Chapter 2 For patients with acute exacerbations of asthma and chronic obstructive pulmonary disease (COPD), accurately estimating the severity of airflow obstruction is a critical component of their care. A focused history plus physical examination is the cornerstone of this assessment in the practice of emergency medicine. The history and physical examination alone, however, cannot reliably quantify airflow obstruction during acute attacks.1–5 In patients with COPD, wide variation exists in the ability to accurately diagnose airway obstruction, and up to 15% of patients with marked airflow obstruction will not be dyspneic.6–9 This blunted perception of disease severity may be a contributor to fatal and near-fatal asthma attacks.10 After therapy for acute exacerbations of asthma, patients may experience subjective resolution of their symptoms even while severe airflow obstruction is still present.11 Given these difficulties in recognizing airflow obstruction, objective measurement provides valuable information. Spirometry is measurement of the volume of air exhaled during forced expiration.12 It can be interpreted as a function of time to determine the flow rate. Spirometry gives the most complete picture of lung mechanics and is the centerpiece of pulmonary function testing. Many parameters can be derived from a spirogram, the most useful of which are forced vital capacity (FVC), which is the total volume exhaled during a forced expiratory maneuver, and forced expiratory volume in 1 second (FEV1), which is the average flow rate during the first second of the forced expiratory maneuver (Fig. 2-1). The advent of small handheld devices allows convenient spirometric evaluation in the emergency department (ED). The most common objective measurement of respiratory mechanics used in the ED is peak expiratory flow rate (PEFR). PEFR is the maximum flow of gas achieved during a forced expiratory maneuver. It correlates well with standard spirometry and has been studied extensively in the ED setting.13–15 Evaluation of Acute Asthma Attacks Currently, no standards exist for the measurement of pulmonary function parameters in ED patients, and practices vary widely. Most patients with asthma exacerbations can be evaluated, treated, and given a disposition with no further pulmonary function testing other than PEFR if quantitative assessment is deemed prudent. Several consensus guidelines recommend obtaining an objective measure of airflow obstruction in all patients seen in the ED with an acute exacerbation of asthma.16–18 Others have proposed that the decision to measure PEFR in patients with acute asthma should be individualized.19 It is reasonable that mild and easily reversible disease be evaluated and treated according to clinical judgment, but if any pulmonary function parameters are to be used, their use is optimized if measured at arrival, after initial treatment, and periodically thereafter.16–18 PEFR and spirometry testing can yield objective data on airflow obstruction during the ED evaluation of COPD exacerbations. Though used by some ED practitioners, consensus guidelines do not recommend routine use of these tests in the acute setting.20–22 PEFR has been studied for its ability to differentiate between COPD and congestive heart failure (CHF).23 Insufficient data exist to recommend its routine use for this purpose in the ED. The most commonly used device to measure PEFR is the “mini-Wright” peak-flow flowmeter (Fig. 2-2). These meters provide accurate and reproducible measurements of PEFR.24 The mini-Wright peak-flow flowmeter retains its accuracy for at least 5 years.25 There is significant variation between types and brands of peak-flow flowmeters, so measurements recorded with the same brand of peak-flow flowmeter are most useful when comparing a patient’s baseline PEFR.11,26,27 After a period of normal breathing, ask the patient to take a maximal inspiration with the lips sealed around the mouthpiece while taking care to keep the tongue from partially obstructing the mouthpiece. Request the patient to initiate a rapid, forceful expiration as soon as possible after reaching maximal inspiration (Fig. 2-3). Coach the patient throughout the procedure and remind the patient to continue to make a forceful and complete exhalation. The PEFR usually occurs during the first 100 msec of expiration. In contrast, when performing spirometry, it is essential that the patient exhale fully. With both tests it is important to have a rapid, forceful exhalation rather than a slow, sustained one. Obtain three separate measurements for both spirometry and PEFR.28,29 PEFR measurements are very sensitive to technique and patient effort. Even a small decrease in effort can lead to considerable degradation of results.11,30 Because airflow is greatest when the lung volumes are highest and the airways are larger, the test is accurate only if performed after a maximal inspiration. Obstructive diseases are characterized by a disproportionate decrease in airflow (FEV1) in relation to the volume of gas exhaled (FVC).31 A decreased FEV1/FVC ratio with preservation of FVC indicates the presence of airflow obstruction. Restrictive diseases decrease total lung capacity and therefore decrease FVC to a greater degree than FEV1. Decreased FVC with a normal or increased FEV1/FVC ratio is indicative of restriction. It is useful to consider the FEV1/FVC ratio when attempting to determine whether a patient has airflow obstruction. In patients with an established diagnosis of obstructive disease, FEV1 is the test that best reflects changes in lung function. Typical values are shown in Table 2-1. These values are dependent on age, gender, ethnicity, and height and can be predicted from mathematical equations.32 Although measures of airflow obstruction are not stand-alone tests, when considered along with other clinical factors, they can guide decisions regarding the disposition of patients with acute asthma exacerbations. The highest of three PEFR or FEV1 measurements should be used and, whenever possible, compared with the patient’s personal best.16–18 In one study of inner-city patients, only 29% knew their personal best PEFR, and even when known, this number may be unreliable.33 In circumstances in which previous best values are unknown or thought to be inaccurate, comparison with predicted values is appropriate. Normal PEFR values for adults are shown in Figure 2-4. Values for children are presented in Tables 2-2 and 2-3. The National Asthma Education and Prevention Program has used the results of FEV1 and PEFR testing to classify the severity of asthma exacerbations (Table 2-4).16 TABLE 2-4 Severity of Asthma Exacerbations according to Objective Measures of Airflow Obstruction FEV1, forced expiratory volume in 1 second; PEFR, peak expiratory flow rate. TABLE 2-2 Predicted Peak Expiratory Flow Rate in Males 8-20 Years of Age* *Based on equations from Hankinson JL, Odencrantz JR, Fedan KB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med. 1999;159:179. TABLE 2-3 Predicted Peak Expiratory Flow Rate in Females 8-18 Years of Age* *Based on equations from Hankinson JL, Odencrantz JR, Fedan KB. Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med. 1999;159:179. Multiple guidelines and articles have advocated specific cutoff values for PEFR and FEV1 to guide decisions on disposition.16–18 There is variation across these guidelines and no consensus that absolute cutoffs should exist.16 When these values are obtained, they should be viewed as additional data points to be considered, along with other clinical variables, in determining the disposition of asthmatics seen in the ED. At the extremes, data may be useful. For example, asthmatic patients with an initial PEFR greater than 70% of personal best or the predicted value will probably be discharged and those below 35% will probably need admission. Beyond the degree of initial airflow obstruction, the response to inhaled bronchodilators is a useful gauge of suitability for outpatient asthma management. A poor response argues in favor of admission, whereas recovery of PEFR or FEV1 to greater than 70% of personal best is a favorable sign. Oximetry is based on the Beer-Lambert law, which states that the concentration of an unknown solute dissolved in a solvent can be determined by light absorption. Pulse oximetry combines the principles of optical plethysmography and spectrophotometry. The probe, set into a reusable clip or a disposable patch, is made up of two photodiodes, which produce red light at 660 nm and infrared light at 900 to 940 nm, and a photodetector, which is placed across a pulsatile vascular bed such as the finger or ear (Fig. 2-5). These particular wavelengths are used because the absorption characteristics of oxyhemoglobin and reduced hemoglobin are quite different at the two wavelengths. The majority of the light is absorbed by connective tissue, skin, bones, and venous blood. The amount of light absorbed by these substances is constant with time and does not vary during the cardiac cycle. A small increase in arterial blood occurs with each heartbeat, thereby resulting in an increase in light absorption (Fig. 2-6). By comparing the ratio of pulsatile and baseline absorption at these two wavelengths, the ratio of oxyhemoglobin to reduced hemoglobin is calculated. Arterial O2 saturation (Sao2) measures the large reservoir of O2 carried by hemoglobin, 20 mL of O2/100 mL of blood, whereas arterial O2 partial pressure (Pao2) measures only the relatively small amount of O2 dissolved in plasma, approximately 0.3 mL of O2/100 mL of blood. Sao2 correlates well with Pao2, but the relationship is nonlinear and is described by the oxyhemoglobin dissociation curve (Fig. 2-7). In hypoxemic patients, small changes in Sao2 represent large changes in Pao2 because these Sao2 values fall on the steep portion of the curve. Conversely, measurements of Sao2 are relatively insensitive in detecting significant changes in Pao2 at high levels of oxygenation because these Sao2 values fall on the plateau portion of the curve. Data on the clinical efficacy of routine pulse oximetry monitoring in the ED are limited, so clinical value has been extrapolated from anesthesia studies.34–36 These studies have demonstrated that continuous monitoring of saturation decreases the incidence and duration of desaturation episodes, thereby resulting in fewer adverse events during recovery and shortening the time to discovery of hypoxia. It follows logically that use in critically ill patients should result in similar benefits, including more rapid recognition of adverse physiologic events and fewer episodes of severe arterial desaturation. Patient outcomes should be improved by initiation of therapeutic interventions following immediate notification of an unfavorable Sao2.37 Recommended uses for pulse oximetry fall into two broad categories: (1) as a real-time indicator of hypoxemia, continuous oximetry monitoring can be used as a warning system because many adverse patient events are associated with arterial desaturation,38 and (2) as an end point for titration of therapeutic interventions to avoid hypoxia (Box 2-1). Pulse oximetry can also be used to assess peripheral perfusion and evaluate for possible ischemia in the extremities. Such use is not standardized, and although clinical experience validates its use, minimal data are available for such utilization in the ED. Vascular surgeons will use a pulse oximetry probe on a finger or toe to assess the results of vascular surgery on the arm or leg. Peripheral artery occlusion from peripheral artery disease may be suggested by comparison of pulse oximetry readings in the extremities. Decreased peripheral oxygenation may be detected in patients with compartment syndrome, traumatic arterial injury, and external compression of the proximal circulation (Fig. 2-8).39,40 The location for the probe is determined by the clinical situation and the probes available. A reusable clip-on probe works well on digits that are easily accessible. Other sites include the earlobe, the nasal bridge, the septum, the temporal artery, and the foot or palm of an infant. A newer probe developed for use on the forehead may provide better readings in cold ambient temperature or during movement.41 Tape and splints can also be used to secure oximetry probes and minimize motion. The computer analyzes the incoming data to identify the arteriolar pulsation and displays this parameter as beats per minute. Newer devices also display a pulse plethysmograph (Fig. 2-9). Simultaneously, O2 saturation is displayed on a beat-to-beat basis. Some machines have hard-copy capability and can provide paper documentation of the patient’s status. Machines differ in their display when a pulsatile flow is not detected. Either the reading will not display at all, or the Sao2 value will be given along with a poor-signal quality warning. It is important to evaluate serial measurements and to verify that the measurements correlate with other clinical markers. Although pulse oximetry represents a significant advance in noninvasive monitoring of oxygenation, clinicians must recognize and understand its limitations.42 Pulse oximetry measures only O2 saturation. In contrast to arterial blood gas determination or capnography, pulse oximetry provides no direct information on pH or the arterial partial pressure of CO2 (Paco2). Witting and Lueck43 empirically demonstrated that a room-air Sao2 value of 97% or higher strongly rules against hypoxemia and moderate to severe hypercapnia. Their validated study of patients with respiratory complaints undergoing arterial blood gas analysis found good discrimination with a room-air Sao2 value of 96% or less. For hypoxemia (Pao2 <70 mm Hg), this value was 100% sensitive and 54% specific. For hypercapnia (Paco2 >50 mm Hg), this value was 100% sensitive and 31% specific. Kelly and colleagues44 found a cutoff value of 92% or less for room-air Sao2 to be more accurate in identifying hypoxemia in patients with COPD. Pulse oximetry is not a substitute for monitoring ventilation because of the variable lag time between the onset of hypoventilation or apnea and a change in oxygen saturation.45 Therefore, during procedural sedation, monitoring of ventilation is a more desirable goal for prevention of hypoxemia and hypercapnia than simple pulse oximetry is (see “Procedural Sedation and Analgesia” under “Carbon Dioxide Monitoring” later in this chapter). Hypoventilation and the resultant hypercapnia may precede a decrease in hemoglobin O2 saturation by many minutes. Furthermore, supplemental O2 may mask hypoventilation by delaying the eventual O2 desaturation that pulse oximetry is designed to monitor and recognize. In preoxygenated animals, airway obstruction was detected within 10 seconds with capnography, but Sao2 values did not change during the 180-second study periods.45 Other limitations of pulse oximetry are summarized in Box 2-2. In patients with methemoglobinemia or elevated carboxyhemoglobin levels, pulse oximetry does not accurately depict quantitative changes in hemoglobin O2 saturation.46,47 Carboxyhemoglobin results in falsely elevated Sao2 estimates of hemoglobin O2 saturation. Low quantities of methemoglobin will reduce pulse oximetry readings by about half the actual methemoglobin percentage. Large quantities of methemoglobin (>10%) can result in a stable pulse oximetry reading of 85% regardless of the actual Sao2. Because pulse oximetry will variably underestimate the percentage of abnormal hemoglobin, a CO-oximeter or blood gas sample is required for confirmation of these conditions and quantitative analysis.
Devices for Assessing Oxygenation and Ventilation
Spirometry
Indications
Evaluation of Exacerbations of COPD
Differentiating Causes of Dyspnea
Contraindications
Equipment
Procedure
Interpretation
Noninvasive Oxygenation Monitoring: Pulse Oximetry
Technology
Physiology
Clinical Utility
Indications
Procedure
Interpretation
Sources of Interference
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