Hypoxia and Equipment Failure



Hypoxia and Equipment Failure


James B. Eisenkraft

Andrew B. Leibowitz





A. Medical Disease and Differential Diagnosis



  • What is hypoxia and what is hypoxemia?


  • Is the partial pressure of oxygen in arterial blood (PaO2) related to age?


  • Was this patient hypoxemic?


  • What is a pulse oximeter, and what is a hemoximeter?


  • How does a pulse oximeter work?


  • How is a two-wavelength pulse oximeter calibrated by the manufacturer?


  • What may affect the accuracy of a two-wavelength pulse oximeter?


  • How do the dyshemoglobins, methemoglobin (metHb) and carboxyhemoglobin (HbCO) affect SpO2 readings?


  • What is a capnometer, and what is capnography? Of what value are they in patient monitoring?


  • What is meant by the term end-tidal carbon dioxide (PETCO2)?


  • What is the appearance of a normal capnogram and what is its significance?


  • What are mainstream and sidestream capnometers?


  • Show some common capnograms and provide a differential diagnosis of each event.


  • What is the arterial-alveolar difference in carbon dioxide (CO2)?


  • What are some of the important safety features of the contemporary anesthesia workstation?


  • What are common sites for gas leakage?


  • How is the anesthesia machine checked for leaks?


B. Preoperative Evaluation and Preparation



  • What should be included in the equipment checkout in preparation for anesthesia?


  • What emergency equipment should be easily available to the anesthesiologist?


  • How should this patient be premedicated?


C. Intraoperative Management



  • How should this patient be monitored?


  • After uneventful inhalation mask induction, cystoscopy was begun, and the SpO2 was noted to decrease to 81% with the patient breathing an FIO2 of 0.4 (oxygen at 2 L per minute and nitrous oxide at 3 L per minute). The patient developed
    respiratory distress. The laryngeal mask airway (LMA) was easily maintained, and no gross secretions were noted. What acute diagnostic and therapeutic interventions would you perform?


  • The patient was tracheally intubated. Squeezing the reservoir bag in the circle system failed to inflate the lungs, and a leak was noted. What are the common sites for gas leaks?


D. Postoperative Management



  • What criteria would you use for tracheal extubation?


  • What are the causes of postoperative hypoxemia?


  • What is the difference between shunt, ventilation/perfusion mismatch, and dead space?


  • What is the differential diagnosis of pulmonary edema?


  • How should the ventilator be set if mechanical ventilation is required postoperatively?


  • If this patient had acute lung injury (ALI) secondary to aspiration, beside low-tidal volume ventilation, what other changes in routine therapy should be considered?


  • What therapies routinely administered by the anesthesiologist may cause ALI?


  • What methods of oxygen administration may be used postoperatively?


A. Medical Disease and Differential Diagnosis


A.1. What is hypoxia and what is hypoxemia?

Hypoxia is defined as reduction of oxygen supply to tissue below physiologic levels. Hypoxemia is defined as deficient oxygenation of the blood. From the anesthesiologist’s perspective, hypoxia is usually considered to be decreased oxygen tension (PO2) inside the body at the tissue level or outside the body (e.g., hypoxic gas mixture), and hypoxemia is decreased oxygen tension in the arterial blood (PaO2).



Dorland WAN. Dorland’s Illustrated Medical Dictionary. 31st ed. Philadelphia, PA: WB Saunders; 2007.


A.2. Is the partial pressure of oxygen in arterial blood (PaO2) related to age?

Yes. There is an age-dependent decrease in the PaO2. In 1972, Marshall and Wyche suggested the following relationship in subjects breathing room air:

mean PaO2 in mm Hg = 102 – 0.33 (age in years) mm Hg

About this regression line, there are 95% confidence limits (two standard deviations [SDs]) of 10 mm Hg.

Cerveri et al. studied PaO2 in normal nonsmoking subjects ages 40 to 90 years. They found that PaO2 was related to age in subjects between 40 and 74 years and constructed the following reference equation:

PaO2 (mm Hg) = 143.6 – (0.39 × age) – (0.56 × BMI) – (0.57 × PaCO2)

For subjects ≥75 years old, there was no correlation with age.



Cerveri I, Zoia MC, Fanfulla F, et al. Reference values of arterial oxygen tension in the middle-aged and elderly. Am J Respir Crit Care Med. 1995;152:934-941.

Marshall BE, Wyche MQ Jr. Hypoxemia during and after anesthesia. Anesthesiology. 1972;37:178-209.

