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Trang 5Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,
M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd
Renee A Bobrowski
Department of Obstetrics and Gynecology, Saint Alphonsus Regional Medical Center, Boise, ID, USA
Introduction
Abnormalities in acid – base and respiratory homeostasis are
common among patients requiring intensive medical support,
but many clinicians fi nd the physiology cumbersome As a result
of both their illness and our therapeutic interventions, critically
ill patients frequently require assessment of metabolic and
respi-ratory status An understanding and clinical application of basic
physiologic principles is therefore essential to the care of these
patients It is also important that clinicians involved in the care
of critically ill gravidas be familiar with the metabolic and
respira-tory changes of pregnancy as well as their effect on arterial blood
gas interpretation
The arterial blood gas provides information regarding acid –
base balance, oxygenation, and ventilation A blood gas should
be considered when a patient has signifi cant respiratory
symp-toms or experiences oxygen desaturation, or as a baseline in the
evaluation of pre - existing cardiopulmonary disease In this
chapter we focus on fundamental physiology, analytic
consider-ations, effective interpretation of an arterial blood gas, and acid –
base disturbances
Essential physiology
Acid – base homeostasis
Normal acid – base balance depends on production, buffering, and
excretion of acid The delicate balance that is crucial for survival
is maintained by buffer systems, the lungs and kidneys Each day,
approximately 15 000 mEq of volatile acids (e.g carbonic acid)
are produced by the metabolism of carbohydrates and fats These
acids are transported to and removed via the lungs as carbon
dioxide (CO 2 ) gas Breakdown of proteins and other substances results in 1 – 1.5 mEq/kg/day of non - volatile or fi xed acids (pre-dominantly phosphoric and sulfuric acids), which are removed
by the kidneys
Buffers are substances that can absorb or donate protons and thereby resist or reduce changes in H + ion concentration Acids produced by cellular metabolism move out of cells and into the extracellular space where buffers absorb the protons These protons are then transported to the kidney and excreted in urine The intra - and extracellular buffer systems that maintain homeo-stasis in the human include the carbonic acid – bicarbonate system, plasma proteins, hemoglobin, and bone
The carbonic acid – bicarbonate system is the principal extracel-lular buffer Its effectiveness is predominantly due to the ability
of the lungs to excrete carbon dioxide In this system, bicarbon-ate, carbonic acid and carbon dioxide are related by the equation:
Gaseous phase
Dissolved Carbonic
acid
Carbonicc anhydrase
Bicarbonate
++ −
3
Carbon dioxide is produced as an end - product of aerobic metabolism and physically dissolves in body fl uids A portion of dissolved CO 2 reacts with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions The concentra-tion of carbonic acid is normally very low relative to that of dis-solved CO 2 and HCO3 − If the H + ion concentration increases, however, the acid load is buffered by bicarbonate, and additional carbonic acid is formed The equilibrium of the equation is then driven to the left, and excess acid can be excreted as carbon dioxide gas
The Henderson – Hasselbalch equation expresses the relation-ship between the reactants of the carbonic acid – bicarbonate system under conditions of equilibrium:
Trang 6Chapter 5
Acid – base disturbances
Disturbances in acid – base balance are classifi ed according to whether the underlying process results in an abnormal rise or fall
in arterial pH The suffi x - osis refers to a pathologic process that causes a gain or loss of acid or base Thus, acidosis describes any
condition that leads to a fall in blood pH if the process continues
uncorrected Conversely, alkalosis characterizes any process that
will cause a rise in pH if unopposed The terms acidosis and
alkalosis do not require the pH to be abnormal The suffi x - emia refers to the state of the blood, and acidemia and alkalemia are
