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CHAPTER 7 Physiologic Monitoring
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179
weights and postnatal ages.2 Pulse oximetry saturation
(SpO2) values vary significantly from measured
arterial tension values obtained with an arterial
blood gas specimen.37 A contributing factor may
be that the calibration of pulse oximeters typically
has been performed on healthy adults. A compelling argument for the use of both pulse oximetry
and transcutaneous oxygen monitoring in critically ill
infants can be made because each monitor has its
own shortcomings.
Pulse oximetry monitoring is common in neonatal care. Many infants in NICUs require prolonged monitoring, and a long-lasting oximeter
probe could offer a substantial cost savings. No
complications are associated with the use of
oxygen saturation monitoring other than the
potential for skin trauma caused by adhesive
on the probe. Newer probes held in position by
gentle elastic pressure have no adhesive touching
the infant’s skin.
In the asymptomatic newly born infant, the incidence of congenital heart anomalies is approximately 1% to 2% of live births, with one-fourth of these
having critical congenital heart defects (CCHDs).
CCHD lesions are ductal dependent or require cardiac catheterization or surgery before 1 year of age,
with most requiring intervention within the first
month. If not detected early, organ hypoperfusion
and hypoxemia occur as the infant continues to transition to adult circulation. Detection of CCHDs
before discharge allows medical and surgical
interventions that may be lifesaving. Multiple
organizations in the United States
25,41,42
ly
have recommended routine screening of all
10,24
and global-
infants after 24 hours of life and before discharge. In
2011, the U.S. Department of Health and Human
Services (USDHHS) added screening for CCHDs
to the Recommended Uniform Screening Panel.48
The American Academy of Pediatrics endorsed the
USDHHS recommendation.23 Refer to a full discussion in Chapter 31.
Noninvasive Oxygen–Carbon Dioxide
Monitoring
END-TIDAL CARBON DIOXIDE
MONITORING
End-tidal CO2 monitors use either sidestream or
mainstream analysis. For sidestream analysis, the
endotracheal tube has a second narrow lumen that
opens at the end of the endotracheal tube. Gases
are analyzed from samples taken from the end of
the tube. The advantages of this system are that
there is no increased dead space in the ventilator
circuit and less chance of inspiratory gases contaminating the sample. The disadvantage to this
method is that secretions may pool at the tip of the
endotracheal tube and occlude the sampling port.
The response time to changes in carbon dioxide
content is slower than when mainstream analysis
is used.
Mainstream analysis of carbon dioxide sam-
ples gases in the ventilator circuit. These gases
are thought to be reflective of gases at the tip of the
endotracheal tube. This method requires a sepa-
rate chamber attached to the end of the endotracheal tube adapter, thus adding increased
dead space and additional weight at the endotracheal tube adapter.
A comparison of sidestream and mainstream
analyses of end-tidal CO2 found that distal values
were higher than proximal values and that distal
values correlated more closely with PaCO2 values.47
This discrepancy was thought to result from the
mixing of end-tidal gases with fresh gases in the
ventilator circuit. In an infant with a large alve-
olar-arterial (A-a) gradient, PetCO2 monitoring
cannot be relied on for accuracy. In premature
infants, it may be useful if the lung disease is
mild to moderate; in infants with normal lung
function, this method is reliable.
45
The waveform output of the end-tidal CO2
monitor can be used clinically if the clinician
understands how the waveform corresponds to
the exchange of gases in the lung (see Fig. 7.2) .
The waveform has a sharp rise on expiration
that reflects the carbon dioxide content of
various lung areas. This expiration is followed
by a plateau that reflects the cessation of dead
space gases and the measurement of alveolar
gas. At the end of the plateau is a sharp drop
that reflects the inspiration of fresh gases with
minimal carbon dioxide content. When using
the monitor, the clinician should recognize that a
sharp rise indicates compromised exhalation, such
as in reactive airway disease. Partially plugged and
dislodged endotracheal tubes will change the
angle of rise on the capnogram. The plateau
phase of the capnogram can be altered by severe
hypotension or decreased cardiac output secondary
to an altered minute ventilation-perfusion (
˙
/
)
mismatch (as in pulmonary embolus, cardiac arrest,
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persistent pulmonary hypertension, atelectasis). No
waveform or failure of the waveform to change
indicates ineffective respiration (dislodged endotracheal tube).
