Postoperative oxygen therapy

Postoperative Oxygen Therapy REX A. MARLEY, MS, CRNA, RRT Much has been pubBshed in the medical Hterature concerning adverse events relating to the surgical patient. Among the notable disorders requiring the expertise of the postanesthesia care unit nurse are the diagnosis and management of respiratory dysfunction acutely attributable to the effects of surgery and anesthesia. Inhalational and/or intravenous anesthetic agents contribute to pathophysiological alterations that lend to the development of hypoxemia in the postoperative period. When patients present with preexisting respiratory disease, their care is frequently more complex and challenging. This review session will address the oxygenation component of respiration and the perioperative influences that alter it as well as treatment considerations for normalizing oxygenation. 9 1998 by American Society of PeriAnesthesia Nurses.

Objectives---Based on the content of the following article, the reader should be able to: (1) describe risk factors predisposing the patient to the development of postoperative hypoxemia, (2) list the various causes of postoperative hypoxemia, (3) cite the associated hazards of oxygen therapy, (4) discuss strategies designed to optimize postoperative oxygenation, and (5) be knowledgeable about the performance of the various of oxygen therapy devices. 9 I have been using, as a means of resuscitating patients, after inhaling the vapour of ether, pure oxygen gas, with the most perfect success. 1 --J. Robinson

ECOGNIZING the value of supplying the human body with additional oxygen immediately in the postoperative period is not new to contemporary patient care as evidenced by the above statement appearing in the British medical journal, The Lancet, over 150 years ago. 1 Supplemental oxygen therapy has continued to be effectively used in the management of the postoperative patient subsequent to this early reference. Hypoxemia is defined as a state of reduced arterial oxygen content (volume of oxygen per unit

R

Rex A. Marley, MS, CRNA, RRT, is a Staff Nurse Anesthetist, in the Department of Anesthesia, Poudre Valley Hospital, Fort Collins, CO. Address correspondence to Rex A. Marley, MS, CRNA, RRT, Department of Anesthesia, Poudre Valley Hospital, 1024 Lemay Ave, Fort Collins, CO 80524. 9 1998 byAmerican Society of PeriAnesthesia Nurses9 1089-9472/98/1306-0005503.00/0 394

of volume of blood) or arterial oxygen partial pressure (amount of oxygen dissolved in plasma [PaO2]). Because the oxyhemoglobin saturation reading (oxyhemoglobin saturation value derived via arterial blood gas analysis [SaO2] and oxyhemoglobin saturation value derived via pulse oximetry [SpO2]) is directly related to arterial partial pressure of oxygen, the definition of hypoxemia is frequently expressed as a value of this saturation. Hypoxemia, which can occur at any time, is a relatively frequent event in the postoperative period and is undetected without the use of pulse oximetry. The associated adverse outcomes after respiratory mishaps represent the largest single class of injury according to the American Society of Anesthesiology Closed Claims Study.2 In this review of closed claims files from 20 major United States insurance carriers, the panel of experts felt that

Journal of PeriAnestheaia Nursing, Vol 13, No 6 (December), 1998: pp 394-412

POSTOPERATIVE OXYGEN THERAPY 72% of the claims should have been preventable had better patient monitoring been used during the anesthesia period. Critical postoperative respiratory events, of which hypoxemia (overall 0.9%) contributes significantly, occur in approximately 1.3% of patients in the PACU. 3 In this review, potential factors contributing to hypoxemia in the postoperative setting will be explored as well as treatment options offered. Supplemental oxygen therapy is one of the most prescribed and effective therapies for patients emerging from the influences of surgery and anesthesia while in the PACU. Practical considerations for the use of supplemental oxygen in the postoperative setting will be detailed.

PATHWAYS OF OXYGENATION

The transfer of oxygen from the atmosphere to the tissue relies on the oxygen cascade principle. The fundamental role of the lungs is to achieve uptake of oxygen from the atmosphere for delivery to the pulmonary capillaries and the removal of carbon dioxide from the pulmonary capillaries for delivery to the atmosphere. Once in the pulmonary capillary, the majority of oxygen combines with hemoglobin (thus the term oxyhemoglobin) present in the red blood cell and is transported to cells as a result of blood flow to the tissues. Once in the tissue capillary beds, oxygen leaves the hemoglobin and diffuses intracellularly where it is consumed by the mitochondria for aerobic metabolism. The goal of oxygen transport into the body is to supply a constant source of oxygen to the mitochondria.

POSTOPERATIVE HYPOXEMIA

Hypoxemia is significant such that insufficient levels of oxygen in the blood can result in inadequate amounts of oxygen available to the tissues. Should this condition persist, cellular hypoxia may ensue resulting in grave neurological or cardiac repercussions, or even death. Hypoxemia, defined as an SpO2 of less than or equal to 9 0 % , 4 o c c u r s during all perioperative phases (Table 1). 48 Relative to the PACU, hypoxemia can be present (1) on arrival to the PACU after transfer from the operating room, (2) at any time during the patient's stay in the PACU, and (3) on discharge from the PACU to the floor.

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Table 1. Incidence of Perioperative Hypoxemia

Perioperative Phase Preoperative Random "spot check" Continuous monitoring (15 min) Intraoperative Healthy ambulatory surgical patients Overall Postanesthesia After supplemental oxygen discontinued Continuous monitoring; overall

Incidence of Hypoxemia

2% 5 21% 0 10%7 53% 4 41%8 Up to 80% 8

Incidence of Postoperative Hypoxemia When reviewing data on the incidence of postoperative hypoxemia, it is important to note whether the observational tool for detecting oxyhemoglobin saturation was used intermittently or continuously. Observational studies reporting discontinuous data collection generally report a lower incidence of hypoxemia than studies that have analyzed data continuously. When continuous pulse oximetry monitoring is used in patients recovering in the PACU, the reported incidence of hypoxemia ranges between 14% and 80% at some point during the patient's stay.4,6,912 It has been shown that PACU personnel are ineffective in detecting oxyhemoglobin desaturation while caring for the recovering patient. In one study, recovery personnel were unable to detect hypoxemia 95% of the time when they were blinded to the pulse oximeter reading.t~ Although supplemental oxygen therapy is effective in alleviating postoperative hypoxemia, 8,~3,H it is not a guarantee of adequate oxygenation. A significant incidence of oxyhemoglobin desaturation, 25% to 64%, still occurs in patients despite receiving supplemental oxygen therapy while in the P A C U . 4,6,9,1~ It is important to remember that a portion of the hypoxemia seen in the PACU will be of a typical abnormality observed during sleep in a small percentage of patients.

Risk Factors for Developing Postoperative Hypoxernia Numerous factors influence the patient's predisposition for the development of hypoxemia postoperatively (Table 2). The risk factors for impaired oxygenation to occur relate to (1) factors unique to the patient (eg, age, body habitus, cardiopulmonary disease), (2) intraoperatively related reasons, or

R E X A. M A R L E Y

396 Table 2. Risk Factors for Developing Hypoxemia

Preexisting Patient age Hypobaric conditions Obesity Cardiopulmonary disease Smoking Intraoperative Duration of anesthesia Type of anesthesia Operative site Postoperative Abdominal distension Pain

(3) events occurring postoperatively as a result of the surgery. Patient age. The extremes of age have been found to place the patient at risk for impaired oxygenation.3,4,9-n,15 There is an inverse relationship between the elderly patient's age and PaO2. Patients over the age of 60 years are at risk 3 and are three times as likely to experience postoperative pulmonary problems than younger patients3 6 Lung maturation processes (ie, increased functional residual capacity [FRC] and residual volume, loss of lung elasticity, blunting of airway reflexes, limited ability to cough and clear airway secretions, reduced airflow rates, increased airway closure) associated with aging account for the increased risk. Infants less than 1 year of age show a greater tendency for oxyhemoglobin desaturation. 17,18Very young children are at risk because of a higher oxygen consumption 19 and propensity for earlier airway closure (lower elastic lung recoil, increased closing capacity) at tidal volume breathing 2~ than older children or adults. Obesity. The obese patient (even as little as 20% overweight doubles risk 16) is likely to experience postoperative complications as a result of the restrictive lung component associated with obesity. 3'7'9'21 Rose et al3 noted adverse respiratory events in the PACU in obese men with a total weight greater than 120 kg and women greater than 100 kg. The supine obese patient has a substantial abdominal mass pushing up against the diaphragm, thus compressing the lungs. The upward shift of the diaphragm effectively reduces FRC while increasing the closing volume. The FRC can be roughly considered as the oxygen reserve within the body.

