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.

FIG. 27-6 Gradual increase in ETCO₂.

A gradual decrease in the ETCO₂ level commonly occurs in the patient who is anesthetized, narcotized, hyperventilated, or hypothermic (Fig. 27-7).

FIG. 27-7 Gradual decrease in ETCO₂.

Assessment of the capnogram can reveal information about the quality of alveolar emptying. For example, the patient with bronchospasm is unable to completely empty the alveoli, and the resulting capnogram does not have an alveolar plateau (Fig. 27-8). The ETCO₂ reported by the capnograph in this instance is not a good estimate of alveolar CO₂. Effective administration of bronchodilator therapy commonly improves alveolar emptying and results in a more normal capnogram.

FIG. 27-8 Incomplete alveolar emptying.

Clinical issues

In addition to the diagnostic usefulness of changes in the capnogram, some specific applications of capnography are particularly valuable in the PACU. Of primary importance is its ability to provide early warning of hypoventilation that, in the PACU, may be the result of anesthesia, sedation, analgesia, or pain. A falling ETCO₂ value may indicate pulmonary hypoperfusion from blood loss or hypotension. During rewarming, ETCO₂ values are likely to increase as metabolic activity increases.

Capnography can signal when shivering produces an unacceptable increase in oxygen consumption and metabolic rate. During ventilator weaning, capnography is valuable in assessing adequacy of ventilation. Recent studies have shown the value of capnography in monitoring the course and efficacy of cardiopulmonary resuscitation (CPR). ETCO₂ measurements, which decrease during cardiac arrest, typically reach approximately 50% of normal levels during effective CPR. When spontaneous circulation is restored, ETCO₂ values increase dramatically. The presence and persistence of normal ETCO₂ values are also useful determinants in confirming tracheal intubation, because CO₂ is not normally found in the esophagus. However, capnography cannot be substituted for chest auscultation and radiography in elimination of the possibility of bronchial intubation.

Importantly in the PACU, capnography can provide critical information about the patient’s ventilatory status, including an early warning of apnea that results in overall patient safety.⁵ Deterioration of a patient is discernable 2 to 3 minutes earlier in a patient with an ETCO₂ reading than with oxygen saturation. Therefore capnography is a helpful assessment for patients who are extremely sedated, who require high doses of opioids, or who have obstructive sleep apnea.⁶

The ASPAN does not currently have a practice recommendation requiring continuous monitoring of ETCO₂ in the phase I PACU. Practice Recommendation 2, Components of Initial, Ongoing, and Discharge Assessment and Management, recommends that vital signs are monitored, to include “end-tidal CO2 (capnography) monitoring if available and indicated.”²^,⁶

Cardiovascular function and perfusion

The three basic components of the circulatory system that must be evaluated are: (1) the heart as a pump; (2) blood; and (3) the arteriovenous system. The maintenance of good tissue perfusion depends on a satisfactory cardiac output; therefore most assessment is aimed at evaluating cardiac output.

Clinical assessment

Observe the overall condition of the patient, especially skin color and turgor. Peripheral cyanosis, edema, dilatation of the neck veins, shortness of breath, and many other findings may be indicative of cardiovascular problems. In addition to checking all operative sites for blood loss, note the amount of blood lost during surgery and the patient’s most recent hemoglobin level.

Blood pressure monitoring

Arterial blood pressure must be assessed in the preoperative physical assessment, on admission to and discharge from the PACU, and at frequent regular intervals during the PACU stay. Arterial blood pressure is the pressure of blood in the arteries and arterioles. It is a pulsatile pressure because of the cardiac cycle, and systolic (peak) and diastolic (trough) numbers are reported in millimeters of mercury. Arterial blood pressure is regulated by the vasomotor tone of the arteries and arterioles, the amount of blood entering the arteries per systole, and blood volume. The pressure is currently measured either noninvasively (indirectly) or invasively (directly). Noninvasive methods include manual cuff measurement with either an aneroid sphygmomanometer or automatic measurement with an electronic blood pressure monitor. Invasive measurement can be accomplished via an arterial line connected to a transducer. A clear understanding of proper technique is essential to ensure accurate and reliable readings with all the blood pressure measurement methods.

Noninvasive measurement

Manual method

An aneroid sphygmomanometer with inflatable cuff and stethoscope is needed for the standard auscultatory blood pressure measurement technique. The cuff is placed on the extremity around the arm or thigh. The pressure may be auscultated over the brachial artery of an arm cuff or popliteal artery at the ankle over the posterior tibial artery (just posterior to the medial malleolus). Systolic pressure in the legs is usually 20 to 30 mm Hg higher than in the brachial artery. Use of the correct cuff size is essential. The width of the inflatable bladder that is encased inside the cuff should be 40% to 50% of the upper arm or thigh circumference. A bladder that is too wide underestimates blood pressure, whereas a bladder that is too narrow overestimates blood pressure. The length of the cuff bladder should be at least 80% of the arm circumference.

The cuff is inflated, and when cuff pressure exceeds the arterial pressure, arterial blood flow ceases and the pulse is no longer palpated. As pressure is released with turning the valve of the inflation bulb, blood flow resumes and audible (Korotkoff) sounds are noted with the stethoscope. These sounds change in quality and intensity throughout further cuff deflation and generally disappear. Systolic pressure is noted as the first audible sound in the cuff-deflating process.⁷ The diastolic pressure is marked by the disappearance of sounds in the adult patient and the muffling of sounds in the pediatric patient.

A common cause of error in blood pressure measurement is an auscultatory gap that may be present, especially in patients with hypertension. This gap is a silent interval between the systolic and diastolic pressures. During this gap, the pulse is palpable. Therefore, to avoid mistakenly low systolic readings, the cuff should be inflated until the pulse is obliterated. Blood pressure readings should be recorded completely, including the systolic pressure, the points at which the sounds become muffled and cease, and the range of the auscultatory gap, if present.

Auscultatory blood pressure measurements can be completed quickly and easily in many circumstances. The accuracy and reliability of the readings can be affected by low flow states (including decreased cardiac output and vasoconstriction) or decreased sound transmission caused by factors related to the patient (edema and obesity) or the environment (noise). Cuff size and placement, user error, and improperly calibrated manometers can also contribute to unreliable readings. Because measurements are intermittent and must be initiated by the user, blood pressure changes may go unnoticed in the postoperative patient with labile hemodynamics or sudden blood loss. The use of automatic blood pressure monitors that can be set to measure blood pressure at regular frequent intervals can minimize some of this risk. Single measurements do not adequately reflect a patient’s blood pressure. Trending blood pressure readings is essential.

Automatic method

Automatic blood pressure monitoring with electronic devices has become increasingly prevalent in the PACU. The devices are commonly used for frequent blood pressure measurements over relatively brief periods, when the need for arterial sampling is minimal to absent, and when the risks of arterial lines cannot be justified.

