Postanesthesia Recovery

The postanesthesia care unit (PACU), sometimes referred to as the recovery room, is designed and staffed to monitor and care for patients who are recovering from the immediate physiologic effects of anesthesia and surgery. PACU care spans the transition from delivery of anesthesia in the operating room to the less acute monitoring on the hospital ward and, in some cases, independent function of the patient at home. Also, PACUs provide critical care to patients for whom there is no intensive care unit bed in busy medical centers. To serve this unique transition period, the PACU must be equipped to monitor and resuscitate unstable patients while simultaneously providing a tranquil environment for the “recovery” and comfort of stable patients. The proximity of the unit to the operating room facilitates rapid access to postoperative patients by anesthesia providers and surgical caregivers.

Admission to the Postanesthesia Care Unit

Upon arrival in the unit, the anesthesia provider should inform the PACU nurse of pertinent details on the patient’s history, medical condition, anesthesia, and surgery. Particular attention is directed to monitoring oxygenation (pulse oximetry), ventilation (breathing frequency, airway patency, capnography), and circulation (systemic arterial blood pressure, heart rate, electrocardiogram [ECG]).

Vital signs are recorded as often as necessary but at least every 15 minutes while the patient is in the unit. The American Society of Anesthesiologists (ASA) has adopted Standards for Postanesthesia Care that delineate the minimal requirements for PACU monitoring and care. More specific recommendations addressing clinical evaluation and therapeutic intervention can be found in the ASA Practice Guidelines for Postanesthesia Care.

Early Postoperative Physiologic Disorders

A variety of physiologic disorders affecting multiple organ systems must be diagnosed and treated in the PACU during emergence from anesthesia and surgery ( Box 39.1 ). Nausea and vomiting, the need for upper airway support, and systemic hypotension are among the most frequently encountered complications. Not surprisingly, serious outcomes may result from airway, respiratory, or cardiovascular compromise. Airway problems and cardiovascular events accounted for the majority (67%) of 419 recovery room incidents reported to the 2002 Australian Incident Monitoring Study (AIMS). In addition, transport of the patient from the operating room to the PACU is also a time when patients are especially vulnerable to airway obstruction, as discussed next.

Box 39.1

Physiologic Disorders Manifested in the Postanesthesia Care Unit

  • Upper airway obstruction

  • Arterial hypoxemia

  • Hypoventilation

  • Hypotension

  • Hypertension

  • Cardiac dysrhythmias

  • Oliguria

  • Bleeding

  • Decreased body temperature

  • Delirium (emergence agitation)

  • Delayed awakening

  • Nausea and vomiting

  • Pain

Upper Airway Obstruction

Loss of Pharyngeal Muscle Tone

Airway obstruction is a common and potentially devastating complication in the postoperative period (also see Chapter 16 ). The most frequent cause of airway obstruction in the PACU is the loss of pharyngeal tone in a sedated or obtunded patient. The residual depressant effects of inhaled and intravenous anesthetics and the persistent effects of neuromuscular blocking drugs (also see Chapter 11 ) contribute to the loss of pharyngeal tone in the immediate postoperative period.

In an awake, unanesthetized patient, the pharyngeal muscles contract synchronously with the diaphragm to pull the tongue forward and tent the airway open against the negative inspiratory pressure generated by the diaphragm. This pharyngeal muscle activity is depressed during sleep, and the resulting decrease in tone promotes airway obstruction. With the collapse of compliant pharyngeal tissue during inspiration, a vicious circle may ensue in which a reflex compensatory increase in respiratory effort and negative inspiratory pressure promotes further airway obstruction. This effort to breathe against an obstructed airway is characterized by a paradoxic breathing pattern consisting of retraction of the sternal notch and exaggerated abdominal muscle activity. Collapse of the chest wall plus 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 face mask (or use of 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 (also see Chapter 16 ).

Residual Neuromuscular Blockade

When evaluating upper airway obstruction in the PACU, the possibility of residual neuromuscular blockade must be considered in any patient who received neuromuscular blocking drugs during anesthesia (also see Chapter 11 ). 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 remain compromised. The stimulation associated with tracheal extubation, followed by the activity of patient transfer to the gurney and subsequent mask airway support, may keep the airway open during transport. 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 (OR).

The association between intermediate-acting neuromuscular blocking drugs and postoperative respiratory complications is dose dependent. Also, inappropriate dosing of the reversal drug neostigmine can cause postoperative respiratory complications. A large prospective study of over 3000 PACU patients showed the unwarranted use or inappropriate dosing of neostigmine to be an independent risk factor for reintubation of the trachea. Therefore, determining the appropriate dose of neostigmine, and specifically avoiding inappropriate dosing or overdosage, is essential to assure full recovery of neuromuscular function in the PACU. Over the years qualitative measurement of the train-of-four (TOF) ratio by tactile response or visualization was the most commonly used method to assess the degree of reversal of neuromuscular blockade at the end of surgery. However, more recent evidence suggests that the qualitative measurement of the TOF ratio may not accurately reflect recovery of neuromuscular function. Instead, the use of quantitative TOF measurement using acceleromyography provides a more objective and accurate method of monitoring neuromuscular function. It is hoped that use of a newly approved reversal drug, sugammadex, will decrease the frequency of inadequate reversal of neuromuscular blockade.

When patients with residual neuromuscular blockade are awake in the PACU, their struggle to breathe may manifest as agitation. 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 is considered the gold standard because it reflects not only generalized motor strength but, more important, the patient’s ability to maintain and protect the airway. In patients whose tracheas have been extubated, the ability to strongly oppose the incisor teeth against a tongue depressor is another reliable indicator of pharyngeal muscle tone in the awake patient. This maneuver correlates with an average TOF ratio of 0.85. Inadequate ventilation or airway obstruction is less likely if the neuromuscular blockade has been reversed with neostigmine or sugammadex (also see Chapter 11 ).

If persistence or return of neuromuscular weakness in the PACU is suspected, prompt review of possible etiologic factors is indicated ( Box 39.2 ). Common factors include respiratory acidosis and hypothermia, alone or in combination. Residual depressant effects of volatile anesthetics or opioids (or both) may result in progressive respiratory acidosis only after the patient is admitted to the PACU and external stimulation is minimized. Similarly, a patient who becomes hypothermic during anesthesia and surgery may show signs of weakness in the PACU that were not noted following extubation in the operating room. Simple measures such as warming the patient, airway support, and correction of electrolyte abnormalities can facilitate recovery from neuromuscular blockade.

Box 39.2

Causes of Prolonged Neuromuscular Blockade

Factors Contributing to Prolonged Nondepolarizing Neuromuscular Blockade

  • Drugs

    • Inhaled anesthetic drugs

    • Local anesthetics (lidocaine)

    • Cardiac antidysrhythmics (procainamide)

    • Antibiotics (polymyxins, aminoglycosides, lincosamines [clindamycin], metronidazole [Flagyl], tetracyclines)

    • Corticosteroids

    • Calcium channel blockers

    • Dantrolene

    • Furosemide

  • Metabolic and physiologic states

    • Hypermagnesemia

    • Hypocalcemia

    • Hypothermia

    • Respiratory acidosis

    • Hepatic/renal failure

    • Myasthenia syndromes

Factors Contributing to Prolonged Depolarizing Neuromuscular Blockade

  • Excessive dose of succinylcholine

  • Reduced plasma cholinesterase activity

    • Decreased levels

    • Extremes of age (newborn, old age)

    • Disease states (hepatic disease, uremia, malnutrition, plasmapheresis)

    • Hormonal changes

    • Pregnancy

    • Contraceptives

    • Glucocorticoids

  • Inhibited activity

    • Irreversible (echothiophate)

    • Reversible (edrophonium, neostigmine, pyridostigmine)

  • Genetic variant (atypical plasma cholinesterase)


Laryngospasm refers to a sudden spasm of the vocal cords that completely occludes the laryngeal opening. It typically occurs in the transitional period when the patient whose trachea has been extubated is emerging from general anesthesia. Although it 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 when awakening.

