Rudolph's Pediatrics, 22nd Ed.

CHAPTER 106. Monitoring of Vital Function

George E. Lister

Patients with serious illness or injury or life-threatening states invariably require close observation to detect changes in function or state. Electronic monitoring complements the information gathered from direct physical examination by providing (1) repetitive or continuous assessment that does not disturb the patient, (2) a means for detecting the effect of interventions, and (3) warning signals for physiological disturbances that permit staff to observe multiple patients simultaneously. Current monitoring devices also frequently have the capacity to store data that can be reviewed subsequently for analysis. Because of the vital importance of circulatory and respiratory function, much of the monitoring in common use tracks activity of these systems, and such monitoring is the focus of this section.


Monitoring of respiratory rate provides valuable clues about disturbances in respiratory function (see Chapter 102). Processes that decrease respiratory system compliance often cause the respiratory rate to increase; processes that depress ventilatory drive cause the respiratory rate to decrease. Such monitoring may be useful both in hospitalized patients and in those at home who are at risk for breathing disturbances. Respiratory rate is assessed by devices that monitor breathing movement, gas flow, or gas exchange. Each approach is described briefly in the following sections and is shown in Figure 106-1 and in the Table 106-1.

It is important to recognize that the methods used to measure respiratory rate track different features of breathing function; each has inherent inaccuracies, so there may be discrepancies when using two or more approaches simultaneously.

The most commonly used device to monitor breathing measures change in transthoracic impedance with the change in thoracic volume. A small current is passed between two electrodes placed on opposite sides of the chest. Increases in the gas volume of the chest with inspiration cause a small increase in impedance to current that can be detected by an electronic circuit, and this is displayed as a wavy line on a monitor. The periodicity in this variation in impedance permits determination of respiratory rate. This approach is simple, safe, readily applicable to patients of all sizes, and is by far the most common approach used for bedside monitoring in the hospital; it has also been widely employed for home monitoring. However, it is essential to recognize important constraints inherent in this technique (see Table 106-1): The signal is not quantitatively related to a change in lung volume, movement unrelated to breathing can be mistaken for breathing, and impedance changes resulting from movement artifact can completely obliterate the breathing signal. Another major limitation of the transthoracic impedance method is that there can be impedance changes associated with breathing effort even though there is no or little ventilation of the lungs. Thus, airway obstruction will not be detected by this method and can confound interpretation of the tracing.

FIGURE 106-1. Common techniques for breath detection. Temperature or CO2 concentration can be measured in gas at the nares or mouth or through a tracheal tube. During inspiration, the gas is at room temperature and has no CO2. During expiration, the gas is warmed and contains CO2; thus, either temperature of CO2 is a signal for the change from inspiration to expiration or vice versa. With transthoracic impedance, two electrodes, placed on opposite sides of the chest, detect a change in impedance as the thoracic volume changes from inspiration to expiration. Inductance plethysmograph uses two bands placed around the chest and abdomen (shown by the coils). With chest and abdominal expansion during inspiration, the bands lengthen, signifying an increase in thoracic or abdominal circumference, and are used to calculate the changes in thoracic (Vthorax) or abdominal volume (Vabd). The sum of these changes is quantitatively related to the volume entering or leaving the lungs with respiration.

Another approach to detect changes in thoracic volume is inductance plethysmography, which is used most commonly in specialized settings, such as a sleep laboratory or intensive care unit. With this technique, the thorax and abdomen are assumed to be a large cylinder that expands circumferentially as air enters the lungs during inspiration. The change in the circumference of the thorax and abdomen is determined from electrical conductors embedded in two thin elastic bands that surround the thorax and abdomen, respectively. The bands contain strain gauges, and the resistance of the bands varies with circumference. By recording changes in both thoracic and abdominal circumference, it is possible to derive information about respiratory rate and tidal volume, which is the sum of the changes in the volume of the thorax and abdomen.3 Inductance plethysmography requires proper positioning of the bands, and it is subject to artifact; however; it has the potential to provide considerable information about mechanical function and mechanisms for breathing disturbances. It may also identify breathing movements when the airway is obstructed.