appropriately used when blood pH is abnormally low ( < 7.36) or high ( > 7.44), respectively [1]
In addition, alterations in acid – base homeostasis are classifi ed based upon whether the underlying mechanism is metabolic or respiratory If the primary abnormality is a net gain or loss of
CO 2, this is respiratory acidosis or alkalosis, respectively Alternatively, a net gain or loss of bicarbonate results in metabolic alkalosis or acidosis, respectively If only one primary process is present, then the acid – base disturbance is simple, and bicarbon-ate and PCO 2 always deviate in the same direction A mixed disturbance develops when two or more primary processes are present, and the changes in HCO3 − and PCO 2 are in opposite directions
The compensatory response attempts to normalize the [HCO3 −]PCO2 ratio and maintain pH Renal and pulmonary function must be adequate for these responses to be effective and adequate time must be allowed for the complete response The compensatory response for a primary respiratory abnormality is via the bicarbonate system or acid excretion by the kidney and requires several days for a complete response Compensation for
a metabolic aberration is through ventilation changes and occurs quite rapidly
Compensatory responses cannot, however, completely return the pH to normal, with the exception of chronic respiratory alka-losis The more severe the primary disorder, the more diffi cult it
is for the pH to return to normal When the pH is normal but PCO 2 and HCO3 − are abnormal or the expected compensatory responses do not occur, then a second primary disorder exists The four types of acid – base abnormalities and the compensatory response associated with each are listed in Table 5.1
Respiratory and acid – base changes during pregnancy
A variety of physiologic changes occur during pregnancy, affect-ing maternal respiratory function and gas exchange As a result,
an arterial blood gas obtained during pregnancy must be inter-preted with an understanding of these alterations Since these changes begin early in gestation and persist into the puerperium, they must be taken into consideration regardless of the stage of pregnancy [2] In addition, the altitude at which a patient lives will affect arterial blood gas values, and normative data for each individual population should be established [3]
Minute ventilation increases by 30 – 50% during pregnancy [4,5] and alveolar and arterial PCO 2 decrease Normal maternal arterial PCO 2 levels range from 26 to 32 mmHg [6 – 8] Since the
P
metabolic respiratory CO
( ) =
−
2
As the equation demonstrates, the ratio of [ HCO3 −] to PCO 2
determines pH (H + ion concentration) and not individual or
absolute concentrations This ratio is infl uenced to a large extent
by the function of the kidneys ( HCO3 −) and lungs (PCO 2 ) The
constant s represents the solubility coeffi cient of CO 2 gas in
plasma and relates PCO 2 to the concentration of dissolved CO 2
and HCO3 − The value of s is 0.03 mmol/L/mmHg at 37 ° C The
dissociation constant (pK) of blood carbonic acid is equivalent
to 6.1 at 37 ° C
The lungs are the second component of acid – base regulation
Alveolar ventilation controls PCO 2 independent of bicarbonate
excretion When the bicarbonate concentration is altered,
respira-tory changes attempt to return the ratio of [HCO3 −] PCO2 toward
the normal 20/1 Thus, in the presence of metabolic
acidosis (decreased HCO3 −), ventilation increases, PCO 2 is
lowered, and the ratio normalizes In metabolic alkalosis, the
increase in HCO3 −
The kidney is the fi nal element of acid – base regulation The
main functions of the renal system are excretion of fi xed acids
and regulation of plasma bicarbonate levels Carbonic acid that
has been transported to the kidney dissociates into H + and HCO3 −
in renal tubular cells Each H + ion secreted into the tubular lumen
is exchanged for sodium, and HCO3 − is passively reabsorbed into
the blood Essentially all bicarbonate must be reabsorbed by the
kidney before acid can be excreted, because the loss of one HCO3 −
is equivalent to the addition of one H + ion Mono - and diphasic
phosphates and ammonia are urinary buffers that combine with
H + ions in the renal tubules and are excreted Under normal