One of the most commonly used automatic noninvasive blood pressure methods is based on oscillometric technology. The cuff is chosen and applied according to conventional technique. Oscillations of the arterial wall are occluded as the cuff is inflated and are detected during cuff deflation. Systolic pressure is indicated at the onset of oscillations. As cuff pressure decreases, oscillations increase in amplitude and peak at the mean arterial pressure. The point at which oscillations disappear is the diastolic pressure (Fig. 27-9). All three pressures are normally reported on oscillometric monitoring devices.

FIG. 27-9 Oscillometric blood pressure measurement. Systolic pressure is indicated at onset of oscillations. Mean arterial pressure occurs when oscillations peak in amplitude. Point at which oscillations disappear is diastolic pressure.

Automatic noninvasive blood pressure monitors can be set to cycle at various measurement periods. The instruments alarm when systolic and diastolic pressures register outside of a preset range. Equipment should be calibrated on a regular basis, and preventive maintenance should include assessment for leaks. The use of automatic devices may be limited in patients with low-flow states or high peripheral vascular resistance and in those who are severely obese or edematous. These devices provide only intermittent measurements and are less desirable for assessment of the patient who is labile.

Newer advances in noninvasive blood pressure technology, currently available for intraoperative monitoring of the patient who is anesthetized, include continuous monitoring capabilities that ensure detection in sudden blood pressure variations. The only other reliable method of continuous blood pressure monitoring currently available is invasive arterial blood pressure technology.

Invasive measurement

Invasive arterial pressure measurements are most commonly obtained via cannulation of the radial artery, but can also be obtained at brachial or femoral sites. A continuous flush solution is connected to the intraarterial catheter and is slowly infused into the arterial vessel under pressure. The pressure within the artery is transmitted through the column of fluid via noncompliant pressure tubing to the transducer. The transducer then converts this pressure to an electric signal that can be converted to millimeters of mercury and displayed on the monitor. A corresponding arterial waveform, or pressure pulse, is also displayed on the monitor.

Arterial blood pressure measurements are continuous and are indicated for patients at high risk hemodynamically. Changes in patient pressures can be observed on an ongoing basis. This technology may also be chosen for patients in whom indirect measurements fail because of diminished or absent Korotkoff sounds (i.e., patients who are obese or edematous) and for those with high peripheral vascular resistance. The direct arterial access is also beneficial if the patient needs frequent blood samples for laboratory analysis.

To ensure more reliable arterial blood pressure readings, the clinician should level and zero the system according to the manufacturer’s specifications. Level the transducer by positioning the open air reference stopcock at the fourth intercostal level at the midaxillary line, known as the phlebostatic axis. The air reference stopcock is when the stopcock is turned off to the patient and opened to air. Depressing the 0 button on the monitor balances the transducer to atmospheric pressure so that it reads 0 mm Hg. Once the monitor is zeroed, turn the stopcock so that it is open to the patient and pressure readings will appear. Aseptic technique must always be used during placement and maintenance of the arterial line and transducer.

Damping of the arterial waveform with subsequent unreliable readings may occur for a variety of reasons, including clotting and kinking of the arterial catheter, positioning of the catheter against the arterial wall, and the presence of air bubbles within the arterial line system. Loose connections, calibration error, and equipment failure can also contribute to unreliable readings. A square-wave test evaluates the dynamic response of the pressure monitoring system. To perform a square-wave test, activate the fast flush device for 1 to 2 seconds and note the monitor configuration. The patient wave form will be replaced with a square wave (Fig. 27-10).

FIG. 27-10 Square wave test using the fast flush valve. A, Normal test and accurate waveform. B, Overdamped. C, Underdamped.

(From Dennison RD: Pass CCRN! ed 3, St. Louis, 2007, Mosby.)

An Allen test should be performed before radial artery cannulation for minimization of the risk of hand ischemia (see Chapter 11). If arterial lines are discontinued in the PACU, constant pressure should be applied to the site for 5 to 10 minutes or until bleeding has ceased. A pressure dressing should be applied, and the site should be checked frequently for any bleeding and radial pulse palpation.

Complications and risks of invasive arterial blood pressure monitoring include infection, thrombosis, emboli, tissue ischemia, hemorrhage, and vessel perforation. Arterial blood pressure monitoring is generally contraindicated in patients with septicemia, coagulopathies, irradiated arterial sites, anatomic anomalies, inadequate collateral blood flow, or thrombosis. No intravenous solution or medications should be administered through the arterial pressure monitoring system at any time. If the catheter patency is in question, blood and fluid are aspirated from the blood drawing port or stopcock and the system is flushed with the fast flush device, not a syringe.⁸

Clinical issues

For assessment of significance, blood pressure readings in the postoperative period must be compared with preoperative baseline measurements. A low postoperative blood pressure may be the result of a number of factors, including the effects of muscle relaxants, spinal anesthesia, preoperative medication, changes in the patient’s position, blood loss, poor lung ventilation, and peripheral pooling of blood. The administration of oxygen to help eliminate anesthetic gases and to assist the patient in awakening causes an increase in blood pressure. Deep breathing, leg exercises, verbal stimulation, and conversation can be instituted to raise the blood pressure. A low fluid volume may be augmented by increasing the rate of intravenous fluids, which helps to maintain the arterial pressure. Any method designed to raise the pressure must be instituted with consideration for the patient’s overall condition.

An increase in blood pressure after surgery is common because of the effects of anesthesia, respiratory insufficiency, or decreased respiratory rate and depth that cause CO₂ retention. The surgical procedure, with the accompanying discomfort, also causes increased blood pressure. Emergence delirium, with its excitement, struggling, and pain, may also be a causative factor in a transient increase in blood pressure. Obviously, determining the cause is important before treatment is instituted. In patients with uncontrolled hypertension, continuous intravenous antihypertensive medications may be necessary. However, diagnosis of the cause of the hypertension is extremely important so that effective therapy can be administered rapidly.

Pulse pressure monitoring

Pulse pressure is an important determinant in the evaluation of perfusion. Because of the pulsatile nature of the heart, blood enters the arteries intermittently, causing pressure increases and decreases. The difference between the systolic and diastolic pressures equals the pulse pressure. The pulse pressure is affected by two major factors: the stroke volume output of the heart and the compliance (total distensibility) of the arterial tree. The pulse pressure is determined approximately by the ratio of stroke output to compliance; therefore any condition that affects either of these factors also affects the pulse pressure.

For accurate evaluation of the patient’s cardiovascular status, all signs and symptoms must be evaluated individually and within the body system as a whole. For example, cool extremities, decreased urine output, and narrowed pulse pressure may be indicative of decreased cardiac output, even in the presence of normal blood pressure.

