Anesthetic Monitoring

The editors and publisher would like to thank Dr. Anil de Silva for contributing to this chapter in the previous edition of this work. It has served as the foundation for the current chapter.


Anesthesiologists have long been at the forefront of patient monitoring. This has been of necessity, because we are responsible for continuously assessing the patient’s physiologic status and the effects of surgery and anesthetic drugs. The following is an introduction to the basic function and utility of the wide array of monitors employed in modern anesthesia care. Monitoring devices will be organized by the organ or organ system that they are monitoring, not the physical property or technique on which that monitor derives its information. Because the monitors for each organ system may employ the same physical properties, such as light absorption or pressure transduction, each monitor will be described as it is used for a specific organ, but the description of the principle may refer to another section within the chapter. For an in-depth review of these principles the reader is referred to a more comprehensive text.


In 1986 the American Society of Anesthesiologists (ASA) established a set of basic monitoring standards, stating that the patient’s oxygenation, ventilation, circulation, and temperature shall be continually evaluated. These standards, the first of their kind (last affirmed in 2015), should be viewed as a minimum requirement and many situations will require additional monitoring. All of the organ systems monitored are perfused by the circulatory system ( Fig. 20.1 ). Monitoring the patient permits the anesthesia provider to continuously assess if the patient’s state is “normal” or “abnormal” and to correct the cause of the abnormality, or at least treat the abnormal number generated by the monitor. However, the limitations of monitors and how to use data from multiple devices must be understood in order to confirm the diagnosis and follow the prescribed treatment.

Fig. 20.1

A summary of monitors and the circulation. Anatomic features are listed around the periphery, with monitored variables central and underlined (see Table 20.1 for normal values of monitored variables). The blood flows in a circuit with a cardiac output of roughly 20% each to the brain, kidneys, liver, GI tract, muscle mass, and other organs (skin, etc.). The systemic vascular resistance (SVR) is a calculated variable, reflecting the totality of blood flow and pressure. Roughly 70% of the blood is on the venous side. The venous capacitance is highly variable and acts as a buffer for changes in volume. Some variables may be measured or derived, depending on methodology. aa, Arteries; ABG, arterial blood gas; BIS, bispectral index; CVP, central venous pressure; DBP, diastolic blood pressure; DBS, double burst stimulation; ECG, electrocardiogram; EEG, electroencephalography; EF, ejection fraction; EMG, electromyography; ETco 2 , end-tidal CO 2 ; F io 2 , fraction of inspired oxygen; GI, gastrointestinal; ICP, intracranial pressure; LA, left atrium; LAP, left atrial pressure; LV, left ventricle; LVEDV, left ventricular end-diastolic volume; LVSV, left ventricular systolic volume; MAP, mean arterial pressure; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PIP, peak inspiratory pressure; Q, cardiac output; RA, right atrium; RR, respiratory rate; RV, right ventricle; SBP, systolic blood pressure; Sp o 2 , arterial O 2 saturation; SPV, systolic pressure variation; SSEP, somatosensory evoked potential; TEE, transesophageal echocardiography; TOF, train-of-four; V t , tidal volume.

Respiratory System

Oxygen (O 2 ) is a colorless, odorless gas critical for cellular respiration. Lack of delivery of oxygen to tissues will result in cellular death. Carbon dioxide is a consequence of cellular metabolism and must be removed from the tissues to maintain acid-based homeostasis. This section will review monitors of patient oxygenation and patient ventilation.


Inspired Oxygen

Inspired oxygen content (or fraction of inspired O 2 , F io 2 ) can be measured by a variety of methods. Anesthesia machines most commonly use an amperometric sensor to measure O 2 in the fresh gas flow. Calibration is recommended, as the sensor, which is basically a fuel cell that consumes oxygen and generates current, has “drift”; that is, the readings in a constant concentration of oxygen will not be constant. It is a slow responding device, meaning that it cannot be used to measure inspired/expired oxygen, which rapidly changes. An alternative method of measuring inspired oxygen uses the fact that oxygen is paramagnetic. A paramagnetic oxygen sensor can be autocalibrating, using room air as a source of 21% O 2 . The gradient between the sample and the room air can be measured by a pressure transducer or a torsion wire. The fast response time allows the measurement of both inspired and expired oxygen content. Measuring expired O 2 (Fe o 2 ) concentration during preoxygenation (just prior to induction of anesthesia) also allows the determination of complete preoxygenation/denitrogenation.

Pulse Oximetry

The pulse oximeter provides a continuous noninvasive estimate of arterial hemoglobin saturation (Sa o 2 ) by analyzing red and infrared light transmitted through living tissue, such as a fingertip or earlobe ( Fig. 20.2 ). It uses the physical principle known as Beer’s law , which relates the concentration of a dissolved substance to the log of the ratio of the incident and transmitted light intensity through a known distance. Because of the differing amounts of red and infrared light absorbed by oxyhemoglobin and reduced hemoglobin the device makes this estimate using only two wavelengths of light emitted by light-emitting diodes, or LEDs (red at 660 nm and infrared at 940 nm) detected by a photodiode. The device determines the signal related to arterial hemoglobin saturation by analyzing the pulsatile component of the absorbents, hence the name pulse oximeter ( Fig. 20.3 ). The device continuously determines the ratio of pulse-added red to pulse-added infrared light absorbance:

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Fig. 20.2

Pulse oximeter. Pulse oximeters (Sp o 2 ) provide an estimate of arterial hemoglobin saturation (Sa o 2 ) by analyzing the pulsatile absorbance of two frequencies of light (660nm and 940 nm) emitted by light-emitting diodes (LEDs), the light source, and detected by a photodiode on the opposite side of the tissue bed of the finger. The photodiode generates a current when it detects any light: red or infrared, or room light. For that reason, the photodiode alternates a pulse of red light and room light with a pulse of infrared light and the room light. Then, when both LEDs are off, it measures room light alone, then subtracts the room light signal from the previous two signals, continuously correcting for changes in room light. It thereby derives a signal associated with the pulsing LED signals. The signal may be improved by decreasing ambient light by covering the probe with an opaque material.

Fig. 20.3

Tissue absorbances. As light is transmitted through tissues and detected by the photodiode it is absorbed by all the tissues between the light source and the detector, that is, skin, muscle, bone, and blood. Because the pulse oximeter wants to determine a signal related only to arterial blood, it analyzes only the pulsatile absorbance noted at the top of the figure. The pulse oximeter, therefore, makes the assumption that whatever is pulsing must be arterial blood. In most cases this is true, but in some situations (e.g., patient motion) there can be large venous pulsations that can produce erroneously low saturation values.

This ratio (R) of absorbance is empirically calibrated to estimate Sa o 2 . That is, the device uses Sa o 2 data derived from human volunteers to determine the relationship between the pulse oximeter saturation (Sp o 2 ) and the ratio of light absorbance ( Fig. 20.4 ).

Fig. 20.4

Pulse oximeter calibration curve. Because of all the absorbances between the light source and the photo detector, the concentrations of oxyhemoglobin and reduced hemoglobin cannot be measured specifically; that is, the exact path length of the light is unknown. Using the pulse-added absorbance from both the infrared and red light source, a ratio of these pulse-added absorbances (see Eq. 1 ) can be empirically related to Sp o 2 . That is, volunteer subjects breathe low inspired oxygen concentrations to produce desaturation while blood samples are obtained for Sa o 2 measurement. These Sa o 2 measurements are calibrated to the ratio of red to infrared pulsatile absorbance to develop the calibration curve, which is incorporated into the device. Note the ratio ranges from approximately 0.4 to 3.4 as the saturation decreases from 100% to 0%. The volunteer data are only available from 100% saturation down to 75% and all values below that are extrapolated from the data. Note that at approximately Sp o 2 85% the ratio of the two absorbances is 1.0. Therefore, any situation that causes the ratio of pulse-added red to pulse-added infrared light to tend toward a ratio of 1.0 produces a saturation of approximately 85%. This occurs with motion artifact, dyes, and methemoglobin toxicity. AC, Alternating current; DC, direct current.

Dyes and Dyshemoglobins

Standard pulse oximeters using two wavelengths of light can determine functional saturation, that is, the percent of oxyhemoglobin (HbO 2 ) over HbO 2 plus reduced hemoglobin (Hb). Two equations are used to solve for two unknowns:

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Functional saturation

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Fractional saturation

Pulse oximeters are calibrated using human volunteers who have little carboxyhemoglobin (COHb) or methemoglobin (MetHb). Therefore, if either carboxyhemoglobin (carbon monoxide poisoning) or methemoglobin (methemoglobin toxicity from benzocaine, for example) is present the devices will produce an erroneous saturation value. In the case of carboxyhemoglobin, because it is red and absorbs red light similarly to that of oxyhemoglobin, the pulse oximeter will give a reading approximately equal to the sum of carboxyhemoglobin and oxyhemoglobin, giving the impression the patient is adequately saturated with oxyhemoglobin even when he has severe carboxyhemoglobin toxicity. In the case of methemoglobin, which is dark and absorbs both red and infrared light to a high degree, it causes the ratio of absorbance to tend toward one. From the calibration curve it can be seen that a ratio of 1 will produce an Sp o 2 of 85% (see Fig. 20.4 [calibration curve]). Therefore, if there is a significant (>20%) amount of methemoglobin present, the pulse oximeter value will tend toward 85%. Thus, it will produce falsely low values when the patient has high Sa o 2 , and falsely “high” values of 85% when the patient is severely hypoxemic. Dyes produce similar errors, as does methemoglobin; that is, they force the saturation toward 85%, although because they are cleared from the circulation quickly this error is only transient. Newer eight-wavelength pulse oximeters are available that can detect all saturations: oxyhemoglobin, carboxyhemoglobin, and methemoglobin. Motion artifact will also cause the Sp o 2 value to tend toward 85% because the motion artifact produces noise in the numerator and denominator, the ratio R is forced toward 1.0, as occurs with methemoglobin. In fact, any situation that results in a small signal-to-noise ratio may cause the Sp o 2 to trend toward 85%.


The respiratory rate, pattern, and depth are all important descriptors of ventilation. Qualitatively, ventilation depth and pattern can be observed by chest rise, auscultation, or reexpansion of the rebreathing bag on the anesthesia machine. In any acute situation in which adequacy of ventilation is an issue, eliminating monitoring devices altogether and going to the source by listening for bilateral clear breath sounds with a stethoscope should be done immediately. This may rule out tension pneumothorax, acute bronchospasm, endobronchial intubation, pulmonary edema, or absence of ventilation altogether.

Airway Pressures

Increases in peak airway pressure, also called peak inspiratory pressure (PIP), merit investigation as they imply an acute increase in airflow resistance or reduction in lung/chest wall compliance. Setting the ventilator to produce an end-inspiratory pause will allow measurement of a plateau pressure, which will be a reflection of lung/chest wall compliance only. The difference between peak and plateau pressure will be a reflection of airway resistance only. If peak airway pressure is increased and plateau pressure is increased a similar amount, this signifies reduced lung/chest wall compliance, which can be caused by conditions such as tension pneumothorax or pulmonary edema. Other clinical findings can help to determine the specific cause, such as accompanying arterial hypotension with tension pneumothorax or visible frothy fluid in the endotracheal tube (ETT) with pulmonary edema. External obstruction of an ETT (from a patient biting on the tube or tube kinking) can cause an increase in PIP with a lesser increase in the plateau pressure. This can be easily ruled out by passing a suction catheter down the ETT. A loss or abrupt decrease in airway pressure is not specific but can indicate a variety of major problems, including circuit disconnections, leaks, extubation of the trachea, failure to deliver fresh gases, failure to set the ventilator properly, excess scavenging, and other anesthesia machine issues. Airway pressure can be measured with analog gauges or electronic pressure transducers.

Tidal Volume

One large study demonstrated improved pulmonary outcomes after major abdominal surgery by using tidal volume of 6 to 8 mL/kg of ideal body weight (based on height and gender) as well as recruitment maneuvers and positive end-expiratory pressure (PEEP). These settings are similar to those associated with improved outcomes in patients with acute respiratory distress syndrome (also see Chapter 41 ). Once these tidal volumes are set, the respiratory rate should be adjusted to maintain an end-tidal CO 2 (ET co 2 ) in the normal range of 35 to 40 mm Hg. Modern ventilators use a variety of modes to achieve this tidal volume ( Fig. 20.5 ). Most ventilators have pressure limits that will alert when peak pressures are exceeded owing to increased airway resistance in the circuit or in the patient ( Fig. 20.6 ). Monitoring the tidal volume and peak airway pressure together will enable the practitioner to quickly detect any changes in resistance to airflow due to resistance in the system or decreased compliance in the lung or chest wall ( Fig. 20.7 ). Tidal volumes can be measured by mechanical vanes rotating in the gas stream, pressure gradients across a flow restriction (fixed or variable), and hot wire anemometers.

Fig. 20.5

Ventilator pressure time curves. Three commonly employed modes of ventilation generate characteristic curves. (A) In volume-controlled ventilation, the pressure and volume smoothly increase until expiration (which is passive). (B) With the addition of an inspiratory pause, the pressure drops with minimal change in volume. (C) In pressure-controlled ventilation, the pressure is constant as volume increases, until expiration. Only four variables determine volume-based mechanical ventilation: (1) inspiratory time (T insp ), (2) inspiratory pause time (T pause ), (3) expiratory time (T exp ,) and (4) inspiratory flow rate. In ventilators that have control loops, faulty monitoring can lead to inadequate or hazardous ventilation. The compliance of the lung can be measured by dividing the tidal volume by the distending pressure (peak or plateau pressure minus PEEP). Dynamic compliance reflects the compliance during airflow, so it includes the resistance of the endotracheal tube as well as the compliance of the lungs. With an inspiratory pause (B), both the dynamic compliance and the static compliance (of the lungs and chest wall) can be measured by using either the peak pressure or the plateau pressure, respectively. The pressure-volume loops are different for the various ventilation modes as well. PEEP, Positive end-expiratory pressure.

Fig. 20.6

Stacking breaths. In both volume control (A) and pressure control (B) ventilation, insufficient expiratory time leads to “stacking” of breaths and changes in the pressure waveform. In the case of volume control ventilation, the pressure can increase, triggering an alarm. With pressure control ventilation, tidal volumes decrease and pressure remains constant (this may trigger a high PEEP alarm). (C) The capnogram also demonstrates decreased ventilation (increasing CO 2 ) and a change in the shape of the CO 2 curve. PEEP, Positive end-expiratory pressure.

Fig. 20.7

Bronchospasm. With volume control ventilation (A), the set tidal volume is attempted to be delivered, with an increase in pressure. This results in the pressure volume loop being shifted to the right and flattened. In pressure control ventilation (B), the stiffness of the lung results in a decreased tidal volume, without a change in the pressure (because that is the ventilator setpoint).

All anesthesia machines require a “disconnect” alarm, usually tied to the airway pressure reading. Inadequate ventilation can occur despite a nominally normal pressure. When using pressure-controlled ventilation, a significant change in ventilator volume can occur without an alarm condition occurring. Mechanical alarms and indicators of ventilation do not ensure tracheal intubation. An esophageal intubation can return “adequate” pressures and volumes and, with transmission of sounds, appear to have bilateral breath sounds. With an intact circulation, measurement of expired CO 2 is the best monitor of ventilation as discussed in detail in the next section.

Capnography/End-Tidal CO 2

Capnography is the analysis of the continuous waveform of expired CO 2 . Gas is continuously sampled from the ventilator circuit just on the patient side of the Y connector. The gas sample is drawn through a small tube into an infrared analyzer and the CO 2 waveform is displayed on the physiologic monitor ( Figs. 20.8 and 20.9 ). Carbon dioxide generated in the tissues is delivered to the right side of the heart through the venous system into the lungs via the pulmonary arteries. Exchange of the carbon dioxide into the alveolar space is fairly efficient because CO 2 has 20 times the solubility in water as does oxygen. Therefore, well-perfused alveoli achieve equilibrium with carbon dioxide in the blood. During expiration alveolar gas leaves the lungs, exiting the trachea through the ETT where the aspirated gas is sampled by the capnometer, producing a peak expired CO 2 close to the arterial carbon dioxide tension (Pa co 2 ) in healthy patients (ETco 2 is usually 3 to 5 mm Hg less than Pa co 2 during general anesthesia).

Fig. 20.8

Apparatus, anatomic, and alveolar dead space. To interpret the capnogram one must first understand alveolar dead space and its components. This schematic shows the heart, lung, and ventilator circuit up to the Y connector. Dead space volume (V DS ) is defined as any portion of the tidal volume that does not participate in gas exchange. V DS is further divided into three components: apparatus dead space (V appsDS ), anatomic dead space (V anaDS ), and alveolar dead space (V alvDS ). Apparatus dead space is the volume of gas between the Y connector and the end of the endotracheal tube. Anatomic dead space is the dead space of the trachea and all connecting airways down to the alveoli. In this figure the lung on the right has no blood flow so all those alveoli are not perfused and at the end of expiration will have zero carbon dioxide. The lung on the left is well perfused and those alveoli can be assumed at end of expiration to equilibrate to the arterial carbon dioxide (Pa co 2 ) value. The expired mixture of the alveolar gas (P aco 2 ) and alveolar dead space gas (no CO 2 ) produces the end-tidal CO 2 (ETco 2 ).

Fig. 20.9

Normal capnogram. A capnogram is a continuous tracing of the carbon dioxide concentration sampled at the Y connector on an intubated, ventilated patient and plotted versus time during the inspiratory and expiratory cycle. It can be divided into three phases. Phase I is the beginning of expiration when the apparatus dead space (V appDS ) and anatomic dead space (V anaDS ) are being sampled, both of which have zero carbon dioxide. Phase II starts when the mixed alveolar gases are detected and the capnogram rises up and reaches a plateau value. Phase III has only a slight rise as the mixed alveolar gases are sampled during the end of the expiratory cycle. With the initiation of inspiration the CO 2 value drops to zero and stays at zero until the next expiration. Note the end peak value is the end-tidal CO 2 (ETco 2 ). The ETco 2 is always lower than the Pa co 2 ; the magnitude of this gap is directly proportional to the ratio of alveolar dead space gas to alveolar gas.

The respiratory tidal volume is composed of alveolar gas volume and dead space. Approximately one third of the tidal volume in healthy patients is dead space (see Fig. 20.8 for details). Because the inspired gas contains no carbon dioxide (unless the CO 2 absorber is malfunctioning and allowing rebreathing of CO 2 to occur), dead space gases will not contain carbon dioxide. When expiration begins in the respiratory cycle, the first gas detected is apparatus dead space, followed by the anatomic dead space. Neither of these spaces contains carbon dioxide, so the capnogram will remain at zero during the initial phase I of the capnogram (see Fig. 20.9 ). As the gas from the alveolar space (well perfused) and the alveolar dead space mix and are detected at the sampling tube, the carbon dioxide waveform will increase from zero up to a plateau value producing a rough square wave until inspiration begins and the CO 2 waveform immediately returns to zero. The final plateau value of the capnogram (ETco 2 ) will approximately equal the arterial CO 2 value if there is no alveolar dead space. The ETco 2 value will always be less than the Pa co 2 value: the degree of this gradient will be in direct proportion to the amount of alveolar dead space in the expired volume, relative to the alveolar gas. The larger the proportion of dead space, the smaller the ETco 2 value. Common abnormalities of the capnogram are depicted in Fig. 20.10 .

Oct 21, 2019 | Posted by in ANESTHESIA | Comments Off on Anesthetic Monitoring

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