Shapiro BA, Peruzzi WT, Kozelowski-Templin R. Clinical Applications of Blood Gases. 5th ed. St. Louis, MO: Mosby-Year Book; 1994:221.

Sorbini CA, Grassi V, Solinas E, et al. Arterial oxygen tension in relation to age in healthy subjects. Respiration. 1968;25:3-13.



A.3. Was this patient hypoxemic?

No. An SpO2 reading of 94% does not signify hypoxemia. This patient is five decades older than a 20-year-old subject; therefore, his mean PaO2 should be 5 × 5 mm Hg per decade, which is 25 mm Hg, less than that (95 mm Hg) expected in a 20-year-old (see section A.2, Sorbini et al.).

95 – 25 = 70 mm Hg

or, using the Marshall and Whyche equation (see section A.2),

102 – 0.33 (70) = 79 mm Hg

Assuming normal adult hemoglobin, temperature, and pH, this PaO2 corresponds to a hemoglobin oxygen saturation of approximately 94% on the normal hemoglobin oxygen saturation versus PO2 curve.

Although the definitions of hypoxemia given in sections A.1 and A.2 must take age into consideration, from a practical point of view, hypoxemia (in the absence of anemia) is generally considered to exist when the PaO2 is less than 60 mm Hg, which is equivalent to a hemoglobin oxygen saturation of 90%.



Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Philadelphia, PA: Elsevier Science; 2010:179-215.


A.4. What is a pulse oximeter, and what is a hemoximeter?

The pulse oximeter is a noninvasive device that provides a real-time estimate (designated the SpO2%) of the arterial hemoglobin saturation with oxygen. It is a transmissive oximeter in which the patient’s fingertip (or other probe site; e.g., earlobe) serves as an in vivo cuvette through which light at two different wavelengths is transmitted.

If one requires an accurate determination of the arterial hemoglobin saturation with oxygen, an arterial blood sample must be drawn and analyzed in a laboratory co-oximeter, sometimes called a hemoximeter. The laboratory co-oximeter is a transmissive oximeter that uses six or more wavelengths of light to measure total hemoglobin (HbTOT), oxygenated hemoglobin (HbO2), deoxygenated (“reduced”) hemoglobin (RHb), metHb, HbCO, and other dyshemoglobins, such as sulfhemoglobin. Because each species of hemoglobin has a characteristic absorbance spectrum (i.e., absorbance vs. wavelength), examination of a sample of blood using these six or eight wavelengths permits identification and quantification of each hemoglobin species. Conventional pulse oximeters use only two wavelengths of light; therefore, they are unable to determine all of the different hemoglobin species and assume that only HbO2 and RHb are present. Fractional saturation (HbO2%) is defined as HbO2 / (HbO2 + RHb + HbCO + metHb)—that is, HbO2 per total Hb. Functional saturation (SaO2) is defined as HbO2 / (HbO2 + RHb). Note that dyshemoglobins are absent from the denominator in the definition of SaO2.



Kurki TS, Eisenkraft JB. Pulse oximetry. In: Reich DL, Kahn R, Mittnacht A, et al, eds. Monitoring in Anesthesia and Perioperative Care. New York: Cambridge University Press; 2011:185-198.


A.5. How does a pulse oximeter work?

The pulse oximeter combines the technologies of spectrophotometry and optical plethysmography. In the pulse oximeter probe, light-emitting diodes transmit red light at wavelength 660 nm and infrared light at wavelength 940 nm through the fingertip or other probe site. Light that passes through the probe site is sensed by a single photodetector and expressed as absorbance at each wavelength. It can be shown that the ratio of absorbances, 660/940 nm, is related to the hemoglobin saturation with oxygen. This is spectrophotometry. Detection of pulsatile flow is by optical plethysmography. With each pulse of arterial blood, the probe site (e.g., fingertip) increases in volume, the path length of the transmitted light increases,
and the absorbance of light at 660 nm and 940 nm increases. This pulse-added absorbance is considered to be due to the pulsatile flow of arterial blood at the probe site, so that the ratio of pulse-added absorbances, 660/940 nm, can be used to provide an estimate of hemoglobin oxygen saturation in arterial blood.



Barker SJ. Pulse oximetry. In: Ehrenwerth J, Eisenkraft JB, Berry JM, eds. Anesthesia Equipment: Principles and Applications. 2nd ed. New York: Elsevier; 2013:256-270.

Kurki TS, Eisenkraft JB. Pulse oximetry. In: Reich DL, Kahn R, Mittnacht A, et al, eds. Monitoring in Anesthesia and Perioperative Care. New York: Cambridge University Press; 2011:185-198.


A.6. How is a two-wavelength pulse oximeter calibrated by the manufacturer?

Each pulse oximeter manufacturer creates an empiric calibration algorithm, that is, one based on observations in human volunteers. The algorithm relates the average ratio of pulseadded absorbances, 660/990 nm, to the actual hemoglobin oxygen saturation in arterial blood samples drawn simultaneously and analyzed in a laboratory hemoximeter. Observations are made with the volunteers breathing varying FIO2 values so that data for saturations as low as 70% are obtained. The calibration algorithm that is created relates the ratio (R) of pulseadded absorbances, 660/940 nm, to the laboratory hemoximeter readings of HbO2 or SaO2%, depending on the pulse oximeter manufacturer. The calibration algorithm is then stored in the software of the pulse oximeter as a “lookup” table. Therefore, the pulse oximeter merely measures R, consults its lookup table, and displays the corresponding saturation reading as SpO2. The pulse oximeter does not actually measure saturation; it infers it from R, and, therefore, it predicts what the laboratory hemoximeter would read if an arterial sample drawn at that moment were analyzed.

A high value for R corresponds to a low SpO2 reading; R = 1 corresponds to an SpO2 reading of 85%, and a low value for R corresponds to a high SpO2 reading. Whenever the SpO2 reading is approximately 85%, one should consider the possibility of a spurious reading as a result of the “R = 1” phenomenon. This is commonly due to malpositioning of the probe on the fingertip.

The pulse oximeter (SpO2) reading is usually specified by the manufacturer to have an SD of ±2%. Therefore, assuming a normal distribution, if the SpO2 reading is 96%, there is a 68% likelihood that the true saturation (as measured by a hemoximeter) is 96 ± 2% (i.e., ±1 SD) and a 95% likelihood that the true saturation is 96 ± 4% (i.e., ±2 SD).



Guan Z, Baker K, Sandberg WS. Misalignment of disposable pulse oximeter probes results in false saturation readings that influence anesthetic management. Anesth Analg. 2009;109:1530-1533.

Kelleher JF, Ruff RH. The penumbra effect: vasomotion-dependent pulse oximeter artifact due to probe malposition. Anesthesiology. 1989;71:787-791.


A.7. What may affect the accuracy of a two-wavelength pulse oximeter?

The two-wavelength pulse oximeter is most accurate when the conditions of its clinical use most closely resemble those of its calibration. Spurious readings or failure may occur during patient movement (e.g., shivering, peripheral nerve stimulation, “twitching”), presence of intense ambient light (low signal/noise ratio), electrocautery use, administration of intravenous dyes with absorbance peaks at 660 nm (e.g., methylene blue), presence of dyshemoglobins (e.g., metHb, HbCO, and sulfhemoglobin), certain colors of nail polish, poor pulsatile flow at the probe site (e.g., hypotension, vasoconstriction, Raynaud disease), and venous pulsations (e.g., tricuspid regurgitation or earlobe placement of the probe in a patient who is in a headdown position).

Recent improvements in pulse oximetry technology include paradigms to increase the signal/noise ratio, thereby permitting motion artifact reduction and increased sensitivity to pulsatile flow. Such pulse oximeters have significantly lower failure rates during patient movement (such as in the postanesthesia care unit) and during conditions of low flow (e.g., hypothermia).



Barker SJ. “Motion-resistant” pulse oximetry: a comparison of new and old models. Anesth Analg. 2002;95:967-972.



A.8. How do the dyshemoglobins, methemoglobin (metHb) and carboxyhemoglobin (HbCO) affect SpO2 readings?

In metHb, iron in the heme moiety is oxidized (such as by dapsone, benzocaine, nitric oxide, prilocaine) to the Fe3+ state rather than being in the normal Fe2+ state. metHb cannot carry oxygen and creates a physiologic anemia. The absorbance spectrum for metHb shows it to have similar absorbances to light at 660 nm and 940 nm. Therefore, the more metHb that is present, the more R tends toward 1 and the SpO2 reading toward 85%. In the presence of metHb, the SpO2 reading overestimates the fractional saturation and underestimates the functional saturation.

In carbon monoxide (CO) poisoning, CO combines with hemoglobin to create a physiologic hypoxemia. HbCO has a similar absorbance to HbO2 at 660 nm but a very low absorbance at 940 nm. In the presence of HbCO, the SpO2 overestimates fractional saturation and underestimates functional saturation. Although blood that is poisoned with CO appears “cherry red” to the naked eye, and therefore may look like it is fully saturated with oxygen, it is important to recognize that the ratio of absorbances 660/940 nm will suggest that the blood hemoglobin oxygen saturation is in the 90s. In a subject breathing FIO2 of 1 (when functional saturation is 100%), as the level of HbCO increases, SpO2 decreases from close to 100% to approximately 91%.

