Care of patients with cardiopulmonary disorders often requires precise knowledge of their oxygenation, ventilatory, and acid-base status. This information is obtained by blood gas and oximetry analysis, mainly of arterial blood samples. To assure comprehensive patient assessment and support good clinical decision making, respiratory therapists (RTs) must know when and how to obtain these measurements and be able to accurately interpret them.
This chapter focuses on the interpretation of arterial blood gas parameters because these measures best reflect the lung’s ability to exchange O2 and CO2 with the blood, the blood’s O2 carrying capacity, and its acid-base status. Table 8-1 outlines the common reference ranges for arterial blood gas measurements.
|Partial pressure of oxygen||Pao2||80-100 mm Hg (room air)|
|Hemoglobin content||Hb||Males: 14-8 g/dL
Females: 12-15 g/dL
|Carboxyhemoglobin saturation||COHb||<3% (nonsmokers)|
|Oxygen content||Cao2||16-20 mL/dL|
|Hydrogen ion concentration (negative log)||pH||7.35-7.45|
|Partial pressure of carbon dioxide||Pco2||35-45 mm Hg|
|Plasma bicarbonate||22-26 mmol/L|
|Base excess||BE||±2 mmol /L|
BE, base excess; , plasma bicarbonate concentration; Pco2, partial pressure of carbon dioxide; pH, hydrogen ion concentration in blood; Po2, partial pressure of oxygen; SO2 oxyhemoglobin saturation.
Peripheral venous blood has passed through the tissue vascular beds, so it reflects local metabolism and is of no value in assessing lung function. On the other hand, mixed venous blood samples from the pulmonary artery can be used to evaluate overall tissue oxygenation. Use of mixed venous blood for this purpose is discussed in Chapter 14.
Blood gas analysis is indicated if the patient’s symptoms, medical history, physical examination, or laboratory data suggest abnormalities in respiratory or acid-base status. Blood gas analysis also can help evaluate treatment effects and thus be used whenever significant changes occur in therapy that affect oxygenation, ventilation, or acid-base balance.
Blood oxygenation can be assessed by arterial blood gas (ABG) analysis, hemoximetry, pulse oximetry, and transcutaneous Po2 monitoring (mainly in infants and children). Ventilation can be measured by ABGs, transcutaneous Pco2 monitoring, or capnography. An ABG is required for accurate assessment of acid-base status. Table 8-2 outlines the key indications for these various measurements, as recommended by the American Association for Respiratory Care.
|Arterial blood gas analysis||Evaluate ventilation (Pco2), acid-base (pH, Pco2 and ), and oxygenation (Po2) status
Assess the patient’s response to therapy and/or diagnostic tests (e.g., O2 therapy, exercise testing)
Monitor the severity and progression of a disease process
|Determine actual blood O2 saturation (as opposed to that computed with a simple blood gas analyzer)
Measure abnormal hemoglobins levels (e.g., COHb, metHb)
|Pulse oximetry||Monitor the adequacy of oxyhemoglobin saturation
Quantify the response of oxyhemoglobin saturation to therapeutic intervention or to diagnostic procedure (e.g., bronchoscopy)
Comply with mandated regulations or recommendations by authoritative groups (e.g., anesthesia monitoring)
Screen infants for critical congenital heart diseases
|Continuously monitor the adequacy of arterial oxygenation and/or ventilation
Continuously monitor for excessive arterial oxygenation (hyperoxemia)
Quantify real-time changes in ventilation and oxygenation due to diagnostic or therapeutic interventions
Screen infants for critical congenital heart diseases
Blood gas sampling and measurement approaches can be broadly classified as being invasive or noninvasive. Invasive approaches require sampling of blood by needle puncture or indwelling catheter. Noninvasive approaches measure blood gas parameters by external skin sensors.
If the goal is to accurately evaluate oxygenation, ventilation, and acid-base status, then analysis of an arterial blood sample is the gold standard against which all other measures are compared. Samples normally are obtained by percutaneous needle puncture of an artery or from an indwelling arterial catheter. Measurement of arterial pH, Paco2, and Pao2 typically is provided by a blood gas analyzer, which also uses programmed equations to compute the and Sao2 values. Standard blood gas analyzers do not measure actual Sao2 or Hb content and cannot detect the presence of abnormal hemoglobins such as carboxyhemoglobin (COHb). Measurement of normal and abnormal hemoglobin (Hb) content and actual saturation usually requires sample analysis by hemoximetry (CO-oximetry).