conditions, the amount of H + excreted approximates the amount
of non - volatile acids produced
The buffer systems, the lungs and kidneys interact to maintain
very tight control of the body ’ s acid – base balance The sequence
of responses to a H + ion load and the time required for each may
be summarized:
Extracellular buffering
by HCO
immediate
Respiratory buf
→
−
3
ffering
minutes to hours
Renal excretion
of H s hour CO
→
↓
↑
+
2
ss to days
In contrast, when P changes
Intracellular b
CO
u
uffering
minutes
Renal excretion of H hours to days
→
+
Unlike the response to an acid load, no extracellular buffering
occurs with a change in PCO 2 Since HCO3 − is not an effective
buffer against H 2 CO 3 , the only protection against respiratory
aci-dosis or alkalosis is intracellular buffering (i.e by hemoglobin)
and renal H + ion excretion
Trang 7Oxygen delivery and consumption
All tissues require oxygen for the combustion of organic com-pounds to fuel cellular metabolism The cardiopulmonary system serves to deliver a continuous supply of oxygen and other essen-tial substrates to tissues Oxygen delivery is dependent on oxy-genation of blood in the lungs, oxygen - carrying capacity of the blood and cardiac output Under normal conditions, oxygen delivery (DO 2) exceeds oxygen consumption (VO 2) by about 75% [17] The amount of oxygen delivered is determined by the cardiac output (CO, L/min) times the arterial oxygen content (CaO 2 mL/O 2 /dL):
DO2=CO C O× a 2×10dL L Arterial oxygen content (CaO 2 ) is determined by the amount
of oxygen that is bound to hemoglobin (S a O 2 ) and by the amount
of oxygen that is dissolved in plasma (P a O 2 × 0.003):
C Oa 2=(1 39 ×Hb S O× a 2) +(P Oa 2×0 003 )
It is clear from this formula that the amount of oxygen dis-solved in plasma is negligible and, therefore, that arterial oxygen
is dependent largely on hemoglobin concentration and arterial oxygen saturation Oxygen delivery can be impaired by condi-tions that affect either cardiac output (fl ow), arterial oxygen content, or both (Table 5.3 ) Anemia leads to low arterial oxygen content because of a lack of hemoglobin binding sites for oxygen [18] The patient with hypoxemic respiratory failure will not have suffi cient oxygen available to saturate the hemoglobin molecule Furthermore, it has been demonstrated that desaturated hemo-globin is altered structurally in such a fashion as to have a dimin-ished affi nity for oxygen [19] It must be kept in mind that the amount of oxygen actually available to tissues also is affected by the affi nity of the hemoglobin molecule for oxygen Thus, the oxyhemoglobin dissociation curve (Figure 5.1 ) and those condi-tions that infl uence the binding of oxygen either negatively or positively must be considered when attempts are made to maxi-mize oxygen delivery [20] An increase in the plasma pH level or
a decrease in temperature or 2,3 diphosphoglycerate (2,3 - DPG) will increase hemoglobin affi nity for oxygen, shifting the curve to the left and resulting in diminished tissue oxygenation If the
fetus depends upon the maternal respiratory system for carbon
dioxide excretion, the decreased maternal PCO 2 creates a gradient
that allows the fetus to offl oad carbon dioxide Thus, fetal PCO 2
is approximately 10 mmHg higher than the maternal level when
uteroplacental perfusion is normal
Maternal alveolar oxygen tension increases as alveolar carbon
dioxide tension decreases, and arterial PO 2 levels rise as high as
106 mmHg during the fi rst trimester [7,9] Airway closing
pres-sures increase with advancing gestation, causing a slight fall in
arterial PO 2 in the third trimester (101 – 104 mmHg) [7,9,10] The
arterial PO 2 level, however, is dependent upon the altitude at
which the patient resides The mean arterial PO 2 for gravidas at
sea level ranges from 95 to 102 mmHg [9,11] , while the average
values reported for those living at 1388 m are 87 mmHg [12] and
61 mmHg at 4200 m [13] As with carbon dioxide transfer, the
fetus depends upon the oxygen gradient for continued diffusion
across the placenta Maternal arterial oxygen content, uterine
artery perfusion and maternal hematocrit contribute to fetal
