Topics in Compan An Med 28 (2013) 124–128
Regular articles
Pulse Oximetry and Capnometry Vincent Thawley, VMD, Lori S. Waddell, DVM, DACVECCn Keywords: oximetry capnometry capnogram Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, Philadelphia, PA, USA
Respiratory dysfunction is common in veterinary patients and various techniques have been developed to rapidly and accurately monitor pulmonary gas exchange. Pulse oximetry and capnometry are tools that allow for continuous evaluation of pulmonary function. Methodology, indications, and limitations of pulse oximetry and capnometry are discussed in this article. Both techniques are useful for monitoring critically ill or anesthetized patients; however, limitations to their use exist which underscore the need for intermittent arterial blood gas analysis. & 2013 Elsevier Inc. All rights reserved.
n
Address reprint requests to Lori Waddell, DVM, DACVECC, Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, 3900 Delancy St, Philadelphia, PA 19143, USA. E-mail: [email protected]
Introduction Pulmonary dysfunction is commonly encountered in critical illness and in anesthetized patients and may lead to hypoxemia, abnormalities in ventilation, or both. Successful management of patients with pulmonary disease frequently involves monitoring techniques that allow for accurate assessment of respiratory function. Although arterial blood gas analysis remains the gold standard in the assessment of oxygenation and ventilation, results provide an assessment of pulmonary function at only 1 moment in time and repeated sampling is necessary to effectively monitor patients with a dynamic disease process. In addition, sample acquisition may be technically challenging and can be stressful for patients that already have respiratory compromise. For these reasons, noninvasive, cageside monitoring tools have gained popularity in recent years. This article discusses pulse oximetry and capnography, 2 monitoring techniques that allow for noninvasive and even continuous assessment of pulmonary gas exchange.
Pulse Oximetry Oximetry is a rapid and noninvasive technique for estimating arterial hemoglobin saturation with oxygen. Pulse oximetry is a transcutaneous bedside tool for measuring functional hemoglobin, which is the hemoglobin that is able to bind, transport, and release oxygen.1 Co-oximetry provides a measurement of both functional hemoglobin and other species of hemoglobin, including methemoglobin, carboxyhemoglobin, and sulfhemoglobin, that are incapable of binding oxygen and thus do not contribute to total arterial oxygen-carrying capacity.2 In most instances, co-oximetry is performed by analyzing a blood sample that precludes continuous use. Pulse co-oximeters, which are bedside, transcutaneous monitors that assess for the presence of various species of hemoglobin using similar methodology as pulse oximeters, have been developed to address this limitation. Pulse co-oximetry is not commonly used in veterinary patients.2 Pulse oximetry was first used clinically in 1964; early oximeters were bulky and expensive but accurate down to a hemoglobin
saturation of 70%.3 Modern oximeters are often compact and handheld, lending themselves to bedside use for quick assessment of arterial oxygenation. Indeed, pulse oximetry is considered a standard-of-care monitoring technique in most human and veterinary critical care settings. According to the Lambert-Beer law, the concentration of a substance is proportional to the absorption of light at a specific wavelength by the substance in question and the length across which the light travels.4 Pulse oximeters operate via this principle; percent hemoglobin saturation with oxygen is determined by analysis of the differential absorption of light by oxygenated and deoxygenated hemoglobin in arterial blood. Modern oximeters emit light in 2 wavelengths—1 in the red region of the light spectrum (660 nm) and 1 in the infrared region (940 nm). Emitted light travels through tissue to reach a photodetector on the opposite side of the device; light with a pulsatile signal is presumed to have traversed arterial blood whereas nonpulsatile light is assumed to have traversed venous blood and connective tissue and is therefore not analyzed by the photodetector.4,5 Oxygenated hemoglobin does not absorb light in the red region of the light spectrum as well as deoxygenated hemoglobin—this accounts for the bright-red appearance of arterial blood. Conversely, deoxygenated hemoglobin does not absorb light in the infrared region as well as oxygenated hemoglobin. Therefore, the amount of oxygenated and deoxygenated hemoglobin present can be determined by the amount of light of each wavelength that is transmitted through the tissue. The amount of oxygenated hemoglobin present, compared with total hemoglobin, is expressed as percent saturation (SpO2).5 The spectral absorption of canine, feline, equine, porcine, and bovine hemoglobin is consistent with that of human hemoglobin, so pulse oximeters designed for human use may be employed in these species.4 Pulse oximeters rely on detection of a pulsating light signal to estimate arterial hemoglobin saturation; as such, obtaining an accurate reading may be difficult in patients that have poor peripheral perfusion due to hypothermia or hypotension.1,6 Likewise, the presence of a cardiac arrhythmia with pulse deficits may result in erroneous results.7 Most monitors display the patient's
1527-3369/$ - see front matter & 2013 Topics in Companion Animal Medicine. Published by Elsevier Inc. http://dx.doi.org/10.1053/j.tcam.2013.06.006
V. Thawley, L.S. Waddell / Topics in Companion An Med 28 (2013) 124–128
heart rate; results must be interpreted with caution should the displayed heart rate not match the patient's actual heart rate. Some oximeters display a plethysmographic pulse waveform that can be examined to ensure accuracy in analysis; others may include pulse signal intensity along with heart rate. If a pulse waveform is displayed it should ideally resemble a normal arterial pulse waveform to ensure accuracy in the calculated hemoglobin saturation. A variety of pulse oximeters are available commercially. Most models employ the use of a clip with a phototransmitter on 1 side and a photoreceptor on the other although some models, designed for use on human foreheads, are flat and have both the phototransmitter and photoreceptor on the same side and utilize light reflection for analysis. Pulse oximeters with probes designed for rectal insertion are also available. When selecting a pulse oximeter, one should give consideration to portability and durability as well as the patient population that it will be used for, particularly if frequent use is anticipated. Anesthetized patients are much easier to monitor with pulse oximetry than are awake, moving patients. In the authors' experience, pulse oximeter probes work best on the tongue, although this site is generally only available in patients that are heavily sedated, anesthetized, or in moribund