The resting respiratory rate of a normal adult is approximately 12 to 20 beats/min. Infants and children have a higher respiratory rate and a lower tidal volume than adults (see Chapter 49). Respirations should be quiet and easy and have a regular rate and rhythm. The chest should move freely as a unit, and expansion should be equal bilaterally. Alterations in symmetry can be caused by many factors, including pain, that may cause splinting at the incision site, consolidation, and pneumothorax. The nurse should note the character of the respirations; intercostal retractions, bulging, nasal flaring, or use of the accessory respiratory muscles, which are signs of respiratory distress. The depth of respiration is as important as the rate. Shallow respirations are the cardinal sign of continuing depression from anesthesia or preoperative medications, but can be caused by many other factors, including incisional pain, obesity, tight binders, and dressings that restrict movements of the thoracic cage or abdomen. Shallow respirations and use of the neck and diaphragmatic muscles may also indicate reparalyzation from the use of skeletal muscle relaxants such as succinylcholine, atracurium, pancuronium, and vecuronium. The presence of chest movements alone does not provide evidence that adequate gas exchange is occurring.

Airway obstruction may be present when the normal duration of inspiration versus exhalation is altered. Restlessness, confusion or anxiety, and apprehension are the earliest signs of hypoxemia and CO₂ retention and should receive immediate attention for determination of cause. The patient’s color is regularly evaluated. Although this assessment is difficult to make, the results provide important information about the respiratory function. Cyanosis is a late sign of severe tissue hypoxia, and if it appears, immediate and vigorous efforts must be instituted to determine and correct the cause of hypoxia. The noninvasive monitors that are increasingly used in the PACU provide an effective means of continuous and objective assessment of gas exchange; pulse oximeters are used for monitoring hemoglobin oxygen saturation, and capnographs are used in evaluation of the adequacy of alveolar ventilation. A discussion of these monitors is forthcoming.

The presence of an artificial airway is noted; airways are used primarily to maintain a patent air passage so that respiratory exchange is not hampered. Five types of airways commonly used are: (1) the balloon-cuffed endotracheal tube (extends from the mouth through the glottis to a point above the bifurcation of the trachea); (2) the balloon-cuffed nasotracheal tube (extends from the nose to the trachea); (3) the laryngeal mask airway (inflatable silicone mask and rubber connecting tubing blindly inserted into the pharynx forming a low pressure seal around the laryngeal inlet); (4) the oropharyngeal airway (extends from the mouth to the pharynx and prevents the tongue from falling back and obstructing the trachea); and (5) the nasopharyngeal airway (extends from the nose to the pharynx). The airway must be kept clear of secretions for adequate gas exchange to occur, and suctioning may be needed if gurgling develops. The airway should not be removed until the laryngeal and pharyngeal reflexes return; these reflexes enable the patient to control the tongue, to cough, and to swallow. If the patient “reacts on the airway” (attempts to eject it), and gags, this can progress to retching and vomiting. The airway should be removed as soon as clinically possible in this instance to avoid aspiration.

An endotracheal tube can be removed as soon as the patient’s condition is adequately reversed, the patient can maintain an airway without the tube, and the danger of aspiration is over. Determination of this point may be difficult; the decision of when a patient needs an airway is usually much easier than the decision of when such an adjunct is not needed. If PACU policy permits removal of an airway, insertion of an airway should definitely be included and both procedures should be accompanied by appropriate education and skill training for the nurses who perform them.

Monitoring of oxygenation with pulse oximetry

A pulse oximeter is used for noninvasive measurement of arterial oxygen saturation (SaO₂) in the blood (SpO₂ when measured with pulse oximetry) and is a valuable adjunct to the clinical assessment of oxygenation. Many clinical indicators, such as the patient’s color and the characteristics of the respirations, are subjective, and the physical signs of cyanosis are not evident until hypoxia is severe. Pulse oximetry monitoring is objective and continuous and provides an early warning of developing hypoxemia, thus allowing intervention before signs of hypoxia appear. Consequently, pulse oximetry has been widely adopted in the PACU as a tool for both safety monitoring and patient management. As a confirmation of the importance of pulse oximetry, the American Society of PeriAnesthesia Nurses (ASPAN) PeriAnesthesia Nursing Standards and Practice Recommendations 2010-2012 recommends evaluation of all PACU patients with pulse oximetry at admission and discharge, and ASPAN recommends a pulse oximeter for every patient in all phases of perianesthesia nursing levels of care.²

A pulse oximeter consists of a microprocessor-based monitor and a sensor (Fig. 27-1). In addition to a SpO₂ display, most oximeters display the pulse rate and have an adjustable alarm system that sounds when values register outside a designated range. A variety of sensors is available, each intended for application to specific sites and for use on patients of various sizes (the manufacturer’s instructions describe these requirements). The sensor is applied to a site with a good arterial supply. The most common application site is a finger or toe (hand or foot in neonates); other sites include the nose, the forehead, the earlobe, or the temple. Both reusable sensors and disposable adhesive sensors are available, and disposable sensors allow for patient-dedicated monitoring when infection control concerns are present.

FIG. 27-1 Pulse oximeter uses two light-emitting diodes and photodiode to determine arterial hemoglobin saturation.

Technology overview

A pulse oximeter uses plethysmography for detection of the arterial pulse and spectrophotometry in determination of SpO₂. The pulse oximetry sensor incorporates a red and an infrared light-emitting diode as light sources and a photodiode as a light detector. In the most common type of sensor, a transmission sensor, the light sources and detector are positioned on opposite sides of an arterial bed, such as around the finger. In a reflectance oximetry sensor, they are positioned on the same surface, such as on the forehead.

With both transmission and reflectance sensors, red and infrared light passes into the tissue, and the detector measures the amount of light absorbed. Because oxyhemoglobin and deoxygenated hemoglobin differ in the absorption of red and infrared light, the detector can determine the percentage of oxyhemoglobin in the arterial pulse.

Applications

Pulse oximetry is used in many clinical settings for safety monitoring and as a patient management tool. As a safety monitor, a pulse oximeter detects hypoxemia caused by unanticipated events such as severe atelectasis, bronchospasm, airway displacement, disconnections or kinks in the breathing circuit, and cardiac arrest. As a patient management tool, pulse oximetry is valuable in titrating oxygen therapy, weaning a patient from mechanical ventilation, and evaluating response to medications or other interventions that are intended for improvement of oxygenation.

In addition to these broad applications, certain uses of pulse oximetry are of particular value in the PACU. For example, patients after surgery can become significantly hypoxemic during transport to or from the PACU. Pulse oximetry during transport can be used to diagnose undetected hypoxemia and to identify a need for supplemental oxygen. As indicated by the ASPAN standards, pulse oximetry is a valuable adjunct to clinical assessments in determination of readiness for PACU discharge. Some patients in the PACU judged to be stable and ready for transfer on the basis of clinical evaluation alone have been found to be hypoxemic after evaluation with pulse oximetry.

Interpretation of pulse oximetry measurements

Consideration of the mechanisms of oxygen transport is essential for adequate interpretation of SpO₂. Approximately 98% of the oxygen in blood is bound to hemoglobin; SaO₂ and SpO₂ reflect this blood oxygen. The remaining blood oxygen is dissolved in plasma; blood gas analysis measures the partial pressure exerted by this oxygen dissolved in plasma (PaO₂ = 80 – 100 mm Hg at sea level). The dissolved oxygen is used to meet immediate metabolic needs. The oxygen bound to hemoglobin serves as the reservoir that replenishes the pool of dissolved oxygen (see Chapter 12).

The rate at which oxygen binds to hemoglobin is primarily controlled by two factors: the PaO₂ and the affinity of hemoglobin for oxygen. This relationship between SaO₂ and PaO₂ is represented by the oxyhemoglobin dissociation curve. The curve is sigmoid in shape, and its position is affected by a number of physiologic variables that change the affinity of hemoglobin for oxygen (Fig. 27-2).

FIG. 27-2 Normal oxyhemoglobin dissociation curve is indicated with the solid line. This curve may shift (indicated with broken lines) whenever pH, temperature, PCO₂, or 2, 3-DPG values are increased or decreased. SO₂, Oxygen saturation; PO₂, partial pressure of oxygen; PCO₂, partial pressure of carbon dioxide; 2, 3-DPG, 2, 3-diphosphoglycerate.

Many factors that shift the oxyhemoglobin dissociation curve are commonly seen in patients in the PACU. For example, a patient with hypothermia may have a left-shifted curve. In such a patient, a given SpO₂ as measured with pulse oximetry may correspond to a lower than normal PaO₂. Although oxygen saturation may be adequate, hemoglobin has a greater affinity for oxygen and is less willing to release oxygen to meet tissue needs. Warming the patient to a normothermic range facilitates oxygen unloading from the hemoglobin molecule and helps to maintain adequate tissue oxygenation.

Clinical issues

As with any technology, important clinical issues must be considered for appropriate use of pulse oximetry. Shifts in the oxyhemoglobin dissociation curve that are caused by abnormal values of pH, temperature, partial pressure of carbon dioxide (PCO₂), and 2,3-diphosphoglycerate must be considered. Consideration of the patient’s hemoglobin level is also important because a pulse oximeter cannot detect depletion in the total amount of hemoglobin. When pulse oximetry is used on a postoperative patient with a low hemoglobin level, a high SpO₂ value might not reflect adequate oxygenation. The amount of hemoglobin, although it is well saturated with oxygen, may be inadequate to meet tissue needs because fewer carriers are available to transport oxygen.

Adequate oxygenation is a factor of not only adequate oxygen saturation and hemoglobin values but also of adequate oxygen delivery, which necessitates appropriate cardiac output, and the ability of the tissues to effectively use oxygen. Tissue hypoxia results when oxygen demand exceeds oxygen supply. Pulse oximetry readings therefore should be assessed in conjunction with all other indices of oxygenation.

Dysfunctional hemoglobin, variants of the hemoglobin molecule that is unable to transport oxygen, present a similar problem. Despite the high SpO₂ level, hemoglobin may be insufficient to carry oxygen. Carboxyhemoglobin is hemoglobin that is bound with carbon monoxide and therefore is unavailable for carrying oxygen. Its effect must be considered in patients with burns or in tobacco smokers with carbon monoxide poisoning. In methemoglobinemia, the iron molecule on the hemoglobin is oxidized from the ferrous to the ferric state. This form of iron is unable to transport oxygen. Methemoglobinemia, although rare, can occur in patients who receive nitrate-based and other drugs and in those who are exposed to a variety of toxins. When dysfunctional hemoglobins are suspected, assessment of oxygenation with pulse oximetry must be supplemented with arterial blood gas saturations measured with a laboratory cooximeter to determine whether dyshemoglobins are present and oxygenation is adequate.

Perfusion at the sensor application site must be sufficient for the pulse oximeter to detect pulsatile flow, which is an important consideration for some patients in the PACU, such as those treated with vasoconstrictors, those with marked hypothermia, and those with significantly reduced cardiac output. A well-perfused site should be selected for application of the sensor. If in doubt, the pulse and adjacent capillary refill can be checked.

If the monitor cannot track the pulse, the patient first is evaluated for adverse physiologic changes. Next, the perianesthesia nurse should ensure that blood flow is not restricted, such as by a flexed extremity, a blood pressure cuff, an arterial line, any restraints, or a sensor that is applied too tightly. Local perfusion to the sensor site can be improved by covering the site with a warm towel or with the use of a forced air warming device. Certain sensors, such as nasal sensors, are designed for application to areas where perfusion is preserved even when peripheral perfusion is relatively poor. Finally, some pulse oximeters use an electrocardiographic signal as an aid in identification of the pulse, thus enhancing the instrument’s ability to detect a weak pulse.

Patient movement can produce false signals that interfere with the ability of the pulse oximeters to identify the true pulse, thus leading to unreliable SpO₂ and pulse rate readings. The sensor should be properly and securely applied; a sensor that is loosely attached or incorrectly positioned can magnify the effect of motion. If the problem persists, consideration should be given to moving the sensor to a less active site. Pulse oximeters that use the electrocardiographic signal as an aid in identification of the pulse can have an enhanced ability to distinguish between the true pulse and artifacts produced by motion. The result is more reliable SpO₂ readings.

Normally, venous blood is nonpulsatile and is not detected with a pulse oximeter. In the presence of venous pulsations, the SpO₂ value provided by the pulse oximeter may be a composite of both arterial and venous saturations. Venous pulsations can occur in patients with severe right-sided heart failure or other pathophysiologic states that create venous congestion and in patients receiving high levels of positive end-expiratory pressure. They can also occur when the sensor is placed distal to a blood pressure cuff or occlusive dressing and when additional tape is wrapped tightly around the sensor. When venous pulsations are present, the perianesthesia nurse should take care in interpreting the SpO₂ readings and, if possible, attempt to eliminate the cause.

Because pulse oximeters are optical measuring devices, the perianesthesia nurse must be aware of additional factors that can influence the reliability of SpO₂ readings. To ensure good light reception, the sensor’s light sources and detector must always be positioned according to the manufacturer’s specifications. In the presence of bright lights, such as infrared warming devices, fluorescent lights, direct sunlight, and surgical lights, the sensor must be covered with an opaque material to prevent incorrect SpO₂ readings. In addition, agents that significantly change the optical-absorbing properties of blood, such as recently administered intravascular dyes, can interfere with reliable SpO₂ measurements. The use of pulse oximetry with certain nail polishes, especially those that are blue, green, and reddish-brown in color, can result in inaccurate readings. If nail polish in these shades cannot be removed, the sensor should be applied to an alternate unpolished site.

Monitoring of ventilation with capnography

Monitoring of end-tidal carbon dioxide (ETCO₂) in respiratory gases provides an early warning of physiologic and mechanical events that interfere with normal ventilation. Capnography, which measures ETCO₂ at the patient’s airway, is increasingly used in the PACU. It allows continuous assessment of the adequacy of alveolar ventilation, cardiopulmonary function, ventilator function, and the integrity of the airway and the breathing circuit. Consequently, it enables early detection of many potentially catastrophic events, including the onset of malignant hyperthermia, esophageal intubation, hypoventilation, partial or complete airway obstruction, breathing circuit leaks or disconnections, a large pulmonary embolus, and cardiac arrest.

Two variants of the instrument are available. A capnometer provides numeric measurement of exhaled CO₂ levels. A capnograph provides the same numeric information, and it also displays a CO₂ waveform. Both types of instruments usually incorporate an adjustable alarm system and often have trending and printing capabilities. The following discussion focuses on the use of capnographs because they allow more complete and effective patient assessment than do capnometers. As discussed subsequently, changes in the shape of the CO₂ waveform can provide crucial diagnostic information about ventilation, similar to the way in which the waveform provided with an electrocardiogram (ECG) can provide crucial diagnostic information about the heart.

Technology overview

For measurement of exhaled CO₂, the most common type of capnograph passes infrared light at a wavelength that is absorbed by CO₂ through a sample of the patient’s respiratory gas. The amount of light that is absorbed by the patient’s gas reflects the amount of CO₂ in the sample.

Capnographs differ in the manner in which they obtain respiratory gas samples for analysis. Sidestream (or diverting) capnographs transport the sample through narrow-gauge tubing to a measuring chamber. Mainstream (or nondiverting) capnographs position a flow-through measurement chamber directly on the patient’s airway. Special adapters are available to allow sidestream capnographs to be used on patients who are not intubated. The sample adapter should be placed as close to the patient’s airway as possible.

Sidestream capnographs incorporate moisture-control features that are designed to minimize clogging of the sample tube, protect the measurement chamber from moisture-induced damage, and minimize the risk of cross contamination. The design of these moisture-control systems significantly affects a monitor’s ease of use. Most systems rely on water traps, which must be emptied routinely. A new technology uses a special system of filters and tubing to dehumidify the sample and thus eliminate the need for water traps.

Capnographs also differ in calibration requirements. Many require removal of the patient from the respiratory circuit and adjustment of the instrument with special mixtures of calibration gases. Advanced capnographic technology includes automatic calibration and does not require any user calibration skills or time.

