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HLA - DR antigen on human trophoblast: a review . Am J Reprod Immunol 1983 ; 3 : 175 – 177 . 53 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 5 Maternal – Fetal Blood Gas Physiology 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: CO H O CO H CO Gaseous phase Dissolved Carbonic acid 22 223 ↔+↔ ↔ Carbonicc anhydrase Lung Kidney HHCO 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 HCO 3 − . 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: Chapter 5 54 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 HCO 3 − and PCO 2 are in opposite directions. The compensatory response attempts to normalize the HCO PCO 32 − [] 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 HCO 3 − 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 pH pK HCO P metabolic respiratory CO =+ [] () = − log 3 2 s As the equation demonstrates, the ratio of [ HCO 3 − ] 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 ( HCO 3 − ) 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 HCO 3 − . 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 HCO PCO 32 − [] toward the normal 20/1. Thus, in the presence of metabolic acidosis (decreased HCO 3 − ), ventilation increases, PCO 2 is lowered, and the ratio normalizes. In metabolic alkalosis, the opposite occurs as PCO 2 rises in response to the primary increase in HCO 3 − . 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 HCO 3 − in renal tubular cells. Each H + ion secreted into the tubular lumen is exchanged for sodium, and HCO 3 − 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 HCO 3 − 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 Ps minutes to hours Renal excretion of H s hour CO → ↓ () ↑ + 2 ss to days In contrast, when P changes Intracellular b CO () 2 : uuffering 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 HCO 3 − 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. Maternal–Fetal Blood Gas Physiology 55 Oxygen 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): DO CO C O dL L a22 10=× × 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): CO Hb SO PO aaa222 1 39 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. Primary disturbance Compensatory response Expected degree of compensation Metabolic acidosis Decreased HCO 3 − 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 HCO 3 − Increased P CO 2 P a CO 2 = [0.7 × (serum bicarbonate)] + 20 Respiratory acidosis Increased P CO 2 Increased HCO 3 − 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 HCO 3 − 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. Parameter Normal range pH 7.40 – 7.46 P CO 2 26 – 32 mmHg P O 2 101 – 106 mmHg HCO 3 − 18 – 21 mEq/L Chapter 5 56 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] . VO C O CO dL L av22 10=×× − () The oxygen extraction ratio (OER) is the fraction of delivered oxygen that is actually consumed: OER VO DO= 22 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 0 20 30 40 50 60 70 80 90 100 P 50 O 2 tension (mmHg) pH pH DPG Temp DPG Temp Percent oxyhemoglobin 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. Formula Normal value Est. alveolar oxygen tension P A O 2 = 145 − P a CO 2 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 × H b × S a O 2 ) + ( P a O 2 × 0.003) 18 – 21 mL/dL Mixed venous oxygen content C O 2 = (1.39 × H b × S O 2 ) + ( P O 2 )(0.003) Oxygen delivery D O 2 = C a O 2 × Q T × 10 640 – 1,200 mLO 2 /min 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 Shunt equation Q sp = C c ′ O 2 − C a O 2 3 – 8% Q t C c ′ O 2 − C O 2 Estimated shunt Est. Qsp/Qt = CC′O 2 – CaO 2 [C C′O 2 – CaO 2 ] + [CaO 2 – CvO 2 ] 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. Maternal–Fetal Blood Gas Physiology 57 catheter [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 oxyhe- moglobin dissociation curve. PCO 2 in the sample decreases 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 measuring 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 - preg- nant patient [24] . Oxygen consumption increases steadily 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 Chapter 5 58 Pulse oximetry is ideal for non - invasive arterial oxygen satura- tion monitoring near the steep portion 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 small changes in oxygen saturation, namely 97 – 99%. Large 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 pres- sure of oxygen. The PO 2 electrode surrounds a membrane 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] . . syndrome . Obstet Gynecol 1988 ; 71 : 872 – 877 . 95 Kinsella SM , Lohmann G . Supine hypotensive syndrome . Obstet Gynecol 1994 ; 83 ( 5 Pt 1 ): 77 4 – 78 8 . 96 Lindheimer MD , Katz AI. Physiol Pharmacol 1968 ; 46 : 573 – 576 . 177 Scott DE , Pritchard JA . Iron defi ciency in healthy young college women . JAMA 19 67 ; 199 : 8 97 – 900 . 178 Pitkin R , Witte D . Platelet. Intrapartum blood volume changes . Am J Obstet Gynecol 1 976 ; 126 : 671 – 677 . 115 Kjeldsen J . Hemodynamic investigations during labor and delivery . Acta Obstet Gynecol Scand 1 979 ;