Table 106-1. Common Techniques for Monitoring Respiratory Function in Children

Breathing can also be detected by measuring the variation in temperature or carbon dioxide tension of gas during respiration. A thermistor placed by the nares detects a difference between the warmed gas breathed out during expiration from the cooler inspired air. Because the temperature signal has no quantitative relation to change in lung volume, this technique can be used only to determine breathing rate. It is primarily used in a laboratory setting rather than for routine monitoring, because breathing through the mouth interferes with the ability to sense a breath, and the equipment requires attention. Measurement of PCO2 at the nares (capnometry) can also be used to sense a breath (see the next section) and to provide information about gas exchange.



The measurement of respiratory gases provides inference about both ventilatory and circulatory function, depending on which gas is considered and where it is sampled. A few general principles help elucidate this point. Because there is no appreciable CO2 in inspired gas, the arterial PCO2 is proportional to the rate of production (metabolic rate) and is inversely proportional to the rate of excretion (ventilation) of CO2 (see Chapter 102). Hence, when metabolism is stable, short-term changes in arterial PCO2 are reflective of changes in ventilation.

Oxygen is taken up in the lungs and is extracted by the tissues at about the same rate that carbon dioxide is produced by the tissues and excreted in the lungs (under normal conditions, the ratio of CO2production to O2consumption ranges from 0.7 to 1.0). The arteriovenous content difference for either gas depends on the relationship between the metabolic rate for that gas and the blood flow rate (metabolic rate/blood flow is proportional to arteriovenous O2 or CO2 content difference). Thus, the difference between arterial and venous blood gas content increases when blood flow is reduced relative to metabolism. Because there is no net storage of O2 or CO2, the decrease in O2 content from arterial to mixed venous blood is roughly the same as the increase in CO2 content from arterial to mixed venous blood (see Fig. 106-2). However, because the relationship between blood PCO2 and content is generally more linear and much steeper than the relationship between PO2 and O2 content, the arteriovenous PCO2 difference is much smaller than the PO2 difference under most conditions. For these reasons, venous PO2is a particularly useful guide to perfusion; when perfusion decreases venous PO2 decreases, which makes an extremity appear cyanotic when blood flow is decreased. The following section addresses means for estimating arterial and venous blood-gas concentrations.


Arterial PCO2 can be measured directly in small samples (< 1 mL) of blood using an electrode (measurement of CO2 content is more technically demanding and not practical for clinical medicine). Because of the rapid response of arterial PCO2 to changes in ventilation, anything that alters ventilation (eg, discomfort, fright) can change the PCO2 and confound interpretation of findings. For these reasons, in critically ill patients, an indwelling catheter is sometimes used, or arterial PCO2 is estimated by techniques that are less likely to disturb the child than arterial puncture. Owing to the narrow difference between arterial and venous PCO2, a reasonable but slightly high estimate of arterial PCO2 can be obtained from freely flowing peripheral venous blood or from capillary blood where skin perfusion is adequate (often achieved by warming of the extremity). Furthermore, when the skin is relatively thin, as in an infant, there is a small amount of CO2 diffusion through warmed superficial capillaries, which can be detected and measured noninvasively using an electrode attached to the skin surface (transcutaneous monitoring).

FIGURE 106-2. Unloading of CO2 and loading of O2 as blood passes through the lung. Left: As CO2 is eliminated from venous blood into the alveoli, the CO2 content and blood PCO2 decrease to arterial levels, as shown at the bottom. Note that this CO2 content–PCO2 relationship is steep, so that arterial and mixed venous PCO2 are quite close under most circumstances. However, when flow slows, the arterial-mixed venous PCO2 difference widens. Right: As O2 is taken up from the alveoli and equilibrated with mixed venous (v) blood, the O2 content and blood CO2 increase to arterial levels, as shown at the bottom. Note that this O2 content–PO2 relationship is more gradual, so that arterial and mixed venous PO2 differ considerably under most circumstances. Normally, arteriovenous O2 contents differ by 4 to 5 mL O2/dL blood. When flow slows, the arterial-mixed venous PO2 difference widens, and mixed venous PO2 decreases, indicating that cardiac output is low in proportion to metabolic demands.