condition. Alternate sites for probe placement include the buccal mucosa, pinna, nonpigmented inguinal skin, and nonpigmented paw pads or interdigital skin webbing. For patients with pigmented oral mucosa, oximetry may be performed using the preputial or vulvar mucosa. An additional site that can be used for flat pulse oximeter probes is the ventral surface of the tail after clipping the hair in this region. The site selected for probe placement should ideally be warm and well perfused. Clipping hair in thick-coated patients so that the phototransmitter is directly on skin is recommended. Moistening the tongue and oral mucosa with saline or water may improve accuracy when these sites are utilized. When long-term, continuous use is anticipated (such as in the mechanically ventilated patient), the oximeter probe site should be inspected every 2-4 hours and the probe moved as necessary to prevent the development of pressure sores.8 Pulse oximetry is a valuable tool in the management of patients with or at risk for developing hypoxemia. Pulse oximetry is routinely used for monitoring sedated or anesthetized patients and as a screening tool to determine whether tachypnea is due to pulmonary compromise or whether diagnostics should be focused elsewhere. Additionally, pulse oximetry is useful to determine whether hypoxemia improves with provision of supplemental oxygen. In humans, it is reported that inaccuracies in pulse oximetry may occur in the presence of hypotension, icterus, anemia, and methemoglobinemia.6,9 However, Hendricks et al10 found that pulse oximetry was a useful monitoring modality in a variety of critically ill canine patients in the intensive care unit. Several of these patients either were anemic, hypothermic, or had increased serum bilirubin. Bright ambient light may interfere with photodetector function so probes should ideally be shielded when in use.7 Excessive patient motion or shivering may preclude continuous pulse oximetry monitoring as the probe is likely to disengage from the site of placement; for these patients, intermittent oximetry readings may be necessary although obtaining any readings can be difficult when motion is present. Carbon monoxide intoxication may result in spuriously high pulse oximetry results as carboxyhemoglobin, formed when carbon monoxide displaces oxygen from hemoglobin molecules, has a similar spectral absorption pattern as oxyhemoglobin. As a result, the machine will mistake carboxyhemoglobin for oxyhemoglobin and report an oxygen saturation that is erroneously
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Fig. 1. A mainstream capnometer inserted between the endotracheal tube and breathing circuit. As exhaled gas passes over the sensor, the concentration of CO2 is measured in real time. CO2SMO (Respironics Novametrix, Andover, MA, USA). (Color version of figure is available online.)
high.1 Co-oximetry can differentiate between oxyhemoglobin and carboxyhemoglobin; if available, use of a co-oximeter is suggested if carbon monoxide intoxication is suspected.1 One of the more important limitations of pulse oximetry stems from the sigmoidal shape of the oxyhemoglobin dissociation curve. When hemoglobin saturation is greater than 90%, the curve is relatively flat, and large increases in the arterial partial pressure of oxygen correspond to only small increases in SpO2. As a result, a patient breathing an oxygen-enriched gas mixture may have a normal SpO2 in the face of significant pulmonary dysfunction that might go unrecognized without arterial blood gas analysis.6 Despite this limitation, pulse oximetry is undoubtedly a useful tool in the management of patients at risk for hypoxemia.
Capnometry Capnometry is the measurement of exhaled carbon dioxide (CO2). CO2 is a major end product of cellular metabolism that is delivered to the lungs via the pulmonary circulation, thus capnometry provides information not only on alveolar ventilation and pulmonary gas exchange, but also on metabolic rate and pulmonary blood flow.11 Capnometry can be utilized to ensure proper placement of endotracheal and nasoesophageal or nasogastric tubes, to monitor adequacy of ventilation, and to detect apnea in patients that are anesthetized and intubated. Capnometry is an extremely useful tool during cardiopulmonary resuscitation (CPR) as delivery of CO2 to the lungs requires adequate pulmonary
Fig. 2. The sampling line of a sidestream capnometer attached to the breathing circuit. Exhaled gas is aspirated at a fixed rate from the breathing circuit and analyzed in a measuring chamber attached to the monitor. Criticare Poet IQ (Criticare Systems, INC, Waukesha WA, USA). (Color version of figure is available online.)
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Fig. 3. Combined capnograph and pulse oximeter. This model allows for visual inspection of the pulse oximetry waveform to ensure accuracy in analysis. CO2SMO (Respironics Novametrix, Andover MA, USA). (Color version of figure is available online.)
perfusion; an increase in exhaled CO2 during the course of CPR suggests that chest compressions are generating sufficient cardiac output to perfuse the lungs or that there has been a return of spontaneous circulation (ROSC).11–13 Colorimetric capnometers are inexpensive, handheld devices that are inserted between the endotracheal tube and breathing circuit in intubated patients. The center of the device contains a paper with a pH-sensitive chemical indicator; a color change from purple to yellow occurs when exhaled gas containing CO2 passes over the paper.5 These devices provide a semi-quantitative assessment of the concentration of CO2 in exhaled gas—a color change to yellow occurs if the exhaled concentration of CO2 is greater than 2%.14 Colorimetric CO2 detectors are best utilized to confirm proper endotracheal tube placement as little to no CO2 is expected within the esophagus or stomach and a lack of color change may suggest esophageal intubation. During cardiopulmonary arrest, absence of a color change does not exclude endotracheal intubation because pulmonary perfusion, and thus delivery of CO2 to the lungs, is inherently compromised. A color change to yellow, however, may suggest some adequacy in resuscitative efforts or ROSC.14 A quantitative measurement of CO2 concentration in exhaled gas can be determined by infrared spectrophotometry, Raman scatter, or mass spectrometry.15,16 CO2 absorbs light in the infrared spectrum; the amount of light absorbed as a beam of infrared light passes through exhaled gas is proportional to the partial pressure
Fig. 4. A normal capnogram. Phase I represents exhalation of gas with an unmeasurable concentration of CO2 from the large airways. Phase II signifies the beginning of exhalation of gas from the alveoli mixing with gas from the conducting airways. Mixed alveolar gas is exhaled in phase III. End-tidal CO2 occurs at the end of phase III. The beginning of the next inspiration occurs during phase IV. (Color version of figure is available online.)