TRANSCUTANEOUS OXYGEN–CARBON
DIOXIDE MONITORING
Skin oxygen tension (TcPO2) and carbon dioxide
tension (TcPCO2) are measured by using one or
two electrodes, depending on the model and brand
of the monitor. The electrodes, once positioned on
the skin, heat the area under the probe and cause
certain physiologic changes as discussed. Oxygen
and carbon dioxide that diffuse through the
heated skin are measured by the electrode, and
the value is digitally displayed on the monitor. If
intervals between calibration are longer than 4
hours, the readings are subject to drift. The cal-
ibration procedures vary with the instruments used.
Inherent in the calibration process is the necessity
to change the position of the skin electrode on the
infant. Better correlations are found when the
instrument is calibrated every 4 hours, the temperature is set correctly, and the infant is well
perfused and normothermic. If the temperature
of the probe cannot be maintained at 43°C to
44°C (109.4°F to 111.2°F), a lower temperature
should be selected to avoid possible burns. At a
lower temperature, the TcPO2 monitor can be used
to monitor trends but should not be interpreted as
actual PaO2 values. The range of accuracy of TcPO2
monitors is limited; hypoxia (less than 40 mm Hg)
and hyperoxia (greater than 120 mm Hg) may not
be accurately reflected.
In an infant with suspected significant rightto-left shunting through a patent ductus arteriosus
such as in persistent pulmonary hypertension, two
transcutaneous oxygen electrodes can be used: one
preductally (right shoulder) and the other postductally (lower abdomen or legs). Significant right-toleft shunting through the patent ductus arteriosus
is present when the preductal oxygen tension is
significantly higher than the postductal oxygen
tension.
The disadvantages of the use of transcutaneous monitoring are that the instrument requires
frequent calibration; requires the use of a heated
electrode, which may burn the skin, especially in
low-birth-weight (LBW) infants; requires a 15-minute period after calibration to heat the skin to the
correct temperature; and has a 15- to 20-second
delay in the readings compared with the patient’s
real-time values. The advantages are that it is not
invasive, does not require the removal of blood for
analysis, and displays a continuous readout of skin
oxygen–carbon dioxide tensions.
NURSING CARE OF INFANTS WITH
NONINVASIVE TRANSCUTANEOUS
OXYGEN AND CARBON DIOXIDE
MONITORS
The electrode can be placed on any portion
of the infant’s body as long as good contact
between the electrode and the skin is maintained. Uneven areas of skin such as over bones and
joints should be avoided because of poor contact
between the membrane and the skin surface. The
infant should not lie on the electrode. Placing the
infant on top of the electrode increases the pressure
on the underlying capillaries, thus affecting the flow
of blood under the probe and resulting in a drop
in TcPO2 values. Because of the heat generated
by the electrode (43°C to 44°C [109.4°F to
111.2°F]), small red areas resembling first-degree burns are produced on the infant’s skin.
To minimize trauma to the infant’s skin, the
electrode should be repositioned every 2 to 4
hours, depending on his or her skin sensitivity. Grouping of nursing interventions has resulted
in minimizing the time that the infant receives
less-than-optimal oxygenation.
Cardiorespiratory Monitoring
The chest leads are applied in a triangular pattern on the infant’s chest. Integrity of the leads
must be ensured. Allowing the contact gel to dry
or inadvertently dislodging the lead during procedures such as x-ray examination, echocardiography,
and lumbar puncture may account for inaccurate
tracings. Various components of the electrocardiogram (ECG) pattern may be diagnostically helpful.
The QRS complex should be monitored for baseline height and width. A sudden decrease in QRS
complex height that is not caused by artifact
may be an indication of pneumothorax. The
QT interval is helpful in diagnosing hypocalcemia
in some infants. Other portions of the strip may
be evaluated for electrolyte imbalance and possible
cardiac ischemia. Hyperkalemia can induce arrhythmias, including heart block, ventricular tachycardia
and fibrillation, and asystole. Initially the ECG will
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181
show peaked T waves with a narrow base. As the
potassium level rises, the P dampens, the PR interval
increases, and the QRS widens. Further increases in
the potassium value lead to absent P waves, QRS
merging with the T wave to form a sine wave, followed by fibrillation, and then asystole.