Pulses

The rate and character of all pulses should be assessed bilaterally. The pulses should be examined simultaneously for determination of equality at time of arrival. Peripheral arterial occlusion is not uncommon; if it is suspected, a Doppler instrument can be of great value in detecting the presence or absence of blood flow. Occlusion is an emergency and must be reported to the surgeon at once. Irregularities in pulse are most commonly caused by premature beats, generally premature ventricular contractions (PVCs) or premature atrial contractions (PACs). These irregular rhythms should be thoroughly investigated before therapy is initiated.

Electrocardiographic monitoring

The perianesthesia nurse must have a basic understanding of cardiac monitoring and should be able to interpret the basic cardiac rhythms and dysrhythmias and correlate them with expected cardiac output and its effects on the patient’s condition. According to the most recent ASPAN standards, ECG monitoring should be performed for each patient during phase I level of care, and an ECG monitor should be readily available for patients in preanesthesia and phase II level of care areas.² Dysrhythmias of any type can occur at any time and in any patient during the postoperative period; therefore accurate ECG monitoring and interpretation are mandatory skills for the perianesthesia nurse. This section is designed to provide an introduction to specific problems of cardiac monitoring in the PACU.

Any type of cardiac dysrhythmia may be seen in the PACU. The causes of specific dysrhythmias must be carefully differentiated before any treatment is instituted. Some commonly encountered problems are reviewed here, but the list is by no means complete.

All abnormal rhythms should be documented with a rhythm strip and recorded in the patient’s progress record. Any questionable rhythms should be documented with a complete 12-lead ECG. Electric monitoring of the patient’s heart is only one assessment parameter and must be interpreted in conjunction with other salient parameters before therapy is initiated. Cardiac monitors generally depict only a single lead. They do not detect all rhythm disturbances and alterations, and a 12-lead ECG is essential for accurate definition of a conduction problem.

Lead placement

The skin where the electrode will be placed should be clean, dry, and smooth. Excessive hair is removed; moisture or skin oils are removed with soap and water or alcohol, and the skin is mildly abraded to obtain good adherence of the electrode.

Site selection on the chest is based on a triangular arrangement of positive, negative, and ground electrodes. Placement of electrodes directly over the diaphragm, areas of auscultation, heavy bones, or large muscles is avoided. Adequate space for application of defibrillator paddles is allowed in the event that defibrillation should become necessary. Fig. 27-11 depicts the most commonly used electrode leads. Lead II is the most commonly used in the PACU because it is the most versatile; it is useful in assessing P waves, P-R intervals, and atrial dysrhythmias. The modified chest lead I is useful for assessing of bundle branch block and differentiation between ventricular dysrhythmias and aberrations. This lead is useful when the patient is known to have preexisting cardiac disease. The Lewis lead is useful when P waves are difficult to distinguish with other leads and is used to detect atrial flutter when it is suspected clinically but not demonstrated on the ECG.

FIG. 27-11 Basic electrode placement.

Sinus dysrhythmias

Sinus bradycardia

Fig. 27-12 shows a slow heart rate, less than 60 beats/min. Sinus bradycardia is a rhythm with impulses that originate at the sinus node at a rate of less than 60 beats/min. Its rhythm may be irregular because of accompanying sinus dysrhythmias. All other complex features are normal.

FIG. 27-12 Sinus bradycardia (lead III).

Sinus bradycardia is commonly encountered in the PACU because of the depressant effects of anesthesia. It can occur normally during sleep, and young healthy adults, especially those who are normally physically active, often have bradycardia. Usually no treatment is necessary except continuation of the stir-up regimen. Excessive parasympathetic stimulation from pain may cause bradycardia, in which case appropriate analgesics and other pain-relieving measures should be initiated. If the patient shows symptoms of low cardiac output, notify the physician; treatment may be initiated with atropine to block vagal effects or epinephrine and dopamine to stimulate the cardiac pacemaker. If temporary pacing wires are available, either atrial or ventricular pacing can be attempted. Bradycardia in conjunction with hypotension is considered an ominous sign for a pediatric trauma patient in shock, because the major component of cardiac output in small children is the heart rate.⁹

Sinus tachycardia

Fig. 27-13 shows a fast heart rate (greater than 100 beats/min). The rhythm may be slightly irregular; all other complex features are normal.

FIG. 27-13 Sinus tachycardia (lead I).

Sinus tachycardia results from any stress and may be encountered in the PACU because of numerous causes, particularly factors relating to an increase in sympathetic tone, including the stress of surgery, anoxia, fever, overhydration, hypovolemia, pain, anxiety, apprehension, or any combination of these factors. Tachycardia is an important postoperative sign and should be fully evaluated before treatment is instituted. Increasing tachycardia is an early sign of shock and must be thoroughly investigated. Treatment must be specific and based on removal of the underlying cause. The patient should be assessed carefully for the ability to tolerate the rapid rate. The deleterious effects of tachycardia are generally related to diminished stroke volume and cardiac output. In general, the patient with previously normal cardiac function can tolerate tachycardia as high as 160 beats/min without manifestation of symptoms. Poor tolerance with a resultant decrease in cardiac output occurs when the diastolic interval, and thus the ventricular filling time, is significantly compromised. Interventions for the compromised condition include beta-adrenergic blockers such as metoprolol and atenolol or calcium channel blockers such as verapamil.

Sinus arrest (atrial standstill)

Sinus arrest is failure of the sinoatrial (SA) node to discharge, with the resulting loss of atrial contraction. The rate remains within normal ranges. The rhythm is regular except when the SA node fails to discharge. P waves and QRS complexes are normal when the SA node is firing and absent when it fails to discharge.

Common causes of sinus arrest in the PACU are the depressant effects of anesthesia or analgesics and electrolyte disturbances. Treatment is aimed at elimination of depressant drugs from the body and correction of electrolyte imbalances. This dysrhythmia must be brought to the attention of the physician immediately, because persistent sinus arrest constitutes an emergency and CPR must be initiated.

Supraventricular dysrhythmias

Supraventricular dysrhythmias are abnormalities in the rhythm of the heart caused by ectopic impulses originating from the SA node, atria, and atrioventricular junction. Supraventricular dysrhythmias occur in 10% to 40% of patients after coronary artery bypass graft surgery. These rhythms should be documented with a 12-lead ECG. Their cause has been related to a number of possible factors, such as an inflammatory reaction to surgical trauma, insufficient protection of the atria during surgery, atrioventricular node ischemia, and sudden withdrawal of beta blockers. A correlation exists between persistent atrial activity during cardioplegia and postoperative supraventricular dysrhythmias.

Premature atrial contraction

Premature atrial contraction, or atrial premature beat, occurs earlier than expected as a result of an irritable focus in the atrium (Fig. 27-14). Cardiac rate and rhythm are normal except for the prematurity. The P wave configuration of the premature beat usually differs from that of the normal beat. The PAC is followed by a pause that is not fully compensatory. This dysrhythmia results from anxiety and is commonly encountered in the PACU. No treatment is necessary unless the PACs become frequent or the patient becomes symptomatic. Pharmacologic therapy may become necessary with agents such as digitalis, beta blockers, or verapamil if hemodynamic function is impaired.