Cardiopulmonary disease. Patients with preexisting pulmonary disease (ie, chronic obstructive pulmonary disease, asthma) typically have comorbid cardiac disease and are at significant risk for developing postoperative problems with ventilation and oxygenation.7,2224 Smoking history. Patients who smoke are more likely to have respiratory compromise postoperatively (nearly sixfold the risk of nonsmokers25). 4,1~ Increased complications are observed once smoking history exceeds 8 to 10 pack years. 27 Postoperatively, smokers have been found to have lower SpO2s than nonsmokers. 28 Smokers typically have several pathophysiologic effects associated with smoking (eg, increased oxygen demand, decreased oxygen supply, carboxyhemoglobin, mucus hypersecretion, impaired tracheobronchial clearance, airway hyperreactivity), most of which predispose the patient to atelectasis and pneumonitis. Children exposed to passive smoking had lower oxyhemoglobin saturations in the PACU than children not exposed to cigarette smoke. 29 Duration of anesthesia. The longer the time (even as little as 60 minutes) the patient is subjected to influences of surgery and anesthesia, the greater the chance of postoperative respiratory impairment including hypoxemia. 4,8,1~176 Emergency surgery, possibly where proper patient evaluation and preparation is limited because of the urgent requirement of the procedure, is associated with more pulmonary problems. 3 Type of anesthesia. The occurrence of postoperative respiratory complications is influenced by the type of anesthesia as well as the specific anesthetic agents. Regional anesthetic techniques (ie, spinal anesthesia), are associated with higher postoperative oxyhemoglobin saturation values than values in patients receiving general anesthesia. 4'9'10'31 Inhalation anesthetics negatively influence pulmonary mechanics by affecting ciliary function with a resultant decrease in mucociliary transport that promotes the retention of airway secretions.27 Sedative and opioid premedication as well as intraoperative opioid usage have been found to increase the incidence of postoperative hypoxemia. 3 Patients receiving postoperative morphine analgesia for pain had a higher incidence of hypoxemia than patients who received regional analgesia for pain management. 32 Opioids may contribute to postoperative hypoxemia by altering the ventila-

POSTOPERATIVE OXYGEN THERAPY tory pattern (ie, obstructive apnea component, thoracoabdominal dyscoordination) and by inhibiting the normal sigh and cough mechanisms. Periodic sighing is fundamental for maintaining alveolar stability postoperatively. Effective sighing has been observed to be reduced from the normal nine to ten sighs per hour to zero in patients receiving opioid analgesia) 3 Operative site. Certain surgical procedures influence the risk of developing postoperative hypoxemia (Table 3). Surgical procedures involving the abdominal or thoracic cavities result in impaired oxygenation for several days postoperatively. 22,34,35 After upper abdominal surgery, reductions in the patient's vital capacity (reduced 25% to 60%) 36,37 and FRC (reduced up to 70%) 38 of awake values have been reported, typically achieving a maximum decrease during the first 2 postoperative days and not returning to normal for at least 7 to 14 days. Generally, nonabdominal or nonthoracic operations impair oxygenation the least. Some studies have noted that the more intravenous fluids a patient received, the higher the incidence of hypoxemia postoperatively. 9,11 The type of operation and duration of surgery might have influenced this observation. Abdominal procedures that were noted to place the patient at risk typically require more intravenous fluid administration to compensate for fluid shifts and losses. Additionally, longer procedures place the patient at risk and permit the opportunity to administer additional intravenous fluids. Hypobaric conditions. Under conditions such as found in Fort Collins, CO (altitude nearly 5,000 feet), where the barometric pressure approximates 636 mm Hg (sea level has a barometric pressure of 760 mm Hg), the total number of oxygen molecules per unit area is less. This results in a reduced alveolar partial pressure of oxygen (unless supple-

Table 3. Influence of Surgical Site on Pulmonary Risk (in Order of Increasing Risk)

Nonabdominal; nonthoracic (eg, head, neck, extremity procedures) Lower abdominal (eg, inguinal herniorrhaphy) Upper abdominal (eg, open cholecystectomy) Thoracic without resection of functional lung tissue {eg, pleural decortication) Thoracic with removal of functional lung (eg, Iobectomy, pneumonectomy)

397 mental oxygen is provided) available for uptake by the blood. Abdominal distension. In instances where significant abdominal distension occurs, there is a reduction in FRC and vital capacity, as well as impedance in effective alveolar ventilation secondary to limited diaphragmatic excursion. Atelectasis and hypoxemia commonly accompany these clinical findings. Uncontrolled pain. Splinting secondary to uncontrolled postoperative pain can contribute to pulmonary complications (ie, alveolar hypoventilation, limited coughing with airway secretion retention, thoracoabdominal dyscoordination, and atelectasis formation). Appropriate analgesic therapy can help optimize respiratory function and improve gas exchange in these patients. 39

Cause of Arterial Hypoxemia In addition to the numerous elements cited that predispose the patient to the development of hypoxemia, several iatrogenic and pathophysiological risk factors contribute to its occurrence. Low inspired oxygen concentration. Fortunately, the delivery of hypoxic gas mixtures to PACU patients is quite rare. Contaminated bulk oxygen delivery systems (ie, crossed medical gas pipelines), have accounted for increased morbidity and mortality in the operative setting. This condition primarily but not always occurs during remodeling or construction of the surgical facility. Thirtyfive crossed pipeline deaths occurred between 1972 and 1982. 4o With the clinical introduction of the inspiratory in-line oxygen analyzer to the modern anesthesia machines and ventilators, the death rate was reduced to four deaths between 1983 and 1993. The in-line oxygen analyzer is effective in the early recognition of contaminated oxygen supply and preventing potentially disastrous consequences. 4~ Failure in anesthesia or ventilator circuit patency, more commonly observed in the PACU, has contributed to reduced alveolar oxygen tensions and resultant hypoxemia. Alveolar hypoventilation. Alveolar hypoventilation can be a result of impaired breathing or increased dead space. The most sensitive clinical marker of hypoventilation is an increase in arterial partial pressure of carbon dioxide (PaCO2). Inadequate ventilation results in an increased alveolar carbon dioxide partial pressure that has a dilutional effect on the alveolar oxygen partial pressure.

398 Perioperatively, the most frequent cause of alveolar hypoventilation is secondary to residual respiratory depressant effects from anesthetic agents (ie, volatile inhalation agents, opioids, sedatives, muscle relaxants). The inhalation anesthetic agents as well as sedatives and opioids can promote alveolar hypoventilation by central nervous system depression or by obtunding the patient sufficiently to cause upper airway obstruction. Residual neuromuscular relaxant effect can lead to peripheral ventilatory depression secondary to respiratory muscle weakness. Ventilation/perfusion abnormalities. Ideally, all alveoli would receive an equal share of inspired gas and cardiac output; however, in reality, some mismatch of ventilation and pulmonary perfusion exists even in normal nonanesthetized individuals. During anesthesia, the normal relationship between pulmonary ventilation and distribution of blood flow to various regions of the lung is altered, leading to a reduction in PaO2. Changes in the shape and dimension of the thoracic cage (depression of rib cage expansion, cephalad diaphragmatic displacement) results in reductions in FRC, residual volume, and lung compliance while also leading to increases in airway resistance. 42 The most common cause of postoperative hypoxemia is primarily a right-to-left intrapulmonary shunt as a result of reduction in the FRC. 43 The maximal decrease in FRC may not be realized until at least 16 hours after surgery. 37 Frank atelectasis is likely to occur secondary to the reduced FRC. Other mechanisms for atelectasis formation postoperatively include inadequate ventilation, main-stem endotracheal intubation, inspissated airway secretions, surgical packing/retraction, pain medication, patient positioning, reduced inhaled nitrogen, abdominal distension, obesity, hemo/pneumothorax, pleural effusions, uncontrolled pain, and phrenic nerve injury. 44 With a preexisting ventilation/ perfusion mismatch, further impairment of gas exchange can occur during anesthesia because of local inhibition of the hypoxic pulmonary vasoconstriction by the inhalational anesthetic agents. 45 Increased oxygen consumption. Hypoxemia can occur if oxygen consumption exceeds oxygen supply. Clinical conditions when increased oxygen consumption is commonly observed include hyperthyroidism, infection, seizures, restlessness, and shivering. A recent evaluation of postoperative shivering found a mean increase in oxygen consumption approaching 40%. 46