Humans display variability in vital signs because
of the constant adjustments by the sympathetic
and parasympathetic nervous systems. Vital sign
variability in the healthy infant is maintained
near a baseline value. When stressful events such
as late-onset sepsis, intraventricular hemorrhage, or
severe chronic lung disease are present, there is a corresponding change in vital signs and diminution in
variability. Infants developing late-onset infection may
exhibit subtle, nonspecific signs in advance of a clinical
diagnosis. To aid in detecting heart rate changes that
may indicate developing infection, some NICUs now
use the HeRO system (Medical Predictive Sciences,
Charlottesville, VA). Heart rate changes over a 5-day
period are tracked allowing health care personnel to
follow patient trends. Loss of beat-to-beat variability
and rising heart rate warrant investigation. As with
any instrument, use of this device requires patient
assessment and judgment.
19
27
to ensure proper diagnosis and treatment, and the
CLIA regulations strive to ensure quality testing.
The accuracy of whole blood glucometers compared with laboratory values may vary depending
on hypoxia, hematocrit, and elevated triglyceride
values. Accuracy also depends on the product that is
being measured, because some glucometers measure
glucose only, whereas others measure total sugars,
including glucose, galactose, maltose, and xylose.
In addition, the clinician must remember that an
approximately 11% difference exists between
plasma glucose (laboratory sample) and wholeblood glucose (POCT device). The POCT value
should be multiplied by 1.11 to determine a
more approximate plasma value.13 A variance
of accuracy also exists with bedside electrolyte
assessment devices. Transcutaneous neonatal bilirubin
assessments require correlation between the serum
bilirubin value and each device, institution, and
patient population for which it is used.11 As neonatal
care advances, rapid availability of patient information
will become more and more crucial. Expect continuous expansion of POCT.
Event Monitoring
Blood Pressure Monitoring
Arterial pressure monitoring may be accomplished
via the UAC attached to a transducer and monitor. Central venous pressure monitoring may be
carried out in the same manner using the UVC.
The same type of transducer may be used for either
arterial or venous pressure recording.
Some research has indicated that the predictive
value of peripheral blood pressure screening for
CCHD is small and that oscillator blood pressure
measurements are less accurate than pulse oximetry
screening to detect CCHD.5 This failure to detect
CCHD is more pronounced in aortic arch obstructive defects.
Point-of-Care Testing
The Centers for Medicare and Medicaid Services
regulates POCT through the Clinical Laboratory
Improvement Act (CLIA).9 Federal regulations
require initial education about POCT procedures, as well as annual reassessment of competency. The quality of these tests is imperative
The advancement of physiologic monitors with
memory capability has enhanced the ability of the
practitioner to review the physiologic status of
the infant as measured by multiple physiologic
parameters for the past 24 to 48 hours. In many
NICUs, the monitor output is integrated into the
electronic or computerized chart. This integration
allows the care provider to retrieve the data from
the monitors into the chart at preselected times,
either prospectively or retrospectively. When the
monitors are programmed with critical value
ranges, any deviation outside these ranges is
noted as an event, which can then be reviewed,
tallied, or otherwise annotated. For care providers
at the bedside, the challenge is to keep iatrogenic
events (e.g., lead removal, excessive activity of the
infant, a stopcock turned the wrong direction)
minimized such that the infant’s record is as valid
a reflection of actual physiologic status as possible.
Any circumstances noted at the time of the event
that may produce false readings should be recorded
so that when the infant’s record is reviewed, these
events can be placed in context of the circumstances
at the time.
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BOX
7.1
• Umbilical artery catheters
• Ischemia from thrombi, emboli, or arterial spasms
• Hemorrhage caused by catheter dislodgement or loose connec-
• Infection
• Malposition
• Umbilical vein catheters
• Thrombus formation leading to pulmonary embolization
• Thrombus formation in portal vessels
• Hepatic necrosis
• Intestinal ischemia
• Hemorrhage caused by catheter dislodgement or loose connections
• Cardiac complications: dysrhythmias, myocardial perforation,
• Infection
• Peripherally inserted central catheter lines
• Occlusion
• Clotting
• Infection
• Malposition
• Cardiac complications: dysrhythmias, myocardial perforation,
• Breakage and leaking
• Phlebitis
• Peripheral edema
• Vascular erosion into the pleural space
CRITICAL FINDINGS
COMPLICATIONS OF
INDWELLING CATHETERS
tions
pericardial effusion
pericardial effusion
4
COMPLICATIONS
UACs act as foreign bodies, causing fibrin depo-
sition and thrombus formation around the catheter. Although most catheters are associated with
thrombus formation, it is of clinical significance in
less than 10% of patients (Box 7.1). A common
problem associated with major complications
of UACs is ischemic disease resulting from
emboli or arterial spasms. In such cases, the
catheter should be removed immediately and
antithrombin therapy should be considered.
Although vasospasm is common, usually it does
not require immediate removal of the catheter.
Blue discoloration, commonly called “catheter
toes,” is seen, rather than blanching. Obviously,
a hemorrhage may occur when the catheter
slips out or when any of the various connections loosen. For reasons such as these, UACs
require constant attention. If the lower extremities or buttocks blanch, the catheter should
be removed immediately and antithrombin
therapy considered. The benefit of antithrombin
therapy must be balanced against the increased risk
for intracranial hemorrhage.
To prevent bleeding once the catheter is
removed, immediately pinch the subumbilical
area with sterile gauze for 5 minutes until hemostasis is achieved. Avoid downward abdomi-
nal pressure that may compromise respiratory
effort. When the color has returned to the
affected area and the infant is stable, replacement
of the catheter can be considered. If vasospasm
occurs in one leg or foot, apply warm wraps
(diapers wetted with warm water or chemical heel warmers) to the opposite leg, or
apply wraps to the upper extremities, thereby
producing a reflex vasodilation to the legs.
However, inherent in this action is the hazard
of obscuring recognition of compromise in
that extremity. The wraps should be reheated
every 10 to 15 minutes until the spasm has
resolved. The skin temperature of the infant
must be greater than 36°C (96.8°F) for wraps
to be effective.
UVCs may cause thrombus formation.
Thrombi can result in pulmonary embolisms. Clots
may form in the portal vessels, resulting in portal
hypertension. Hepatic necrosis, gut ischemia, and
hemorrhage have been associated with UVCs.
Other complications include dysrhythmias, myocardial perforation, pericardial effusion, and endocarditis.
PICCs that are placed in central veins have
complication rates lower than those placed in
noncentral veins.51 Complications include occlu-
sion, clotting, infection, sepsis, phlebitis, leakage,
extravasation, peripheral edema, malposition, catheter migration, cardiac tamponade, and catheter
breakage.52 Bacteremia, always a major con-
cern, will require the removal of the catheter
if the blood culture remains positive for more
than 24 hours. To prevent central line–associated bloodstream infection (CLABSI), establishment of and strict adherence to a care
bundle is beneficial.8 Bundle items for insertion
include a procedure cart with sterile perimeter,
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183
skin disinfection, and strict sterile technique.
Maintenance items include handwashing, use of
gloves, attention to PICC access and fluid tubing
changes, and daily CLABSI surveillance. Refer to
a full discussion in Chapter 16. Occlusion sometimes may be treated with clot-dissolving agents.
Establishment of a PICC team to insert and manage these devices, catheter tip placement in the
superior or inferior vena cava, and heparinized
solutions have been shown to reduce complications. In an emergent situation, evaluate catheter
tip placement before administering medications or
fluid boluses in case of catheter malposition and
cardiac tamponade.
CONTROVERSIES
Clinicians continue to disagree on the optimal
placement site for UACs. However, a Cochrane
review and subsequent update determined that
high UACs resulted in fewer vascular complications than did low UACs and recommended
the exclusive use of high placement for UACs.3
Prophylactic administration of antibiotic agents is
not indicated.33 Use of the UAC for infusion of
antibiotic agents, calcium, hyperalimentation solutions, or blood varies, and no definitive studies are
available. Blood cultures can be drawn from the
UAC for up to 6 hours after insertion. The use
of heparin in the infusate has been controversial
because heparin decreases catheter occlusion but
not thrombosis.34 In addition, heparin use in a flush
solution alone is not beneficial in preventing catheter occlusion.
Enteral feeding with an umbilical line in
place lacks definitive studies; however, this prac-
tice is more common than was previously thought.
A Cochrane review found that trophic enteral feedings were not detrimental.30 Select NICUs provided trophic and more substantial enteral feedings
with umbilical catheters in place.
Routine monitoring of all infants receiving
intermediate or intensive care is the standard of
care. Indwelling catheters for blood pressure mon-
itoring have the advantage of continuous readout,
but external cuffs are less invasive. There is a continued need for research into the efficacy and safety
of umbilical catheters. Box 7.2 cites new research
into future possibilities for neonatal physiologic
monitoring.
21
BOX
7.2
1. Intelligent monitoring systems. Rather than signal when a single pa-
2. Telemedicine has demonstrated success in examining and diagnosing
3. Telemedicine to provide follow-up care of newborns discharged from
4. Use of nasogastric tubes to monitor intraabdominal pressure of VLBW
5. Electrode-free, noninvasive wireless vital signs monitoring systems.
6. Artificial womb for preterm infants <26 weeks of gestation.
BOX
7.3
Physiologic Monitoring
1. Placement of umbilical lines is invasive. Educate parents about the
• Placement is painless because the umbilical cord contains no nerves.
• The point of catheter insertion and where the tip of the catheter
• The umbilical catheter can be used for numerous functions: ad-
• Care should be taken when holding or manipulating the infant to
• Holding the infant out of the incubator and wrapped in blankets
2. The NICU environment can be frightening. Educate parents about the
• The baby is being monitored by various methods, including car-
• The purpose and a short description of each monitor.
WHAT’S NEXT IN PHYSIOLOGIC
MONITORING?
rameter exceeds a preset threshold, these monitors would integrate
multiple data, including patient medications and laboratory results,
to provide a more complete view of the patient’s status.
retinopathy of prematurity and genetic and neurologic abnormalities.51
It will now evolve to allow a remote neonatal intensive care unit model
where a neonatologist can simultaneously monitor multiple infants
continuously—visually and by the integration of multiple data. Virtual
rounds as needed, as well as care direction, can occur.
NICU, resulting in a decreased need for hospital visits.
preterm infants (<1500 g) to evaluate for feeding intolerance.
PARENT/CAREGIVER TEACHING
PHYSIOLOGIC MONITORING
following:
is located.
ministering IV fluid, medications, and blood products; monitoring;
and obtaining laboratory specimens.
prevent catheter dislodgement and blood loss.
obscures visualization of the catheter and connections.
following:
diorespiratory, blood pressure, and transcutaneous monitors.
2
47,50
37
7
32,44
15,35,49
PARENT TEACHING
Important elements of parent teaching are listed in Box 7.3. As with the many other invasive
procedures in neonatology, the clinician obtains
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permission from the parents for umbilical vessel
catheterization and PICC placement. This may be
the clinician’s first contact with the family and thus
sets the atmosphere for future contacts. Although
parents initially are hesitant about umbilical catheter
placement, generally they are comforted to learn
that it will result in a painless way of drawing blood;
there are no nerves in the umbilical cord to sense
pain. Parents also appreciate that PICC placement
will reduce the number of peripheral IV attempts.
Before parents visit the infant, providers need
to inform parents about the technology that is
being used to monitor the infant (i.e., umbilical
catheter, transcutaneous monitors, cardiorespiratory
monitors, blood pressure monitors), including what
the technology is registering. Often parents are confused about where the catheter goes once it enters
the umbilicus and the purposes of other monitoring
devices.
Parents need to be instructed on how to hold
their infant while an umbilical catheter or PICC
is in place because manipulating the infant may
accidentally dislodge the catheter and result
in blood loss and potential infection. When
the infant is being held out of the incubator and
wrapped in blankets, the integrity of the catheter
and connections is not easily evaluated. The parents’ vigilance around the technology used on their
infant can potentially avoid these incidents.
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39. Ross PA, Newth CJ, Khemani RG. Accuracy of pulse oximetry
in children. Pediatrics. 2014;133(1):22.
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Assoc Neonatal Nurses (NANN) Conference. 2017.
41. Sanchez Luna M, Perez Munuzuri A, Sanz Lopez E, et al,
Comite de Estandares de la Sociedad Espanola de Neonatologia.
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the neonatal period. The Spanish National Neonatal Society
recommendations. An Pediatr (Barc). 2018;88(2):112.