An arterial blood sample may be obtained from the radial, brachial, dorsalis pedis, or femoral arteries. The radial artery is preferred because it is readily accessible, easy to stabilize, and least likely to cause loss of distal perfusion if it become obstructed (normally the ulnar artery provides collateral circulation to the hand). Box 8-1 outlines the key steps involved in obtaining an arterial blood sample via percutaneous puncture.
Coagulation-related laboratory tests should be checked to assess for risk for bleeding. Specifically, low platelet counts or increased bleeding times (high prothrombin time, partial thromboplastin time, or international normalized ratio values) may indicate a propensity for bleeding and the need to pressurize the puncture site longer than usual to prevent hemorrhage. See Chapter 7 for more detail on these tests.
In terms of infection control, standard precautions are a must. Given that blood splashes can occur during arterial puncture, in addition to wearing gloves, clinicians should wear a face shield and consider using a gown to protect the skin and clothing (see Chapter 1). When expelling any air bubbles from the sample, one also must avoid discharge of blood droplets into the environment. This important step is accomplished by either (1) using a filter cap on the syringe, or (2) expelling the bubble-containing portion of the sample slowly into sterile gauze pad contained in a sealable plastic bag.
When the radial artery is selected, a modified Allen test must be performed to evaluate the adequacy of collateral circulation to the hand (Fig. 8-1). To perform this test, the patient is instructed to make a tight fist. Then the RT compresses both the radial and ulnar arteries, after which the patient is told to open and relax the hand, which should reveal a blanched palm and fingers. Next, the RT releases pressure over the ulnar artery while observing the patient’s hand for color changes. If collateral flow is adequate, the patient’s hand will “pink up” within 10 to 15 seconds—a positive Allen test. A positive result confirms adequate collateral flow and that the radial artery is an acceptable sampling site. If the test is negative (the hand does not pink up rapidly), the radial artery is not an acceptable site for puncture. In such cases, the other wrist is evaluated, or the brachial artery is used to obtain the sample.
After the sample is obtained and the puncture site stabilized, the sample is either sent to the laboratory or analyzed at the bedside using a point-of-care analyzer. When using a point-of-care analyzer, the instrument needs to be properly prepared before obtaining the blood sample. Normally, this involves verifying its power-up operation, inserting the needed cartridge, and confirming internal calibration. After the sample is obtained, it should be thoroughly mixed and dispensed into the cartridge within 3 minutes (do not place it in ice!). If the analysis results fall outside the analyzer’s reportable ranges (results “flagged”), the remaining sample should be sent to the central laboratory for analysis.
Of course, the RT should never wait for the repeat results if the findings indicate a life-threatening problem. For example, if the bedside results indicate oxygen levels below the analyzer’s reportable ranges and the patient is cyanotic, the RT should immediately start oxygen administration or raise the FIo2 while awaiting test results from the central laboratory.
Arterial puncture causes trauma, so an indwelling arterial catheter, or A-line, should be used when frequent sampling is necessary. As a result of the potential hazards of hemorrhage and bloodstream infection, A-lines require careful management, and their use generally is limited to patients undergoing intensive care.
An A-line system consists of a pressurized infusion set connected to a pressure transducer, intraflow flush device, and sampling port. Two different approaches are used for blood sampling: a three-way stopcock and a closed reservoir. Figure 8-2 depicts the design and operation of a typical three-way stopcock sampling port.
The preparatory and follow-up steps for obtaining and processing a blood sample from an A-line are similar to those for radial arterial puncture, and an Allen test is obviously not needed. Instead, to confirm perfusion at the site of cannulation and proper continuous blood pressure measurement, one should observe the monitor and verify a satisfactory arterial waveform (see Chapter 15 for details on assessing arterial pressure waveforms). After gathering the needed equipment, the RT can proceed to obtain the sample using the applicable procedure, as outlined in Table 8-3.
