Arterial Puncture

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.

Fine points involved in arterial puncture include checking coagulation-related tests, applying appropriate infection control standards, and assessing for collateral circulation.

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 F_Io₂ while awaiting test results from the central laboratory.

Indwelling Catheter (A-Line)

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.

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.

Pulse Oximetry

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:

Pulse saturation(SpO2as%)=HbO2HbO2+HHb×100

Computed in this manner, the Spo₂ often is called the functional saturation because it is based solely on the presence of normal Hb, that is, the amount available for binding with oxygen.

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:

CO-oximeter SaO2=HbO2HbO2+HHb+Dyshemoglobins×100

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%.

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/HCO3−) 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 F_Io₂.

Transcutaneous Analysis

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

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.

Alveolar Air Equation

Assuming normal lung function and taking into account the environmental factors, we can compute the partial pressure of oxygen in the alveoli (P_Ao₂) using the alveolar air equation:

PAO2=FIO2(PB−PH2O)−(PaCO2×1.25)

where P_Ao₂ = partial pressure of oxygen in the alveoli; F_Io₂ = fraction of inhaled oxygen; P_B = 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 P_Ao₂ of a patient breathing room air (F_Io₂ = 0.21) at sea level (P_B = 760 mm Hg) with a Paco₂ of 40 mm Hg would be computed as follows:

PAO2=0.21(760mm Hg−47mm Hg)−(40×1.25)=(0.21×713mm Hg)−50mm Hg=149.7mm Hg−50mm Hg=99.7mm Hg≈100mm Hg

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 P_Ao₂ 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.

Hypoxemia: Severity and Causes

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.

Causes of hypoxemia include hypoventilation, ventilation-perfusion (V˙/Q˙) mismatch, pulmonary shunting, diffusion defect, and breathing gas with a low partial pressure of oxygen (P_Io₂). Table 8-6 summarizes these causes, identifies some example conditions, and specifies how to differentiate among them. The V˙/Q˙ mismatch is the most common cause of hypoxemia seen by RTs, with pure diffusion defects being relatively rare in general clinical practice.

TABLE 8-6

Causes of Hypoxemia

Type of Hypoxemia	Underlying Cause	Clinical Examples	Differential Assessment
			P(A-a)o2	Response to O2 therapy
Hypoventilation	Rise in PAco2 reduces PAo2 (alveolar air equation)	Drug overdose Neuromuscular disorders	Normal∗	Marked
V˙/Q˙ mismatch	Blood flows through underventilated regions of the lung	COPD Asthma	Increased	Marked
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 Equipment failure	Normal	Marked

ARDS, acute respiratory distress syndrome; COPD, chronic obstructive pulmonary disease.

^∗Normal P(A-a)o₂ but P_ao₂ decreased in proportion to rise in P_aco₂. Breathing room air, the two gas partial pressures normally sum to about 140 mm Hg. Thus, with pure hypoventilation, if the P_aco₂ rises from 40 to 70 mm Hg (+30 mm Hg), the P_ao₂ 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.