Fig. 5. The capnogram does not return to baseline, indicating that the patient is rebreathing CO2. This may be owing to faulty 1-way valves within the breathing circuit or because the soda lime is exhausted.
of CO2 (PCO2) in the sample. This method of capnometry is used most frequently in the clinical setting. Raman scattering measures PCO2 by exposing gas within the analyzer to a high-intensity argon laser beam; CO2 molecules absorb and then re-emit some energy from the beam at a distinctive wavelength.15 Mass spectrometers measure concentration of CO2 by exposing exhaled gas to an ionizing electron beam; ions are subsequently subjected to a magnetic field and separated based on mass and charge. This type of capnometer is expensive and is therefore infrequently used clinically.15 Capnometers are further classified by location at which CO2 is measured. Mainstream capnometers (Fig 1) measure CO2 concentration at their insertion site between the endotracheal tube and breathing circuit whereas sidestream capnometers (Fig 2) siphon exhaled gas from the breathing circuit for analysis in an optical chamber located away from the patient.17 Mainstream analyzers allow for preservation of a closed breathing system and readings are instantaneous as the analyzer is part of the breathing circuit; however, these analyzers increase dead space and the weight of the analyzer may lead to inadvertent extubation especially when connected to very small endotracheal tubes. Newer mainstream capnometers are designed with this limitation in mind; an attempt has been made in some models to reduce equipment dead space added to the breathing circuit.11 Mainstream capn-
Fig. 6. An increase in the slope of the alveolar plateau may result from bronchoconstriction or obstruction of the endotracheal tube.
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Fig. 7. A spontaneous breath from a patient that is being mechanically ventilated, indicating patient-ventilator dyssynchrony, is demonstrated by this capnogram.
ometers should be inspected frequently for accumulation of condensation within the analyzer as water vapor absorbs infrared light and may lead to a falsely high CO2 reading.15 Compared with mainstream analyzers, sidestream analyzers are less bulky and in-line moisture traps may be utilized to prevent inaccuracies due to condensation.11,15 Sidestream monitors may have some utility in nonintubated patients as the sampling line may be connected to nasal catheters or simply inserted into the nostril.16 In some instances, the small diameter sampling line may become occluded by respiratory secretions necessitating replacement. Because exhaled gas is removed from the breathing circuit and analyzed remotely, results are not obtained instantaneously and they may be slightly out of synch with patient respiration. Gas is withdrawn from the breathing circuit at a fixed rate per minute that may exceed the respiratory minute volume in very small patients necessitating a compensatory increase in fresh gas flow rates for these patients.11 Sidestream capnometers continuously vent exhaled gas into the environment after analysis; when used for patients breathing an inhaled anesthetic gas, a scavenging system must be in place to prevent inadvertent staff exposure and environmental contamination. When the concentration of CO2 in exhaled gas is displayed graphically over time, the resulting waveform is known as a capnogram. Capnometers that display a capnogram (Fig 3) are typically more expensive than those that just provide end-tidal
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CO2 (PETCO2) concentration; however, these devices are extremely useful monitoring tools as analysis of the capnogram waveform frequently can diagnose problems with either the patient or equipment that might go unrecognized otherwise. A normal capnogram waveform (Fig 4) is generated by the measurement of CO2 (PCO2) at various points during the respiratory cycle. Phase I occurs during the initial part of exhalation; gas measured at this point typically contains no or an unmeasurable concentration of CO2 because it is coming from dead space—from the circuit as well as physiologic from the large airways that do not participate in gas exchange. Phase II represents the transition between gas from the airway dead space to alveolar gas, which contains CO2. Phase III, known as the alveolar plateau, occurs when all the gas is coming from the alveoli. PETCO2 occurs at the end of the alveolar plateau and represents the concentration of CO2 at the end of expiration. Phase IV, the inspiratory downstroke, occurs at the beginning of the next inspiration.18 Changes in capnogram waveform may signify a disturbance in respiratory function, metabolic rate or pulmonary perfusion, or patient-ventilator dyssynchrony during mechanical ventilation. Likewise, malfunction of part of the breathing circuit may be first identified by an alteration in the capnogram (Figs 5-9). For example, rebreathing CO2, which might occur when 1-way valves within the breathing circuit fail or when soda lime is exhausted, may be identified by an inspiratory baseline that does not reach 0 and progressively increases. PETCO2 may increase over time because of hypoventilation or when production of CO2 is increased, such as with fever, sepsis, malignant hyperthermia, thyroid storm, or with excessive overfeeding (typically with parenteral nutrition). A gradual decrease in PETCO2 may be the result of hyperventilation, hypothermia, or declining cardiac output. A sudden decline in PETCO2 may suggest extubation, equipment failure, massive pulmonary embolism, or cardiopulmonary arrest.19 PETCO2 is often slightly less than PaCO2 owing to dilution of alveolar gas by gas in the dead space.16,17 When pulmonary perfusion and gas exchange are normal, PETCO2 correlates well with PaCO2 and, in most patients, the PaCO2-PETCO2 gradient is less than 5 mm Hg. As such, PETCO2 may be a useful surrogate for a continuous estimate of PaCO2. When gas exchange is compromised by pulmonary pathology, pulmonary embolism, poor cardiac output, or excessive dead space (physiologic or mechanical), the PaCO2-PETCO2 gradient will increase and can be as high as 20 mm Hg or more in severe pulmonary disease.16,17 In this situation, an elevated PETCO2 indicates increased PaCO2 but a normal or low PETCO2 does not rule out hypercapnea. For this reason, the need for periodic arterial blood gas analysis to establish the actual gradient cannot be overemphasized.