oxy-genation and compromise of any of these factors can cause fetal
hypoxemia and eventually acidemia [14]
Despite the increased ventilation, maternal arterial pH remains
essentially unchanged during pregnancy [7,15] A slightly higher
pH value has been noted in women living at a moderate altitude,
with a reported mean of 7.46 at 1388 m above sea level [3]
Bicarbonate excretion by the kidney is increased during normal
pregnancy to compensate for the lowered PCO 2 , and serum
bicar-bonate levels are normally 18 – 21 mEq/L [2,7,8,16] Thus, the
metabolic state of pregnancy is a chronic respiratory alkalosis
with a compensatory metabolic acidosis (Table 5.2 )
Table 5.1 Summary of acid – base disorders: the primary disturbance, compensatory response, and expected degree of compensation
Metabolic acidosis Decreased HCO3 − Decreased P CO 2 P a CO 2 = [1.5 × (serum bicarbonate)] + 8
P a CO 2 = last two digits of pH Metabolic alkalosis Increased HCO3 − Increased P CO 2 P a CO 2 = [0.7 × (serum bicarbonate)] + 20 Respiratory acidosis Increased P CO 2 Increased HCO3 −
Acute: pH ∆ = 0.08 × (measured P a CO 2 − 40)/10
Chronic: pH ∆ = 0.03 × (measured P a CO 2 − 40)/10 Respiratory alkalosis Decreased P CO 2 Decreased HCO3 − Acute: pH ∆ = 0.08 × (40 − measured P a CO 2 )/10
Chronic: pH ∆ = 0.03 × (40 − measured P a CO 2 )/10
Table 5.2 Arterial blood gas values during pregnancy at sea level
Normative data should be established for individual populations residing
at high altitude
HCO3 −
Trang 8Chapter 5
to some areas, with relative hypoperfusion of other areas, limiting optimal systemic utilization of oxygen [21]
The patient with diminished cardiac output secondary to hypovolemia or pump failure is unable to distribute oxygenated blood to tissues Therapy directed at increasing volume with normal saline, or with blood if the hemoglobin level is less than
10 g/dL, increases oxygen delivery in the hypovolemic patient The patient with pump failure may benefi t from inotropic support and afterload reduction in addition to supplementation
of intravscular volume
Relationship of oxygen delivery to consumption
Oxygen consumption (VO 2 ) is the product of the arteriovenous oxygen content difference (C (a – v) O 2 ) and cardiac output Under normal conditions, oxygen consumption is a direct function of the metabolic rate [22]
VO2=C( a v − )O2×CO×10dL L The oxygen extraction ratio (OER) is the fraction of delivered oxygen that is actually consumed:
OER=VO DO2 2 The normal OER is about 0.25 A rise in the OER is a compen-satory mechanism employed when oxygen delivery is inadequate for the level of metabolic activity An OER of less than 0.25 sug-gests fl ow maldistribution, peripheral diffusion defects, or frac-tional shunting [22] As the supply of oxygen is reduced, the fraction extracted from blood increases and oxygen consumption
is maintained If a severe reduction in oxygen delivery occurs, the limits of oxygen extraction are reached, tissues are unable to sustain aerobic energy production, and consumption decreases The level of oxygen delivery at which oxygen consumption begins
to decrease has been termed the “ critical DO 2 ” [23] At the critical
DO 2, tissues begin to use anerobic glycolysis, with resultant
plasma pH level or temperature falls, or if 2,3 - DPG increases,
hemoglobin affi nity for oxygen will decrease and more oxygen
will be available to tissues [20]
In certain clinical conditions, such as septic shock and adult
respiratory distress syndrome, there is maldistribution of fl ow
relative to oxygen demand, leading to diminished delivery and
loss of vascular autoregulation, producing regional and
microcir-culatory imbalances in blood fl ow [21] This mismatching of
blood fl ow with metabolic demand causes excessive blood fl ow
10
10
20
30
40
50
60
70
80
90
100
P50 O2 tension (mmHg)
pH
pH
DPG Temp
DPG Temp
Figure 5.1 The oxygen binding curve for human hemoglobin A under
physiologic conditions (middle curve) The affi nity is shifted by changes in pH,
diphosphoglycerate (DPG) concentration, and temperature, as indicated P 50
represents the oxygen tension at half saturation (Reproduced by permission from
Bunn HF, Forget BG Hemoglobin: molecular, genetic, and clinical aspects
Philadelphia: WB Saunders, 1986.)