REX A. MARLEY

Decreased cardiac output. Reductions in pulmonary perfusion secondary to dysrhythmias, myocardial depression, or hypovolemia will increase pathophysiological shunting and continued oxyhemoglobin desaturation of the shunted blood. Prolonged Postoperative Hypoxemia When describing postoperative hypoxemia, two classic phases (the early or late phases) are commonly used. The late postoperative phase, defined as the phase occurring greater than 12 hours after the discontinuation of anesthesia, sees the immediate influence of anesthetic drugs diminish and other factors (ie, patient's general medical condition, developing complications of surgery) assuming the causative role. Persistent late postoperative hypoxemia after major abdominal and thoracic surgery has been evaluated using continuous pulse oximetry to document hypoxemic episodes. Detailed patient observation with pulse oximetry has found oxyhemoglobin desaturation to be quite common up to postoperative day 7. 47 The propensity for atelectasis after abdominal and thoracic procedures plus side effects attributable to opioid analgesic administration (ie, impaired ventilatory control, upper airway obstruction during sleep) account for this prolonged oxygenation impairments Recall that the maximal reduction in FRC does not occur until approximately 16 hours postoperatively.43 A gradual improvement in FRC occurs normally during the first week after surgery. Additionally, morphine abolishes rapid eye movement sleep and once opioid analgesia is discontinued, it is felt that a "catching up" of rapid eye movement sleep occurs, resulting in even more profound hypoxemia secondary to a sleep apnea component. 47 This episodic oxyhemoglobin desaturation (13% of patients had SpO2 < 85%) commonly occurs at night during the first 5 postoperative days. 48 Hypoxemia has been found to occur most often during the first postoperative day48; however, several evaluations have noted oxyhemoglobin levels to be lowest during the second, 49-51 third, 52,53and up to the fifth54 postoperative night. Continued supplemental oxygen therapy beyond the early phase (which includes normal PACU recovery time) has been shown to be effective in preventing late nocturnal hypoxemia55 and appears warranted in these circumstances.

Consequences of Hypoxia Several deleterious effects of hypoxia have been identified in the perioperative setting. Hypoxemia

POSTOPERATIVE OXYGEN THERAPY and its contribution to postoperative neurological and cardiac impairment have received the most attention in an attempt to clarify its influence. Cardiac dysrhythmia. Perioperative hypoxemia has been associated with an increase in the incidence of dysrhythmias, ST segment depression, and tachycardia. 56 Improving oxyhemoglobin saturations in hypoxemic patients has been shown to reduce the incidence of cardiac dysrhythmias 57 and tachycardia. 58 Myocardial ischemia. Persistent postoperative hypoxemia may contribute to the genesis of myocardial ischemia or infarction especially in instances associated with increased oxygen demand. 59 Myocardial ischemia is likely to occur under clinical conditions where hypoxemia is severe (SpO2 < 85%) and protracted (>5 min). 6~ Eighty-five percent of perioperative myocardial infarctions occur between postoperative days 1 and 3, 6t which corresponds with the highest incidence of prolonged postoperative hypoxemia (see Prolonged Postoperative Hypoxemia Section earlier in this article). Mental confusion. Brain dysfunction is known to occur postoperatively, secondary to multiple mechanisms. In the elderly, the incidence of acute postoperative delirium has been observed to be as high as 41%.62 Factors contributing to an altered mental status postoperatively are frequently multifactorial and include (1) extensive surgery, (2) pain, (3) perioperative medications (ie, sedative drugs), (4) increased patient age, (5) male gender, (6) consuming more than three alcoholic drinks per week, (7) sleep disturbances, (8) metabolic and electrolyte disturbances, (9) change of environment, (10) acute withdrawal from alcohol and benzodiazepines, (11) hypotension or hypovolemia, and (12) hypoxemia. 62-66 Rosenberg and Kehlet 66 found the highest incidence of postoperative mental confusion to occur on the third postoperative day that coincided with low SpO2s observed on the second postoperative night. Postoperative hypoxemia may play an important role in the development of cerebral dysfunction; however, further systematic evaluations are warranted to define this relationship. 67 Postoperative wound complications. Wound healing requires adequate tissue perfusion and oxygen. Inadequate tissue perfusion and reduced subcutaneous oxygen partial pressure are known to diminish wound healing and increase the risk of postoperative infection. 68,69 Supplemental oxygen

399 therapy has been suggested to be beneficial in promoting wound healing and resistance to infection. 7~ It is not apparent whether postoperative hypoxemia specifically contributes to delayed wound healing or reduces resistance to bacterial infection; further investigation of this issue is necessary to elucidate a relationship. MONITORING OXYGENATION

Clinical Assessment of Oxygenation The ability to rapidly and efficiently evaluate a patient remains an essential art and science and cannot be overemphasized. These are the indicators that the clinician relies on to seek more definitive data. Oftentimes, subjective and objective clinical signs are the initial presenting symptom that prompts more definitive evaluation (Table 4). 75,76 The clinical signs and symptoms of hypoxemia can be misleading at times. An evaluation of cardiovascular effects in healthy volunteers subjected to acute normocarbic hypoxemia failed to show any discernable hemodynamic or respiratory changes that could serve as reliable indicators of hypoxemia. 77 Gross cyanosis can easily be detected by the trained practitioner, yet mild cyanosis may be difficult to detect and has proven an unreliable indicator of hypoxemia. Over 50 years ago, it was shown that cyanosis was unreliable as a clinical assessment tool in the detection of hypoxemia. 7~ Kelman and Nunn 79 showed that lighting condiTable 4. Clinical Signs of Acute Hypoxemia

Subjective Signs Anxiety; restlessness; inattentiveness Mental confusion Altered mental status Dyspnea Dimmed peripheral vision Objective Signs Diaphoresis Seizures; unconsciousness Cyanosis Increased cardiac output Increased stroke volume Hypertension--early sign Hypotension--late sign Tachypnea* Dysrhythmias Tachycardia-- early signt Bradycardia--late sign *Secondary to carotid body chemoreceptor stimulation and lactic acidosis. l-Secondary to sympathetic stimulation.

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tions common to the PACU setting impaired the ability of care givers to accurately access cyanosis. 79

Physiological Measurement of Oxygenation The ability to monitor the patient's oxygenation status has improved immensely during the past 30 years to where measurement requirements are rudimentary and readily available. Several methods are available for quantifying oxygenation. A brief review of methods applicable to the postoperative setting will be offered. Pulse oximetry. The routine assessment of oxygenation in the PACU is best achieved with the pulse oximeter and should be implemented whenever possible. The pulse oximeter is advantageous in that it offers continual, noninvasive, and instantaneous oxyhemoglobin saturation determination. Although studies showing a reduction in postoperative complications (cardiovascular, respiratory, neurological, infectious) are lacking, the use of pulse oximeters in the PACU have resulted in changes in patient care. 4 Moiler observed that pulse oximetry monitoring postoperatively (1) enabled the early detection and correction of potentially harmful events; (2) reduced the incidence, severity, and duration of hypoxemia; and (3) led to changes in patient care when hypoxemia was detected.4,8~ Interestingly, Moller4 found that when pulse oximetry was used in the PACU there was an increase in (1) the flow rate of supplemental oxygen therapy, (2) continued supplemental oxygen therapy to the ward, and (3) the use of naloxone. Personnel who are entrusted with patient evaluation based on data offered from the pulse oximeter should be versed in its use and limitations and inaccuracies. Although the accuracy of oxyhemoglobin saturation determination via the pulse oximeter is deemed to be within - 2% to 3% between an SaO2 of 70% to 100%, 81 the clinician must have an understanding of factors affecting accuracy (Table 5). 82-1~ Whenever suspicion exists about the accuracy of pulse oximetric readings, an arterial blood gas should be obtained to confirm or disprove that suspicion. Arterial blood gas analysis. Arterial blood gas (ABG) analysis, considered the "gold standard" test to assess oxygenation, may be useful to confirm abnormal SpO2 findings. Additional information is provided with routine ABG analysis (ie, pH, PaCO2, SaO2, bicarbonate, base status), which may prove

REX A. MARLEY Table 5. Factors Influencing the Accuracy of Pulse Oximetry Fingernail polish 82,83 Blue, green, and black nail polish interfere more than purple and red nail polish. Clear acrylic nails do not affect SpO2 Falsely low readings Venous pulsation84-86 Tricuspid regurgitation or venous engorgement may be problematic Falsely low readings Skin pigmentation 87-89 Finger probe more accurate than ear probe in deeply pigmented skin Falsely high readings or unobtainable Exogenous and endogenous dyes9~ Methylene blue greater effect than indocyanine green, which is greater than indigo carmine Falsely low readings Anemia92,93 Hemoglobin <8 g/dL and low SaO2, or hematocrit <10% Falsely low readings at low SaO2 values Reduced pulsatile component94 Secondary to hypotension, vasoconstriction, hypothermia Ear probe more accurate than finger probe in this instance Inaccurate, unobtainable, or falsely low reading Hypoxemia95,96 More inaccurate at SaO2 <75%-80% Falsely low or high readings during profound hypoxemia Carboxyhemoglobinemia97 Falsely high readings Motion artifact98 Falsely low readings Methemoglobinemia99-101 Falsely high readings at high SaO2s;variable readings at low SaO2s Ambient light 1~176 Minimal interference in well-designed probes Falsely low readings Penumbra effect106 Incorrectly fitting probe Falsely low readings

useful for the clinician. Limitations of ABG analysis include its invasiveness and injury potential, intermittent monitoring capability, and a lag time of several minutes is likely before results are available for interpretation. HAZARDS OF OXYGEN THERAPY

Although supplemental oxygen is administered for the beneficial effect of preventing or relieving tissue hypoxia, there are potential problems and concerns associated with its administration.

POSTOPERATIVE OXYGEN THERAPY

Pulmonary Oxygen Toxicity As with most drugs, when oxygen is administered in high concentrations, it can initiate cellular toxicity consisting of inflammatory, destructive, and proliferative cellular changes. 1~ The lungs are affected more than other organ systems because they are exposed to the highest oxygen concentration. 1~ The pathogenesis of oxygen toxicity is believed to be the result of the cellular production of toxic oxygen free radicals, m8 The development of oxygen toxicity is dependent on the inspired partial pressure of oxygen, and the duration of time the patient is exposed to the additional oxygen. The precise circumstances that lead to pulmonary oxygen toxicity in patients have proven difficult to define. Generally, patients with healthy lung parenchyma can tolerate inspired oxygen concentrations approaching 60%, whereas in patients with underlying lung disease, inspired oxygen concentrations greater than 50% may lead to further parenchymal damage, m9 It is known that prolonged exposure to less than 50% oxygen is well tolerated for extended periods of time without apparent pulmonary injury.Ira Obviously, the lowest supplemental oxygen concentration that relieves tissue hypoxia is to be recommended for delivery to patients.

Retinopathy of Prematuri~. Severe eye injury can occur predominantly in preterm (< 36 weeks gestational age) and low-birthweight (<2 kg) infants who are exposed to excessive amounts of oxygen in the blood. It has been theorized that the insult to the retina is a result of vasoconstriction once the PaO: exceeds 100 mm Hg and leads to disruption in the normal development of retinal blood vessels, tll In susceptible neonates, the immature retina is vulnerable to damage from excessive partial pressures of oxygen in the blood. H2 Depending on the neonate's condition, the inspired oxygen concentration should be adjusted to maintain a PaO2 between 60 mm Hg and 100 mm Hg. n3,1t4

Oxygen-InducedHypoventilation Rarely, patients with severe chronic obstructive pulmonary disease will have an abnormal drive to breathe. Patients normally breathe in response to changes in the partial pressure of carbon dioxide within the blood that directly influences pH level

401 changes within the medulla. In patients whose work of breathing to normalize the partial pressure of carbon dioxide in the blood requires too much energy expenditure, they will reset their threshold of tolerance (eg, PaCO2 > 50 mm Hg) to a higher level. It then becomes possible that a secondary stimulus to breathe, a lowered partial pressure of oxygen sensed by aortic and carotid chemoreceptors, becomes the dominant stimulus. When supplemental oxygen therapy is initiated in this circumstance, there is the possibility of blunting the patient's drive to breathe by increasing the blood oxygen partial pressure to above the stimulus point for taking a breath. If the patient's normal baseline PaCO2 is greater than 50 mm Hg and SaO2 is less than 90%, then supplemental oxygen therapy may cause oxygen-induced breathing impairment, n5 In patients in whom this condition is suspected, maintaining the SpO2 at 90% is desirable.

Absorption Atelectasis The inhalation of 100% oxygen can contribute to atelectasis formation. Nitrogen, the major component of gas in the alveoli when breathing air, is inert and relatively insoluble in the blood. Because it is not absorbed into the blood like oxygen, it maintains a residual gas volume in the alveoli. If nitrogen is removed from the alveoli as when the patient breathes 100% oxygen, this residual gas volume may no longer exist. Oxygen is rapidly absorbed into the blood and if the composition of the alveoli gas is primarily oxygen, a reduction in alveolar volume will occur. This is particularly pronounced in regions of the lung where airway narrowing or obstruction occur.

CONVENTIONAL MANAGEMENT OF POSTOPERATIVE OXYGENATION

The postoperative respiratory care of patients may range from instituting no additional measures if the low-risk patient maintains sufficient oxyhemoglobin saturations while breathing room air to the initiation of mechanical ventilation with positive end-expiratory pressure (PEEP) in the patient who fails to maintain sufficient oxygen levels while spontaneously breathing with conventional oxygen delivery devices. The exact respiratory therapy will depend on the individual patient and associated risk factors.

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Preoperative Counseling and Preparation In the patient with preexisting pulmonary disease or who is at risk for the development of postoperative pulmonary complications, a means to systematically screen and counsel the patient preoperatively is important. Instruction in measures that promote normal oxygenation (eg, incentive spirometry, ambulation, pain control, supplemental oxygen therapy) should be introduced to the patient before surgery. A companion article in this issue (Preoperative Evaluation of the Pulmonary Patient Undergoing Nonpulmonary Surgery, by Marienau and Buck) delves into the preoperative assessment of the pulmonary patient presenting for surgery.

Supplemental Oxygen Therapy Increasing the ambient concentration of inspired oxygen is an effective means of reducing the occurrence of hypoxemia in the postoperative patient. Certain high-risk groups of patients with concurrent pathophysiology (eg, anemia, cerebrovascular ischemia, chest trauma, hypotension, hypovolemia, increased oxygen consumption [ie, pyrexia], myocardial ischemia, sickle cell disease) will require the routine administration of postoperative oxygen.65 Continuous pulse oximetric evaluation should be used to monitor the oxyhemoglobin saturation in all patients while recovering in the PACU. This monitoring tool will help determine the extent and duration of supplemental oxygen therapy required. Patient transport considerations. With the advent of portable pulse oximeters, numerous investigators have looked into oxyhemoglobin saturation levels during patient transport from the operating room to the PACU. The overall reported incidence of oxyhemoglobin desaturation (-<90%) during transport after surgery and anesthesia from operating room to PACU ranges between 8% and 28% for children 116-12~and 23% and 35% for adults. 121-124 Predisposing factors influencing the development of transport hypoxemia include (1) an age of less than or equal to 2 years, 117 (2) longer transport times, 117,121and (3) patient position. TM Hypoxemia is prevalent in the period immediately after the cessation of anesthetic agent administration secondary to central nervous system depression and obstructive airway components. Based on the higher-than-expected incidence of hypoxemia, supplemental oxygen therapy in conjunction with