Fig. 8. Gradually increasing PETCO2. This may be the result of hypoventilation, hyperthermia, fever, sepsis, or thyroid storm.
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Fig. 9. A rapid decline in PETCO2, seen during mechanical or manual ventilation, may suggest severe pulmonary hypoperfusion, massive pulmonary embolism, or cardiopulmonary arrest. Extubation or equipment failure may also result in a sudden decrease in PETCO2.
In addition to its role in the management of the anesthetized or mechanically ventilated patient, PETCO2 monitoring may be useful in the placement of nasoesophageal or nasogastric feeding tubes, as a measurable concentration of CO2 through the feeding tube suggests inadvertent endotracheal placement.20 During CPR endtidal capnography provides information about the efficacy of resuscitative efforts. PETCO2 is often very low or 0 initially owing to pulmonary hypoperfusion; an increase in PETCO2 during CPR suggests that chest compressions have achieved some degree of forward blood flow. In fact, an increase in PETCO2 greater than 10 mm Hg above baseline during the first 20 minutes of CPR has been shown to predict ROSC in humans with high sensitivity and specificity.21 Ineffective CPR will result in failure to increase PETCO2 and the resuscitative strategy should be reevaluated.13 Conclusion Pulse oximetry and capnometry are rapid, noninvasive and useful techniques with many applications in clinical practice. Clinicians should be aware of the limitations that exist with these monitoring tools and interpret results carefully in the context of history, physical examination findings, and arterial blood gas analysis. References 1. Sotirios F, Prifits KN, Anthracopoulos MB. Pulse oximetry in pediatric practice. Pediatrics 128:740–753, 2011 2. Ayres DA. Pulse oximetry and CO-oximetry. In: Burkitt Creedon JM, Davis H, editors. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. West Sussex: Wiley-Blackwell; 2012. p. 274–285 3. Severinghaus JW. History and recent developments in pulse oximetry. Scand J Clin Lab Invest 53:105–111, 1993 4. Grosenbaugh DA, Alben JO, Muir WW. Absorbance spectra of inter-species hemoglobins in the visible and near infrared regions. J Vet Emerg Crit Care 7:36–42, 1997
5. Marino PL. Oximetry and capnography. In: The ICU Book. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2007, p. 385–401 6. Jubran A. Pulse oximetry. Crit Care 3:R11–R17, 1999 7. Matthews NS, Hartke S, Allen JC. An evaluation of pulse oximeters in dogs, cats and horses. Vet Anaesth Analg 30:3–14, 2003 8. Fairman NB. Evaluation of pulse oximetry as a continuous monitoring technique in critically ill dogs in the small animal intensive care unit. J Vet Emerg Crit Care 2:50–56, 1992 9. Proulx J. Respiratory monitoring: arterial blood gas analysis, pulse oximetry, and end-tidal carbon dioxide analysis. Clin Tech Small Anim Pract 14:227–230, 1999 10. Hendricks JC, King LG. Practicality, usefulness, and limits of pulse oximetry in critical small animal patients. J Vet Emerg Crit Care 3:5–12, 1993 11. Anderson CT, Breen PH. Carbon dioxide kinetics and capnography during critical care. Crit Care 4:207–215, 2000 12. Lewis LM, Stothert J, Standeven J, et al. Correlation of end-tidal CO2 to cerebral perfusion during CPR. Ann Emerg Med 21:1131–1134, 1992 13. Brainard BM, Boller M, Fletcher DJ, et al. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 5: monitoring. J Vet Emerg Crit Care 22: S65–S84, 2012 14. Ornato JP, Shipley JB, Racht EM, et al. Multicenter study of a portable, handsize, colorimetric end-tidal carbon dioxide detection device. Ann Emerg Med 21:518–523, 1992 15. Barter LS. Capnography. In: Burkitt Creedon JM, Davis H, editors. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. West Sussex: Wiley-Blackwell; 2012. p. 340–348 16. Hendricks JC, King LG. Practicality, usefulness, and limits of end-tidal carbon dioxide monitoring in critical small animal patients. J Vet Emerg Crit Care 4:29–39, 1994 17. Teixeira Neto FJ, Carregaro AB, Mannarino R, et al. Comparison of a sidestream capnography and a mainstream capnography in mechanically ventilated dogs. J Am Vet Med Assoc 221:1582–1585, 2002 18. Bhavani-Shankar K, Philip JH. Defining segments and phases of a time capnogram. Anesth Analg 91:973–977, 2000 19. Raffe MR. End tidal capnography. In: King LG, editor. Textbook of Respiratory Disease in Dogs and Cats. St Louis: Elsevier-Saunders; 2004. p. 198–201 20. Johnson PA, Mann FA, Dodam J, et al. Capnographic documentation of nasoesophageal and nasogastric feeding tube placement in dogs. J Vet Emerg Crit Care 12:227–233, 2002 21. Cantineau JP, Lambert Y, Merckx P, et al. End-tidal carbon dioxide during cardiopulmonary resuscitation in humans presenting mostly with asystole: a predictor of outcome. Crit Care Med 24:791–796, 1996
Regular articles
Pulse Oximetry and Capnometry Vincent Thawley, VMD, Lori S. Waddell, DVM, DACVECCn Keywords: oximetry capnometry capnogram Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, Philadelphia, PA, USA
Respiratory dysfunction is common in veterinary patients and various techniques have been developed to rapidly and accurately monitor pulmonary gas exchange. Pulse oximetry and capnometry are tools that allow for continuous evaluation of pulmonary function. Methodology, indications, and limitations of pulse oximetry and capnometry are discussed in this article. Both techniques are useful for monitoring critically ill or anesthetized patients; however, limitations to their use exist which underscore the need for intermittent arterial blood gas analysis. & 2013 Elsevier Inc. All rights reserved.