|Three-Way Stopcock Sampling||In-line Closed Reservoir Sampling|
|Swab sample port with alcohol
Attach waste syringe and turn stopcock off to flush solution/bag
Aspirate 5-6 mL blood (at least 6 times the system “dead” volume)
Turn stopcock off to port
Remove waste syringe, properly discard
Secure heparinized syringe to port, reopen stopcock, collect sample
Turn stopcock off to port, remove syringe
Flush line until clear
Turn stopcock off to patient, briefly flush sampling port, reswab with alcohol
Turn stopcock off to port and confirm restoration of arterial pulse pressure waveform
|Slowly draw blood into the reservoir to the needed fill volume
Close the reservoir shut-off valve
Swab sample port with alcohol
Attach the blunt/needleless sampling syringe to the valved sampling port
Aspirate the needed volume of blood
Open the reservoir shut-off valve
Slowly depress reservoir plunger to reinfuse blood into patient
Reswab port and flush line until clear
Confirm restoration of arterial pulse pressure waveform
Given that closed reservoir sampling minimizes blood waste, reduces the potential for line contamination, and better protects against exposure to bloodborne pathogens than the stopcock method, it is becoming the standard approach in many intensive care units.
Noninvasive blood gas analysis uses external skin sensors to measure relevant parameters. By far, pulse oximetry is the most common noninvasive method for ABG-related measurements. An alternative approach, transcutaneous Po2/Pco2 monitoring, is used mainly with infants and children.
Pulse oximetry is a noninvasive technique for measuring oxygen saturation of hemoglobin (Hb) in the blood, with the reported measure being abbreviated as Spo2. When compared with analysis of arterial blood Hb saturation by invasive sampling and hemoximetry (Sao2) among patients with good perfusion, pulse oximeters exhibit an overall accuracy in the 2% to 4% range.
As the “fifth vital sign,” pulse oximetry commonly is used in intensive care units, the emergency department, operating rooms, during patient transport, and during special procedures such as bronchoscopy, computed tomography scanning, sleep studies, exercise testing, and weaning from supplemental O2 and mechanical ventilation. Pulse oximetry also provides the basis for prescribing and adjusting O2 therapy in both the hospital and home care settings.
Proper use of pulse oximeters and the data they provide requires basic knowledge of their operation and limitations. Pulse oximeters use the spectrophotometric principle of light absorption. The standard device probe transmits two wavelengths of light—red and infrared—through capillary beds such as the earlobe or digit. A more or less constant level of light is absorbed by the tissues and venous blood. However, a portion of the light is absorbed by the pulsatile flow of arterial blood, yielding variable rates of absorption for oxygenated Hb (HbO2) and reduced Hb (HHb). The oximeter circuitry then compares these differences in light absorption and computes the Spo2 as follows:
Abnormal hemoglobin combinations or dyshemoglobins such as carboxyhemoglobin (Hbco) cannot be measured by standard pulse oximeters that emit only two wavelengths of light. To measure dyshemoglobins requires at least four wavelengths of light, as provided by bench-top hemoximeters (CO-oximeters) and some multifunction blood gas analyzers. The Sao2 measured by a CO-oximeter is called the fractional saturation because it compares the proportion of Hb saturated with oxygen with the total amount of Hb present, including any dyshemoglobins:
Thus, because CO-oximeters measure the total complement of Hb and standard pulse oximeters do not, in the presence of dyshemoglobins, pulse oximetry will overestimate the true Sao2. Other factors that can result in erroneous estimation of Sao2 using pulse oximetry are summarized in Table 8-4. Pulse oximeter accuracy also is affected by the Sao2 level, with the range of error increasing substantially when saturations drop below 65% to 70%.
|Presence of COHb||Falsely high Spo2|
|Presence of metHb||Falsely low Spo2 if Sao2 > 85%
Falsely high Spo2 if Spo2 < 85%
|Vascular dyes (e.g., methylene blue)||Falsely low Spo2|
|Dark skin pigmentation||Falsely high Spo2 (3%-5%)|
|Nail polish||Falsely high Spo2 (especially black)|
|Poor local perfusion (vasoconstriction and/or hypothermia)||Possible loss of signal, falsely low Spo2 (may be falsely high is sepsis)|
|Motion artifact||Unpredictable spurious readings or false alarms|
|Ambient light||Varies (e.g., falsely high Spo2 in sunlight); may also cause falsely high pulse reading|
To overcome errors associated with the presence of dyshemoglobins (such as a patient with suspected CO poisoning), one normally would obtain an arterial blood sample and analyze it using a laboratory hemoximeter. More recently, portable multiwavelength pulse oximeters have become available that can provide relatively accurate noninvasive measurement of common dyshemoglobins at the bedside. Likewise, technological advances in sensor design and circuitry have helped decrease the spurious readings and false alarms associated with motion artifact. Simply shielding the sensor from ambient light can eliminate that source of error. More problematic are the errors that occur with poor perfusion at a peripheral sampling site. In these cases, placement of a reflectance (as opposed to an absorption-type) probe on a core body site such as the forehead or chest will provide more accurate estimates of Hb saturation.