Table 5.3 Commonly used formulas for assessment of oxygenation
Pulmonary capillary oxygen content C c ′ O 2 = [Hb](1.39) + ( P A O 2 )(0.003)
Arterial oxygen content C a O 2 = (1.39 × Hb × S a O 2 ) + ( P a O 2 × 0.003) 18 – 21 mL/dL Mixed venous oxygen content C O 2 = (1.39 × Hb × S O 2 ) + ( P O 2 )(0.003)
Oxygen consumption V O 2 = Q T ( C a O 2 − C v O 2 ) = 13.8 (Hb) (Q T ) ( S a O 2 − S v O 2 )/100 180 – 280 mLO 2 /min
Estimated shunt
Est Qsp/Qt = C
C′O2 – CaO2
[CC′O2 – CaO2] + [CaO2 – CvO2]
P a CO 2 , partial pressure of arterial carbon dioxide; P a O 2 , partial pressure of arterial oxygen; P O 2 , partial pressure of venous oxygen; Hb, hemoglobin; S a O 2 , arterial oxygen saturation; S O 2 , venous oxygen saturation; Q T , cardiac output
Trang 9catheter [29] An adequate volume of maintenance fl uid or fl ush solution must be withdrawn from the catheter and discarded before obtaining the sample for analysis But the diffi culty is estimating the appropriate amount to withdraw Although a 2.5
mL discard volume has been suggested, it has also been recom-mended that each intensive care unit establish its own policy based upon individual catheter and connection systems [1,30,31] Air bubbles in the collection syringe cause time - dependent changes in the arterial blood gas Air trapped as froth accelerates these changes because of the increased surface area [32] The degree of change in PO 2 depends upon the initial PO 2 of the sample Since an air bubble has a PO 2 of 150 mmHg (room air), the bubble will cause a falsely elevated PO 2 if the sample PO 2 is
< 150 mmHg The opposite occurs if the sample has an initial
PO 2 > 150 mmHg [1,33] Oxygen saturation is most signifi cantly affected when the sample PO 2 is < 60 mmHg since saturation changes rapidly with changes in PO 2 , as predicted by the
within several minutes of exposure to ambient air [32,34] When a blood sample remains at room temperature following collection, PO 2 and pH may decrease while PCO 2 increases Specimens analyzed within 10 – 20 minutes of collection give accu-rate results even when transported at room temperature [35,36]
In most clinical settings, however, the time between sampling and laboratory analysis of the specimen exceeds this limit Therefore, the syringe should be placed into an ice bath immediately after sample collection The combination of ice and water provides better cooling of the syringe than ice alone, and a sample may be stored for up to 1 hour without adversely affecting blood gas results [34]
Several additional factors can infl uence blood gas results Insuffi cient time between an adjustment in fractional inspired oxygen or mechanical ventilator settings and blood gas analysis may not accurately refl ect the change Equilibration is quite rapid, however, and has been reported to occur as soon as 10 minutes after changing ventilator settings of postoperative cardiac patients [37] General anesthesia with halothane will falsely elevate PO 2 determination as it mimics oxygen during sample analysis [38 – 41] Finally, severe leukocytosis causes a false lowering of PO 2 due
to consumption by the cells in the collection syringe [42] The effect of the white blood cells may be minimized, but not neces-sarily eliminated, by cooling the sample immediately after it is obtained
The blood gas analyzer
The blood gas analyzer is designed to simultaneously measure the
pH, PO 2 , and PCO 2 of blood An aliquot of heparinized blood is injected into a chamber containing one reference and three mea-suring electrodes Each meamea-suring electrode is connected to the reference electrode by a Ag/AgCl wire The electrodes and injected sample are kept at a constant 37 ° C by a warm water bath or heat exchanger The accuracy of the measurements depends upon routine calibration of equipment, proper sample collection, and constant electrode temperature
lactate production and metabolic acidosis [23] If this oxygen
deprivation continues, irreversible tissue damage and death
ensue
Oxygen delivery and consumption in pregnancy
The physiologic anemia of pregnancy results in a reduction in the
hemoglobin concentration and arterial oxygen content Oxygen
delivery is maintained at or above normal despite this because