REX A. MARLEY oxygenation monitoring has been advocated during patient transport to the PACU. 116,123,125 When transporting the patient after anesthesia, children are typically transported in the lateral decubitus position to help maintain airway patency. In hemodynamically stable adult patients, the semirecumbent position should be instituted during transport when appropriate. Using this position while encouraging the patient to breathe deeply every 10 to 15 seconds during transport improves oxygenation and may negate the need for supplemental oxygen) 24 Oxygen therapy during early recovery. Supplemental oxygen therapy should be available for all patients recovering from the influences of surgery and anesthesia. This additional oxygen will not correct the underlying cause of hypoxemia, yet in treatable circumstances, it will increase the margin of patient safety until the treatable cause is found. Whether or not all patients should routinely receive supplemental oxygen therapy after anesthesia is controversial. Gift et a1126 challenged the conventional practice of supplementing oxygen postoperatively in patients considered low risk for developing hypoxemia. In their evaluation, they found it acceptable to omit supplemental oxygen therapy in patients presenting to the PACU with an oxyhemoglobin saturation of greater than 92%. The patient should be determined to be healthy and not at risk for the development of hypoxemia if supplemental oxygen therapy is to be omitted, yet supplemental oxygen should be immediately available should hypoxemia develop. Continual pulse oximetric monitoring is required, and ongoing respiratory nursing assessment is afforded the patient. If routine supplemental oxygen therapy is not afforded every patient after undergoing general anesthesia or deep sedation, an institutional policy addressing this and requisite patient monitoring is desirable.

Continued oxygen therapy during late recovery. As stated earlier in this report, certain patients are at risk for protracted arterial oxygen desaturation during the first postoperative week. 52 Continued supplemental oxygen therapy is appropriate in these patients at risk (ie, after major abdominal or thoracic surgery, patients with preexisting risk factors) along with follow-up patient evaluation to determine the duration that supplemental oxygen is required. Supplemental oxygen therapy is effective in reducing the incidence of postoperative hypoxemia yet does not correct the underlying cause of

POSTOPERATIVE OXYGEN THERAPY the hypoxemia. 127 Supplemental oxygen therapy has been advocated in high-risk patients for a period of 2 to 4 days postoperatively.67 Cost of supplemental oxygen therapy. An argument for selectively prescribing oxygen to postoperative patients often relates to theoretical or actual cost savings to the patient. To help in finding an answer in this situation, it is necessary to appreciate the actual cost of supplying oxygen to the patient. As of mid-1998, the local hospital cost to provide the rudimentary oxygen supplementation to the patient include the following (personal communication, Linda Sylvain, Surgical Services, Poudre Valley Hospital, Fort Collins, CO): 9 Oxygen source--pipeline, 0.02r "E" size cylinder, 1.6r 9 Oxygen therapy device--nasal cannula, 36r patient; simple oxygen mask, 56C/patient For example, the cost of providing oxygen to a patient via the nasal cannula at 3 L/min for a 45minute PACU stay would approach 39r

Enhance Alveolar Ventilation The primary means of preventing hypoxemia in the immediate postoperative period, when residual anesthetic agents impact pulmonary function, is to assure sufficient spontaneous ventilation. Residual anesthetic agents (eg, opioids) may exert a depressant effect on the medullary drive to breathe and thus reduce the patient's minute ventilation. Appropriate management is based on the magnitude of hypoventilation. The use of low-dose reversal agents (eg, opioid or benzodiazepine antagonists if these agents were administered perioperatively), or anticholinesterase to reverse residual nondepolarizing muscle relaxant, may be indicated. Pharmacologically induced respiratory stimulation has been suggested to enhance postoperative ventilation and assist in removing the inhaled volatile agents. Doxapram, a central nervous system stimulant, has been found to reduce postoperative pulmonary complications 128 and improve oxygenation during the first 5 days 129 after major abdominal surgery. A recent study evaluating the efficacy of doxapram administered postoperatively via continuous infusion was terminated early after three of the nine patients receiving the stimulant developed complications (including brain stem infarction). 13~ Patients exhibiting signs of hypoxemia secondary to alveolar hypoventilation readily

40a respond to supplemental oxygen therapy, TM yet, normalization of the PaCO2 by improving alveolar ventilation should be the principal goal of patient management.

Appropriate Pain Management Incisional discomfort is the predominant factor leading to ineffective cough, inability or unwillingness to take a sigh breath, and impaired ventilation after surgery. 132 Pain was the most pronounced reason for restriction of patient movement in bed after major abdominal surgery. 133Appropriate postoperative pain management may facilitate earlier patient mobilization. After abdominal surgery, it has been shown that the more opioid the patient receives, the greater the respiratory depression will be, TM including apnea and episodic hypoxemia. 32 ,135 Opioid analgesic therapy should be judiciously administered and tapered when it is no longer required.

Periodic Alveolar Expansion/Lung Hyperinflation Inspiratory maneuvers (eg, periodic deep breathing or incentive spirometry) are designed to help maintain terminal airway and alveolar patency, thus minimizing the occurrence of microatelectasis. Prophylactic deep breathing in low-risk patients and incentive spirometry in high-risk patients has been shown to reduce postoperative complications alter abdominal surgery. 136,137

Continuous positive airway pressure (CPAP)/ PEEP. CPAP and PEEP refer to above ambient pressure maintained within a closed ventilation system. PEEP implies positive pressure maintained during the expiratory phase of the mechanically ventilated patient, whereas CPAP is above ambient pressure applied throughout the ventilatory cycle of the spontaneously breathing patient. CPAP and PEEP are treatment modalities designed to prevent terminal airway and alveolar collapse, thus resulting in improved ventilation/perfusion relationships. In patients in whom persistent hypoxemia is problematic secondary to a reduction in FRC, the use of CPAP or PEEP may be beneficial to help normalize FRC. Patient Positioning Whenever practical, the patient should be positioned in the semirecumbant position. The sitting position when compared with the supine position has been found to (1) increase the FRC 138for up to

REX A. MARLEY

404

5 days after surgery, 139'140 (2) decrease pulmonary shunt after abdominal surgery, 141 and (3) improve oxygenation in the markedly obese patient on postoperative days 1 and 2.142 A similar improvement in oxygenation has been observed in low-risk patients who sat or stood after abdominal surgery on postoperative days 1 and 4.143

Table 6. Low-Flow Oxygen Therapy Devices Device

FiO2

02 Flow R a t e

Nasal cannula

0.24-0.44

1-6 L/min

Simple oxygen mask

0.40-0.60

5-10 L/min

Partial rebreathing mask

0.60-0.80

10-15 L/rain

>0.80

>15 L/rain

POSTOPERATIVE OXYGEN THERAPY DEVICES

The conventional tools necessary for augmenting oxygen to the recovering patients have been available for several decades. Typically, these devices have been categorized into two oxygen delivery systems (low-flow or high-flow) based on their perceived ability to maintain a consistent inspired oxygen concentration. Inconsistencies in oxygen delivery is apparent with both systems. It is important to be knowledgeable of the described oxygen delivery capabilities and of mitigating influences that impact on both oxygen delivery systems.

Nonrebreathing mask

Low-Flow Systems (Variable Performance Devices) Low-flow oxygen delivery devices, often referred to as variable performance devices, as the name implies do not deliver consistent inspired oxygen concentrations to the patient (Table 6). 144 Several factors influence the oxygen delivery ability of the low-flow devices: 9 Oxygen flow rate. Generally, the higher the oxygen flow rate, as determined by the oxygen flowmeter setting, the higher the inspired oxygen concentration available to the patient. 9 Inspiratory flow rate. Slower inspiratory flow rates result in less air entrainment and thus a higher concentration of delivered oxygen. 9 Tidal volume. A larger tidal volume will result in more room air being entrained in the inspired gas and thus dilute the oxygen concentration. 9 Size of reservoir (appliance or anatomic). The greater the oxygen reservoir, the less dilution from room air. The nasal cannula for example, relies on the nasopharynx as an anatomic oxygen reservoir (approximately 50 mL) and thus has a smaller oxygen reservoir than the nonrebreathing mask that has the mask reservoir of 100 mL to 200 mL plus the attached bag that approximates 600 mL to 800 mL.