42. Saxena A, Mehta A, Ramakrishnan S, et al. Pulse oximetry as
a screening tool for detecting major congenital heart defects in Indian newborns. Arch Dis Child Fetal Neonatal Ed.
2015;100(5):F416.
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44. Silverman DG, Banack T. Patient monitoring: wide potential
for non-invasive brain temperature monitoring system. ASA
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45. Smith L, Dills R. Survey of medication administration through
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47. Tingay DG, Mun KS, Perkins EJ. End tidal carbon dioxide is as
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mittees/heritable-disorders/rusp/index.html. Accessed October
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49. Usuda H, Watanabe S, Miura Y, et al. Successful maintenance
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50. Wang SK, Callaway NF, Wallenstein MB, et al. SUNDROP: six
years of screening for retinopathy of prematurity with telemedicine. Can J Opthalmol. 2015;50(2):101.
51. Wenger TL, Gerdes J, Taub K, et al. Telemedicine for genetic
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Association of Neonatal Nurses; 2015.
ACID-BASE HOMEOSTASIS
pH = − log [H+]
pH = − log [0.0000001]
pH = − [–7]
pH=7
base
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8
AND OXYGENATION
JAMES S. BARRY, JANE DEACON, CARMEN HERNANDEZ, AND M. DOUGLAS JONES, JR.
ccurate interpretation of blood gas values and an understanding of acid-base
A
and oxygenation physiology are essential
to the proper diagnosis or management of an
ill neonate.
blood gases allows an analysis of two interrelated but separate processes: acid-base homeostasis and oxygen-carrying capacity.
chapter considers the parameters that describe these
processes, their measurements, and the effects of
proposed treatment on homeostasis.
abbreviations and their meanings are listed in
Box 8.1.
Components of arterial blood gases include (1)
measured values (Pao2, Paco2, and pH) and (2) calculated values (oxygen saturation, bicarbonate concentration, and base excess). Some analyzer systems
also estimate hemoglobin concentration. The pH,
Paco2, base excess, and bicarbonate components
are used to assess acid-base homeostasis,
whereas Pao2, saturation (Sao2), and hemoglobin concentration
quacy of oxygen-carrying capacity (Table 8.1).
9,33,53
The measurement of arterial
1,53
Common
1,9
are used to assess the ade-
1,32,44
This
32,44,56
PHYSIOLOGY
Acid-Base Homeostasis
To review basic chemistry, an acid is a hydrogen ion donor, and a base is a hydrogen ion
acceptor. The pH refers to the concentration
of hydrogen ions [H+] in a liquid and reflects
the acid-base balance in liquid.56 The quantity of
hydrogen ions is minute, approximately 0.0000001
mole/L. Therefore, the negative log of the hydrogen
ion concentration is used to define pH and create a
positive, workable number (pH = 7) (Equation 1).
A pH of 7 represents a neutral solution, a pH
of less than 7 represents acidity, and a pH of
greater than 7 represents alkalinity:
(1)
The Henderson-Hasselbalch equation describes
pH as equal to a constant (pK) plus the logarithm
of the ratio of the base-to-acid concentration
(Equation 2).
concentration of hydrogen ions (reflected in the
denominator), the blood pH value decreases, and
acidemia results. Conversely, if there is less acid or
more base, the blood pH increases, and alkalemia
results.
The first step in determining acid-base homeostasis
is the measurement of pH. The normal human pH is
between 7.35 and 7.45. Acidemia and acidosis are often
used interchangeably, but strictly speaking, a pH of less
than 7.35 is acidemia, and the process that caused it is
acidosis; a pH of greater than 7.45 is alkalemia, and the
process that caused it is alkalosis.33 Arterial carbon
dioxide (Paco2) and bicarbonate [HCO
represent the two main components of acidbase homeostasis: (1) the respiratory contribution
(Paco2) controlled by alveolar ventilation
(2) the nonrespiratory or metabolic contribution
controlled primarily by renal excretion, retention,
or production of HCO
affect the nonrespiratory components of acid-base
10,36
Thus, if there is an increase in the
10
pH = pK + log
–.1,30,50
3
/
(2)
acid
3
1,17,20
Other factors that
–
] values
and
BLUE type highlights content that is particularly applicable to clinical settings.