When accuracy is essential (as in some critically ill patients), Spo2 should be compared to simultaneous hemoximetry analysis. The discrepancy between the Sao2 and Spo2 can then be used to “calibrate” the pulse oximetry reading. For example, if the Spo2 reading is 93% and hemoximetry analysis reveals an Sao2 of 90%, subtracting 3% from the subsequent Spo2 measurements will provide a more valid estimate of arterial oxygen saturation.
Pulse oximetry has dramatically reduced the need for invasive sampling of arterial blood. However, it should never be substituted for actual blood sample analysis when the clinical situation demands accurate and complete assessment of oxygenation. In addition, because pulse oximeters only provide oxygenation data, abnormalities in ventilation (Pco2) or acid-base balance (pH/) can go undetected unless they, too, are measured. Standard pulse oximetry only measures the relative proportion of O2Hb and not the actual amount of circulating Hb in the blood, so anemia also can be missed if not separately assessed. Finally, as a result of the relationship between Hb saturation and O2 partial pressures, pulse oximetry is of limited utility for detecting abnormally high Po2 values (hyperoxemia). For this reason, RTs should be extra careful when using pulse oximetry to monitor oxygenation in newborn infants at risk for retinopathy of prematurity, one cause of which is hyperoxemia. In these cases, the upper limit for Spo2 should be in the 93% to 95% range, with higher values the basis for lowering the FIo2.
As a noninvasive measure of blood gas tensions, the transcutaneous measurement of oxygen (Ptco2) and carbon dioxide (Ptcco2) partial pressures has been available for more than 30 years. A typical transcutaneous blood gas sensor includes an O2 and CO2 electrode and a heating element. These electrodes measure gas pressures using the same electrochemical principles used in bench-top blood gas analyzers. However, instead of measuring the gas partial pressures in a blood sample, the electrodes measure the Po2 and Pco2 in an electrolyte gel at the skin surface. The heating element warms the underlying skin to 40°C to 42°C, which increases blood flow and thus “arterializes” the blood. Warming also increases skin permeability and enhances diffusion of O2 and CO2 from the capillaries into the electrolyte gel under the sensor.
Transcutaneous blood gas analysis generally has been limited to use with infants and small children in need of continuous monitoring of oxygenation and ventilation (see Chapter 12 for details). However, with the notable exception of monitoring for hyperoxemia, Ptco2 monitoring been replaced by pulse oximetry. This is because the accuracy of Ptco2 measures is highly dependent on the adequacy of perfusion. Low cardiac output, peripheral vasoconstriction, and dehydration all decrease capillary flow, which lowers Ptco2. And as with Pao2, Ptco2 does not fully reflect total oxygen content of the blood. As discussed subsequently, complete assessment of blood oxygen content also requires knowledge of Hb content and saturation.
On the other hand, the Ptcco2 can be reliably measured in patients in most age groups, making it a good choice for the continuous noninvasive monitoring of ventilation. Ptcco2 monitoring is particularly useful when capnography is unavailable or impractical, such as during noninvasive ventilation. In general, in properly calibrated systems with good sensor placement, Ptcco2 values will fall within 3 to 5 mm Hg of the measured Paco2.
As a result of the lengthy set-up, calibration, and stabilization times needed by transcutaneous monitors, they have no place in assessing patients during emergencies. In these cases, pulse oximetry is a better choice for assessing oxygenation, with arterial sampling and point-of-care ABG analysis used to obtain a quick but complete picture of oxygenation, ventilation, and acid-base balance.
Capnography involves the measurement of CO2 concentrations or partial pressures in the respired gases and their real-time graphic display during breathing. Measurement is based on the fact that CO2 gas absorbs light in the infrared spectrum in proportion to its concentration. Using this principle, a capnograph employs a photodetector that measures changes in the intensity of infrared light passed through an analysis chamber.