n
Address reprint requests to Lori Waddell, DVM, DACVECC, Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, 3900 Delancy St, Philadelphia, PA 19143, USA. E-mail: [email protected]
Introduction Pulmonary dysfunction is commonly encountered in critical illness and in anesthetized patients and may lead to hypoxemia, abnormalities in ventilation, or both. Successful management of patients with pulmonary disease frequently involves monitoring techniques that allow for accurate assessment of respiratory function. Although arterial blood gas analysis remains the gold standard in the assessment of oxygenation and ventilation, results provide an assessment of pulmonary function at only 1 moment in time and repeated sampling is necessary to effectively monitor patients with a dynamic disease process. In addition, sample acquisition may be technically challenging and can be stressful for patients that already have respiratory compromise. For these reasons, noninvasive, cageside monitoring tools have gained popularity in recent years. This article discusses pulse oximetry and capnography, 2 monitoring techniques that allow for noninvasive and even continuous assessment of pulmonary gas exchange.
Pulse Oximetry Oximetry is a rapid and noninvasive technique for estimating arterial hemoglobin saturation with oxygen. Pulse oximetry is a transcutaneous bedside tool for measuring functional hemoglobin, which is the hemoglobin that is able to bind, transport, and release oxygen.1 Co-oximetry provides a measurement of both functional hemoglobin and other species of hemoglobin, including methemoglobin, carboxyhemoglobin, and sulfhemoglobin, that are incapable of binding oxygen and thus do not contribute to total arterial oxygen-carrying capacity.2 In most instances, co-oximetry is performed by analyzing a blood sample that precludes continuous use. Pulse co-oximeters, which are bedside, transcutaneous monitors that assess for the presence of various species of hemoglobin using similar methodology as pulse oximeters, have been developed to address this limitation. Pulse co-oximetry is not commonly used in veterinary patients.2 Pulse oximetry was first used clinically in 1964; early oximeters were bulky and expensive but accurate down to a hemoglobin
saturation of 70%.3 Modern oximeters are often compact and handheld, lending themselves to bedside use for quick assessment of arterial oxygenation. Indeed, pulse oximetry is considered a standard-of-care monitoring technique in most human and veterinary critical care settings. According to the Lambert-Beer law, the concentration of a substance is proportional to the absorption of light at a specific wavelength by the substance in question and the length across which the light travels.4 Pulse oximeters operate via this principle; percent hemoglobin saturation with oxygen is determined by analysis of the differential absorption of light by oxygenated and deoxygenated hemoglobin in arterial blood. Modern oximeters emit light in 2 wavelengths—1 in the red region of the light spectrum (660 nm) and 1 in the infrared region (940 nm). Emitted light travels through tissue to reach a photodetector on the opposite side of the device; light with a pulsatile signal is presumed to have traversed arterial blood whereas nonpulsatile light is assumed to have traversed venous blood and connective tissue and is therefore not analyzed by the photodetector.4,5 Oxygenated hemoglobin does not absorb light in the red region of the light spectrum as well as deoxygenated hemoglobin—this accounts for the bright-red appearance of arterial blood. Conversely, deoxygenated hemoglobin does not absorb light in the infrared region as well as oxygenated hemoglobin. Therefore, the amount of oxygenated and deoxygenated hemoglobin present can be determined by the amount of light of each wavelength that is transmitted through the tissue. The amount of oxygenated hemoglobin present, compared with total hemoglobin, is expressed as percent saturation (SpO2).5 The spectral absorption of canine, feline, equine, porcine, and bovine hemoglobin is consistent with that of human hemoglobin, so pulse oximeters designed for human use may be employed in these species.4 Pulse oximeters rely on detection of a pulsating light signal to estimate arterial hemoglobin saturation; as such, obtaining an accurate reading may be difficult in patients that have poor peripheral perfusion due to hypothermia or hypotension.1,6 Likewise, the presence of a cardiac arrhythmia with pulse deficits may result in erroneous results.7 Most monitors display the patient's
1527-3369/$ - see front matter & 2013 Topics in Companion Animal Medicine. Published by Elsevier Inc. http://dx.doi.org/10.1053/j.tcam.2013.06.006
V. Thawley, L.S. Waddell / Topics in Companion An Med 28 (2013) 124–128
heart rate; results must be interpreted with caution should the displayed heart rate not match the patient's actual heart rate. Some oximeters display a plethysmographic pulse waveform that can be examined to ensure accuracy in analysis; others may include pulse signal intensity along with heart rate. If a pulse waveform is displayed it should ideally resemble a normal arterial pulse waveform to ensure accuracy in the calculated hemoglobin saturation. A variety of pulse oximeters are available commercially. Most models employ the use of a clip with a phototransmitter on 1 side and a photoreceptor on the other although some models, designed for use on human foreheads, are flat and have both the phototransmitter and photoreceptor on the same side and utilize light reflection for analysis. Pulse oximeters with probes designed for rectal insertion are also available. When selecting a pulse oximeter, one should give consideration to portability and durability as well as the patient population that it will be used for, particularly if frequent use is anticipated. Anesthetized patients are much easier to monitor with pulse oximetry than are awake, moving patients. In the authors' experience, pulse oximeter probes work best on the tongue, although this site is generally only available in patients that are heavily sedated, anesthetized, or in moribund condition. Alternate sites for probe placement include the buccal mucosa, pinna, nonpigmented inguinal skin, and nonpigmented paw pads or interdigital skin webbing. For patients with pigmented oral mucosa, oximetry may be performed using the preputial or vulvar mucosa. An additional site that can be used for flat pulse oximeter probes is the ventral surface of the tail after clipping the hair in this region. The site selected for probe placement should ideally be warm and well perfused. Clipping hair in thick-coated patients so that the phototransmitter is directly on skin is recommended. Moistening the tongue and oral mucosa with saline or water may improve accuracy when these sites are utilized. When long-term, continuous use is anticipated (such as in the mechanically ventilated patient), the oximeter probe site should be inspected every 2-4 hours and the probe moved as necessary to prevent the development of pressure sores.8 Pulse oximetry is a valuable tool in the management of patients with or at risk for developing hypoxemia. Pulse oximetry is routinely used for monitoring sedated or anesthetized patients and as a screening tool to determine whether tachypnea is due to pulmonary compromise or whether diagnostics should be focused elsewhere. Additionally, pulse oximetry is useful to determine whether hypoxemia improves with provision of supplemental oxygen. In humans, it is reported that inaccuracies in pulse oximetry may occur in the presence of hypotension, icterus, anemia, and methemoglobinemia.6,9 However, Hendricks et al10 found that pulse oximetry was a useful monitoring modality in a variety of critically ill canine patients in the intensive care unit. Several of these patients either were anemic, hypothermic, or had increased serum bilirubin. Bright ambient light may interfere with photodetector function so probes should ideally be shielded when in use.7 Excessive patient motion or shivering may preclude continuous pulse oximetry monitoring as the probe is likely to disengage from the site of placement; for these patients, intermittent oximetry readings may be necessary although obtaining any readings can be difficult when motion is present. Carbon monoxide intoxication may result in spuriously high pulse oximetry results as carboxyhemoglobin, formed when carbon monoxide displaces oxygen from hemoglobin molecules, has a similar spectral absorption pattern as oxyhemoglobin. As a result, the machine will mistake carboxyhemoglobin for oxyhemoglobin and report an oxygen saturation that is erroneously
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Fig. 1. A mainstream capnometer inserted between the endotracheal tube and breathing circuit. As exhaled gas passes over the sensor, the concentration of CO2 is measured in real time. CO2SMO (Respironics Novametrix, Andover, MA, USA). (Color version of figure is available online.)
high.1 Co-oximetry can differentiate between oxyhemoglobin and carboxyhemoglobin; if available, use of a co-oximeter is suggested if carbon monoxide intoxication is suspected.1 One of the more important limitations of pulse oximetry stems from the sigmoidal shape of the oxyhemoglobin dissociation curve. When hemoglobin saturation is greater than 90%, the curve is relatively flat, and large increases in the arterial partial pressure of oxygen correspond to only small increases in SpO2. As a result, a patient breathing an oxygen-enriched gas mixture may have a normal SpO2 in the face of significant pulmonary dysfunction that might go unrecognized without arterial blood gas analysis.6 Despite this limitation, pulse oximetry is undoubtedly a useful tool in the management of patients at risk for hypoxemia.
Capnometry Capnometry is the measurement of exhaled carbon dioxide (CO2). CO2 is a major end product of cellular metabolism that is delivered to the lungs via the pulmonary circulation, thus capnometry provides information not only on alveolar ventilation and pulmonary gas exchange, but also on metabolic rate and pulmonary blood flow.11 Capnometry can be utilized to ensure proper placement of endotracheal and nasoesophageal or nasogastric tubes, to monitor adequacy of ventilation, and to detect apnea in patients that are anesthetized and intubated. Capnometry is an extremely useful tool during cardiopulmonary resuscitation (CPR) as delivery of CO2 to the lungs requires adequate pulmonary
Fig. 2. The sampling line of a sidestream capnometer attached to the breathing circuit. Exhaled gas is aspirated at a fixed rate from the breathing circuit and analyzed in a measuring chamber attached to the monitor. Criticare Poet IQ (Criticare Systems, INC, Waukesha WA, USA). (Color version of figure is available online.)
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Fig. 3. Combined capnograph and pulse oximeter. This model allows for visual inspection of the pulse oximetry waveform to ensure accuracy in analysis. CO2SMO (Respironics Novametrix, Andover MA, USA). (Color version of figure is available online.)
perfusion; an increase in exhaled CO2 during the course of CPR suggests that chest compressions are generating sufficient cardiac output to perfuse the lungs or that there has been a return of spontaneous circulation (ROSC).11–13 Colorimetric capnometers are inexpensive, handheld devices that are inserted between the endotracheal tube and breathing circuit in intubated patients. The center of the device contains a paper with a pH-sensitive chemical indicator; a color change from purple to yellow occurs when exhaled gas containing CO2 passes over the paper.5 These devices provide a semi-quantitative assessment of the concentration of CO2 in exhaled gas—a color change to yellow occurs if the exhaled concentration of CO2 is greater than 2%.14 Colorimetric CO2 detectors are best utilized to confirm proper endotracheal tube placement as little to no CO2 is expected within the esophagus or stomach and a lack of color change may suggest esophageal intubation. During cardiopulmonary arrest, absence of a color change does not exclude endotracheal intubation because pulmonary perfusion, and thus delivery of CO2 to the lungs, is inherently compromised. A color change to yellow, however, may suggest some adequacy in resuscitative efforts or ROSC.14 A quantitative measurement of CO2 concentration in exhaled gas can be determined by infrared spectrophotometry, Raman scatter, or mass spectrometry.15,16 CO2 absorbs light in the infrared spectrum; the amount of light absorbed as a beam of infrared light passes through exhaled gas is proportional to the partial pressure
Fig. 4. A normal capnogram. Phase I represents exhalation of gas with an unmeasurable concentration of CO2 from the large airways. Phase II signifies the beginning of exhalation of gas from the alveoli mixing with gas from the conducting airways. Mixed alveolar gas is exhaled in phase III. End-tidal CO2 occurs at the end of phase III. The beginning of the next inspiration occurs during phase IV. (Color version of figure is available online.)