186
CHAPTER 8 Acid-Base Homeostasis and Oxygenation
CO
co
o
o
o
o
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187
BOX
8.1
A Alveolar
a Arterial
D Difference
F Fraction
I Inhalation, inspired
P Partial pressure (tension, driving force)
pH Negative log of hydrogen ion concentration
ABBREVIATIONS
Combined Abbreviations
Pa
Partial pressure of arterial oxygen
2
Fi
Fraction of inspired oxygen
2
Pi
Partial pressure of inspired oxygen
2
P50 Partial pressure at which hemoglobin is 50% saturated
balance cause a change in [HCO
–
]; thus, [HCO
3
an indicator of the nonrespiratory component.
–
3
30,35,50
] is
RESPIRATORY CONTRIBUTION
Carbon dioxide is produced from cellular
metabolism.
1,46
As carbon dioxide is produced,
it dissolves in intracellular fluid and can be measured as the partial pressure (P) of the dissolved gas
(CO2). As the pressure of the dissolved gas increases
inside the cell, carbon dioxide moves out of the
cell and into the blood. Blood transports dissolved
carbon dioxide (some combined with hemoglobin
as carboxyhemoglobin, most as bicarbonate) to
the lung, where the partial pressure in the pulmonary capillary is greater than that in the alveoli,43
causing carbon dioxide to move into the alveoli
down a concentration gradient. Ventilation is the
only method of removing carbon dioxide. The
amount of carbon dioxide in the blood is the
net result of the body’s metabolism (production)
and alveolar ventilation (clearance). Because
metabolism does not change greatly and CO2 diffuses easily across membranes, the only clinically
important limitation to CO2 removal is at the lungs.
Thus, Paco2 reflects alveolar ventilation.
10,17,20,33
In the red blood cell, the enzyme carbonic anhy-
drase promotes the combination of a fraction of
dissolved CO2 with water to form carbonic acid
(H2CO3), which then dissociates into a hydrogen
ion [H+] and a bicarbonate ion [HCO
+ H2O = CO3 = [H+] + [HCO
2
2
–]1,46
3
–
]H
3
(3)
TABLE
8.1
BLOOD GASES VALUES
pH 7.35–7.45
Pa
HCO
Base excess (–5) to (+5)
Pa
O2 saturation 92%–94%
NORMAL (ARTERIAL) BLOOD GAS
VALUES
2
–
3
2
35-45 mm Hg
18-26 mEq/L
60–80 mm Hg
Therefore, an increase in Paco2 (hypoventila-
tion) causes pH to fall. This is called respiratory
acidosis.17 A decrease in Paco2 (hyperventilation)
results in less acid formation in the blood and
causes pH to rise. This pathophysiologic process
is known as respiratory alkalosis.
NONRESPIRATORY (METABOLIC)
CONTRIBUTION
Nonrespiratory (metabolic) derangements can also
disturb acid-base homeostasis. Normal metabolism
produces hydrogen ions. Blood pH is maintained
within normal limits by renal mechanisms for
excreting hydrogen ions. Increased production
of [H+] may occur in conditions such as shock
with poor peripheral tissue perfusion or genetically determined aberrations of metabolism.52
The hydrogen ions produced must be eliminated to
avoid a fall in blood pH. Derangements also occur
when hydrogen ions are lost (e.g., in gastric fluids)
or when bicarbonate is lost (e.g., in diarrheal fluid
or ileostomy drainage).
53
Authorities differ as to the best way to describe
nonrespiratory derangements in acid-base status.
The traditional approach relies on the measurement of pH, Pco2, and [HCO
–
]. An alternative
3
description is of acid-base status in terms of (1)
strong ions (Na+, K+, Ca2+, Mg2+, Cl–), strong
because they remain dissociated at normal human
blood pH, and (2) weak acids (hemoglobin, albumin, inorganic phosphate), weak because they
are partially dissociated at the normal human
blood pH. Blood pH in this conceptualization is
a function of the difference between strong cations and strong anions, the strong ion difference
(SID). As an example, the alkalosis associated
188 UNIT TWO Support of the Neonate
pH – 6.1 + log (20/1.2)
pH = 6.1 + 1.3 = 7.4
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with the loss of gastric fluid would be described
exclusively in terms of the loss of [Cl–], with the
loss of [H+] making no independent contribution
to the resulting alkalemia. Advocates maintain
that the measurement of SID leads to a greater
understanding of the causes of nonrespiratory and
mixed acid-base derangements.