The primary application of capnography is to monitor patients during general anesthesia, mechanical ventilation, or resuscitation. As a noninvasive substitute for Paco2 to assess ventilation, we use the end-tidal level of CO2, either its partial pressure (Petco2) or %CO2. Normally, the Petco2 averages about 2 to 5 mm Hg less than the Paco2, or between 30 and 43 mm Hg (about 4.0% to 5.6%). Ventilation-perfusion imbalances can alter the difference between the Paco2 and Petco2, and these imbalances are common in patients with respiratory disorders; therefore, we normally focus on trending of the end-tidal CO2 levels when using capnography for continuous monitoring. On the other hand, discrete breath analysis can be used to identify abnormal events such as extubation or rebreathing. Chapter 14 provides more detail on the use of capnography to monitor patients in intensive care.
A complete assessment of arterial blood gas parameters indicating the state of patient oxygenation includes the arterial partial pressure of oxygen (Pao2), hemoglobin content (Hb) and Hb saturation (Sao2, Spo2), and arterial O2 content (Cao2).
The Pao2 is the pressure exerted by dissolved oxygen in the arterial blood. The Pao2 reflects the lung’s ability to transfer O2 from the inspired gas into the circulating blood. Thus, the Pao2 depends on both environmental factors (O2 concentration and barometric pressure) and lung function, as determined by both age and the presence of disease.
where PAo2 = partial pressure of oxygen in the alveoli; FIo2 = fraction of inhaled oxygen; PB = barometric pressure; Ph2o = water vapor pressure in alveoli, 47 mm Hg at BTPS; Paco2 = arterial partial pressure of CO2 (assumed to approximate the alveolar Pco2); and 1.25 = factor based on the ratio of CO2 production to O2 consumption (respiratory quotient). For example, the PAo2 of a patient breathing room air (FIo2 = 0.21) at sea level (PB = 760 mm Hg) with a Paco2 of 40 mm Hg would be computed as follows:
Even in healthy lungs gas transfer is imperfect, so not all of the O2 in the alveoli diffuses into the pulmonary capillaries. How much of the O2 in the lungs actually diffuses into the blood depends on both age and the presence of disease. In children and young adults with normal lungs breathing at sea level, there exists on average a 10 mm Hg gradient between the PAo2 and Pao2, yielding a normal Pao2 in the 90- to 100 mm Hg range. This difference—called the alveolar-arterial oxygen tension gradient and abbreviated as P(A-a)o2—increases with increasing age, owing to a progressive decline in lung function. For patients breathing room air, this increase in P(A-a)o2 is estimated by multiplying their age by 0.3. For example, we would estimate the P(A-a)o2 of an otherwise healthy 70-year-old patient as being 0.3 × 70, or about 20 mm Hg. This would yield an expected Pao2 for this patient of about 100 − 20 = 80 mm Hg. Note that recent epidemiologic studies suggest that the age-associated increase in P(A-a)o2 levels off at about 70 years of age, making about 80 mm Hg the lower limit of the Pao2 reference range for essentially all age groups breathing air at sea level. Of course, the lower bound of the reference range for Pao2 decreases for individuals living at high altitudes in direct proportion to the decrease in barometric pressure.
When the Pao2 is below 80 mm Hg, a condition of hypoxemia exists. As indicated in Table 8-5, the Pao2 level determines whether hypoxemia is classified as mild, moderate, or severe.
|Pao2 (mm Hg)||Relative Severity|
Causes of hypoxemia include hypoventilation, ventilation-perfusion () mismatch, pulmonary shunting, diffusion defect, and breathing gas with a low partial pressure of oxygen (PIo2). Table 8-6 summarizes these causes, identifies some example conditions, and specifies how to differentiate among them. The mismatch is the most common cause of hypoxemia seen by RTs, with pure diffusion defects being relatively rare in general clinical practice.
|Type of Hypoxemia||Underlying Cause||Clinical
|P(A-a)o2||Response to O2 therapy|
|Hypoventilation||Rise in PAco2 reduces PAo2 (alveolar air equation)||Drug overdose
|mismatch||Blood flows through underventilated regions of the lung||COPD
|Pulmonary shunting||Blood flows by alveoli that are not ventilated, does not pick up any oxygen||Atelectasis Pneumonia Pulmonary edema ARDS||Increased||Minimal|
|Diffusion defect||Impaired gas transfer across alveolar-capillary membrane||Interstitial lung diseases (e.g., pulmonary fibrosis, sarcoidosis)||Increased||Marked|
|Low PIo2||Decreased PIo2 lowers PAo2||Altitude sickness
ARDS, acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease.
