Indications

Contraindications

Equipment

Spirometers can be divided into two categories. Volume spirometers measure the amount of gas exhaled as a function of time. These devices, however, tend to be cumbersome and are not ideally suited to the ED. Flow spirometers measure the flow of gas past a certain point and use that information to extrapolate volume and time data. These machines are smaller, simpler to use, and more portable. Flow spirometers determine gas flow by measuring the difference in pressure between two points in a tube (pneumotachograph), cooling of a heated wire (hot wire anemometer), or revolutions of a rotating vane. Most handheld spirometers also measure PEFR.

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

Procedure

Calibrate the spirometer in accordance with the manufacturer’s directions and examine the peak-flow flowmeter to ensure that the measurement bar is resting at the zero line before beginning the procedure. For multipatient devices, attach a disposable mouthpiece to the input orifice.

Before starting the test, explain the procedure and allow unfamiliar patients to practice a few times. Ideally, the patient should be in the standing position or, if not feasible, be seated upright in bed. Ask the patient to elevate the chin and hold the neck in a slightly extended position. A nose clip is not required for PEFR measurements but may be useful when performing formal spirometry testing.

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.

Interpretation

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

Isolated measurements of PEFR are not reliable in making the diagnosis of asthma because of significant variation between individuals. However, it is appropriate to use PEFR to monitor the degree of airflow obstruction in known asthmatics.

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

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.

Technology

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.

Because the pulse oximeter uses only two wavelengths of light, it can distinguish only two substances. As a result, pulse oximeters measure “functional saturation,” which is the concentration of oxyhemoglobin divided by the concentrations of oxyhemoglobin plus reduced hemoglobin. The disadvantage of functional saturation is that the denominator does not include other hemoglobin species that may be present, such as carboxyhemoglobin and methemoglobin. The advantage of using only two wavelengths in the oximeter is that the cost, size, and weight of the device are reduced. The CO-oximeter, one example of a commercially available in vitro oximeter and the standard by which pulse oximetry is calibrated, uses four or more wavelengths, measures “fractional saturation,” and is able to quantify additional hemoglobin species.

Physiology

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.

Currently available pulse oximeters are accurate and precise when saturation ranges from 70% to 100%. This range is satisfactory because for most patients an O₂ saturation of 80% is as much an urgent warning as is one lower than 70%. Testing of pulse oximeters has shown that at 75% saturation, bias is scattered uniformly, with 7% underestimation and 7% overestimation.

Clinical Utility

Pulse oximetry offers an advantage in assessing the adequacy of oxygenation over arterial blood gas analysis by providing continuous estimated Sao₂ measurements. Direct measurement of Sao₂ is determined from blood gas values coupled with knowledge of the actual hemoglobin levels in a patient’s blood. Sao₂ measurement is estimated with pulse oximetry (Spo₂). In this chapter we equate Sao₂ and Spo₂.

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

Indications

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

Procedure

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.

Interpretation

Patients with normal physiologic gas exchange have an O₂ saturation between 97% and 100%. When Sao₂ falls below 95%, hypoxemia may be present, although this may be baseline for some patients with cardiac or lung disease. Oxygen saturation below 90% represents significant hypoxemia. As with spirometry, an isolated, low early measurement of Sao₂ does not mandate admission because of the potential for rapid response to therapy. Low Sao₂ readings should be heeded as important clinical warning signs. Pulse oximetry may be affected by numerous extrinsic factors, but a decline in oxygen saturation with serial measurements should always prompt an evaluation of respiratory status and adequacy of circulation.

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.

Sources of Interference

Conclusions

Pulse oximetry is a widely available technology that provides an easy, noninvasive, and generally reliable method of monitoring oxygenation. Because measurements are continuous, pulse oximetry allows earlier detection of hypoxic episodes than intermittent arterial blood gas analysis does. Frequent measurements can lead to earlier corrective measures and prevention of adverse consequences.

Terminology

The ancient Greeks believed there was a combustion engine inside the body that gave off smoke (capnos in Greek) in the form of a breath. A capnometer is a CO₂ monitor that displays a number (i.e., Petco₂). A capnograph is a CO₂ monitor that displays a number and a waveform (i.e., the capnogram).

Technology

Capnography became a routine part of anesthesia practice in Europe in the 1970s and in the United States in the 1980s.⁵⁴ Capnography was incorporated into the American Heart Association (AHA) guidelines in 2000 and the American College of Emergency Physicians (ACEP) guidelines in 2001 and has become the standard of care for verification of endotracheal (ET) tube placement in the operating room, the ED, and the prehospital setting.

Most capnography technology is built on infrared (IR) radiation techniques. These techniques are based on the fact that CO₂ molecules absorb IR radiation at a very specific wavelength (4.26 µm), with the amount of radiation absorbed having a close to exponential relationship to the CO₂ concentration present in the breath sample. Detecting these changes in IR radiation levels by using appropriate photodetectors sensitive in this spectral region allows the CO₂ concentration in the gas sample to be calculated.

CO₂ monitors measure gas concentration or partial pressure by using one of two configurations, depending on the location of the sensor: mainstream or sidestream (Fig. 2-11). Mainstream devices measure CO₂ directly from the airway, with the sensor located at the proximal end of the ET tube. Sidestream devices measure CO₂ by aspirating a small sample from the exhaled breath through tubing and a sensor located inside the monitor. Mainstream systems are configured only for intubated patients because the sensor is located on the ET tube. Sidestream systems do not require an ET tube because the sensor is located inside the monitor and may therefore be used in either intubated or nonintubated patients. The airway interface for intubated patients is an airway adapter placed on the hub of the ET tube. For spontaneously breathing patients, a nasal-oral cannula is used. This allows concomitant CO₂ sampling and delivery of low-flow oxygen to the patient.

Sidestream systems can be high flow (requiring 150 mL/min of CO₂ in the breath sample to obtain an accurate reading) or low flow (requiring 50 mL/min of CO₂). Low-flow sidestream systems have a lower occlusion rate (from moisture or patient secretions) and are more accurate in patients with low tidal volumes (neonates, infants, and patients with hypoventilation and low–tidal volume breathing).⁵⁵

CO₂ monitors can be either quantitative or qualitative (Fig. 2-12). Quantitative devices measure the precise Petco₂ as either a number (capnometry) or a number and a waveform (capnography). Qualitative devices measure the range in which Petco₂ falls (e.g., 0 to 10 mm Hg, >35 mm Hg) as opposed to a precise value (e.g., 38 mm Hg). The most commonly used qualitative device is the colorimetric Petco₂ detector, which consists of a piece of specially treated litmus paper that turns color when exposed to CO₂. Its primary use is for verification of ET tube position. If the tube is in the trachea, the resultant exhalation of CO₂ will change the color of the litmus paper; if the tube is in the esophagus with no CO₂ in the breath, no change in color will take place.

Physiology

The capnogram, which corresponds to a single tidal breath, consists of four phases (ascending phase, alveolar plateau, inspiratory limb, dead space ventilation) (see Fig. 2-10). Each phase has conventionally been approximated as a straight line.^54–56 Phase I (dead space ventilation, A to B) represents the beginning of exhalation in which dead space is cleared from the upper airway. Phase II (ascending phase, B to C) represents the rapid rise in CO₂ concentration in the breath stream as CO₂ from the alveoli reaches the upper airway. Phase III (alveolar plateau, C to D) represents the CO₂ concentration reaching a uniform level in the entire breath stream (from alveolus to nose) and concludes with a point of maximum CO₂ pressure (Petco₂). This is the number that appears on the monitor display. Phase IV (D to E) represents the inspiratory cycle in which the CO₂ concentration drops to zero as atmospheric air enters the airway.

A normal capnogram, for patients of all ages, is characterized by a specific set of elements: it includes the four distinct phases just described, the CO₂ concentration starts at zero and returns to zero (i.e., there is no rebreathing of CO₂), a maximum CO₂ concentration is reached with each breath (i.e., Petco₂), the amplitude is dependent on Petco₂, the width is dependent on the expiratory time, and there is a characteristic shape for all subjects with normal lung function.

Patients with normal lung function, irrespective of age, will have a characteristic rectangular- or trapezoidal-shaped capnogram and a narrow Petco₂-Pco₂ gradient (0 to 5 mm Hg), with Petco₂ accurately reflecting Paco₂.⁵⁷ Patients with obstructive lung disease will have a more rounded ascending phase and an upward slope in the alveolar plateau (Fig. 2-13).⁵⁸ In patients with abnormal lung function from mismatch, the gradient will widen, depending on the severity of the lung disease, and Petco₂ will be useful only for trending ventilatory status over time and not as a spot check because it may not correlate with Paco₂.^59,60

Indications for Intubated Patients

Indications for Capnography in Spontaneously Breathing Patients

In spontaneously breathing, nonintubated patients, capnography can be used for

Limitations

Significant technical problems have historically restricted the effective clinical use of capnography. Such problems include interference with the sensor by condensed water and patient secretions in both mainstream and high-flow sidestream devices, cross-sensitivity with anesthetic gases in conventional CO₂ sensors, lack of ruggedness for intrahospital and interhospital transport, and power consumption issues related to portable battery operation time. These issues have largely been resolved in the newer-generation capnography monitors.

Problems with accuracy continue to affect high-flow sidestream systems. When the tidal volume of the patient drops below the flow rate of the system (e.g., neonates, infants, hypoventilating patients with low–tidal volume breathing), the monitor will entrain room air, thereby falsely diluting Petco₂ and slurring the ascending phase of the waveform.88–90

Early capnography airway interfaces (i.e., nasal cannula) had difficulty providing consistent measurements in mouth-breathing patients and those who alternated between mouth and nose breathing. The newer oral-nasal interface has addressed these problems.

Capnography is most effective when assessing a pure ventilation, perfusion, or metabolism problem. Capnographic findings in patients with mixed ventilation, perfusion, or metabolism problems are difficult to interpret. For example, in patients with complex pathophysiology, a ventilation problem may elevate Petco₂, whereas a perfusion problem may simultaneously lower Petco₂. Absolute values and even trends over time may be difficult to interpret in these situations.

Although capnography in patients in cardiac arrest is 100% specific for tracheal placement of the ET tube, its sensitivity for esophageal placement is uncertain.

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70. Silvestri, S, Ralls, GA, Krauss, B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med. 2005;45:497.

71. Falk, JL, Rackow, EC, Weil, MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318:607.

72. Garnett, AR, Ornato, JP, Gonzalez, ER, et al. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987;257:512.

73. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:729.

74. Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury. 3rd ed. J Neurotrauma. 2007;24:S1.

75. Davis, DP, Dunford, JV, Ochs, M, et al. The use of quantitative end-tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004;56:808.

76. Hoffmann, RA, Krieger, BP, Kramer, MR, et al. End-tidal carbon dioxide in critically ill patients during changes in mechanical ventilation. Am Rev Respir Dis. 1989;140:1265.

77. Helm, M, Schuster, R, Hauke, J, et al. Tight control of prehospital ventilation by capnography in major trauma victims. Br J Anaesth. 2003;90:327.

78. Deakin, CD, Sado, DM, Coats, TJ, et al. Prehospital end-tidal carbon dioxide concentration and outcome in major trauma. J Trauma. 2004;57:65.

79. Swedlow, DB. Capnometry and capnography: the anesthesia disaster early warning system. Semin Anesth. 1986;3:194.

80. Weil, MH, Bisera, J, Trevino, RP, et al. Cardiac output and end-tidal carbon dioxide. Crit Care Med. 1985;13:907.

81. Abramo, TJ, Wiebe, RA, Scott, S, et al. Noninvasive capnometry monitoring for respiratory status during pediatric seizures. Crit Care Med. 1997;25:1242.

82. Krauss, B. Capnography as a rapid assessment and triage tool for chemical terrorism. Pediatr Emerg Care. 2005;21:493.

83. Krauss, B, Hess, DR. Capnography for procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2007;50:172.

84. Soto, RG, Fu, ES, Vila, H, et al. Capnography accurately detects apnea during monitored anesthesia care. Anesth Analg. 2004;99:379.

85. Fearon, DM, Steele, DW. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002;9:1373.

86. Estevan, G, Abramo, TJ, Okada, P, et al. Capnometry for noninvasive continuous monitoring of metabolic status in pediatric diabetic ketoacidosis. Crit Care Med. 2003;31:2539.

87. Nagler, J, Wright, RO, Krauss, B. End-tidal carbon dioxide as a measure of acidosis in children with gastroenteritis. Pediatrics. 2006;117:260.

88. Friesen, RH, Alswang, M. End-tidal Pco₂ monitoring via nasal cannulae in pediatric patients: accuracy and sources of error. J Clin Monit. 1996;12:155.

89. Gravenstein, N. Capnometry in infants should not be done at lower sampling flow rates. J Clin Monit. 1989;5:63.

90. Sasse, FJ. Can we trust end-tidal carbon dioxide measurements in infants? J Clin Monit. 1985;1:147.

Pulse Oximetry

McMorrow, RC, Mythen, MG. Pulse oximetry. Curr Opin Crit Care. 2006;12:269.

New, W. Pulse oximetry. J Clin Monit. 1985;1:126.

Sinex, JE. Pulse oximetry: principles and limitations. Am J Emerg Med. 1999;17:59.

The Technology Assessment Task Force of the Society of Critical Care Medicine. A model for technology assessment applied to pulse oximetry. Crit Care Med. 1993;21:615.

Witting, MD, Lueck, CH. The ability of pulse oximetry to screen for hypoxemia and hypercapnia in patients breathing room air. J Emerg Med. 2001;20:341.

CO₂ Monitoring

Falk, JL, Rackow, EC, Weil, MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318:607.

Krauss, B. Capnography as a rapid assessment and triage tool for chemical terrorism. Pediatr Emerg Med. 2005;21:493.

Krauss, B, Deykin, A, Lam, A, et al. Capnogram shape in obstructive lung disease. Anesth Analg. 2005;100:884.

Krauss, B, Hess, DR. Capnography for procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2007;50:172.

Silvestri, S, Ralls, GA, Krauss, B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med. 2005;45:497.