Fig. 5. The capnogram does not return to baseline, indicating that the patient is rebreathing CO2. This may be owing to faulty 1-way valves within the breathing circuit or because the soda lime is exhausted.
of CO2 (PCO2) in the sample. This method of capnometry is used most frequently in the clinical setting. Raman scattering measures PCO2 by exposing gas within the analyzer to a high-intensity argon laser beam; CO2 molecules absorb and then re-emit some energy from the beam at a distinctive wavelength.15 Mass spectrometers measure concentration of CO2 by exposing exhaled gas to an ionizing electron beam; ions are subsequently subjected to a magnetic field and separated based on mass and charge. This type of capnometer is expensive and is therefore infrequently used clinically.15 Capnometers are further classified by location at which CO2 is measured. Mainstream capnometers (Fig 1) measure CO2 concentration at their insertion site between the endotracheal tube and breathing circuit whereas sidestream capnometers (Fig 2) siphon exhaled gas from the breathing circuit for analysis in an optical chamber located away from the patient.17 Mainstream analyzers allow for preservation of a closed breathing system and readings are instantaneous as the analyzer is part of the breathing circuit; however, these analyzers increase dead space and the weight of the analyzer may lead to inadvertent extubation especially when connected to very small endotracheal tubes. Newer mainstream capnometers are designed with this limitation in mind; an attempt has been made in some models to reduce equipment dead space added to the breathing circuit.11 Mainstream capn-
Fig. 6. An increase in the slope of the alveolar plateau may result from bronchoconstriction or obstruction of the endotracheal tube.
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Fig. 7. A spontaneous breath from a patient that is being mechanically ventilated, indicating patient-ventilator dyssynchrony, is demonstrated by this capnogram.
ometers should be inspected frequently for accumulation of condensation within the analyzer as water vapor absorbs infrared light and may lead to a falsely high CO2 reading.15 Compared with mainstream analyzers, sidestream analyzers are less bulky and in-line moisture traps may be utilized to prevent inaccuracies due to condensation.11,15 Sidestream monitors may have some utility in nonintubated patients as the sampling line may be connected to nasal catheters or simply inserted into the nostril.16 In some instances, the small diameter sampling line may become occluded by respiratory secretions necessitating replacement. Because exhaled gas is removed from the breathing circuit and analyzed remotely, results are not obtained instantaneously and they may be slightly out of synch with patient respiration. Gas is withdrawn from the breathing circuit at a fixed rate per minute that may exceed the respiratory minute volume in very small patients necessitating a compensatory increase in fresh gas flow rates for these patients.11 Sidestream capnometers continuously vent exhaled gas into the environment after analysis; when used for patients breathing an inhaled anesthetic gas, a scavenging system must be in place to prevent inadvertent staff exposure and environmental contamination. When the concentration of CO2 in exhaled gas is displayed graphically over time, the resulting waveform is known as a capnogram. Capnometers that display a capnogram (Fig 3) are typically more expensive than those that just provide end-tidal
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CO2 (PETCO2) concentration; however, these devices are extremely useful monitoring tools as analysis of the capnogram waveform frequently can diagnose problems with either the patient or equipment that might go unrecognized otherwise. A normal capnogram waveform (Fig 4) is generated by the measurement of CO2 (PCO2) at various points during the respiratory cycle. Phase I occurs during the initial part of exhalation; gas measured at this point typically contains no or an unmeasurable concentration of CO2 because it is coming from dead space—from the circuit as well as physiologic from the large airways that do not participate in gas exchange. Phase II represents the transition between gas from the airway dead space to alveolar gas, which contains CO2. Phase III, known as the alveolar plateau, occurs when all the gas is coming from the alveoli. PETCO2 occurs at the end of the alveolar plateau and represents the concentration of CO2 at the end of expiration. Phase IV, the inspiratory downstroke, occurs at the beginning of the next inspiration.18 Changes in capnogram waveform may signify a disturbance in respiratory function, metabolic rate or pulmonary perfusion, or patient-ventilator dyssynchrony during mechanical ventilation. Likewise, malfunction of part of the breathing circuit may be first identified by an alteration in the capnogram (Figs 5-9). For example, rebreathing CO2, which might occur when 1-way valves within the breathing circuit fail or when soda lime is exhausted, may be identified by an inspiratory baseline that does not reach 0 and progressively increases. PETCO2 may increase over time because of hypoventilation or when production of CO2 is increased, such as with fever, sepsis, malignant hyperthermia, thyroid storm, or with excessive overfeeding (typically with parenteral nutrition). A gradual decrease in PETCO2 may be the result of hyperventilation, hypothermia, or declining cardiac output. A sudden decline in PETCO2 may suggest extubation, equipment failure, massive pulmonary embolism, or cardiopulmonary arrest.19 PETCO2 is often slightly less than PaCO2 owing to dilution of alveolar gas by gas in the dead space.16,17 When pulmonary perfusion and gas exchange are normal, PETCO2 correlates well with PaCO2 and, in most patients, the PaCO2-PETCO2 gradient is less than 5 mm Hg. As such, PETCO2 may be a useful surrogate for a continuous estimate of PaCO2. When gas exchange is compromised by pulmonary pathology, pulmonary embolism, poor cardiac output, or excessive dead space (physiologic or mechanical), the PaCO2-PETCO2 gradient will increase and can be as high as 20 mm Hg or more in severe pulmonary disease.16,17 In this situation, an elevated PETCO2 indicates increased PaCO2 but a normal or low PETCO2 does not rule out hypercapnea. For this reason, the need for periodic arterial blood gas analysis to establish the actual gradient cannot be overemphasized.