∗Normal P(A-a)o2 but Pao2 decreased in proportion to rise in Paco2. Breathing room air, the two gas partial pressures normally sum to about 140 mm Hg. Thus, with pure hypoventilation, if the Paco2 rises from 40 to 70 mm Hg (+30 mm Hg), the Pao2 should fall by a roughly comparable amount, that is, from 100 to 70 mm Hg.
The clinical recognition of hypoxemia often is first suggested by the patient complaining of shortness of breath, especially with exertion. Additional common clinical manifestations of hypoxemia include mental confusion, tachycardia, tachypnea, hypertension, and cyanosis.
Although universally used as a measure of pulmonary gas exchange, the Pao2 provides only a limited picture of patient oxygenation. Indeed, dissolved oxygen represents only 1% to 2% of the total normally transported to the tissues. A full picture of patient oxygenation requires assessment of Hb content and saturation, total O2 content, and actual O2 transport and delivery to the tissues.
Normally, more than 98% of the O2 in arterial blood is chemically bound to hemoglobin. How much oxygen Hb carries in a given volume of blood depends on (1) the total hemoglobin concentration and (2) the proportion of oxygen bound to it (the Hb saturation or Sao2). The Sao2 in turn depends on the Pao2 and a number of other factors affecting O2 binding with hemoglobin.
It is important to note that the Sao2 reported by standard ABG analysis is a calculated value and that the Spo2 represents only the functional saturation of normal Hb with O2. For this reason, to obtain true Sao2 values (as well as measures of common dyshemoglobins) requires that blood samples undergo hemoximetry analysis.
Each gram of normal hemoglobin has the capacity to bind with 1.34 mL O2. With an average Hb content of 15 g/dL, this means that each 100 mL of blood has the potential for carrying about 20 mL O2 (1.34 mL/g × 15 g/dL = 20.1 mL/dL). If the Hb content is lower than normal (as in anemia), the maximal O2 carried is reduced proportionately. For example, if a patient’s Hb were to drop by 50% from 15 g/dL to 7.5 g/dL, the O2 carrying capacity of Hb would also be reduced in half, from about 20 mL/dL to about 10 mL/dL. For this reason, a complete assessment of patient oxygenation must include knowledge of Hb content, as determined by either CO-oximetry or a complete blood cell count (CBC).
Sao2 is a measure of how well Hb molecules are “filled” with O2. The primary factor determining Sao2 is the blood Pao2. The oxyhemoglobin dissociation curve quantifies the relationship between Pao2 and Sao2 (Fig. 8-3). This curve is composed of an upper flat portion and a lower steep portion, with a Pao2 of 60 mm Hg and Sao2 of 90% marking the dividing point between the two. Looking at the upper flat portion, as the Pao2 drops 40 mm Hg from 100 mm Hg down to 60 mm Hg, the Sao2 decreases very little, by only about 5% to 7%. On the other hand, when the Pao2 falls below 60 mm Hg onto the steep portion of the curve, the Sao2 decrease is much more precipitous. For example, on this portion of the curve, a decrease in Pao2 of only 20 mm Hg (from 60 to 40 mm Hg) causes a 15% to 20% drop in Sao2.
In patients with normal Hb content, if the Sao2 drops below 80% (equivalent to a Pao2 of about 50 mm Hg), the amount of desaturated Hb in the capillaries is sufficient to cause central cyanosis, the bluish discoloration of the capillary beds observed most easily around the lips and oral mucosa. However, because cyanosis requires an absolute quantity of desaturated Hb (about 5 g/dL HHb), if the total Hb content is low (anemia), this sign may not be apparent, even if the hypoxemia is severe.
In addition to Pao2, Sao2 is affected by a number of other factors, the most important of which are body temperature, blood pH, and Paco2 (Box 8-2). Alkalosis, hypocapnia, hypothermia, and the presence of fetal Hb and carboxyhemoglobin shift the oxyhemoglobin dissociation curve to the left, resulting in a higher Sao2 for a given Pao2. Shifts to the left cause oxygen to bind more tightly to Hb, which facilitates O2 uptake in the lungs but can impair unloading at the tissues. Conversely, acidosis, hypercapnia, and fever shift the curve to the right and result in lower Sao2 values for the same Pao2. Shifts to the right have the opposite effect, resulting in decreased oxygen affinity for Hb. Although this facilitates unloading of O2 at the tissues, it can impair uptake in the pulmonary capillaries.