FIG. 27-14 Atrial premature beat (lead I).

Atrial tachycardia

Atrial tachycardia is a rhythm disturbance that is a rapid regular supraventricular heart rate that results from an irritable focus of five or more PACs in succession (Fig. 27-15). The rate is 150 to 200 beats/min with a regular rhythm.

FIG. 27-15 Atrial paroxysmal tachycardia: onset in middle of record (lead I).

This rhythm should be documented with a full 12-lead ECG. The physician should be notified for institution of therapy. Maneuvers that enhance vagal tone such as the Valsalva maneuver and carotid sinus massage may be successful in termination of this dysrhythmia. Antiarrhythmic agents such as digitalis, quinidine, and verapamil may cause atrial tachycardia to revert to normal sinus rhythm. Adenosine can be used to stop atrial tachycardia, and quinidine or procainamide can be used to establish normal sinus rhythm. If these measures are unsuccessful, synchronized cardioversion is necessary.

Atrial flutter

Atrial flutter consists of rapid supraventricular contractions that result from an ectopic focus with varying degrees of ventricular blocking (Fig. 27-16). Its cause is the same as that of PAC and atrial tachycardia. The rhythm is usually regular; the atrial rate is 250 to 350 beats/min. Treatment is the same as for atrial tachycardia.

FIG. 27-16 Atrial flutter: 2:1 and 3:1 rhythm (lead I).

Atrial fibrillation

In atrial fibrillation, one or more irritable atrial foci discharge at an extremely rapid rate that lacks coordinated activity (Fig. 27-17). Atrial fibrillation occurs commonly in patients with atrial enlargement from mitral valve disease or from long-standing coronary artery disease and is often preceded by PACs, tachycardia, or flutter. Clinically, the patient has an irregular heartbeat, pulse rate, and usually, a noticeable pulse deficit. Cardiac output decreases in varying degrees. Normally, atrial filling and contraction account for 30% of ventricular filling. Without this atrial filling, or “atrial kick,” of volume into the ventricle, stroke volumes and thus cardiac outputs are diminished. Treatment involves digitalis, quinidine, verapamil, atrial pacing, ablation, or cardioversion.

FIG. 27-17 Atrial fibrillation (lead I).

Ventricular dysrhythmias

Myocardial ischemia and perioperative myocardial infarction remain the two major causes of ventricular dysrhythmias; however, bradycardia, hypokalemia, hypoxemia, acidosis, and hypothermia are also potential causes.

Premature ventricular contraction

Premature ventricular contraction is a rhythm disturbance that involves an earlier-than-expected ventricular contraction from an irritable focus in the ventricle (Fig. 27-18). The rhythm is regular except for the premature beat, and the rate is normal.

FIG. 27-18 Premature ventricular contractions (leads II and III).

(From Hall J: Guyton and Hall textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)

The P wave is absent from the premature beat. A wide, bizarre, notched QRS complex that may be of greater-than-normal amplitude is present. A widened T wave of greater-than-normal amplitude is present after the premature beat and is of opposite deflection to that of the QRS complex.

The PVC is followed by a pause that is fully compensatory (i.e., the time of the PVC plus the pause time equals the time of two normal beats). PVCs are commonly encountered in the PACU and can occur in any patient. Occasional PVCs occur normally and need no treatment. Multiple PVCs may indicate inadequate oxygenation; when they occur, the patient’s respiratory status should be assessed thoroughly. Other causative factors of PVCs include electrolyte disturbances, acid-base imbalance, drug toxicity, and hypoxemia of the myocardium.

Treatment of PVCs is based on the underlying cause and obliteration of the irritable focus. Occasional isolated PVCs need not be treated. If PVCs occur more frequently than five per minute, if a successive run of two or more occurs, if they are multifocal, or if they occur during the vulnerable period on the ECG complex, they must be treated because they are the precursors of the more lethal ventricular dysrhythmias.

Ventricular dysrhythmias present in the setting of bradycardia should be treated with atropine or with overdrive pacing for elimination of ventricular escape rhythms.

Ventricular tachycardia

Three or more consecutive PVCs constitute ventricular tachycardia (Fig. 27-19). The rhythm is fairly regular, and P waves are not seen. Occasionally, patients may have ventricular tachycardia and be asymptomatic, but usually they have anxiety, palpitations, fluttering, pounding in the chest, dizziness, faintness, and precordial pain. If ventricular tachycardia is prolonged, cyanosis, mental confusion, convulsions, and unconsciousness develop as a result of decreased blood and oxygen supply to the brain.

FIG. 27-19 Ventricular paroxysmal tachycardia (lead III).

The causative factors of ventricular tachycardia are essentially the same as those for PVCs. Most commonly, ventricular tachycardia in the PACU is the result of hypoxia, drug toxicity, or underlying heart disease.

Ventricular tachycardia must be treated immediately. If the patient initially tolerates the dysrhythmia, treatment should be instituted with amiodarone or lidocaine. If the patient has cardiac decompensation and circulatory insufficiency, cardioversion with direct current electric countershock should be immediately instituted. Immediate notification of the physician is essential.

Ventricular fibrillation

Ventricular fibrillation is characterized by a rapid irregular quivering of the ventricles that is uncoordinated and incapable of pumping blood (Fig. 27-20). This rhythm disturbance is the major death-producing cardiac dysrhythmia. The immediate initial treatment is external direct current countershock (Fig. 27-21). Ventricular fibrillation may occur spontaneously without any forewarning, or it may be preceded by evidence of ventricular irritability. Patients in whom ventricular fibrillation is likely to develop include those with underlying heart disease, those with ventricular irritability in the operating room during surgery, and those with symptoms of shock. All these patients should be monitored continuously throughout the recovery period. If ventricular fibrillation is not immediately terminated with countershock, CPR and a cardiac code must be initiated without delay (see Chapter 57).

FIG. 27-20 Ventricular fibrillation (lead II).

FIG. 27-21 Emergency administration of external direct-current countershock.

(From Miller RD, Pardo Jr MC: Basics of anesthesia, ed 6, Philadelphia, 2011, Saunders.)

Hemodynamic monitoring

Although more prominent in cardiac surgery, hemodynamic monitoring using pulmonary artery catheters are commonly used with patients of higher acuity who receive care in many PACUs. Minimally invasive monitoring techniques include use of the esophageal Doppler, arterial pressure-based cardiac output, impedance cardiography, or ultrasound cardiac output monitoring. These minimally invasive techniques reflect cardiac output and assessment of fluid requirements by volumetric means.