Comments More comfortable; better tolerated than other oxygen delivery devices. Reservoir: nasopharynx Oxygen flow rate should be at least 5 L/min to prevent a buildup of carbon dioxide within the mask. Adjust oxygen flow rate to keep reservoir bag partially inflated at peak inspiration avoid room air entrainment. Leaflet valves closing both exhalation ports are not recommended because of risk of suffocation.

Abbreviation: FiO2, fractional concentration of inspired oxygen.

9 Respiratory rate. The faster the respiratory rate, the faster will be the inspiratory flow rate and an increased likelihood of diluting the oxygen with entrained room air. The net effect would be a lower inspired oxygen concentration in the patient with a rapid respiratory rate and taking a large breath as opposed to the patient taking small tidal volumes at a slow respiratory rate. If the patient has an unstable ventilatory pattern, the inspired oxygen concentration will change according to their breathing pattern. Nasal cannula. The nasal cannula is quite appropriate for the routine administration of postoperative oxygen. It has the advantages of costeffective oxygen delivery, comfort for the patient, and the ability to provide sufficient oxyhemoglobin saturations. When compared with the nasal catheter or simple oxygen mask, the nasal canuula was found to afford greater comfort and compliance (ie, more likely to keep the appliance in proper position), for postoperative oxygen therapy. 145-147 The

POSTOPERATIVE OXYGEN THERAPY nasal cannula has also been found to increase postoperative oxyhemoglobin saturations comparable with that of the simple oxygen mask 145,147-149 or 40% face tent. 15~ Practical points regarding the nasal cannula include the following: 9 The nasal cannula is not an appropriate oxygen therapy device in patients with blocked nasal passages. 9 The patient may breathe through the mouth or nose while receiving nasal cannula supplemented oxygen provided the nasal passages are patent. The inspired oxygen concentration might be higher if the conscious patient is encouraged to breath through the nose.151-152 9 Avoid oxygen flow rates greater than 6 L/min because this (1) affords minimal increases in inspired oxygen concentration, and (2) increases nasal irritation and decreases patient comfort. 9 In newborns and infants, limit the oxygen flow rate to 2 L/min. 153-154 9 In the adult patient, it has been recommended that humidification is unnecessary at oxygen flow rates of less than or equal to 4 L/min. 155-157 However, these evaluations were on patients receiving chronic supplemental oxygen therapy via the nasal cannula and not in patients whose airways were acutely instrumented or subjected to the influences of general anesthesia.

Simple oxygen mask. The simple oxygen mask is capable of delivering more oxygen to the patient than the nasal cannula but is not as well tolerated in the postoperative period (eg, certain patients experience claustrophobia)) 46 Practical points regarding the simple oxygen mask include the following: 9 The simple oxygen mask is not tolerated as well as the nasal cannula. Airway access and care is limited with the masks. 9 The minimum oxygen flow rate setting for the simple oxygen mask is 5 L/min to assure exhaled carbon dioxide washout from the previous exhaled breath. 155,158-16~

Partial rebreathing mask. The partial rebreathing mask has the appliance reservoir of the mask (100 mL to 200 mL) plus the attached bag (600 mL to 800 mL). The mask derives the name "partial rebreathing" because the first portion of the patient's exhaled breath aids in filling the reservoir

,,0~ bag. This portion of the patient's tidal volume is deadspace gas that did not participate in gas exchange and is thus high in oxygen and low in carbon dioxide. Practical points regarding the partial rebreathing mask include the following: 9 The partial rebreathing mask is not tolerated as well as the nasal cannula. Airway access and care is limited with the masks. 9 Oxygen flow rate should be sufficient to prevent reservoir bag collapse during inspiration.

Nonrebreathing mask. The nonrebreathing mask has a one-way valve between the reservoir bag and mask to prevent the patient's exhaled gas from entering the reservoir bag. The true nonrebreathing mask is not as commonly used as it once was because it has been noted that the partial rebreathing mask appears to offer comparable inspired oxygen concentrations. 155 Practical points regarding the nonrebreathing mask include the following: 9 The nonrebreathing mask is not tolerated as well as the nasal cannula. Airway access and care is limited with the masks. 9 Oxygen flow rate should be sufficient to prevent reservoir bag collapse during inspiration.

High-flow systems (fixed perfi)rmance devices). The high-flow oxygen delivery devices, often referred to as fixed performance devices, are designed to meet the inspiratory gas demands of the patient and keep the oxygen concentration constant. These devices have a means of blending room air with oxygen to provide an exact oxygen concentration with sufficient total gas flow available to the patient to meet the peak inspiratory flow rates. The high-flow system devices include the air entrainment mask, aerosol mask, face tent, tracheostomy collar, and the " T " piece (Briggs adaptor). A common misconception regarding the highflow system devices relates to their ability to deliver the stated oxygen concentration under all conditions. In patients with an above normal inspiratory flow rate (ie, 100 L/min) or when the desired inspired oxygen concentration exceeds 50%, 155 the total gas flow to the patient may be insufficient to prevent room air dilution. A bench evaluation of the

406

R E X A. M A R L E Y

aerosol face mask interfaced with two jet nebulizers (inspired oxygen concentration set at 80%), found less than 70% oxygen delivered during nearly 90% of the breathing patterns. 161

GUIDELINES FOR POSTOPERATIVE OXYGEN THERAPY In the postoperative respiratory care of the surgical patient, the following basic recommendations should be established by each department as part of patient care regimens. 1. Pulse oximetry should be used to monitor all postoperative patients while recovering in the PACU. 2. Certain groups of patients are at risk to prolonged hypoxemia and will require extended monitoring and oxygen supplementation. This will include but not be limited to patients who are obese, have received major abdominal or thoracic procedures, have received generous or continual opioid analgesic therapy, have acute or chronic airway disease, are hypovolemic, are hypotensive, are anemic, have myocardial ischemia, have cerebrovascular ischemia, have increased oxygen consumption (eg, pyrexia), or have sickle cell disease. 3. Oxyhemoglobin saturation monitoring and a means of providing supplemental oxygen therapy should be available for patient transport from the operating room to the PACU. 4. Supplemental oxygen therapy should be provided such that h y p o x e m i a is relieved. This

m a y entail using delivery devices that have greater oxygen delivery capabilities than currently used devices. 5. If continual oxyhemoglobin saturation monitoring is unavailable in the PACU, supplemental oxygen therapy should be instituted and oxyhemoglobin levels spot checked immediately on arrival, as needed during recovery, and once oxygen therapy has been discontinued before dismissal from the PACU. 6. Exercise caution regarding supplemental oxygen therapy in the patient with COPD who retains carbon dioxide and relies on the hypoxic ventilatory drive.

SUMMARY Hypoxemia continues to be a relatively common complication in the immediate and extended period after surgery and anesthesia. H y p o x e m i a occurs regularly during sleep in certain individuals and occasional episodes can be anticipated postoperatively. Detection is a crucial component in the effective management o f postoperative hypoxemia. The clinician must be able to recognize the at-risk situations and while following appropriate monitoring and management protocol he or she must be able to treat the patient early and effectively. We are yet to adequately define when hypoxemia will become problematic and result in adverse patient outcomes. In the postoperative setting, it is important to have an organized and rational approach to oxygen therapy.

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oximetry with methemoglobinemia. Anesth Analg 67:10991101, 1988 100. Barker SJ, Tremper KK, Hyatt J: Effects ofmethemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 70:112-117, 1989 10l. Eisenkraft JB: Pulse oximeter desaturation due to methemoglobinemia. Anesthesiology 68:279-282, 1988 102. Brooks TD, Paulus DA, Winkle WE: Infrared heat lamps interfere with pulse oximeters [letter]. Anesthesiology 61:630, 1984 103. Hanowell L, Eisele JH Jr, Downs D: Ambient light affects pulse oximeters [letter]. Anesthesiology 67:864-865, 1987 104. Amar D, Neidzwski J, Wald A, et al: Fluorescent light interferes with pulse oximetry. J Clin Monit 5:135-136, 1989 105. Kelleher JF, RuffRH:Thepenumbraeffect: Vasomotiondependent pulse oximeter artifact due to probe malposition. Anesthesiology 71:787-791, 1989 106. Crapo JD: Morphologic changes in pulmonary oxygen toxicity. Annu Rev Physio148:721-731, 1986 107. Klein J: Normobaric pulmonary oxygen toxicity. Anesth Analg 70:195-207, 1990 108. Sen CK: Oxygen toxicity and antioxidants: State of the art. Indian J Physiol Pharmacol 39:177-196, 1995 1(/9. Shapiro BA, Cane RD: Metabolic malfunction of lung: Noncardiogenic edema and adult respiratory distress syndrome. SurgAnnu 13:271-298, 1981 110. Clark JM, Lambertsen C J: Puhnonary oxygen toxicity: A review. Pharmacol Rev 23:37 133, 1971 111. Aranda JV, Saheb N, Stern L, et al: Arterial oxygen tension and retinal vasoconstriction in newborn infants. Am J Dis Child 122:189-194. 1971 112. Zierler S: Causes of retinopathy of prcmatnrity: An epidemiologic perspective. Birth Defects 24:23 33, 1988 113. James I~S, Lanman JT: llistory of oxygen therapy and retrolental fibroplasia. Pediatrics 57:591-642, 1976 (suppl 2) 114. Phibbs RH: Oxygen therapy: A continuing hazard to the premature infant [editorial]. Anesthesiology 47:486-487, 1977 115. Youtsey JW: Oxygen and mixed gas therapy, in Barnes TA (ed): Respiratory Care Practice. Chicago, IL, Year Book, 1988, pp 131-163 116. Pullerits J, Burrows FA, Roy WL: Arterial dcsaturation in healthy children during transfer to the recovery room. Can J Anaesth 34:470-473, 1987 117. Fossum SR, Knowles R: Perioperative oxygen saturation levels of pediatric patients. J Post Anesth Nuts 10:313-319, 1995 118. Motoyama EK, Glazener CH: Hypoxemia after general anesthesia in children. Anesth Analg 65:267-272, 1986 119. Kataria BK, Harnik EV, Mitchard R, et al: Postoperative arterial oxygen saturation in the pediatric population during transportation. Anesth Analg 67:280-282, 1988 120. Chripko D, Bevan JC, Archer DR et al: Decreases in arterial oxygen saturation in paediatric outpatients during transfer to the postanaesthetic recovery room. Can J Anaesth 36:128-132, 1989 121. Blair 1, Holland R, Lau W, et al: Oxygen saturation during transfer from operating room to recovery after anaesthesia. Anaesth Intensive Care 15:147-150, 1987 122. Smith DC, Crul JF: Early postoperative hypoxia during transport. Br J Anaesth 61:625-627, 1988 123. Tyler IL, Tantisira B, Winter PM, et al: Continuous

4o9 monitoring of arterial oxygen saturation with pulse oximetry during transfer to the recovery room. Anesth Analg 64:11081112, 1985 124. Biddle CJ, Holland MS, Schreiber TR, et al: Prevention of hypoxemia in good-risk patients during postoperative transport by positioning and deep breathing. Respir Care 32:24-28, 1987 125. Badgwell JM, Savage GT, Kelley EL: A case for delivering supplemental oxygen to postoperative patients during transport to the PACU. J Peri Anesth Nurs 11:295-297, 1996 126. Gift AG, Stanik J, Karpenick J, et al: Oxygen saturation in postoperative patients at low risk for hypoxemia: Is oxygen therapy needed? Anestb Analg 80:368-372, 1995 127. Rosenberg J, Pedersen MH, Gebuhr P, et al: Effect of oxygen therapy on late postoperative episodic and constant hypoxaemia. Br J Anaesth 68:18-22, 1992 128. Steele RJ, Walker WS, Irvine MK, et al: The use of doxapram in the prevention of postoperative pulmonary complications. Surg Gynecol Obstet 154:510-512, 1982 129. Jansen JE, Sorensen AI, Naesh O, et al: Effect of doxapram on postoperative pulmonary complications after upper abdominal surgery in high-risk patients. Lancet 335:936938, 1990 130. Rosenberg J, Kristensen PA, Pedersen MH, et al: Adverse events with continuous doxapram infusion against late postoperative hypoxaemia. Eur J Clin Pharmacol 50:191 194, 1996 131. West JB: Respiratory Physiology--The Essentials. Baltimore, MD, Williams & Wilkins, 199(/, pp 51-68 132. Richardson J. Sabanathan S, Mearns AJ, et al: Efficacy of preemptive analgesia and continuous extrapleural nerve block on post thuracotomy pain and pulmonary mechanics. J Cardiovase Surg 35:219-228. 1994 133. Rosenberg-Adamsen S, Staushohn K, Edvardsen 1,, el al: Body position and late postoperative nocturnal hypoxaemia. Anaesthesia 52:586 602, 1997 134. Catling JA, Pinto DM, Jordan C, et al: Respiratory effects of analgesia after cholecystectomy: Comparison of continuous and intermittent papaveretum. BMJ 281:478-480, 1980 135. Clyburn PA, Rosen M, Vickers MD: Comparison of the respiratory effects of i.v. infusions of morphine and regional analgesia by extradural block. Br J Anaesth 64:446-449, 1991) 136. Hedstrand U, Liw M, Rooth G, et al: Effect of respiratory physiotherapy on arterial oxygen tension. Acta Anaesthesiol Scand 22:349-352, 1978 137. Hall JC, Tarala RA, Tapper J, et al: Prevention of respiratory complications after abdominal surgery: A randomised clinical trial. BMJ 312:148-153, 1996 138. Craig DB, Wahba WM, Don HF, Couture JG, et al: Closing volume and its relationship to gas exchange in seated and supine positions. J Appl Physiol 31:717-721, 1971 139. Hsu HO, Hickey RF: Effect of posture on functional residual capacity postoperatively. Anesthesiology 44:520-521, 1976 140. Meyers JR, Lembeck L, O'Kane H, et al: Changes in functional residual capacity of the lung after operation. Arch Surg 110:576-583, 1975 141. Bonnet F, Bourgain JL, Matamis D, et al: The influence of position on ventilation-perfusion distribution after abdominal surgery. Acta Anaesthesiol Scand 32:585-589, 1988 142. Vaughan RW, Wise L: Postoperative arterial blood gas

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measurements in obese patients: Effect of position on gas exchange. Ann Surg 182:705-709, 1976 143. Mynster T, Jensen LM, Jensen FG, et al: The effect of posture on late postoperative oxygenation. Anaesthesia 51:225227, 1996 144. Wilson BG, Bone RC: Administration of oxygen and other medical gases, in Eubanks DH, Bone RC, (eds): Principles and Applications of Cardiorespiratory Care Equipment. St Louis, MO, Mosby-Year Book, 1994, pp 27-47 145. Nolan KM, Winyard JA, Goldhill DR: Comparison of nasal cannulae with face mask for oxygen administration to postoperative patients. Br J Anaesth 70:440-442, 1993 146. McBrien ME, Sellers WF: A comparison of three variable performance devices for postoperative oxygen therapy. Anaesthesia 50:136-138, 1995 147. Stausholm K, Rosenberg-Adamsen S, Skriver M, et al: Comparison of three devices for oxygen administration in the late postoperative period. Br J Anaesth 74:607-609, 1995 148. Hudes ET, Marans HJ, Hirano GM, et al: Recovery room oxygenation: A comparison of nasal catheters and 40 per cent oxygen masks. Can J Anaesth 36:20-24, 1989 149. Williams AB, Jones PL, Mapleson WW: A comparison of oxygen therapy devices used in the postoperative recovery period. Anaesthesia 43:131-135, 1988 150. Scudefi PE, Mims GRIlI, Weeks DB, et al: Oxygen administration during transport and recovery after outpatient surgery does not prevent episodic arterial desaturation. J Clin Anesth 8:294-300, 1996 151. Dunlevy CL, Tyl SE: The effect of oral versus nasal breathing on oxygen concentrations received from nasal cannu1as. Respir Care 37:357-360, 1992