Fig. 8. Gradually increasing PETCO2. This may be the result of hypoventilation, hyperthermia, fever, sepsis, or thyroid storm.
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Fig. 9. A rapid decline in PETCO2, seen during mechanical or manual ventilation, may suggest severe pulmonary hypoperfusion, massive pulmonary embolism, or cardiopulmonary arrest. Extubation or equipment failure may also result in a sudden decrease in PETCO2.
In addition to its role in the management of the anesthetized or mechanically ventilated patient, PETCO2 monitoring may be useful in the placement of nasoesophageal or nasogastric feeding tubes, as a measurable concentration of CO2 through the feeding tube suggests inadvertent endotracheal placement.20 During CPR endtidal capnography provides information about the efficacy of resuscitative efforts. PETCO2 is often very low or 0 initially owing to pulmonary hypoperfusion; an increase in PETCO2 during CPR suggests that chest compressions have achieved some degree of forward blood flow. In fact, an increase in PETCO2 greater than 10 mm Hg above baseline during the first 20 minutes of CPR has been shown to predict ROSC in humans with high sensitivity and specificity.21 Ineffective CPR will result in failure to increase PETCO2 and the resuscitative strategy should be reevaluated.13 Conclusion Pulse oximetry and capnometry are rapid, noninvasive and useful techniques with many applications in clinical practice. Clinicians should be aware of the limitations that exist with these monitoring tools and interpret results carefully in the context of history, physical examination findings, and arterial blood gas analysis. References 1. Sotirios F, Prifits KN, Anthracopoulos MB. Pulse oximetry in pediatric practice. Pediatrics 128:740–753, 2011 2. Ayres DA. Pulse oximetry and CO-oximetry. In: Burkitt Creedon JM, Davis H, editors. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. West Sussex: Wiley-Blackwell; 2012. p. 274–285 3. Severinghaus JW. History and recent developments in pulse oximetry. Scand J Clin Lab Invest 53:105–111, 1993 4. Grosenbaugh DA, Alben JO, Muir WW. Absorbance spectra of inter-species hemoglobins in the visible and near infrared regions. J Vet Emerg Crit Care 7:36–42, 1997
5. Marino PL. Oximetry and capnography. In: The ICU Book. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2007, p. 385–401 6. Jubran A. Pulse oximetry. Crit Care 3:R11–R17, 1999 7. Matthews NS, Hartke S, Allen JC. An evaluation of pulse oximeters in dogs, cats and horses. Vet Anaesth Analg 30:3–14, 2003 8. Fairman NB. Evaluation of pulse oximetry as a continuous monitoring technique in critically ill dogs in the small animal intensive care unit. J Vet Emerg Crit Care 2:50–56, 1992 9. Proulx J. Respiratory monitoring: arterial blood gas analysis, pulse oximetry, and end-tidal carbon dioxide analysis. Clin Tech Small Anim Pract 14:227–230, 1999 10. Hendricks JC, King LG. Practicality, usefulness, and limits of pulse oximetry in critical small animal patients. J Vet Emerg Crit Care 3:5–12, 1993 11. Anderson CT, Breen PH. Carbon dioxide kinetics and capnography during critical care. Crit Care 4:207–215, 2000 12. Lewis LM, Stothert J, Standeven J, et al. Correlation of end-tidal CO2 to cerebral perfusion during CPR. Ann Emerg Med 21:1131–1134, 1992 13. Brainard BM, Boller M, Fletcher DJ, et al. RECOVER evidence and knowledge gap analysis on veterinary CPR. Part 5: monitoring. J Vet Emerg Crit Care 22: S65–S84, 2012 14. Ornato JP, Shipley JB, Racht EM, et al. Multicenter study of a portable, handsize, colorimetric end-tidal carbon dioxide detection device. Ann Emerg Med 21:518–523, 1992 15. Barter LS. Capnography. In: Burkitt Creedon JM, Davis H, editors. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. West Sussex: Wiley-Blackwell; 2012. p. 340–348 16. Hendricks JC, King LG. Practicality, usefulness, and limits of end-tidal carbon dioxide monitoring in critical small animal patients. J Vet Emerg Crit Care 4:29–39, 1994 17. Teixeira Neto FJ, Carregaro AB, Mannarino R, et al. Comparison of a sidestream capnography and a mainstream capnography in mechanically ventilated dogs. J Am Vet Med Assoc 221:1582–1585, 2002 18. Bhavani-Shankar K, Philip JH. Defining segments and phases of a time capnogram. Anesth Analg 91:973–977, 2000 19. Raffe MR. End tidal capnography. In: King LG, editor. Textbook of Respiratory Disease in Dogs and Cats. St Louis: Elsevier-Saunders; 2004. p. 198–201 20. Johnson PA, Mann FA, Dodam J, et al. Capnographic documentation of nasoesophageal and nasogastric feeding tube placement in dogs. J Vet Emerg Crit Care 12:227–233, 2002 21. Cantineau JP, Lambert Y, Merckx P, et al. End-tidal carbon dioxide during cardiopulmonary resuscitation in humans presenting mostly with asystole: a predictor of outcome. Crit Care Med 24:791–796, 1996
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