Hemodynamic monitoring can be accomplished via the following invasive lines: a flow-directed pulmonary artery catheter, a central venous pressure catheter, a left-atrial or right-atrial catheter, a pulmonary artery thermistor catheter, or a peripheral arterial catheter (A-line). The parameters obtained from these various lines, the catheter insertion sites, and the placement and monitoring methods are presented in Table 27-1 and depicted in Fig. 27-22. Problems associated with maintenance of these lines are summarized in Table 27-2.

Table 27-1 Methods for Invasive Monitoring of Hemodynamic Parameters

FIG. 27-22 Schematic view of anatomy of pulmonary catheterization.

(From Papadakos P, Szalados J: Critical care: the requisites in anesthesiology, St. Louis, 2005, Mosby.)

Table 27-2 Potential Problems Associated with Invasive Hemodynamic Monitoring

POTENTIAL PROBLEMS	ETIOLOGY	PRECAUTIONS AND TREATMENT
Alterations in Pressure Wave Configurations
Dampened tracings	*Technical*
	Air in system	Check system for bubbles; flush bubbles out of system.
	Disconnection in system	Inspect and tighten all connections. Check that stopcocks are positioned correctly and covered with dead-end stopcock port covers (no holes).
	Kinked catheter	Remove dressing to ascertain whether catheter is kinked externally.
	Catheter tip against wall	Turn patient’s head or reposition extremity in which that catheter is inserted; watch for improvement in tracing. Gently aspirate catheter from various angles to determine at which angle best flow is achieved; tape and redress catheter at angle at which best flow is achieved. Gently flush catheter in an attempt to push tip away from vessel wall. Never flush catheter in which clotting is suspected.
	*Physiologic*
	Clot on catheter tip	Attempt to aspirate blood from catheter. If possible, keep aspirating until clot is retrieved or blood no longer seems thickened, then flush system until line is cleared and readable tracing reappears. If blood cannot be aspirated, do not flush system and notify physician.
	With FDPAC, this may also indicate that catheter has advanced forward and is in wedged position*	Ensure balloon is deflated. Recheck system and line. If no improvement, obtain chest radiograph and notify physician.
	*Technical*
Abrupt exaggeration of pressure tracings	Loss of calibration of level of transducer	Re-zero and re-level transducer. Check that balloon has not accidentally inflated. Check for dysrhythmia.
	*Physiologic*
	Slippage of catheter out of chamber or vessel	Avoid traction on intravascular lines; tape catheter to skin or secure with suture.
	FDPAC slipping from pulmonary artery to right ventricle; characterized by systolic pressure that remains same while diastolic pressure falls into range of right-ventricular end-diastolic pressure	Inflate balloon in an attempt to let catheter float back into pulmonary artery. If catheter does not migrate back into pulmonary artery, obtain chest radiograph and notify physician.
	RAC, PAC, or PATC has slipped out of vessel wall into thoracic cavity	Attempt to aspirate to see whether catheter is still in vessel. If blood returns, flush system and attempt to obtain readable pressure tracings. If no blood return is achieved, notify physician and remove catheter, per protocol.
Alterations in Vascular Integrity
Venous and arterial spasms	Trauma to vessels during prolonged insertion attempts; artery irritated by catheter	Apply local anesthetic to catheter surface or administer anesthetic via intravenous route. Use guidewire to facilitate insertion. Cool catheter to make it less flexible and easier to insert.
Thrombophlebitis	Irritation to vessels from prolonged insertion attempts or from constant motion of catheter against vessel	See Venous and Arterial Spasms, discussed previously. Secure catheter in place with either tape or suture. Avoid prolonged infusions of chemically irritating medications. Maintain adequate dilutions and observe for signs and symptoms of phlebitis and change flush solution bag before it empties. Notify physician for possible withdrawal of catheter. Distal placement of stopcocks, connecting catheters, and tubing permits atraumatic blood sampling and flushing.
Embolization	Clot embolization from thrombophlebitis or from clot on catheter tip	Always aspirate catheter first if clot is suspected. Never flush.
	Pulmonary embolism with infarct from FDPAC	Observe for changes in chest radiograph that indicate pulmonary embolization.
	Cerebral embolization from LAC	Observe for neurologic changes that may indicate embolization from LAC.
	Peripheral embolization with extremity ischemia from peripheral arterial lines	Observe for ischemic changes of extremity in which catheter is located.
Air embolization	Loose connections	Secure and tighten all connections. Vigilantly observe LAC, because even minute amounts of air in this system can lead to serious neurologic complications.
	Rupture of balloon on FDPAC caused by overinflation	Inflate balloon slowly, and do not overinflate. Limit inflations. Allow balloon to empty air passively back into syringe. Avoid aspirating air back because this weakens integrity of balloon. Aspirate only if air fails to return passively. If air does not return and rupture is questioned, sterile saline solution can be injected into balloon and attempts made to aspirate it back. Failure to aspirate fluid back indicates leak; physician should be notified.
Vessel erosion or hemorrhage	Inadequate hemostasis after insertion	Apply firm pressure for 15 to 20 minutes.
Bleeding from insertion site: Rupture of branch of pulmonary artery	Overinflation of balloon in normal-sized vessel Normal inflation of balloon in too-small vessel Repeated normal inflations in brittle or susceptible vessel

Do not attempt to inflate balloon if tracing already appears wedged. Inject only prescribed amount of air into balloon.

Inject air slowly, and stop injecting if resistance is felt. Inject only amount of air necessary to obtain wedge tracing.

Limit wedge intervals in patients at high risk, such as patients with pulmonary hypertension or long-standing mitral valve disease.

Atrial dysrhythmias Irritation of right atrium from RAC or during insertion of FDPAC Withdraw CVP catheter to level of superior vena cava, and obtain readings from that area. Continue with insertion of FDPAC because dysrhythmias are usually self limiting and stop once catheter tip exits right atrium. Ventricular dysrhythmias Irritation of right ventricle from tip of FDPAC during insertion procedure or from catheter tip slipping out of pulmonary artery and back into right ventricle Continue with insertion of FDPAC because dysrhythmias are usually self limiting and stop once catheter passes into pulmonary artery. If catheter tip falls back into right ventricle from pulmonary artery, inflate balloon because this cushions tip of catheter and may alleviate dysrhythmias. Administer antidysrhythmic if ventricular dysrhythmias continue. Notify physician, obtain chest radiograph, and manipulate catheter, per hospital policy. Infections Local infection Faulty aseptic techniques during insertion or during subsequent dressing changes Maintain sterility during insertion. Change dressings with sterile technique and tubings, per hospital policy. Systemic infection Faulty aseptic technique during insertion Avoid spasms during insertion. Avoid development of thrombophlebitis along vessel. Change indwelling catheters and insertion sites every 48 to 72 hours, which may be impossible in patients with difficult vascular access sites. In these situations, rethreading new catheter over guidewire at previous insertion site can be done every 48 to 72 hours. However, once site is questionable or patient has symptoms of sepsis develop, such as elevated temperatures and white blood cell count, new line at new site is necessary. Endocarditis Extension of local insertion site; infection along catheter and into circulation Culture per hospital policy. Observe for development of new murmurs.