152. Poulton TJ, Comer PB, Gibson RL: Tracheal oxygen concentrations with a nasal cannula during oral and nasal breathing. Respir Care 25:739-741, 1980 153. Vain NE, Prudent LM, Stevens DP, et al: Regulation of oxygen concentration delivered to infants via nasal cannulas. Am J Dis Child 143:1458-1460, 1989 154. Fan LL, Voyles JB: Determination of inspired oxygen delivered by nasal cannula in infants with chronic lung disease. J Pediatr 103:923-925, 1983 155. Fulmer JD, Snider GL: American College of Chest Physicians (ACCP)-National Heart, Lung, and Blood Institute (NHLBI) Conference on Oxygen Therapy. Arch Intern Med 144:1645-1655, 1984 156. Estey W: Subjective effects of dry versus humidified low-flow oxygen. Respir Care 25:1143-1144, 1980 157. Cambell EJ, Baker MD, Crites-Silver P: Subjective effects of humidification of oxygen for delivery by nasal cannula. A prospective study. Chest 93:289-293, 1988 158. JensenAG, JohnsonA, Sandstedt S: Rebreathing during oxygen treatment with face mask: The effect of oxygen flow rates on ventilation. Acta Anaesthesiol Scand 35:289-292, 1991 159. Robertson GS: Cricothyroid puncture in the assessment of equipment for postoperative oxygen therapy. Lancet 1:801803, 1969 160. Campkin NTA, Ooi RG, Soni NC: The rebreathing characteristics of the Hudson oxygen mask. Anaesthesia 48:239242, 1993 161. Goust GN, Potter WA, Wilons MD, et al: Shortcomings of using two jet nebulizers in tandem with an aerosol face mask for optimal oxygen therapy. Chest 99:1346-1351, 1991

POSTOPERATIVE OXYGEN THERAPY POSTTEST 1.8 CONTACT HOUR

Directions: T h e m u l t i p l e - c h o i c e e x a m i n a t i o n b e l o w is d e s i g n e d to test y o u r u n d e r s t a n d i n g o f t h e b a s i c s o f p o s t o p e r a t i v e o x y g e n t h e r a p y a c c o r d i n g to t h e o b j e c t i v e s listed. To e a r n c o n t a c t h o u r s f r o m t h e A m e r i c a n S o c i e t y o f P e r i A n e s t h e s i a ( A S P A N ) C o n t i n u i n g E d u c a t i o n P r o v i d e r P r o g r a m : (1) r e a d t h e article; (2) c o m p l e t e the p o s t t e s t b y i n d i c a t i n g the a n s w e r s o n test grid p r o v i d e d ; (3) t e a r o f f the b o t t o m p o r t i o n a n d s u b m i t p o s t m a r k e d b e f o r e D e c e m b e r 31, 2000, w i t h c h e c k p a y a b l e to A S P A N ( A S P A N m e m b e r , $ 1 2 . 0 0 p e r test; n o n m e m b e r , $ 1 5 . 0 0 p e r test); a n d r e t u r n to A S P A N , 6 9 0 0 G r o v e Rd, T h o r o f a r e , N J 0 8 0 8 6 . N o t i f i c a t i o n o f c o n t a c t h o u r s will b e s e n t to y o u in 4 to 6 w e e k s . POSTTEST QUESTIONS 1. Which of the following is false regarding postoperative hypoxemia: a. Studies monitoring continuous oxyhemoglobin saturation find a higher incidence of hypoxemia than studies where discontinuous monitoring techniques are used. b. The only at-risk time for hypoxemia to occur is during the first 15 minutes after the discontinuation of anesthesia. c. The incidence of postoperative hypoxemia in the PACU has been reported as high as 80%. d. Hypoxemia is defined as a decrease in the arterial oxygen partial pressure. 2. The most common cause of postoperative hypoxemia is: a. A left-to-right intrapulmonary shunt as a result of a reduction in the FRC. b. A right-to-left intrapulmonary shunt as a result of a reduction in the FRC. c. A right-to-left intrapulmonary shunt as a result of an increase in the FRC. d. A left-to-right intrapulmonary shunt as a result of an increase in the FRC.

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3. Risk factors for the development of postoperative hypoxemia include all of the following except: a. Obese patients are at risk because of the associated obstructive lung disease component that reduces FRC. b. Very young children (<1 yr of age) have a lower elastic lung recoil than the older child. c. Children exposed to passive smoke have lower oxyhemoglobin saturations in the PACU. d. The inhalation anesthetic agents (ie, isoflurane) inhibit mucociliary transport. 4. Which surgical site is associated with the highest risk of pulmonary complications? a. Upper abdominal (eg, open cholecystectomy) b. Lower abdominal (eg, inguinal herniorrhaphy) c. Thoracic without resection of functional lung tissue (eg, pleural decortication). d. Thoracic with removal of functional lung (eg, lobectomy). 5. Which statement is not true regarding opioid administration. a. Normal sighs and cough mechanisms are inhibited by opioid administration. b. Opioid administration may increase thoracoabdominal dyscoordination. c. Central nervous system depression secondary to opioid administration contributes to alveolar hypoventilation. d. Rapid eye movement sleep augmentation occurs secondary to opioid administration. 6. Which of the following does not affect the accuracy of pulse oximetry? a. Elevated carboxyhemoglobin levels. b. Elevated oxyhemoglobin levels. c. Elevated methemoglobin levels. d. Methylene blue dye. 7. Which of the following is false regarding the hazards of oxygen therapy? a. The infant less than 36 weeks' gestational age and weighing less than 2 kg receiving supplemental oxygen therapy is at risk for retinopathy of prematurity. b. Replacing nitrogen with oxygen in the lung alveoli may contribute to absol-ption atelectasis. c. Pulmonary oxygen toxicity is minimized if the inspired oxygen concentration is less than 50%. d. In patients suspected of having oxygen induced hypoventilation, ideally the SpO2 should be greater than 96%. 8. Effective measures to increase postoperative oxygenation might include all of the following e.rcept: a. Placing the adult patient in the semirecumbant position to increase FRC. b. The use of PEEP to increase FRC by preventing alveolar collapse. c. Appropriate pain management to facilitate patient mobilization. d. The use of low-dose doxapram to reverse residual nondepolarizing muscle relaxant. 9. All of the following are true regarding oxygen therapy devices except: a. The nasal cannula is better tolerated by the awakening patient than the other oxygen therapy devices. b. The oxygen flow rate for the partial rebreathing mask should be adjusted to where the reservoir bag totally collapses during inspiration, thus using all of the stored oxygen. c. The minimum oxygen flow rate for the simple oxygen mask should be 5 L/min to prevent buildup of carbon dioxide within the mask. d. Oxygen flow rates exceeding 6 L/min through the nasal cannula are irritating to the nasal passages. 10. Which statement is true regarding oxygen delivery of low-flow devices: a. The higher the oxygen flow rate, the higher the inspired oxygen concentration. b. The higher the inspiratory flow rate, the higher the inspired oxygen concentration. c. The larger the tidal volume, the higher the inspired oxygen concentration. d. The faster the respiratory rate, the higher the inspired oxygen concentration.

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ANSWERS: System #W011200. Please circle the correct answer. 1.

a b c d

2.

a b c d

3.

a, b c d

6.

a b c d

7.

a b c d

8.

a b c d

5.

a b c d

10.

a b c d

Please Print Name

Nursing License No. and State

Address City Social Security #

State

Zip ASPAN Member Number

EVALUATION: Postoperative Oxygen Therapy (SD, strongly disagree; D, disagree; ?, uncertain; A, agree; SA, strongly agree)

1. To what degree did the content meet the objectives? a. Objective #1 was met. b. Objective #2 was met. c. Objective #3 was met. d. Objective #4 was met. e. Objective #5 was met, 2. The program content was pertinent, comprehensive, and useful to me. 3. The program content was relevant to my nursing practice. 4. Self-study/home study was an appropriate format for the content. 5. Identify the amount of time required to read the article and take the test. 25 rain 50 min 75 min 100 rain 125 min

SD

D

?

A

SA

1 1 1 1 1 1

2 2 2 2 2 2 2 2

3 3 3 3 3 3 3 3

4 4 4 4 4 4 4 4

5 5 5 5 5 5 5 5

1 1

Test answers must be submitted before December 31, 2000, to receive contact hours.