The normal capnogram

For effective use of capnography, it is important to understand the components of the normal CO₂ waveform (capnogram)—a square wave pattern with a plateau (Fig. 27-3). Early in exhalation, air from the anatomic dead space, which is virtually CO₂ free, is measured with the instrument. As exhalation continues, alveolar gas reaches the sampling site, and the CO₂ level increases rapidly. The CO₂ concentration continues to increase throughout exhalation and reaches the alveolar plateau because alveolar gas dominates the sample. At the end of exhalation, the ETCO₂ occurs, which in the normal lung is the best approximation of alveolar CO₂ levels. The CO₂ concentration then drops rapidly as the next inhalation of CO₂-free gas begins.

FIG. 27-3 Normal capnogram. AB, Beginning exhalation, dead space; BC, initial alveolar emptying; CD, end-alveolar emptying; D, end tidal CO₂; E, inspiration (CO₂-free gas).

End-tidal versus arterial carbon dioxide

In normal conditions, when ventilation and perfusion are well matched, ETCO₂ closely approximates arterial CO₂ (PaCO₂). The difference between the PaCO₂ and the ETCO₂ level is the alveolar-arterial CO₂ difference (a-ADCO₂). ETCO₂ is usually as much as 5 mm Hg lower than PaCO₂. When the two measurements differ significantly, an anomaly in the patient’s physiology, the breathing circuit, or the capnograph is usually present. Significant divergence between ETCO₂ and PaCO₂ is often attributable to increased alveolar dead space. CO₂-free gas from nonperfused alveoli mixes with gas from perfused regions, thus decreasing the ETCO₂ measurement. Clinical conditions that cause increased dead space, such as pulmonary hypoperfusion, cardiac arrest, and embolic conditions (e.g., air, fat thrombus, amniotic fluid), can increase the a-ADCO₂. Changes in the a-ADCO₂ can be used in assessing the efficacy of the treatment; as the patient’s dead space improves, the partial pressure of the alveolar carbon dioxide less the partial pressure of arterial carbon dioxide (PACO₂ – PaCO₂) narrows. Increases in dead space ventilation lower ETCO₂ and therefore increase the PaCO₂ – ETCO₂ gradient. Widened PaCO₂ – ETCO₂ examples include embolic phenomena, hypoperfusion, and chronic obstructive pulmonary disease. Alternatively, a significant PACO₂ – PaCO₂ value can indicate incomplete alveolar emptying (e.g., with reactive airway disease), a leak in the gas-sampling system that allows loss of respiratory gas, and contamination of respiratory gas with fresh gas.⁴

Interpretation of changes in the capnogram

An abnormal capnogram provides an initial warning of many events that warrant immediate intervention. Abnormalities may be seen on a breath-by-breath basis or when the CO₂ trend is examined. For this reason, visualization is preferable of both the real-time waveform and the CO₂ trend on the monitor display. Examples follow for a look at changes produced by significant events that commonly occur in the PACU.

A sudden decrease in ETCO₂ to a near-zero level indicates that the monitor is no longer detecting CO₂ in exhaled gases (Fig. 27-4). Immediate action is crucial for detection and correction of the cause of this loss of ventilation. Possible causes include a completely blocked endotracheal tube, esophageal intubation, a disconnection in the breathing circuit, and inadvertent extubation. The latter three possibilities are particularly likely if the decrease in ETCO₂ coincides with movement of the patient’s head. First, after elimination of possible clinical causes for this decrease in ETCO₂, a clogged sampling tube or instrument malfunction is investigated as the cause of the problem.

FIG. 27-4 Sudden decrease in ETCO₂ to near-zero level.

An exponential decrease in ETCO₂ over a small number of breaths usually signals a life-threatening cardiopulmonary event that has dramatically increased dead space ventilation (Fig. 27-5). Sudden hypotension, pulmonary embolism, and circulatory arrest with continued ventilation must be considered.

FIG. 27-5 Exponential decrease in ETCO₂.

A gradual increase in the ETCO₂ level while the capnogram retains its normal shape usually indicates that ventilation is inadequate to eliminate the CO₂ that is produced (Fig. 27-6). This situation can be the result of a small ventilator leak or a partial airway obstruction that reduces minute ventilation. It can also reflect increased CO₂ production associated with increased body temperature, the onset of sepsis, or shivering. Of particular importance, a large increase in ETCO₂ can be one of the earliest signs of malignant hyperthermia, which may not begin until after emergence from anesthesia.