Another noninvasive approach is derived from the fact that the PCO2 of the gas in an ideal alveolus equilibrates with that in the adjacent pulmonary capillary blood (which eventually contributes to the systemic arterial blood). This alveolar gas can be sampled at end-expiration to estimate arterial PCO2, when some practical conditions are satisfied (see Fig. 106-3). The gas is analyzed by a capnometer, which monitors the inspiratory and expiratory PCO2 and either provides a continuous recording or the value at end-expiration. However, with airflow obstruction processes, such as asthma or bronchopulmonary dysplasia, the end-tidal PCO2 can underestimate arterial PCO2 by a variable amount. The end-tidal PCO2 may also be factitiously reduced if there is contamination of expired gas from air drawn into the system (in the patient whose trachea is not intubated or who has an air leak around the tracheal tube), which occurs particularly when the sample rate is high relative to alveolar ventilation.

The expiratory gas can be sampled through a small nasopharyngeal catheter using a withdrawal pump or, in an intubated patient, by withdrawing gas from the side of the tube (side-stream) or by having the sensor in series with the tracheal tube (in-stream). Typically, the PCO2 of the gas is measured by infrared sensor or, less commonly, by mass spectrometry.

Finally capnometry may be particularly susceptible to underestimation of arterial PCO2 in the small infant who breathes at such a high rate that a plateau is not achieved. Despite these important constraints, capnography is a valuable technique for monitoring gas exchange noninvasively, especially because of the risks and difficulties in maintaining an indwelling arterial catheter in many infants and children.


Measuring oxygen in arterial blood provides information about the adequacy of gas exchange in the lung and can be useful for quantifying the impairment in pulmonary function. Because arterial oxygenation can be decreased by an intra-cardiac right-to-left shunt, it is also useful for detecting certain cardiac defects. Oxygen can be measured from small volumes of blood using electrodes that detect PO2. The fractional hemoglobin O2 (HbO2) saturation (often expressed as a percentage) can also be measured in blood using an oximeter that compares the transmitted light at different wavelengths to determine the proportions of oxyhemoglobin and, if needed, COHb and MetHb, relative to total hemoglobin. Machines that measure PO2 may also provide a calculated value for HbO2 that is based on the measured PO2 and pH and on assumptions about the position and shape of the oxygen dissociation curve. The HbO2values obtained from the blood gases in this manner are only estimates and are not as valid as those obtained from a blood oximeter. It is important to remember the relation between PO2, HbO2 saturation, and O2 content ([HbO2 × Hb × 1.34 + PO2 × 0.003] = O2 content, where HbO 2is expressed as a fraction, Hb is expressed in mL/dL, and PO2 is expressed in mmHg) and to remember that the relationship between HbO2 and PO2 is not linear.

FIGURE 106-3. Expired PCO2 (PECO2) shown as a function of time. The shaded gas represents CO2 as it moves from the alveoli to the bronchioles and to the trachea. The dark line shows the mixed expired PCO2, which is derived from multiple alveoli as they empty. Left: Because the alveoli and conducting airways normally eliminate CO2 at relatively similar rates, the PECO2 is initially 0 as dead space gas is exhaled; it rises abruptly and then reaches a plateau (end-tidal PECO2) close to the value for the arterial PCO2Right: When there is airflow obstruction or marked heterogeneity in the emptying of alveoli, mixing of gas from units that have different rates of CO2elimination produces a gradually rising PECO2, and the end-tidal underestimates arterial PCO2.

Owing to the large arteriovenous difference, venous PO2 is rarely useful for estimating arterial PO2 except under unusual circumstances. O2 can be measured in arterial blood from an indwelling catheter or by arterial puncture, with many of the same constraints raised for CO2. However, when skin blood flow is adequate, capillary PO2 will provide a reasonable estimate of arterial PO2. Within the last 30 years, the advent of noninvasive techniques has dramatically simplified the estimation and monitoring of arterial oxygenation. However, the information provided can also be confusing, because even healthy subjects have episodes when arterial oxygenation transiently decreases below what is perceived to be normal, and the implications of periods when arterial oxygenation decreases in potentially unhealthy infants, especially premature babies, is often unclear.4 As with CO2, placing an electrode on warmed skin allows for detection of O2 diffusing from the superficial capillaries, although this technique is only practical in the small infant.

Pulse oximetry has virtually replaced all other methods of monitoring arterial blood oxygenation. With pulse oximetry, a small band is placed on the skin, usually on a digit, and a light beam with two different wavelengths is periodically emitted from a light source on one side of the digit. The band also contains a light detector that is sensitive to both wavelengths and is located on the opposite side of the finger. The light detector picks up the light transmitted through the finger from the light source. The pulsating arterial blood in the tissue between the light source and the detector absorbs some of the light, causing small variations in detected light intensity at the patient’s pulse rate. The instrument analyzes these pulsations to determine the relative fraction of oxygenated to total hemoglobin. This ratio (HbO2/total Hb) is usually reported as HbO2saturation, or SaO2, when referring to arterial blood HbO 2saturation.5

However, because only two wavelengths are used, there can be interference caused by absorption by hemoglobin in other forms (particularly COHb, which causes artificially high readings, and MeHb) and by external light.

Pulse oximeters also detect heart rate from the pulse. Some devices display a pulse waveform, but this should not be interpreted as a tracing of pulse pressure, because it is amplified and not calibrated to pressure. Although relatively insensitive to modest changes in circulation, the oximeter must be able to detect a pulse to determine arterial SaO2; therefore, states with poor peripheral perfusion can interfere with this technique and give a value unpredictably lower than arterial SaO2. Normal arterial SaO2 is close to 95% in healthy children and adults, but studies of infants have shown that there may be periodic decreases to below 90% even in the absence of respiratory illness.4

Although venous PO2 is generally much lower than arterial PO2 and is not useful for gauging gas exchange, it is quite valuable for judging perfusion (see Fig. 106-2). Whenever flow decreases relative to metabolic rate, arteriovenous O2 content difference increases. Therefore, in subjects with normal arterial oxygenation, a decrease in cardiac output is detected by a decline in mixed systemic venous PO2, which is approximately 39 to 40 mm Hg (equivalent to a fractional HbO2 of ∼ 0.75) in the normal individual. Mixed venous blood can be sampled in critically ill patients from a catheter placed in the pulmonary artery or in the superior vena cava or right atrium. The latter two sites are easier to access but may not provide as representative a sample as the pulmonary artery.

In recent years, near-infrared spectroscopy has been used in specialized circumstances to judge tissue perfusion, particularly cerebral perfusion. This technique assesses the relative concentration of oxyhemoglobin to hemoglobin and oxidation of cytochrome aa3 from reflected light that is emitted in the near-infrared spectrum (650–1000 nm) at the surface of the tissue of interest. Because this light can pass through bone and other tissues, it provides a measure of tissue oxygenation and, as such, is a means for assessing tissue perfusion. Just as mixed venous blood provides a useful estimate of system perfusion, this technique is gaining increased use in intensive care units, especially as a guide to monitor cerebral perfusion. However, there are still technical hurdles that limit determination of anything but relative values, and it is not clear whether tracking this information makes a difference in patient outcome.6,7


Electrocardiograms (ECG) can be monitored continuously from electrocardiographic electrodes generally placed on the chest, and a cardiotachometer determines heart rate from the frequency of the “QRS” signal. Although an invaluable tool for monitoring and for observing responses to therapy, there are important sources of error. When the signal is large, the T wave and QRS may both be detected, and the cardiotachometer may show a value that is twice normal. Failure to detect a signal can occur when the QRS amplitude changes—for example, with respiration, repositioning of the leads, or changes in posture. Finally, it is essential to recognize that the ECG recording used in patient monitoring is filtered to help reduce the amount of artifact and does not provide a complete view of cardiac forces. It is quite easy to misinterpret rhythm disturbances or even fail to detect them by observing the monitor or by reading a single “rhythm strip.”8 Whenever an arrhythmia is suspected or the rate of the peripheral pulse does not concur with the monitor, a complete ECG should immediately be obtained.


Measuring arterial pressure is essential for detecting abnormalities in the circulation and determining responses to therapy. It can be measured continuously in patients by using an indwelling arterial catheter attached to an electronic manometer, or it can be measured intermittently by several techniques. Determining pressure using a sphygmomanometer in conjunction with a cuff that occupies about two-thirds of the length of the limb segment remains the standard approach. The cuff is inflated to a pressure well above that occluding the arterial systolic pulse and is gradually deflated while listening for Korotkoff sounds. The first sound corresponds to arterial systolic pressure, and the muffling of the second sound corresponds to the arterial diastolic pressure. The systolic pressure can also be determined by palpating the artery distal to the cuff and noting the pressure at which the pulse is first felt when the cuff is deflated. Alternatively, a Doppler device can be used to detect arterial blood flow when the cuff is deflated; this is particularly useful when the pulse is weak and difficult to feel consistently. A similar approach relies on using a pulse oximeter to detect the return in the arterial waveform at the systolic pressure when a blood pressure cuff is deflated. There are several devices that can automatically inflate a cuff and determine the Korotkoff sounds or arterial pulsations as the cuff is deflated. These instruments can be programmed to measure blood pressure at regular and very frequent intervals. Some of these devices tend to yield diastolic pressures lower than those obtained from auscultation or with an indwelling arterial catheter.9

It is important to recognize that there are some regional variations in blood pressure and that these can be accentuated in pathological states. Normally, mean blood pressures are equal throughout the large arteries, although systolic pressure is higher and diastolic is lower when comparing the large arteries of the legs to the brachial or radial artery. However, in states of low cardiac output, systolic and mean blood pressure from a large central artery is often higher than values from more peripheral arteries by a variable amount that depends on how impaired perfusion is and how constricted the peripheral arteries are in response. It is also important to realize that central systolic blood pressure may be sustained near normal levels even in the presence of shock, owing to severe vasoconstriction of peripheral arteries and arterioles.


Central venous pressure is used as a proxy for central vascular volume. In general, as the volume in the vasculature increases, the central venous pressure rises. The pressure from a catheter in the right atrium or large central vein is used to monitor cardiac filling. Because systemic perfusion depends on left ventricular filling, there are conditions when measuring right atrial pressure is insufficient. Specifically, when there is any site of obstruction between the chambers, dysfunction of one of the ventricles, or pulmonary vascular disease, the pressure in the right atrium may not reliably reflect that in the left atrium. For these reasons, a catheter may be placed in the pulmonary artery, which is then used to estimate left atrial pressure by measuring the wedge or occlusion pressure (obtained by inflating a small balloon at the tip of the catheter that propels the catheter into a small distal vessel while occluding flow there). It is important to recognize that in certain circumstances, venous and atrial pressures can be elevated, because the atrium is compressed by air (pneumothorax), fluid (pericardial or pleural), or even inflated lungs, all of which will impede cardiac filling but will create an erroneous impression that the atrium is filled (see Chapter 103).

With these constraints in mind, central venous pressure can serve as a useful guide for determining how interventions are affecting cardiac filling in patients in whom responses are not very predictable (eg, the child with congestive circulatory failure whose positive end-expiratory pressure is initiated or adjusted) or in patients in whom there is a narrow margin of safety (eg, the child with elevated intracranial pressure and low cardiac output). Normal values for central venous pressure range from −3 to +3 mm Hg in the infant to 5 to 10 mm Hg in the child and young adult. These values, however, can be greatly affected by the use of positive-pressure breathing. Accordingly, it is usually more useful to judge relative changes rather than to rely on absolute targets for therapy. Monitoring of pulmonary arterial or wedge pressures and sampling of mixed venous blood from the catheter also can provide valuable data regarding the mechanism for circulatory dysfunction or the response to therapy, especially in the patient who has suspected dysfunction of the left or right ventricle. Proper placement of a central venous or pulmonary arterial catheter is essential to reduce the risk of arrhythmias or untoward complications. The contour of the pressure tracing during placement of the catheter provides essential information to discern this position and is an invaluable aid in the process of catheter insertion (eFig. 106.1 ). In recent years, widespread availability of noninvasive techniques (Doppler ultrasound) for assessing cardiac filling and ventricular function has decreased the use of the pulmonary arterial catheter except in the most critically ill children or those who are susceptible to complex cardiac dysfunction. Although this technique does not provide cardiac filling pressures, it can assess the volume in the right and left atrium, cardiac function, and the presence or degree of valvar obstruction.