RAC, Right-atrial catheter; PATC, pulmonary artery thermistor catheter; LAC, left-atrial catheter. FDPAC, flow-directed pulmonary artery catheter; CVP, central venous pressure.

* Wedging of catheter in postoperative patient may be common occurrence for two reasons: (1) catheter may have advanced forward during operative procedure when chest was open and lungs were not fully inflated, because less resistance to forward advancement was found; and (2) as hypothermia is reversed and patient and catheter rewarm, its increased flexibility may allow it to float forward.

Adapted from Cole D, Schlunt M: Adult perioperative anesthesia: the requisites in anesthesiology, Philadelphia, 2004, Mosby; and Dennison R: Pass CCRN! ed 3, St. Louis, 2007, Mosby.

Right-atrial pressure

The normal right-atrial pressure ranges from 2 to 6 mm Hg. Pressures that exceed that level can be the result of fluid overload, right-ventricular failure, tricuspid valve abnormalities, pulmonary hypertension, constrictive pericarditis, or cardiac tamponade. Values in the lower range are usually indicative of hypovolemia.

Pulmonary artery pressure

Pulmonary artery systolic pressures normally range from 15 to 30 mm Hg, whereas a normal pulmonary artery diastolic pressure is 5 to 15 mm Hg. Mean pulmonary artery pressures range from 10 to 20 mm Hg. Hypovolemia contributes to low pressure readings. Increased volume loads that can develop with an atrial or ventricular septal defect or left-ventricular failure can create elevations in pressure. In addition, obstructions to forward flow that can be caused by mitral stenosis or pulmonary hypertension can lead to an elevation in pulmonary artery pressures.

Pulmonary capillary wedge pressure

Normal pulmonary capillary wedge pressure (PCWP) recordings are between 8 and 12 mm Hg. Values in this range can be caused by an increased volume load, as is seen in left-ventricular failure, or they can be created by an obstruction to forward flow. Such obstructions may be caused by mitral stenosis, mitral regurgitation, or pulmonary embolism. Lower values may result from hypovolemia or indicate an obstruction to left-ventricular filling, which could occur with a pulmonary embolism, pulmonary stenosis, or right-ventricular failure.

Left-atrial pressure

Normal left-atrial pressures range from 8 to 12 mm Hg. As is seen with the PCWP, elevations in left-atrial pressure are associated with volume overloads or obstructions to forward flow, the latter of which may consist of left-ventricular failure states, mitral or aortic valve dysfunctions, or constrictive pericarditis. Lower recordings are generally a consequence of hypovolemia from inadequate volume or are related to an obstruction to forward flow. Such an obstruction may be a pulmonary embolism or pulmonic valve stenosis, or it may result from right-ventricular failure.

Mean arterial pressure

Normal mean arterial pressures generally range between 80 and 120 mm Hg. In a postoperative cardiac surgical case, pressures less than 60 mm Hg are generally avoided because coronary artery filling may be limited or impeded when parameters reach this level and may contribute to an ischemic or infarction state. Conversely, pressures greater than 120 mm Hg are avoided because they place too much stress on newly created suture lines that could readily rupture with sustained pressures.

Cardiac output and cardiac index

Cardiac output is the amount of blood ejected by the ventricle in 1 minute. Normal cardiac output is 4 to 8 L/min; it is calculated with the following formula:

in which SV is stroke volume, HR is heart rate, and CO is cardiac output.

Cardiac index is calculated with the following formula:

in which BSA is body surface area in square meters and CI is cardiac index. Normal CI ranges from 2.5 to 4 Lmin/m ². Because CI takes body size into consideration, it is a better indicator of the patient’s perfusion status.¹^,⁶^,⁸^,⁹

Systemic vascular resistance

Systemic vascular resistance (SVR) is the resistance the left ventricle must work against to eject its volume of blood. Normal SVR is 900 to 1400 dynes/s/cm^–5. An elevated SVR can create enough resistance to left-ventricular ejection that cardiac output and cardiac index decrease, which leads to a state of hypoperfusion or shock. Infusion of vasodilators and afterload-reducing agents can counteract this elevation. SVR is calculated with the following formula:

in which MAP is mean arterial pressure and CVP is central venous pressure.¹^,⁸^,¹⁰^,¹¹

Pulmonary vascular resistance

Pulmonary vascular resistance (PVR) is the resistance the right ventricle must work against to eject blood into the pulmonary bed. Normal PVR is 80 to 240 dynes/s/cm^–5. An elevated PVR can create enough resistance to right-ventricular ejection that right-sided failure or infarction can develop. Infusion of vasodilators or pulmonary artery dilators such as aminophylline can counteract these elevations. PVR is calculated with the following formula:

in which PAM is pulmonary artery mean pressure and LAP is left-atrial pressure.¹^,⁸^,¹⁰^,¹¹

Central nervous system function

All anesthetics affect the central nervous system (CNS), and one can assume for the present, although it is not known exactly how narcosis occurs, that anesthetics are general nonselective depressants. The complexity of the CNS, coupled with our incomplete knowledge of how it functions, makes it a most difficult system to evaluate.

Assessment of the CNS in the PACU generally involves only gross evaluation of behavior, level of consciousness, intellectual performance, and emotional status. A more detailed assessment of CNS function is necessary for patients who have undergone CNS surgery; that discussion occurs in Chapters 10 and 38.

Emergence from anesthesia

Patients arrive in the PACU at all levels of consciousness, from fully awake to completely anesthetized. With modern anesthesia techniques, however, most patients respond appropriately by the time they are established in the PACU and become oriented quickly when the stir-up regimen is begun (see Chapter 28). With the use of fluorinated and opioid anesthetics, emergence is generally quiet and uneventful. Occasionally, a patient becomes agitated and thrashes about; this situation seems to occur more often in adolescents and young adults than in patients of other age groups. Emergence delirium also tends to occur more frequently in patients who have undergone intraabdominal and intrathoracic procedures (see Emergence Excitement in Chapter 29).

The perianesthesia nurse can facilitate patient orientation by telling the patient where he or she is, that the surgery is over, and what time it is as a part of the stir-up regimen. Reorientation occurs in reverse order from anesthesia; the patient first becomes oriented to person, then place, then time. This order, of course, may not hold true for the patient who was somewhat confused or disoriented before surgery, which emphasizes the importance of recording accurate information about the mental status of the patient before anesthesia.