Dyshemoglobins such as COHb and metHb affect oxygenation in much the same way as anemia. Every gram of Hb chemically bound to a molecule other than O2 is equivalent to an absolute reduction of 1 g/dL of circulating Hb. For example, if a smoke inhalation patient with normal Hb content has a COHb saturation of 40%, it would be as if he had only 9 g/dL circulating Hb, instead of 15 g/dL.
As already noted, the presence of carboxyhemoglobin also shifts the oxyhemoglobin dissociation curve to the left, which further impairs oxygenation by inhibiting the unloading of oxygen at the tissues. Normal COHb levels for nonsmokers are less than 3% and have a minimal impact on oxygenation. Smokers typically exhibit COHb levels in the 5% to 10% range. Higher levels of COHb occur with inhalation of fire smoke or engine exhaust, typically in enclosed spaces. In such cases, the Sao2 (but not necessarily Pao2) will be significantly reduced; the conscious patient may complain of headache, dyspnea, and nausea; and signs of hypoxemia such as tachypnea and tachycardia may be present. However, because carboxyhemoglobin is cherry red in color, cyanosis does not occur. At COHb levels above 40%, visual disturbance, myocardial damage, coma, and eventually, death may occur.
Another common dyshemoglobin is methemoglobin (metHb). metHb is a variant of hemoglobin in which the iron in the heme group has been oxidized from its normal Fe2+ (ferrous) state to the Fe3+ (ferric) state, which is incapable of binding with O2. As with CO poisoning, increased levels of metHb have the same effect as an absolute anemia, causing a reduction in Cao2 called methemoglobinemia.
Patients with high metHb levels can be found in every clinical service department of the hospital. Indeed, as many as one in five of all patients evaluated with traditional CO-oximetry exhibit a metHb above the reference range. Methemoglobinemia can be inherited (cytochrome reductase deficiency, hemoglobin M disease) or acquired by exposure to Hb-oxidizing agents. Environmental exposure to nitrates, nitrites, aniline, or benzene can induce methemoglobinemia, as can inhaling fumes containing nitric oxide (NO). More common is methemoglobinemia caused by the administration of nitrogen-based cardiac medications (e.g., nitroglycerin, nitroprusside), local anesthetic agents (e.g., benzocaine, prilocaine, lidocaine, EMLA creams), and selected antibiotics (e.g., dapsone, sulfonamides). Also, patients treated with inhaled NO are susceptible to acquired methemoglobinemia.
The Pao2 in patients with methemoglobinemia generally is normal, and standard pulse oximetry cannot measure metHb; therefore, detection requires either laboratory CO-oximetry or multiwavelength pulse oximetry. As a result of its dark reddish brown color, metHb levels as low as 15% can cause cyanosis. Indeed, the presence of central cyanosis in patients with normal Pao2 strongly suggests methemoglobinemia. Signs and symptoms like those due to CO poisoning occur at metHb levels in the 25% to 50% range. Above 50%, metHb cardiac dysrhythmias, severe central nervous system (CNS) depression, and profound metabolic acidosis can develop, leading to death if not treated. Treatment involves removing the causative factors and administering a reducing agent such as methylene blue. Supplemental O2 therapy is commonly used to maximize the O2 carrying capacity of the remaining normal hemoglobin but is of little value until the normal state of the Hb molecule is restored.
Cao2 represents the total oxygen content in the arterial blood, measured in mL/dL. It consists of both physically dissolved O2 and that chemically bound to Hb. The vast proportion of the O2 carrried in the blood is bound to Hb; therefore, a normal Cao2 requires a normal volume of circulating red blood cells containing normal quantities of Hb.
Cao2 is calculated by summing its component parts, that is, dissolved O2 and O2 chemically bound to Hb. Dissolved O2 is computed by multiplying the solubility coefficient of O2 in plasma at 37°C (0.003 mL/dL/mm Hg) times the Pao2. At a normal Pao2 of 100 mm Hg, the dissolved O2 would therefore be calculated as follows:
The volume of O2 chemically bound to Hb is computed by multiplying the Hb content by its carrying capacity (1.34 mL/g) by the Sao2. With 15 g/dL Hb normally saturated to 97%, the amount of chemically bound O2 would therefore be calculated as follows: