Loss of Pharyngeal Muscle Tone

The most frequent cause of airway obstruction in the immediate postoperative period is the loss of pharyngeal muscle tone in a sedated or obtunded patient. The persistent effects of inhaled and intravenous anesthetics, neuromuscular blocking drugs, and opioids all contribute to the loss of pharyngeal tone in the PACU patient.

In an awake patient, opening of the upper airway is facilitated by the contraction of the pharyngeal muscles at the same time that negative inspiratory pressure is generated by the diaphragm. As a result, the tongue and soft palate are pulled forward, tenting the airway open during inspiration. This pharyngeal muscle activity is depressed during sleep, and the resulting decrease in tone can promote airway obstruction. A vicious cycle then ensues wherein the collapse of compliant pharyngeal tissue during inspiration produces a reflex compensatory increase in respiratory effort and negative inspiratory pressure that promotes further airway obstruction.

The effort to breathe against an obstructed airway is characterized by a paradoxical breathing pattern consisting of retraction of the sternal notch and exaggerated abdominal muscle activity. Collapse of the chest wall and protrusion of the abdomen with inspiratory effort produces a rocking motion that becomes more prominent with increasing airway obstruction. Obstruction secondary to loss of pharyngeal tone can be relieved by simply opening the airway with the “jaw thrust maneuver” or continuous positive airway pressure (CPAP) applied via a facemask (or both). Support of the airway is needed until the patient has adequately recovered from the effects of drugs administered during anesthesia. In selected patients, placement of an oral or nasal airway, laryngeal mask airway, or endotracheal tube may be required.

Residual Neuromuscular Blockade

Postoperative residual neuromuscular blockade is unfortunately very common ( Box 80.2 ). The literature reports incidences between 20% and 40% and a recent study even found that 56% of patients had residual neuromuscular blockade upon arrival in the PACU. When evaluating upper airway obstruction in the PACU, the possibility of residual neuromuscular blockade should be considered in any patient who received neuromuscular blocking drugs during anesthesia. Residual neuromuscular blockade may not be evident on arrival in the PACU because the diaphragm recovers from neuromuscular blockade before the pharyngeal muscles do. With an endotracheal tube in place, end-tidal carbon dioxide concentrations and tidal volumes may indicate adequate ventilation while the ability to maintain a patent upper airway and clear upper airway secretions remains compromised. The stimulation associated with tracheal extubation, followed by the activity of patient transfer to the gurney and subsequent encouragement to breathe deeply may keep the airway open during transport to the PACU. Only after the patient is calmly resting in the PACU does upper airway obstruction become evident. Even patients treated with intermediate- and short-acting neuromuscular blocking drugs may manifest residual paralysis in the PACU despite what was deemed clinically adequate pharmacologic reversal in the operating room.

Measurement of the train-of-four (TOF) ratio is a subjective assessment that is often misleading when done by touch or observation alone. A decline in this ratio may not be appreciated until it reaches a value less than 0.4 to 0.5, whereas significant signs and symptoms of clinical weakness persist to a ratio of 0.7. Pharyngeal function is not restored to normal until an adductor pollicis TOF ratio is greater than 0.9.

In the anesthetized patient, a quantitative TOF measurement showing a TOF ratio ≥0.9 is the most reliable indicator of adequate reversal of drug-induced neuromuscular blockade. Qualitative TOF measurement and 5-second sustained tetanus at 50 Hz are insensitive and will not allow detection of fade above an average TOF ratio of 0.31 ± 0.15; 5-second sustained tetanus at 100 Hz is unreliable. In an awake patient, clinical assessment of reversal of neuromuscular blockade is preferred to the application of painful TOF or tetanic stimulation. Clinical evaluation includes grip strength, tongue protrusion, the ability to lift the legs off the bed, and the ability to lift the head off the bed for a full 5 seconds. Of these maneuvers, the 5-second sustained head lift has been considered to be the standard, reflecting not only generalized motor strength but, more importantly, the patient’s ability to maintain and protect the airway. However, studies have shown that the 5-second head lift is remarkably insensitive and should not routinely be used to assess recovery from neuromuscular blockade. The ability to strongly oppose the incisor teeth against a tongue depressor is a more reliable indicator of pharyngeal muscle tone. This maneuver correlates with an average TOF ratio of 0.85 as opposed to 0.60 for the sustained head lift. In a year-long study of 7459 PACU patients who had received general anesthesia, Murphy et al. reported critical respiratory events (CREs) in 61 of them. These events occurred within the first 15 minutes of PACU admission, at which time a TOF ratio was measured. When compared with matched controls, these patients had a significantly lower TOF ratio (0.62 [+0.20]) compared to controls 0.98 [+0.07]). In a recent study, Bulka and associates were able to demonstrate that patients who had received neuromuscular blocking drugs, but did not receive reversal agents, had a 2.26 times higher risk of developing postoperative pneumonia compared to those who did receive reversal agents.

When a PACU patient demonstrates signs and/or symptoms of muscular weakness in the form of respiratory distress and/or agitation, one must suspect that there could be a residual neuromuscular blockade and prompt review of possible etiologic factors is indicated (see Box 80.2 ). Common factors include respiratory acidosis and hypothermia, alone or in combination. Upper airway obstruction as a result of the residual depressant effects of volatile anesthetics or opioids (or both) may result in progressive respiratory acidosis after the patient is admitted to the PACU and external stimulation is minimized. Simple measures such as warming the patient, airway support, and correction of electrolyte abnormalities can facilitate recovery from neuromuscular blockade. The approval of sugammadex in the United States by the FDA in December 2015 may have a major impact on residual paralysis in patients who were paralyzed with aminosteroid neuromuscular blocking drugs (sugammadex does not work with benzylisoquinolinium neuromuscular blocking drugs). While reversal with neostigmine requires a baseline twitch response, and the duration until the patient has a TOF ratio of ≥0.9 is highly variable, sugammadex can be administered at any depth of neuromuscular blockade and most commonly produces full recovery within several minutes after administration. In a recent study, reversal with sugammadex resulted in a return of TOF ratio to greater than 0.9 within 5 minutes in 85% of patients with no twitches on TOF stimulation. It is anticipated that the increased availability and use of sugammadex, as an alternative to neostigmine, will result in a decreased incidence of residual neuromuscular blockade in the PACU.

Laryngospasm

Laryngospasm refers to a sudden spasm of the vocal cords that completely occludes the laryngeal opening via forceful tonic contractions of the laryngeal muscles and descent of the epiglottis over the laryngeal inlet. It typically occurs in the transitional period when the extubated patient is emerging from general anesthesia yet not fully awake. Although laryngospasm is most likely to occur in the operating room at the time of tracheal extubation, patients who arrive in the PACU asleep after general anesthesia are also at risk for laryngospasm upon awakening, which is often triggered by airway irritants, such as secretions or blood. Treatment of laryngospasm involves removal of the stimulus (suctioning of secretions, blood) and the application of a jaw thrust maneuver with CPAP (up to 40 cm water [H ₂ O]) is often sufficient stimulation to break the laryngospasm. However, if jaw thrust maneuver and CPAP fail, then immediate skeletal muscle relaxation can be achieved with succinylcholine (0.1-1.0 mg/kg intravenously [IV] or 4 mg/kg intramuscularly [IM]). If these maneuvers fail, one should proceed with a full dose of an induction agent and intubating dose of a muscle relaxant to enable the practitioner to perform an emergent tracheal intubation; attempting to pass a tracheal tube forcibly through a glottis that is closed because of laryngospasm is not acceptable.

Edema or Hematoma

Airway edema is a possible surgical complication in patients undergoing prolonged procedures in the prone or Trendelenburg position, procedures involving the airway and neck (including thyroidectomy, carotid endarterectomy, and cervical spine procedures ), as well as those in which the patient receives a large volume resuscitation. Although facial and scleral edema is an important physical sign that can alert the clinician to the presence of airway edema, visible external signs may not accompany significant edema of pharyngeal tissue (see also Chapter 44 ). Patients who have had a difficult intraoperative intubation and/or airway instrumentation may also have increased airway edema from direct injury. If tracheal extubation is to be attempted in these patients in the PACU, then evaluation of airway patency must precede removal of the endotracheal tube. The patient’s ability to breathe around the endotracheal tube can be evaluated by suctioning the oral pharynx and deflating the endotracheal tube cuff. With occlusion of the proximal end of the endotracheal tube, the patient is then asked to breathe around the tube. Good air movement suggests that the patient’s airway will remain patent after tracheal extubation. An alternative method involves measuring the intrathoracic pressure required to produce a leak around the endotracheal tube with the cuff deflated. This method was originally used to evaluate pediatric patients with croup before extubation. When used in patients with general oropharyngeal edema, the safe pressure threshold can be difficult to identify. Lastly, when ventilating patients in the volume control mode, one can measure the exhaled tidal volume before and after cuff deflation. Patients who require reintubation generally have a smaller leak (i.e., less percentage difference between exhaled volume before and after cuff deflation) than those who do not. A difference greater than 15.5% is the advocated cutoff value for extubation of the trachea. The presence of a cuff leak demonstrates the likelihood of successful extubation, not a guarantee, just as a failed cuff leak does not rule out a successful extubation. The cuff leak test does not and should never take the place of sound clinical judgment, as it is neither sensitive nor specific; it may be used as an adjunct to aid in providing another layer of guidance.

In order to facilitate the reduction of airway edema, one may sit the patient upright to ensure adequate venous drainage, and consider administering a diuretic and intravenous dexamethasone (4-8 mg every 6 hours for 24 hours), which may help decrease airway swelling.

External airway compression is most often caused by hematomas following thyroid, parathyroid, or carotid surgical procedures. Patients may complain of pain and/or pressure, dysphagia, and can demonstrate signs of respiratory distress as the pressure from the expanding hematoma within the tissue can disrupt both venous and lymphatic drainage, both of which can further exacerbate airway swelling. Mask ventilation may not be possible in a patient with severe upper airway obstruction resulting from edema or hematoma. In the case of a hematoma, an attempt can be made to decompress the airway by releasing the clips or sutures on the wound and evacuating the hematoma. This maneuver is recommended as a temporizing measure, but it will not effectively decompress the airway if a significant amount of fluid or blood (or both) has infiltrated the tissue planes of the pharyngeal wall. If emergency tracheal intubation is required, then ready access to difficult airway equipment and surgical backup to perform an emergency tracheostomy are crucial, as one should assume increased difficulty secondary to laryngeal and airway edema, possible tracheal deviation, and a compressed tracheal lumen. If the patient is able to move adequate air via spontaneous ventilation, then an awake technique is often preferred as visualization of the cords by direct laryngoscopy may not be possible.

Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) syndrome is an often overlooked cause of airway obstruction in the PACU, given that most patients are actually not obese and the vast majority of patients are undiagnosed at the time of surgery.

It is well known that patients with OSA are at an increased risk of suffering from cardiopulmonary complications as compared to the general population not affected by OSA syndrome. Patients with OSA are particularly prone to airway obstruction and should not be extubated until they are fully awake and following commands. Any redundant compliant pharyngeal tissue in these patients not only increases the incidence of airway obstruction, but can also increase the difficulty of intubation by direct laryngoscopy. Once in the PACU, a patient with OSA whose trachea has been extubated is exquisitely sensitive to opioids and, when possible, continuous regional anesthesia techniques should be used to provide postoperative analgesia. Other opioid-sparing techniques should be utilized, such as scheduled acetaminophen, and use of nonsteroidal antiinflammatory drugs (NSAIDs) when not contraindicated. One may also employ the use of ketamine, dexmedetomidine, and clonidine, all of which can also decrease postoperative opioid requirements. Interestingly, benzodiazepines can have a greater effect on pharyngeal muscle tone than opioids, and the use of benzodiazepines in the perioperative setting can significantly contribute to airway obstruction in the PACU.

Another strategy to employ when caring for a patient with OSA is to position them in either an upright (seated, reverse Trendelenburg) or semi-upright position whenever possible, as the supine position is known to worsen OSA.

In addition, the use of goal-directed fluid strategies should be utilized with consideration of lower salt-containing substances, as these patients are more prone to fluid shifts, which can worsen airway edema.

When caring for a patient with OSA, plans should be made preoperatively to provide CPAP in the immediate postoperative period. Patients should be asked to bring their own CPAP machines with them on the day of surgery to enable the equipment to be set up before the patient’s arrival in the PACU. Patients who do not routinely use CPAP at home or who do not have their machines with them may require additional attention from the respiratory therapist to ensure proper fit of the CPAP delivery device (mask or nasal airways) and to determine the amount of positive pressure needed to prevent upper airway obstruction.

In patients with OSA who are morbidly obese, immediately applying CPAP postextubation in the operating room rather than waiting to apply positive pressure in the PACU may offer additional benefits. In patients undergoing laparoscopic bariatric surgery, Neligan and colleagues compared the application of 10 cm H ₂ O CPAP immediately postextubation to instituting the same CPAP 30 minutes later in the PACU. When compared with matched controls, patients who received immediate CPAP demonstrated improved spirometric lung function (i.e., functional residual capacity [FRC], peak expiratory flow [PEF], and forced expiratory volume [FEV]) at 1 hour and 24 hours postoperatively.

Two large cohort studies demonstrated that patients with OSA who are not treated with positive airway pressure (PAP) preoperatively are at increased risk for cardiopulmonary complications after general and vascular surgery and that PAP therapy was associated with a reduction in postoperative cardiovascular complications. If the patient can tolerate PAP, and their surgical procedure is not a contraindication to its application, patients with OSA should use a PAP device postoperatively.

Alveolar Hypoventilation

Review of the alveolar gas equation demonstrates that hypoventilation alone is sufficient to cause arterial hypoxemia in a patient breathing room air ( Fig. 80.2 ). At sea level, a normocapnic patient breathing room air will have an alveolar oxygen pressure (PAO ₂ ) of 100 mm Hg. Thus, a healthy patient without a significant alveolar-arterial gradient will have a Pao ₂ near 100 mm Hg. In the same patient, an increase in Paco ₂ from 40 to 80 mm Hg (alveolar hypoventilation) results in a Pao ₂ of 50 mm Hg. Hence, even a patient with normal lungs will become hypoxic if allowed to significantly hypoventilate while breathing room air.

Hypoventilation as a cause of arterial hypoxemia.

From Nicholau D. Postanesthesia recovery. In: Miller RD, Pardo MC Jr, eds. Basics of Anesthesia. 7th ed. Philadelphia: Elsevier; 2018.

Normally, minute ventilation increases linearly by approximately 2 L/min for every 1-mm Hg increase in Paco ₂ . In the immediate postoperative period, the residual effects of inhaled anesthetics, opioids, and sedative-hypnotics can significantly depress this ventilatory response to carbon dioxide. In addition to depressed respiratory drive, the differential diagnosis of postoperative hypoventilation includes generalized weakness due to residual neuromuscular blockade or underlying neuromuscular disease. The presence of restrictive pulmonary conditions, such as preexisting chest wall deformity, postoperative abdominal binding, or abdominal distention, can also contribute to inadequate ventilation.

Arterial hypoxemia secondary to hypercapnia can be reversed by the administration of supplemental oxygen ( Fig. 80.3 ) or by normalizing the patient’s Paco ₂ by external stimulation of the patient to wakefulness, pharmacologic reversal of opioid or benzodiazepine effect, or controlled mechanical ventilation of the patient’s lungs.

Alveolar partial pressure of carbon dioxide (Pco ₂ ) as a function of alveolar ventilation at rest. The percentages indicate the inspired oxygen concentration required to restore alveolar partial pressure of oxygen (Po ₂ ) to normal.

Adapted from Nunn JF. Nunn’s Applied Respiratory Physiology. 6th ed. Philadelphia: Butterworth-Heinemann; 2005, with permission.

Decreased Alveolar Oxygen Pressure

Diffusion hypoxia refers to the rapid diffusion of nitrous oxide into alveoli at the end of a nitrous oxide anesthetic. Nitrous oxide dilutes the alveolar gas and produces a transient decrease in Pao ₂ and Paco ₂ . In a patient breathing room air, the resulting decrease in Pao ₂ can produce arterial hypoxemia while decreased Paco ₂ can depress the respiratory drive. In the absence of supplemental oxygen administration, diffusion hypoxia can persist for 5 to 10 minutes after discontinuation of a nitrous oxide anesthetic; therefore, it may contribute to arterial hypoxemia in the initial moments in the PACU.

Ventilation-Perfusion Mismatch and Shunt

Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion. This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood flow to well-ventilated alveoli. In the PACU, the residual effects of inhaled anesthetics and vasodilators such as nitroprusside and dobutamine used to treat systemic hypertension or improve hemodynamics will blunt hypoxic pulmonary vasoconstriction and contribute to arterial hypoxemia.

Unlike a mismatch, a true shunt will not respond to supplemental oxygen. Causes of postoperative pulmonary shunt include atelectasis, pulmonary edema, gastric aspiration, pulmonary emboli, and pneumonia. Of these, atelectasis is probably the most common cause of pulmonary shunting in the immediate postoperative period. Mobilization of the patient to the sitting position, incentive spirometry, and PAP by facemask can be effective in treating atelectasis.

Increased Venous Admixture

Increased venous admixture typically refers to low cardiac output states. It is due to the mixing of desaturated venous blood with oxygenated arterial blood. Normally, only 2% to 5% of cardiac output is shunted through the lungs, and this shunted blood with a normal mixed venous saturation has a minimal effect on Pao ₂ . In low cardiac output states, blood returns to the heart severely desaturated. Additionally, the shunt fraction increases significantly in conditions that impede alveolar oxygenation, such as pulmonary edema and atelectasis. Under these conditions, mixing of desaturated shunted blood with saturated arterialized blood decreases Pao ₂ .

Decreased Diffusion Capacity

A decreased diffusion capacity may reflect the presence of underlying lung disease such as emphysema, interstitial lung disease, pulmonary fibrosis, or primary pulmonary hypertension. In this regard, the differential diagnosis of arterial hypoxemia in the PACU must include the contribution of any preexisting pulmonary condition.

Finally, keep in mind that inadequate oxygen delivery may result from an unrecognized disconnection of the oxygen source or empty oxygen tank.

Postobstructive Pulmonary Edema

Postobstructive pulmonary edema (also referred to as negative pressure pulmonary edema, NPPE) is a rare, but significant consequence of laryngospasm and other upper airway obstruction that may follow tracheal extubation at the conclusion of anesthesia and surgery. Laryngospasm is likely the most common cause of postobstructive pulmonary edema in the PACU, but postobstructive pulmonary edema may result from any condition that occludes the upper airway. The etiology of NPPE is multifactorial, but is clearly correlated with the generation of exaggerated negative intrathoracic pressure attributable to forced inspiration against a closed glottis. The resulting negative intrathoracic pressure augments blood flow to the right side of the heart, which in turn dilates and increases hydrostatic pressure gradient across the pulmonary vascular bed, promoting the movement of fluid into the interstitial and alveolar spaces from the pulmonary capillaries. Negative inspiratory pressure will also increase left ventricular afterload, thus decreasing the ejection fraction, which heightens left ventricular end diastolic pressure, left atrial pressure, and pulmonary venous pressure. This chain of events further escalates the development of pulmonary edema via increase of pulmonary hydrostatic pressures. Patients who are muscularly healthy are at increased risk of postobstructive pulmonary edema secondary to their ability to generate significant inspiratory force.

The resulting arterial hypoxemia develops relatively quickly (usually observed within 90 minutes of the upper airway obstruction), and is accompanied by dyspnea, pink frothy sputum, and bilateral fluffy infiltrates on the chest radiograph. Treatment is generally supportive and includes supplemental oxygen, diuresis, and, in severe cases, initiation of positive-pressure ventilation. The general consensus of postoperative monitoring in these patients ranges anywhere from 2 to 12 hours. Resolution of NPPE typically occurs within 12 to 48 hours when recognized and treated immediately; however, if diagnosis and resulting therapy is delayed, mortality rates can reach 40%. Although it is quite uncommon, pulmonary hemorrhage and hemoptysis have been observed.

Transfusion-Related Acute Lung Injury

The differential diagnosis of pulmonary edema in the PACU should include transfusion-related lung injury in any patient who intraoperatively received blood products. Transfusion-related lung injury is typically exhibited within 2 to 4 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets. TRALI occurs when recipient neutrophils become activated by constituents of the donor blood products. These neutrophils then release inflammatory mediators which initiate the cascade of pulmonary edema and resulting lung injury via increasing the permeability of the pulmonary vasculature. Given that presenting symptoms (sudden onset of hypoxemic respiratory failure) can appear up to 6 hours after the conclusion of the transfusion, the syndrome may develop during the patient’s stay in the PACU. The resulting noncardiogenic pulmonary edema is often associated with fever, pulmonary infiltrates on chest radiograph (without signs of left heart failure), cyanosis, and systemic hypotension. If a complete blood cell count is obtained with the onset of symptoms, then documenting an acute drop in the white blood cell count (leukopenia) is possible, reflecting the sequestration of granulocytes within the lung and exudative fluid.

Treatment is supportive and includes supplemental oxygen and diuresis. It is estimated that up to 80% of patients will recover within 48 to 96 hours. Mechanical ventilation may be needed to support hypoxemia and respiratory failure. Vasopressors may be required to treat refractory hypotension.

In past years, the lack of specific diagnostic criteria has resulted in the underdiagnosing and underreporting of this syndrome. Recently, a group of transfusion experts in the American-European Consensus Conference developed and implemented diagnostic criteria that have raised the awareness of the syndrome ( Box 80.4 ).

Transfusion-Associated Circulatory Overload (Taco)

TACO may be difficult to distinguish from TRALI, however TACO should be highly considered in patients who have diminished cardiac function at baseline, renal insufficiency, and in surgical procedures where there is both rapid and large-volume fluid and blood product administration. Patients with TACO are essentially unable to manage the rate and/or volume of product received secondary to their underlying comorbidities, and tend to develop symptoms of respiratory distress, hypoxemia, and signs of left and/or right heart failure within 2 to 6 hours of the transfusion. TACO is commonly associated with physical manifestations of fluid overload and these patients frequently are hypertensive during the onset of dyspnea. The chest radiograph may demonstrate findings of preexisting cardiac disease and a possible cardiogenic component, such as cardiomegaly and pleural effusions. Elevated levels of BNP are suggestive of TACO. TACO and TRALI may indeed coexist. Treatment is mainly supportive and should focus on treatment of supplemental oxygen for hypoxemia and diuresis for acute volume overload. Positive pressure ventilation can be employed as well.

Oxygen Supplementation

In the era of cost containment, it has been suggested that the routine delivery of supplemental oxygen to all patients recovering from general anesthesia is a costly and unnecessary practice. The argument against the use of routine oxygen supplementation relies on the fact that continuous pulse oximetry, now a PACU standard, readily identifies those patients who will require oxygen therapy. Supporting this argument is the observation that after general anesthesia a majority of patients do not become hypoxic (63% at threshold of Sao ₂ <90%, and 83% at threshold of Sao ₂ <94%) when breathing room air in the PACU. Although the authors of this observational study predict that the elimination of routine oxygen supplementation in the PACU would result in significant cost savings, others assert that the economic benefit of limited oxygen therapy is likely to be offset by the cost of complications.

Although the practice of providing prophylactic oxygen therapy to all patients after general anesthesia is controversial, most would argue that the benefits outweigh the risks. Even with oxygen supplementation, a significant percentage of patients will become hypoxic at some point during their PACU stay. Russell and associates studied 100 patients who were transferred to the PACU breathing room air before receiving at least 40% oxygen by aerosol face tent in the unit. All patients had an Sao ₂ greater than 97% before the 2-minute transport to the PACU. Fifteen percent of patients experienced transient desaturation on arrival in the PACU (<92% saturation for >30 seconds). This immediate desaturation correlated positively with patient age, body weight, ASA classification, general anesthesia, and increased volume of intravenous fluid greater than 1500 mL. An even larger percentage of patients (25%) desaturated 30 to 50 minutes later in their PACU stay despite prophylactic oxygen administration. These later desaturations were more severe (71%-91%) and lasted longer (5.8 ± 12.6 minutes) than those that occurred on admission. Additional correlating factors included duration of anesthesia and female gender.

The safe practice of postanesthesia care without oxygen supplementation requires ideal conditions at all times; that is, functioning oxygen delivery apparatus at every bedside as well as sufficient manpower for observation and immediate intervention. Gravenstein argues that this degree of vigilance is likely unrealistic and the risk of adverse outcome to even a small number of patients is unwarranted.

Limitations of Pulse Oximetry

The ASA Standards for Postanesthesia Care require that patients be observed and monitored with “particular attention given to” both oxygenation and ventilation. The pulse oximeter is a standard monitor in the PACU for the detection of hypoxemia, but it does not reflect the adequacy of ventilation. Although several studies have demonstrated oximetry’s limited ability to detect hypoventilation in patients breathing room air, they confirm that it does not reliably detect hypoventilation in patients breathing oxygen. When monitoring ventilation in the PACU, pulse oximetry is not a substitute for close observation by trained personnel.

Supplemental Oxygen

The degree of hypoxemia, the surgical procedure, and patient compliance determine the oxygen delivery system of choice in the PACU. Regardless of the delivery system, oxygen should be humidified in order to prevent the subsequent dehydration of the nasal and/or oral mucosa. Patients who have just undergone head and neck surgery may not be candidates for facemask oxygen because of the risk of pressure necrosis on incision sites and microvascular muscle flaps, whereas nasal packing prohibits the use of nasal cannulas in others. Face tent oxygen or blow-by setups are viable alternatives in cases in which tight-fitting masks and straps are contraindicated. In an elderly patient, or one who is at an increased risk of delirium, nasal cannula may be selected over a facemask, as long as their oxygenation saturation levels are adequate.

Simple facemasks are generally used in the postoperative setting in patients who are breathing spontaneously yet require a higher oxygen flow rate and/or concentration in order for them to maintain their oxygenation saturation. The practitioner should ensure the proper size, as the mask should fit comfortably over the patient’s nose and mouth. Oxygen flow rates should be at least 5 L/min in order to preclude rebreathing of CO ₂ . Nonrebreather masks have traditionally been known to deliver the highest concentration (up to 95%) in spontaneously breathing patients.

The delivery of oxygen through a traditional nasal cannula with bubble humidifier is usually limited to a maximum flow of 6 L/min to minimize the discomfort and complications that result from inadequate humidification. As a general rule, each liter per minute of oxygen flow through nasal cannula increases the FiO ₂ by 0.04, with 6 L/min delivering an FiO ₂ of approximately 0.44.

Until recently, maximum oxygen delivery to extubated patients required delivery by facemask through a nonrebreather system or high-flow nebulizer. These systems can be inefficient, however, because of inadequate mask fit and/or high-minute ventilation requirements that result in significant entrainment of room air. The newer high-flow nasal cannula (HFNC) devices can comfortably deliver oxygen at 40 L/min, 37°C, and 99.9% relative humidity. The delivery of high-flow oxygen directly to the nasopharynx produces an FiO ₂ equal to that delivered by traditional mask devices. HFNC is an appropriate alternative in patients with hypoxemic respiratory failure without hypercapnia. In fact, the Vapotherm system has been shown to deliver a higher FiO ₂ than a nonrebreather mask at similar flow ranges (10-40 L/min). Unlike the nonrebreather mask, these devices deliver high-flow oxygen directly to the nasopharynx throughout the respiratory cycle. The efficacy of these devices may be enhanced by a CPAP effect resulting from the high gas flow.

In a recent meta-analysis by Zhao et al., it was concluded that HFNC, when compared to conventional oxygen therapy systems, reduced the need for mechanical ventilation ; however outcomes were similar when compared to noninvasive ventilation.

Continuous Positive Airway Pressure

An estimated 8% to 10% of patients who undergo abdominal surgery subsequently require intubation and mechanical ventilation in the PACU. As discussed earlier in this chapter, respiratory failure in the immediate postoperative period is often due to transient and rapidly reversible conditions such as splinting from pain, diaphragmatic dysfunction, muscular weakness, and pharmacologically depressed respiratory drive. Readily reversible hypoxemia may be due to hypoventilation, atelectasis, or volume overload. The application of CPAP in this setting can potentially decrease hypoxemia as a result of atelectasis by recruiting alveoli. The resulting increase in functional reserve capacity may also improve pulmonary compliance and decrease the work of breathing.

A large percentage of patients who are obese and undergoing Roux-en-Y gastric bypass surgery have OSA and stand to benefit significantly from postoperative CPAP therapy. Yet surgeons were initially hesitant to embrace this modality for fear that applying positive pressure to the airway would inflate the stomach and proximal intestine and result in anastomotic disruption. In a single-center study of 1067 patients undergoing gastro-jejunostomy bypass and 420 diagnosed with OSA, CPAP did not increase the risk of postoperative anastomotic leaks.

Noninvasive Positive-Pressure Ventilation

Even with the application of CPAP in the PACU, a number of patients will require additional ventilatory support. Noninvasive positive-pressure ventilation (NIPPV) has been shown to be an effective alternative to endotracheal intubation in the intensive care unit (ICU) setting. Although the use of NIPPV in both chronic and acute respiratory failure is well established, its application in the PACU is limited.

In the past, the use of NIPPV was avoided in the immediate postoperative period because of the potential for gastric distention, aspiration, and wound dehiscence. These potential complications were especially true in patients who had undergone esophageal or gastric surgery. Careful consideration of both the patient and the surgical factors must guide the decision to use noninvasive modes of ventilation in the PACU. Relative contraindications include hemodynamic instability or life-threatening arrhythmias, altered mental status, high risk of aspiration, inability to use nasal or facial mask (head and neck procedures), and refractory hypoxemia.

NIPPV can be delivered by facemask using the pressure support mode of a mechanical ventilator. Alternatively, the use of a biphasic PAP machine allows the delivery of positive pressure by either nasal cannula or facemask. An example protocol for instituting NIPPV in patients with acute respiratory failure is shown in Box 80.5 .

NIPPV should be considered postoperatively in patients with OSA, COPD, and cardiogenic pulmonary edema. Utilization of PPV postextubation in the immediate postoperative periods may aid in the prevention of atelectasis as well as ensuing respiratory failure. There have been several studies that investigated the prophylactic use of NIPPV in the bariatric, general, thoracic, and vascular surgical populations. Despite the fact that there is lack of data demonstrating succinct results and large RCTs, NIPPV has shown to be beneficial in distinctive patient populations.

Patients who are able to cooperate and tolerate PPV, as well as those with an intact mental status, moderate hypercarbia and academia (PaCO ₂ 45-92, pH 7.1-7.35), and physiologic improvement within 2 hours are often associated with higher rates of success with NIPPV. Relative contraindications to PPV include copious secretions, lack of an intact mental status, cardiac or respiratory arrest, and those who are considered to be high aspiration risks or are unable to protect their airway.

Systemic Hypertension

Patients with a history of essential hypertension are at greatest risk for significant systemic hypertension in the PACU, especially if they did not take their morning antihypertensive medications. Additional factors include pain (which is usually associated with tachycardia +/− tachypnea), nausea and vomiting, hypoventilation and associated hypercapnia, hypoxia, emergence excitement, anxiety, agitation, advanced age, urinary retention (secondary to large intraoperative administration of IV fluids), and preexisting renal disease ( Box 80.6 ). One must also not forget the possibility of alcohol withdrawal (which can occur as early as 24 hours after the patient’s last alcohol consumption). Drug withdrawal must also be considered as a possibility; this can be secondary to β-blocker withdrawal, or opioid or benzodiazepine withdrawal as well. Recent use/abuse of certain recreational drugs, such as cocaine, methamphetamines, or LSD/PCP can all produce exaggerated sympathetic states and patients under the influence of these will present with tachycardia and hypertension.

The surgical procedures most commonly associated with postoperative hypertension are carotid endarterectomy and intracranial procedures. A significant number of patients, especially those with a known history of hypertension, will require pharmacologic blood pressure control in the PACU.

Systemic Hypotension

Postoperative systemic hypotension may be characterized as (1) hypovolemic (decreased preload), (2) distributive (decreased afterload), (3) cardiogenic (intrinsic pump failure), and/or (4) extracardiac/obstructive. ( Box 80.7 ).

Regardless of the type of shock the patient is in postoperatively, the underlying cause must be identified and treated. Fluids, blood products, and vasopressors can be used as needed to restore intravascular volume and support adequate perfusion while the patient is being assessed or undergoing a subsequent therapeutic procedure.

Evaluation

Patients who complain of chest pain in the recovery room should have a 12-lead ECG performed and a troponin level drawn. A physical exam and further workup, as indicated, should be done in order to rule out other causes for chest pain (e.g., pulmonary embolus, aortic dissection, tension pneumothorax, cardiac tamponade, esophageal rupture, etc.). ECG changes, such as ST-segment changes, may not necessarily represent myocardial ischemia (especially in younger patients with no known cardiac disease and no cardiac risk factors), however, should associated signs and symptoms point toward cardiac ischemia, further workup is certainly warranted.

Presently, myocardial ischemia after non-cardiac surgery (MINS) has been established as an entity in itself. MINS is defined as elevated postoperative troponin levels without any clinical symptoms or any changes in the ECG, provided there is no other nonischemic cause for the elevated troponin level (e.g., chronic troponin elevation, pulmonary embolism, sepsis, rapid atrial fibrillation). Elevated troponin levels are independently associated with poor outcomes. An international prospective cohort study found that postoperative elevated troponin after noncardiac surgery was a strong independent predictor of 30-day mortality.

The most recent guidelines established by the American Heart Association/American College of Cardiology (AHA/ACC) recommend obtaining a troponin level for all patients who present with ECG changes suggestive of ischemia or exhibit typical ischemic chest pain after surgery. Furthermore, they recommend drawing serial troponin levels for stable patients after vascular or intermediate risk surgery. A recent multicenter study investigated the association between postoperative high-sensitivity troponin (hsTnT) levels with myocardial injury and 30-day mortality after noncardiac surgery. The authors confirmed that postoperative myocardial injury is most commonly silent, as 93% of patients with MINS did not experience any symptoms. Furthermore, they found that elevated hsTnT levels without an ischemic feature in the first 3 days after noncardiac surgery were associated with a significantly increased 30-day mortality. These newer studies may even warrant a more liberal approach to drawing postoperative hsTnT levels in the PACU.

Treatment

Once the diagnosis of myocardial ischemia/injury has been made, the primary surgical team should immediately be notified and a cardiology consult should be obtained.

After ruling out other life-threatening causes, the patients should receive oxygen, and blood pressure and heart rate should be controlled. If there are no absolute contraindications to their administration, the patient should be given nitroglycerin, a β blocker, a statin, and aspirin. Pain and anxiety should be treated with an opioid and a benzodiazepine, and anemia should be corrected, if present. One should be prepared for further decompensation of the patient and have a code cart readily available. Should the patient become hemodynamically unstable, echocardiography may help in guiding next steps (e.g., placing an IABP, emergent interventions).

Depending on the acuity of the situation, further interventions like fibrinolysis, percutaneous coronary intervention (PCI), or revascularization should be considered and discussed. However, since these patients just had surgery, there are conflicting goals in terms of postoperative bleeding versus coronary blood flow. A mutual approach between surgeon, cardiologist, anesthesiologist, and patient should be chosen to determine the best course of action.

Tachycardia

Common causes of tachycardia in the PACU include pain, agitation, hypoventilation with associated hypoxia and hypercapnia, hypovolemia, PONV, and shivering. Less common but serious causes include hemorrhage; cardiogenic, septic, or anaphylactic shock; pulmonary embolism; pneumothorax; thyroid storm; and malignant hyperthermia.

When evaluating postoperative tachycardia, the most important question is whether or not the patient is hemodynamically stable. If the patient is stable, oxygen should be administered, a 12-lead ECG obtained, and the underlying rhythm determined. Unstable patients typically present with a heart rate greater than 150 bpm, are hypotensive, and may exhibit other signs of decreased perfusion, for example, altered mental status, chest pain, or shock. These patients should undergo immediate synchronized cardioversion. There are various different causes of tachyarrhythmia in the PACU which warrant individualized approaches regarding the medications to administer and the energy doses to use for cardioversion. A comprehensive overview can be found in the American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care 2015.

Bradycardia

Bradycardia in the PACU is often iatrogenic. Drug-related causes include β-blocker therapy, anticholinesterase reversal of neuromuscular blockade, opioid administration, and treatment with clonidine or dexmedetomidine. Procedure- and patient-related causes include bowel distention, increased intracranial or intraocular pressure, hypoxia, hypothermia, hypothyroidism, and spinal anesthesia. A high spinal block can impede the cardioaccelerator fibers originating from T1 through T4, resulting in severe bradycardia. The ensuing sympathectomy and possible intravascular fluid volume depletion along with decreased venous return can produce sudden bradycardia and cardiac arrest, even in young healthy patients.

When evaluating postoperative bradycardia, vital signs and hemodynamic stability should be immediately assessed. Underlying causes should be corrected, if possible. Asymptomatic bradycardia may not need to be treated at all, however, if the patient is unstable and hypotensive, or shows signs of shock, altered mental status, ischemic chest discomfort, or acute heart failure, urgent intervention is indicated. According to the ACLS guidelines, first-line treatment is atropine IV. If this is ineffective, transcutaneous pacing or initiation of a vasopressor (dopamine, epinephrine infusion) is indicated. Eventually, expert consultation and transvenous pacing should be considered.

Atrial Arrhythmias

The most common atrial arrhythmia is atrial fibrillation, which affects approximately 4% of patients following major noncardiac surgery. The overall incidence of new postoperative atrial arrhythmias may be as high as 10% in this patient population. The incidence is even higher after cardiac and thoracic procedures when the cardiac arrhythmia is often attributed to atrial irritation. The risk of postoperative atrial fibrillation is increased by preexisting cardiac risk factors, positive fluid balance, electrolyte abnormalities, and oxygen desaturation. These new-onset atrial arrhythmias are not benign as they are associated with a longer hospital stay and increased mortality.

Control of the ventricular response rate is the immediate goal in the treatment of new-onset atrial fibrillation. Hemodynamically unstable patients may require prompt electrical cardioversion, but most patients can be treated pharmacologically with an intravenous β-adrenergic blocker or calcium channel blocker. If hemodynamic instability is a concern, the short-acting β-blocker esmolol can be considered. Rate control with these agents is often enough to chemically cardiovert the postoperative patient whose arrhythmia may be catecholamine driven. If the goal of therapy is chemical cardioversion, an amiodarone load can be initiated in the PACU with the knowledge that QT prolongation, bradycardia, and hypotension may accompany the intravenous infusion of this drug.

Ventricular Arrhythmias

Premature ventricular contractions (PVCs) and ventricular bigeminy commonly occur in the PACU. PVCs most often reflect increased sympathetic nervous system stimulation that may accompany tracheal intubation, pain, and transient hypercapnia. They commonly resolve on their own, but this can be facilitated by administering analgesics and ensuring proper ventilation. True ventricular tachycardia is rare and is indicative of underlying cardiac pathology. In the case of torsades de pointes (polymorphic ventricular tachycardia), underlying QT prolongation on the ECG may be intrinsic or drug related. The most commonly administered QT prolonging drugs in PACU are 5-HT3 receptor antagonists (e.g., ondansetron, dolasetron), haloperidol, droperidol, albuterol, methadone, and amiodarone. Treatment with 1 to 2 g of magnesium IV over 5 minutes should be initiated and potentially repeated, if necessary.

Treatment

Early postoperative arrhythmias often require immediate electrolyte correction as well as pharmacologic and nonpharmacologic interventions. In general, the urgency of treatment of a cardiac arrhythmia depends on the physiologic consequences of the arrhythmia, basically hypotension, cardiac ischemia, or both. Tachyarrhythmias decrease coronary perfusion time and increase myocardial oxygen consumption. Their impact depends on the patient’s underlying cardiac function, and they are most harmful in patients with coronary artery disease. Bradycardia has a more deleterious effect in patients with a fixed stroke volume, such as infants and patients with restrictive pericardial disease or cardiac tamponade. For the most part, treatment relies on identifying and correcting the underlying cause (i.e., hypoxemia or electrolyte abnormalities). The possible role of myocardial ischemia or the occurrence of pulmonary embolism must be considered when contemplating treatment options.