If the presence of dyshemoglobins is suspected, arterial blood must be drawn and analyzed in a laboratory hemoximeter to obtain accurate readings of saturation.

Pulse oximetry technology has evolved rapidly, and multiwavelength pulse oximeters, called pulse co-oximeters, are clinically available. They use more than seven wavelengths of light (Masimo Rainbow SET Pulse CO-Oximetry, Masimo Company, Irvine, CA), similar to the laboratory hemoximeter. This technology makes it possible to measure CO (SpCO), methemoglobin (SpMet), and total hemoglobin (SpHbt), all noninvasively and in real time.



Barker SJ, Badal JJ. The measurement of dyshemoglobins and total hemoglobin by pulse oximetry. Curr Opin Anaesthesiol. 2008;21:805-810.

Barker SJ, Curry J, Redford D, et al. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study. Anesthesiology. 2006;105:892-897.

Shamir MY, Avramovich A, Smaka T. The current status of continuous noninvasive measurement of total, carboxy, and methemoglobin concentration. Anesth Analg. 2012;114:972-978.


A.9. What is a capnometer, and what is capnography? Of what value are they in patient monitoring?

A capnometer is a device that measures the tension (in units of millimeters of mercury [mm Hg] or kilopascals [kPa]) or concentration (volumes %) of CO2 in the gas near the patient’s airway throughout the respiratory cycle. Capnography is the graphic display of the CO2 concentration on the y-axis against time on the x-axis.

Capnometry may be achieved using different technologies that can monitor CO2. Most capnometers now use infrared spectroscopy to measure the PCO2 (i.e., CO2 partial pressure in millimeters of mercury). A built-in barometer measures barometric pressure (PB) so that CO2 can also be displayed as a percentage (PCO2 × 100/PB = %CO2).

Capnography is one of the American Society of Anesthesiologists’ standards for basic anesthetic monitoring (i.e., “Continual monitoring for the presence of expired CO2 shall be performed unless invalidated by the nature of the patient, procedure or equipment.”). It is the “gold standard” for establishing the presence of ventilation.



American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. Schaumburg, IL: American Society of Anesthesiologists; 2010.

Ehrenwerth J, Eisenkraft JB, Berry JM, eds. Anesthesia Equipment: Principles and Applications. 2nd ed. New York: Elsevier; 2013:245-254.


A.10. What is meant by the term end-tidal carbon dioxide (PETCO2)?

PETCO2 is the tension of CO2 in the exhaled gas at the end of an exhalation. Because this gas originates from the alveoli, it is considered to represent the CO2 tension in the alveolar gas (PACO2). The PACO2 results from the combination of gases coming from ideal alveoli, where ventilation and perfusion are perfectly matched and the CO2 concentration is the same as
arterial (PACO2), and alveolar dead space (alveoli that are ventilated but not perfused) where CO2 concentration is the same as inspired (PICO2) and is normally zero.

The presence of a normal capnogram and PETCO2 depends on (1) production of CO2 by the tissues, (2) cardiac output and pulmonary blood flow to carry CO2 to the lungs, and (3) ventilation. Monitoring of PETCO2 can be used to adjust the setting of a mechanical ventilator and monitor ventilation as well as to detect ventilator malfunctions and breathing system problems, such as leaks, incompetent unidirectional valves, exhausted CO2 absorbent, metabolic problems (e.g., malignant hyperthermia), and gas embolism.



Ehrenwerth J, Eisenkraft JB, Berry JM, eds. Anesthesia Equipment: Principles and Applications. 2nd ed. New York: Elsevier; 2013:245-254.

Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Philadelphia, PA: Elsevier Science; 2010:159-177.


A.11. What is the appearance of a normal capnogram and what is its significance?

A typical normal capnogram (PCO2 vs. time) is shown in Figure 59.1. Four phases have been described.

Phase I. This is the expiratory baseline. During exhalation, CO2-free gas from the mechanical (apparatus) dead space (e.g., flexible or “goose-neck” connector) and anatomic dead space (large conducting airways) flows past the CO2 sampling port.

Phase II. This is the expiratory upstroke. It is due to CO2 from alveoli mixed with anatomic dead space gas passing the gas sampling port and is usually a steep upslope.

