosis
FromChatbum RL, Carlo WA: Assessment of neonatal
Chicago,.1988.
Arrows,elevated or depressed values; N, normal; lICO) -, bicarbonate; BE, base excess.
metabolicacid-base disorders are further classified as
uncompensated, partly compensated, or completely
compensated. Primary respiratory acid-base disorders
are compensated by metabolic adjustments, and vice
versa. This compensatory effect is evident from the
Henderson-Hasselba1ch equation, which shows that a
I relativelyconstant ratio of [HCO] -] to PC02 is necessary
to maintain pH in the normal range. By examining the
pH, 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 may
k ariseis the determination of which abnormality is the
primaryacid-base problem and which is the compensa-
torymechanism. For example, if a particular patient has
a normal pH, but both the PC02 and [HCO] -] are
elevated,the blood gas disturbance may represent either
a 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 bicarbonate
E 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 of
g {: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-
' 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
I}'Ja&d-basestatus, because
.
alterations in respiratory acid-
t basebalance (that is, changes in PC02) will also have a
. small effect on [HC03 - V This
effect is evident from
i,;~mining the hydrolysis reaction, which shows that as
f Peo2 and [dissolved CO2] vary, so does [HCO]
~;,
Chapter 38 Blood gas interpretation 453
pH Pan)1 HCOJ- BE
t N N
t 1-
I t
N t t t
t N N
t
N
N
N
t N t t
t t t t
N t t t
gas exchange. In Carlo WA, Chatburn RL (eds): Neo1latal respiratory care, ed 2, Year Book,
. ratio between changes in PC02 to changes in [HC03 -]
is about 10:1 when Peo2 increases greater than 40 mm
Hg, and is about 5: I when Peo2 falls below this value.51
There needs to be significant hypercarbia or hypocarbia,
therefore, for [HCO~ -1 to be substantially affected by
changes in Peo2.
The measurement of standard bicarbonate is de-
signed to obviate the effect of Peo7 on [HCO~ -] and
is included in the Iypical blood gas report. In this in
vitro test, blood is equilibrated to a Peo2 of 40 mm
Hg at 37°C, and Ihe rHCO] -] is determined. "his
method theoretically provides 'a more accurate index
of metabolic acid-base balance than does actual bi-
carbonate. Standard bicarbonate rel1ects in vitro con-
ditions, however, and the results can differ somewhat
from the "true" value for standard bicarbonate if the
measurement could be performed in vivo.9 Under most
circumstances, standard and actual bicarbonate values
will be similar, unless there is significant hypercarbia
or hypocarbia.
Base excess ([BE]) is another metabolic acid-base
index.17 [BE] is equal to the observed blood buffer base
minus the normal blood buffer base. It is a reflection of
the effect of all oluod buffers, not just bicarbonate;
Under conditions of metabolic acidosis, buffering capac-
ity will be consumed, and the base excess will be
negative; this condition is also referred to as a base
deficit. [BE] is calculated from a Siggaard-Anderson
nomogram, which relates Peo2, pH, hemoglobin con-
centration, and base excess. This nomogram was devel-
oped from data ootained in vitro.') As such, and like
standard bicarbonate, the determination of [BE] may
not exactly reflect the "true" [BE] in vivo.
Primary respiratory disorders and compensatory
mechanisms. Respiratory acidosis is the most important
disorder in this group because of its frequency and
potentially life-threatening nature. Uncompensated, or
acute, respiratory acidosis is due to alveolar hypoventi-
lation, and is heralded by an elevation in Peo2 with a fall
in pH. For every increase in PC02of 10 mm Hg, the pH
will fall by about 0.07 units.4u Causes for hypoventilation
]. The
 Chapter 38 Blood gas interpretation 455 I'i'
I
l.
1 "
100 I I I / A
7.0
L
Mixed 18 24 ; I
,; j:
90 -I I 'iij'" respiratory
0 and ["
-C metabolic t"
'u
80-1 0 acidosis/ g;c.nirntn,.v / 1-7.1
Partly compensated . I.:
metabolicacidosis .B I'
70 -I .E
Q)
~ It!
I:
.j
I- 7.2
60 Partly compensated
respiratory acidosis f I
~
::;- I':
+
J:
........
50 7.3 =a. f, .,
..s Compensated II
I.
metabolic Compensated I
40-1 acidosis respiratory acidosis 7.4 !.

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

10-1 ///
("0
alkalosis
..D
0
Qj [ 76
8.0
"'<,; J/
9-1 ana meraOOIlCI I I- 8.5
o 10 20 30 40 50 60 70 80 90
PC02(torr)

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.)

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

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

, I
Hypoventilation
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

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
Pneumothorax
, ,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,
however. In adults, liver disease and certain drugs and
toxins can elevate blood lactic acid levels.35.46.76Also,
elevations in blood pyruvate will cause lactic acid levels
to rise. Lactic acidosis is therefore not a specific marker
for hypoxia.22 Additionally, some studies have shown a
poor correlation between decreased tissue oxygen de-
livery and increased lactic acid levels, suggesting that
lactic acidosis is not a sensitive marker for hypoxia.3 This
~' lack of sensitivity may, in part, be due to the nonlinear
rise in lactic acid levels that occur during progressive
I hypoxia.36 Also, because lactic acid is normally metabo-
,, ,
lized by the liver, elevated levels can be temporary.22
Therefore, the absence of lactic acidosis does not imply
b, the absence of hypoxia.
V The measurement of mixed venous P02 and mixed
Jl venous oxygen saturation (SV02)is another method used
to assess for hypoxia. In adults, normal Pv02 is about 40
if I
I
mm Hg (range 35 to 45 mm Hg),46.73and normal SV02is
.
!~
about 75% (range 68% to 77%).53 The value of these
L mixed venous oxygen indices is that they reflect the
equilibrium between oxygen delivery to the tissues and
tissue oxygen consumption. If oxygen consumption
., I
remains constant, conditions that decrease oxygen de-
livery to the tissues (either decreased arterial
content or decreased cardiac output) willcausethc- ','
and Svo2 to fall; these decreases are evident from~
examination of the Fick equation. Low Pvoz and
values are therefore felt to indicate tissue h)i
Although some believe that Pv02 or Svoz are the.
overall inriicators of tissue hypoxia,26others have! .
a poor wrrelation between these indices and
indicators of tissue hypoxia. 54 There is also some'~ ..
as to which of these two indices is superior in
tissue oxygenation.7.73Uthe oxyhemoglobindu
curve 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~
is hypoxanthine. Hj
most studied of these markers
anthine is a breakdown product of adenosine' .
phate. Under aerobic conditions, hypoxanthinc.js,