cardiac output increases 50% It is important to remember,
there-fore, that the pregnant woman is more dependent on cardiac
output for maintenance of oxygen delivery than the non -
throughout pregnancy and is greatest at term, reaching an average
of 331 mL/min at rest and 1167 mL/min with exercise [10]
During labor, oxygen consumption increases by 40 – 60%, and
cardiac output increases by about 22% [25,26] Because oxygen
delivery normally far exceeds consumption, the normal pregnant
patient usually is able to maintain adequate delivery of oxygen to
herself and her fetus, even during labor When a pregnant
patient ’ s oxygen delivery decreases, however, she can very quickly
reach the critical DO 2 , especially during labor, compromising
both herself and her fetus The obstetrician, therefore, must make
every effort to optimize oxygen delivery before allowing labor to
begin in the compromised patient
Blood gas analysis
The accuracy of a blood gas determination relies upon many
factors, including blood collection techniques, specimen
trans-port, and laboratory equipment Up to 16% of specimens may be
improperly handled, diminishing diagnostic utility in a number
of cases [27] Factors that can infl uence blood gas results include
excessive heparin in the collection syringe, catheter dead space,
air bubbles in the blood sample, time delays to laboratory analysis
as well as other less common causes This section highlights
con-siderations for obtaining a blood sample and potential sources of
error, and briefl y describes laboratory methods
Sample collection
The collection syringe typically contains heparin to prevent
clot-ting of the specimen Excessive heparin in the syringe before
blood collection, however, can signifi cantly decrease the PCO 2
and bicarbonate of the sample The spurious PCO 2 level results
in a falsely lowered bicarbonate concentration when calculated
using the Henderson – Hasselbalch equation Although sodium
heparin is an acid, pH is minimally affected because whole blood
is an adequate buffer Expelling all heparin except that in the dead
space of the syringe and needle will ensure adequate dilution by
obtaining a minimum of 3 mL of blood and reduce or avoid
anticoagulant - related errors [28]
In the intensive care setting, an arterial catheter is often placed
when frequent blood sampling is anticipated Dilutional errors
occur when a blood sample is contaminated with fl uids in the
Trang 10Chapter 5
Pulse oximetry is ideal for non - invasive arterial oxygen satura-tion monitoring near the steep porsatura-tion of the oxyhemoglobin dissociation curve, namely at a P a O 2 less than or equal to 70 mmHg [44] P a O 2 levels greater than or equal to 80 mmHg result in very
changes in the P a O 2 from 90 mmHg to 60 mmHg can occur without signifi cant change in arterial oxygen saturation This technique, therefore, is useful as a continuous monitor of the adequacy of blood oxygenation and not as a method to quantitate the level of impaired gas exchange [45]
Poor tissue perfusion, hyperbilirubinemia, and severe anemia may cause inaccurate oximetry readings [44] Carbon monoxide poisoning leads to an overestimation of the P a O 2 When methe-moglobin levels exceed 5%, the pulse oximeter cannot reliably predict oxygen saturation Methylene blue, the treatment for methemoglobinemia, will also lead to inaccurate oximetry read-ings Normal values for maternal pulse oximetry readings (S p O 2 ) are dependent upon gestational age, position, and altitude of residence [46 – 48]
Mixed venous oxygenation
The mixed venous oxygen tension (P V O 2) and mixed venous oxygen saturation (S V O 2 ) are parameters of tissue oxygenation [22] P V O 2 is 40 mmHg with a saturation of 73% Saturations less than 60% are abnormally low These parameters can be measured directly by obtaining a blood sample from the distal port of the pulmonary artery catheter The S V O 2 also can be measured con-tinuously with a fi beroptic pulmonary artery catheter Mixed venous oxygenation is a reliable parameter in the patient with hypoxemia or low cardiac output, but fi ndings must be inter-preted with caution When the S V O 2 is low, oxygen delivery can
be assumed to be low However, normal or high does not guar-antee that tissues are well oxygenated In conditions such as septic shock and adult respiratory distress syndrome, the maldistribu-tion of systemic fl ow may lead to abnormally high S V O 2 in the face of severe tissue hypoxia [21] The oxyhemoglobin dissocia-tion curve must be considered when interpreting the S V O 2 as an indicator of tissue oxygenation [19] Conditions that result in a left shift of the curve cause the venous oxygen saturation to be normal or high, even when the mixed venous oxygen content is low The S V O 2 is useful for monitoring trends in a particular patient, because a signifi cant decrease will occur when oxygen delivery has decreased secondary to hypoxemia or a fall in cardiac output
Blood gas interpretation
The processes leading to acid – base disturbances are well described, and blood gas analysis may facilitate identifi cation of the cause of
a serious illness Since many critically ill patients have metabolic and respiratory derangements, correct interpretation of a blood gas is fundamental to their care Misinterpretation, however, can result in treatment delays and inappropriate therapy Several
Blood pH and PCO 2 are potentiometric determinations, with
the potential difference between each electrode and the reference
electrode quantitated The pH electrode detects hydrogen ions,
and the electrical potential developed by the electrode varies with
the H + ion activity of the sample The potential difference between
the pH and reference electrode is measured by a voltmeter and
converted to the pH The PCO 2 electrode is actually a modifi ed
pH electrode A glass electrode is surrounded with a weak
bicar-bonate solution and enclosed in a silicone membrane Carbon
dioxide in the sample diffuses through this membrane which is
permeable to CO 2 but not water and H + ions As CO 2 diffuses
through the membrane, the pH of the bicarbonate solution
changes Thus, the pH measured by the electrode is related to
CO 2 tension
The measurement of PO 2 is amperometric, as the current
gen-erated between an anode and cathode estimates the partial
permeable to oxygen but not other blood constituents The
elec-trode consists of an anode and a cathode, and constant voltage is
maintained between them An electrolytic process that occurs
in the presence of oxygen produces current, and the magnitude
of the current is proportional to the partial pressure of oxygen in
the sample As oxygen tension increases, the electrical current
generated between the anode and cathode increases
Bicarbonate concentration as reported on a blood gas result is
not directly measured in the blood gas laboratory Once pH and
PCO 2 are determined, bicarbonate concentration is calculated
using the Henderson – Hasselbalch equation or determined from
a nomogram In contrast, the total serum CO 2 (tCO 2 ) content is
measured by automated methods and reported with routine
serum electrolyte measurements
Oxygen saturation (SO 2 ) is the ratio of oxygenated hemoglobin
to total hemoglobin It can be plotted graphically once PO 2 is
determined, calculated using an equation that estimates the
oxy-hemoglobin dissociation curve, or determined
spectrophoto-metrically by a co - oximeter The latter is the most accurate
method since saturation is determined by a direct reading
Pulse oximetry
The oximetry system determines arterial oxygen saturation by
measuring the absorption of selected wavelengths of light in
pul-satile blood fl ow [43] Oxyhemoglobin absorbs much less red and
slightly more infrared light than reduced hemoglobin Oxygen
saturation is therefore the ratio of red to infrared absorption
Red and infrared light from light - emitting diodes are projected
across a pulsatile tissue bed and analyzed by a photodetector The
absorption of each wavelength of light varies cyclically with pulse
The patient ’ s heart rate, therefore, is also determined When
assessing the accuracy of the arterial saturation measured by the
pulse oximeter, correlation of the oximeter determined heart rate
and the patient ’ s actual pulse rate indicates proper electrode
placement The oximetry probe is usually placed on a nail bed or
ear lobe Under ideal circumstances, most oximeters measure
saturation (S p O 2 ) to within 2% of S a O 2 [43]