16,24,29,46
Others
favor staying with the traditional bicarbonate-centered model.
15,34
The present discussion focuses
on the traditional bicarbonate-centered approach.
Readers are referred to recent reviews for comparisons of the two methods.
A fall in blood [HCO
29,34
–
] might indicate that
3
bicarbonate, a base and therefore a hydrogen ion
acceptor, has been used up by the addition of [H+].
As shown in Equation 3, a change in [HCO
–
]
3
might also reflect a change in Pco2. This difficulty
is overcome in blood gas analyzers by correcting
the Pco2 (graphically) to 40 mm Hg, yielding a
“standard bicarbonate” concentration.46 The standard bicarbonate concentration and the buffering
properties of hemoglobin are combined in the
concept of base excess (BE). BE is strictly defined
as the amount of base or acid that is needed
to restore blood to a pH of 7.4 at a normal
Pco2 of 40 and temperature of 37°C.2 A positive value suggests a deficit of fixed (i.e., not
volatile as with H2CO3) acid or an excess of
base; a negative value indicates an excess of
fixed acid or a deficit of base.46 An abnormality of the standard bicarbonate concentration
or BE indicates a process of nonrespiratory
(metabolic) alkalosis30 or nonrespiratory (metabolic) acidosis.49 Caution is needed because
various blood gas analyzers do not calculate BE in
a similar manner and can vary by 3 to 9 mmol/L.2
Additionally, BE is commonly calculated using
assumptions from adult physiology with a normal
bicarbonate of 26, which is significantly higher
than what would be considered normal for a premature neonate.
39
In the Henderson-Hasselbalch equation (see
Equation 2), the pH is equal to a constant, pK, plus
the logarithm of the base:acid ratio.
tuting [HCO
the acid
–
] for the base and dissolved CO2 for
3
17,46
and multiplying CO2 by its solubility
1,33,46
By substi-
coefficient (0.03 mEq/L/mm Hg), the equation
becomes the following:
pH = pK + log [HCO
–
/ (Pco2 × 0.03)]
3
(4)
The value of pK is 6.1; the normal [HCO
3
–
] is
24 mEq/L, and the normal Paco2 is 40 mm Hg.
Substituting, we obtain the following:
(5)
or
Changes in the 20:1.2 ratio have profound effects
on the pH.
1. Hypoventilation of sufficient degree that Paco2
is doubled from 40 to 80 (respiratory acidosis)
results in a ratio of 24:2.4, or 10. The logarithm
of 10 is 1, and the pH would be 6.1 + 1, or 7.1.
2. If a metabolic acidosis reduced [HCO
to 12 mEq/L, the ratio would be 12:1.2 or 10:1,
and the pH would be 7.1.
MIXED CONTRIBUTIONS
The two most common reasons for acid-base
disturbance in humans are the accumulation
of carbon dioxide and the production of lactic
acid through anaerobic metabolism as a consequence of tissue oxygen deprivation. Thus far,
these derangements (Fig. 8.1) have been discussed
as if they happened in isolation, but respiratory
and nonrespiratory problems often occur simultaneously depending on pathologic processes in the
body. Besides the four single acid-base derange-
ments, there are combined acid-base derangements: (1) respiratory acidosis and metabolic
acidosis, (2) respiratory acidosis and metabolic
alkalosis, (3) respiratory alkalosis and metabolic acidosis, and (4) respiratory alkalosis and
metabolic alkalosis. The combined acidoses or
combined alkaloses have a cumulative effect on
the pH, whereas a combination of acidosis and
alkalosis tends to negate the effects of each on the
pH value.
COMPENSATION
Acid-base homeostasis maintains pH near the nor-
mal range. The body attempts to maintain equi-
librium by balancing a pathologic process with
a physiologic process or predictable buffering
response.
nonrespiratory components of the acid-base system
are deranged, the other system will compensate to
counterbalance the primary process. For example,
any respiratory process that leads to retention of carbon dioxide (respiratory acidosis) stimulates a nonrespiratory system, in this case the renal system, to
1,29
The following are two examples:
32,33,44,56
10,33,53
Thus, if either the respiratory or
–
] from 24
3
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