Alterations in cerebral function are often the first signs of impaired oxygen delivery to the tissues; therefore an orderly and periodic assessment of mental function is necessary for detection of early evidence of abnormal cerebral function. Restlessness, agitation, and disorientation in the PACU can be ascribed to a number of other causes and are often difficult to evaluate. The use of continuous pulse oximetry can assist the perianesthesia nurse in determination of whether symptoms may be related to hypoxemia.

Thermal balance

The measurement of the patient’s body temperature in the PACU is particularly important. The most recent ASPAN standards state that, at minimum, the preoperative assessment, initial postoperative physical assessment, and discharge evaluation of the patient in phases I and II Level of care should include documentation of temperature.² Normal body temperature may vary from 36° to 38° C (96.8° to 100.4° F). In the healthy adult, body temperature remains fairly constant because of the balance between heat production and heat loss. Alterations in body temperature occur often in the postoperative patient. Factors that affect the body temperature in the PACU patient are listed in Box 27-1.

Premedications, anesthesia, and the stress of surgery all interact in a complex fashion to disrupt normal thermoregulation. Both hypothermia (temperature less than 36° C) and hyperthermia (temperature greater than 38° C) are associated with physiologic alterations that may interfere with recovery (Box 27-2). Patients at the age extremes and those with extreme debilitation are at even greater risk for postoperative development of temperature abnormalities.

BOX 27-2 Physiologic Alterations Associated with Hypothermia and Hyperthermia

Hypothermia	Hyperthermia
Bluish tint to skin (cyanosis)	Pale skin (mottled)
Increased metabolic rate with shivering, then decreased metabolic rate	Increased metabolic rate
Decreased oxygen consumption	Increased oxygen consumption
Decreased muscle tone	Decreased muscle tone
Decreased heart rate	Increased heart rate (rapid and bounding)
Dysrhythmias	Dysrhythmias
Decreased level of consciousness	Alterations in central nervous system (patient may be agitated)

Core temperature (approximate value of temperature of blood perfusing the major metabolically active organs) is measured via the pulmonary artery, distal esophagus, nasopharynx, or tympanic membrane (using infrared thermistor). Monitoring the true core temperature is unrealistic and not clinically feasible for use on all patients in the PACU. Therefore, other measurement techniques (axillary, rectal, tympanic, temporal artery, oral) are required in the PACU even while their correlation to core temperature is debated. Consistency in use of the same method of measurement is required so that trends can be spotted and management of hypothermia begun.

Evidence-Based Practice

ASPAN’s evidenced-based clinical practice guideline for the promotion of perioperative normothermia recommends, as supported by strong evidence, that near core measures of oral temperatures best approximate core readings, the same route of temperature measurement should be used throughout the perianesthesia period; and caution should be taken in interpreting extreme values from any site with near core instruments. Temperature measurement recommendations supported by weak evidence suggests that temporal artery measurements approximate core temperature at normothermic temperature but not extremes outside of normothermia; and that infrared tympanic thermometry does not provide accurate temperature measurements during the perianesthesia period. Temperature measurement recommendations supported by conflicting evidence suggests that oral chemical dot thermometers are acceptable near-core alternatives.

Implications for practice

Overall, the research on perianesthesia temperature measurement is weak because of a lack of controls, insufficient statistical analysis, and lack of replication. Perianesthesia nurses should keep up to date with research in the area of accurate temperature measurements during the perianesthesia period. Consideration for the use of oral temperatures is important because that route has the strongest evidence. Consistency of temperature measurement is of utmost importance throughout the perianesthesia period to reflect an accurate picture of the patient’s body temperature.

Source: Hooper VD et al: ASPAN’s evidence-based clinical practice guideline for the promotion of perioperative normothermia, ed 2, J Perianesth Nurs 25:346-365, 2010.

Management of the patient with hypothermia is directed toward the restoration of normothermia and the avoidance of shivering. Warm blankets can be placed over the patient as specific hospital protocol allows. Forced air warming systems provide a safe and effective means of gradually rewarming the patient. Hypothermia and hyperthermia are discussed in greater detail in Chapter 53.

Fluid and electrolyte balance

Evaluation of a patient’s fluid and electrolyte status involves total body assessment. Imbalances readily occur in the postoperative patient for a number of reasons, including the restriction of food and fluids before surgery, fluid loss during surgery, patient’s physical status, and stress. The normal body response to stress of surgery is renal retention of water and sodium. In addition, patients often have abnormal avenues of postoperative fluid loss (see Chapter 14).

Fluid intake

Each patient must be evaluated for determination of baseline requirements and the fluid needed to replace abnormal losses. The healthy adult who is deprived of oral intake needs 2000 to 2200 mL of water per day to compensate for urinary output and insensible loss.

Intravenous fluids

Most patients admitted to the PACU from the operating room are receiving intravenous fluids. The anesthesia care provider must have an open intravenous line for the administration of necessary medications and replacement fluids during surgery, and an open line is needed after surgery for supply of necessary fluids, electrolytes, and medications. Because all efforts to substitute for normal oral intake of electrolytes and adequate volumes of fluid are at best temporary and inadequate, the first objective is to return the patient to adequate oral intake as soon as possible. Until this objective can be attained, an intravenous line must be maintained. The nurse should be aware of the type and amount of any fluid administered and any medications that may have been added to it.

The intravenous site should be checked to ensure that the needle or cannula is still in the vein and that no extravasation has occurred. Watch for kinks or disconnected tubing, and ensure that the rate of infusion is accurate. The intravenous site should be positioned comfortably; a board may be helpful in maintaining the intravenous site if the patient should become restless.

Pediatric patients may need a protective device over the site or soft protective devices to prevent dislodging of the needle or cannula. A simple paper cup device can be helpful in preventing dislodgement of the intravenous line from the scalp veins of small infants. Snip the bottom out of the cup; thread the cup over the tubing; place the large opening over the intravenous site; and secure the cup to the baby’s head with tape crisscrossed over the entire cup. In addition to providing protection for the intravenous site, this method allows the nurse to check the insertion site frequently.

After ensuring that the intravenous fluids are infusing correctly, check to see what fluids, if any, are to follow or if the infusion is to be discontinued. If the patient is receiving total parenteral nutrition and intralipids, only feeding solutions should go through this line; another intravenous pathway must be secured for other uses. Multilumen catheters allow for the administration of multiple fluids and medications, and central line catheters can be connected to a transducer to provide continuous hemodynamic monitoring, if indicated.

The flow of intravenous fluids in the patient receiving hyperalimentation, the patient who is fluid-restricted, the infant or small child, and the patient who is receiving intravenous analgesia or vasopressors should always be regulated with electronic fluid administration devices.

Oral fluids

Oral intake must be prohibited after anesthesia until the laryngeal and pharyngeal reflexes are fully regained, as evidenced by the patient’s ability to gag and swallow effectively. If the patient is permitted oral intake, starting with small amounts of ice chips is best because they are less likely to cause nausea and vomiting. Some PACUs use isotonic ice chips that are made from a balanced electrolyte solution, such as Lytren, Pedialyte, and Ricelyte. If ice chips are well tolerated, the patient can progressively increase oral intake to include water and other clear liquids. Kool-Aid and fruit-flavored popsicles are well tolerated and accepted by children and adults. In addition, carbonated beverages may be soothing to a patient who feels slightly nauseated. The management of postoperative nausea and vomiting is discussed in Chapters 16 and 29.

Fluid output

Normal output in the average adult results from obligatory urinary output and insensible avenues of loss, including evaporation of water from the skin and exhalation during respiration. The amount of urine necessary for the normal renal system to excrete waste products of a day’s metabolism is approximately 600 mL. Optimally, 30 mL/h or more of urine should be obtained from an adult who is catheterized to ensure proper hydration and kidney function. Urinary output should be closely monitored in the recovery phase; measurement of urinary output and urine specific gravity yields important clues to the overall status of the patient and may alert the nurse to overhydration or dehydration or the development of shock.

A lower than normal urinary output can be expected in the postoperative patient as a result of the body’s normal reaction to stress; however, an unduly small volume of urine (less than 500 mL in 24 hours) may indicate the presence of renal insufficiency, and the physician should be notified.

If a urinary catheter is in place, a more accurate observation of hourly output is available. If urine volume is low and specific gravity remains fixed at a low level, renal insufficiency is indicated. A small urine volume plus a high specific gravity indicates dehydration. In addition to the volume and specific gravity of urinary output noted, the urine should be examined for the presence of pus, blood, or casts.

The perianesthesia nurse must evaluate abnormal and normal avenues of output. Abnormal ways include external losses from vomiting, nasogastric tubes, T-tubes, and fistula or wound drainage and temporary functional losses from fluid shifting within the body, such as hemorrhage into soft tissues and the edema of surgical wounds.

The surgical site should be noted on admission to the PACU, and the dressing should be checked for drainage. The perianesthesia nurse must be aware of the presence of any drains and the expected amount of drainage. Drainage tubes should be checked to ensure patency, and the amount, color, and odor of any drainage should be observed and documented. All tubes should be secure and either clamped shut or connected to drainage apparatus as ordered by the physician. A summary of imbalances that may occur with abnormal avenues of output is presented in Table 27-3. Any deviations from the normally expected drainage in a specific route should be reported promptly to the surgeon.

Table 27-3 Imbalances that May Occur with Abnormal Avenues of Output*

Obviously, the accurate measurement and recording of all intake and output is vital to the assessment of each patient’s fluid and electrolyte status. A running total kept on the postanesthesia flow sheet or online documentation system is essential for quick assessment of fluid status. In addition to observation and assessment of avenues of intake and output, the perianesthesia nurse should be alert to symptoms of fluid and electrolyte imbalance, which are summarized in Table 27-4.

Table 27-4 Signs and Symptoms of Acute Fluid and Electrolyte Imbalance

IMBALANCE	SYMPTOMS AND FINDINGS
Hyperosmolarity
Water excess, sodium deficit	Polyuria (if kidneys are healthy), twitching, hyperirritability, disorientation, nausea, vomiting, weakness, serum Na < 120 mEq/L
Isotonic Disturbances
Dehydration	Weakness, nausea, vomiting, oliguria, postural drop in systolic BP, elevated hematocrit, normal serum Na⁺
Circulatory collapse	Shock
Volume excess	Dyspnea, cough, sweating, edema
Hydrogen Ion Imbalances
Metabolic acidosis	Bicarbonate loss: nausea, vomiting, abdominal discomfort, Weakness, tremors, malaise, headache, Kussmaul respiration, hypotension, tachycardia and other dysrhythmias, confusion, drowsiness, lethargy leading to coma Symptoms of K⁺ excess, ABG pH < 7.35, HCO⁻³ < 25, acid urine with pH < 6.0; increased rate and depth of breathing

Metabolic alkalosis Increased bicarbonate, slow breathing, nausea, vomiting, diarrhea, paresthesia of mouth and extremities, confusion, dizziness, muscle irritability, tetany, seizures, coma; decreased rate and depth of breathing to retain CO₂ (hypoventilation) Respiratory acidosis (CO₂ retention) Hypoventilation: tachycardia, tachypnea initially; bradypnea, hypotension, dysrhythmias, confusion, headache, blurred vision ABG pH < 7.4, PCO₂ > 40, HCO⁻³ 25-35 Respiratory alkalosis

Hyperventilation: tachycardia, palpitations, dry mouth, anxiety, profuse perspiration, paresthesia of mouth and extremities, dizziness, vertigo, increased muscle twitching, tetany, inability to concentrate, seizures, coma

Increased irritability, disorientation, shallow slow respirations, periods of apnea, irregular pulse, muscle twitch, ABG pH > 7.45, HCO⁻³ > 29, alkaline urine with pH > 7.0

Potassium Imbalances Deficit (hypokalemia)

Weakness, mental confusion, shallow respirations, hypotension, dysrhythmias, serum K⁺ < 3.5 (measurement of extracellular K⁺ and only gives vague reflection of intracellular balance)

Four common causes of hypokalemia: reduced intake, GI losses, excessive renal loss of K⁺, K⁺ shifts from extracellular to intracellular, metabolic alkalosis

Excess (hyperkalemia)

Intestinal colic, oliguria, bradycardia, cardiac arrest, serum K⁺ > 5 mEq/L

Metabolic acidosis

Calcium Imbalances Deficit (hypocalcemia) Tingling of fingers, laryngospasm, facial spasms, painful muscle spasms, positive Trousseau sign, positive Chvostek sign, convulsions, palpitations, cardiac dysrhythmias, serum Ca⁺⁺ < 4.5 mEq/L Excess (hypercalcemia) Drowsiness, lethargy and headaches. Weakness and muscle flaccidity, heart block, anorexia, nausea, vomiting, constipation and dehydration

BP, Blood pressure; ABG, arterial blood gas; GI, gastrointestinal; PCO₂, partial pressure of carbon dioxide.

Musculoskeletal assessment

An increase of orthopedic surgical procedures for both ambulatory and hospitalized patients provides a challenge to the perianesthesia nurse. Primary risk factors for complications in those with musculoskeletal injuries include the patient’s multiple comorbid conditions, age, and the multiple types of drugs used, including anticoagulants, steroids, estrogens, and opioids. Assessment and care of these patients include consideration for circulation, reflexes, positioning, transfer, and ambulation. See Chapter 37 for more specifics.

Integumentary system

Chapters 5 and 17 address aspects of the integumentary system. The integumentary system can be injured by the physical forces used in positioning and maintaining the patient position during and after surgery. Pressure, shear, friction, and maceration can cause damage to tissue integrity. The perianesthesia nurse must assess the patient’s skin and positioning to prevent integumentary complications from occurring.