Phase III. This is the expiratory or alveolar plateau and is due to alveolar CO2.

In patients with healthy lungs, it is nearly horizontal, but in patients with obstructive airway disease, there is a more pronounced upward slope. The maximum expired CO2 is usually considered as the PETCO2.

Phase IV. This is the inspiratory downstroke. During the commencement of inspiration, fresh (i.e., CO2-free) gas is inhaled past the sensor, and the capnogram falls sharply to baseline.

The angle between the upstroke of phase II and the plateau of phase III is referred to as the α angle. The angle between phase III and IV is the β angle. An increase in the α angle and slope of phase III is seen commonly in acute bronchospasm. The angle usually decreases with treatment of the bronchospasm.



Ehrenwerth J, Eisenkraft JB, Berry JM, eds. Anesthesia Equipment: Principles and Applications. 2nd ed. New York: Elsevier; 2013:245-254.

Lumb AB. Nunn’s Applied Respiratory Physiology. 7th ed. Philadelphia, PA: Elsevier Science; 2010:174.






FIGURE 59.1 Phases of the normal capnogram. (Phase I) inspiratory baseline. (Phase II) expiratory upstroke. (Phase III) expiratory plateau. (Phase IV) inspiratory downstroke. (From Good ML. Capnography. Uses, interpretation, and pitfalls. In: ASA Refresher Courses in Anesthesiology. Park Ridge, IL: American Society of Anesthesiologists; 1990:179, with permission.)



A.12. What are mainstream and sidestream capnometers?

In a mainstream or nondiverting type of analyzer, the gas analyzer sensor is brought to the airway itself, and no gas is removed from the breathing system. A cuvette with a quartz window is placed between the breathing system Y-piece and the tracheal tube connector. As respired gases flow past the window in the cuvette, a beam of infrared radiation (wavelength 4.3 µm) is directed through the window. Absorbance of infrared radiation at 4.3 µm is used to measure PCO2. Advantages of the nondiverting analyzer are rapid response time, accurate waveform, and no need to scavenge gases. Disadvantages are that this additional device in the airway can be a site for a disconnect and needs sterilization (or replacement of a disposable single-use cuvette) between cases, needs to be heated because water vapor condensing on the window causes error, and can be blocked by secretions or blood on its window. A very lightweight (25 g) mainstream analyzer (IRMA, Masimo, Danderyd, Sweden) capable of measuring CO2, nitrous oxide, and all five potent inhaled anesthetics is available.

A sidestream or diverting gas analyzer aspirates gas from the breathing circuit through a sampling adapter placed by the airway. The sampled gas passes through a sampling catheter (usually 6 to 10 ft in length) to reach the gas analyzer. Advantages of diverting analyzers are that the breathing circuit adapter is disposable. The analyzer, being remote from the airway, can be more versatile and incorporate several technologies in one “box” to analyze multiple gases (e.g., infrared analysis for CO2, nitrous oxide, anesthetic agents; paramagnetic sensor or fuel cell for oxygen). Disadvantages of sidestream sampling analysis are slower response times, the possibility of sampling leaks, errors resulting from the length of the gas sampling tube, the need to scavenge gases from the analyzer after analysis, and susceptibility of the sampling tube to becoming clogged by water or secretions. Because of their versatility in regard to gas monitoring, most anesthetizing locations now use sidestream sampling analyzers.



Ehrenwerth J, Eisenkraft JB, Berry JM, eds. Anesthesia Equipment: Principles and Applications. 2nd ed. New York: Elsevier; 2013:191-221.


A.13. Show some common capnograms and provide a differential diagnosis of each event.

Elevated baseline equals the amount of CO2 present in inspired gas (Fig. 59.2A)



  • Capnometer not properly calibrated to zero


  • Delivery of CO2 to breathing system through fresh gas inflow


  • Incompetent unidirectional valves


  • Failure of CO2 absorber (channeling, exhaustion, bypass) Prolonged expiratory plateau and expiratory upstroke (Fig. 59.2B)


  • Mechanical obstruction to exhalation


  • Chronic obstructive pulmonary disease


  • Bronchospasm Dips in expiratory plateau (Fig. 59.2C[1])


  • Patient making spontaneous inspiratory effort


  • “Curare cleft” Cardiogenic oscillations if synchronized with electrocardiogram (Fig. 59.2C[2])


  • Ventilator pressure relief valve perturbations

Elevated expiratory plateau (Fig. 59.2D)

Mar 18, 2021 | Posted by in ANESTHESIA | Comments Off on Hypoxia and Equipment Failure
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