Jaw thrust with CPAP (up to 40 cm H 2 O) is often sufficient stimulation to “break” the laryngospasm. If jaw thrust and CPAP maneuvers fail, immediate skeletal muscle relaxation can be achieved with intravenously (IV) or intramuscularly (IM) administered succinylcholine (0.1 to 1.0 mg/kg IV or 4 mg/kg IM). A tracheal tube should not be passed forcibly through a glottis that is closed because of laryngospasm.

Airway Edema

Airway edema is a possible postoperative complication in patients undergoing prolonged procedures in the prone or Trendelenburg position and in procedures with large amounts of blood loss requiring aggressive intravascular fluid resuscitation. Surgical procedures on the tongue, pharynx, and neck, including thyroidectomy, carotid endarterectomy, and cervical spinal procedures, can result in upper airway obstruction because of tissue edema or hematoma, or both. Although facial and scleral edema are important physical signs that can alert the clinician to the presence of airway edema, significant edema of pharyngeal tissue is often not accompanied by visible external signs. If tracheal extubation is attempted in these patients in the PACU, evaluation of airway patency must precede removal of the endotracheal tube (ETT). The patient’s ability to breathe around the ETT can be evaluated by suctioning the oral pharynx and deflating the ETT cuff. With occlusion of the proximal end of the ETT, the patient is then asked to breathe around the tube. This qualitative assessment of adequate air movement suggests that the patient’s airway will remain patent after tracheal extubation. More quantitative methods include (1) measuring the intrathoracic pressure required to produce an audible leak around the ETT when the cuff is deflated and (2) measuring the exhaled tidal volume before and after ETT cuff deflation in a patient receiving volume control ventilation. Though helpful, none of these cuff leak “tests” takes the place of sound clinical judgment when deciding when to safely extubate the patient. If concern for airway compromise is significant, a tracheal tube exchange catheter can be used.

Obstructive Sleep Apnea

Special consideration must be given to patients with obstructive sleep apnea (OSA) in the PACU (also see Chapter 27, Chapter 50 ). Patients with OSA have a more frequent risk for postoperative desaturation, respiratory failure, postoperative cardiac events, and the need for intensive care unit transfer. As such, it is important to recognize and diagnose OSA in the preoperative setting and be mindful of its implications in the intraoperative and postoperative settings. Many screening tools such as the STOP-BANG questionnaire are effective in predicting OSA. Because patients with OSA are particularly prone to airway obstruction, their tracheas 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 also makes mask ventilation and intubation by direct laryngoscopy difficult or at times impossible. Once in the PACU, a patient with OSA whose trachea has been extubated is exquisitely sensitive to opioids, and, when possible, regional anesthesia and multimodal analgesia techniques should be used to provide postoperative analgesia and minimize opioid consumption. The combination of benzodiazepines and opioids can cause significant episodes of hypoxemia and apnea in patients with OSA.

For patients with OSA, plans should be made preoperatively to provide CPAP in the immediate postoperative period. Patients are often asked to bring their CPAP machines with them on the day of surgery so that the equipment can 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. For patients with known or suspected OSA, consideration should also be given to postoperative continuous pulse oximetry monitoring.

Management of Airway Obstruction

A patient who has an obstructed upper airway requires immediate attention. Efforts to open the airway by noninvasive measures should be attempted before reintubation of the trachea. Jaw thrust with CPAP (5 to 15 cm H 2 O) is often enough to tent the upper airway open in patients with decreased pharyngeal muscle tone. If CPAP is not effective, an oral, nasal, or laryngeal mask airway can be inserted rapidly. After successfully opening the upper airway and ensuring adequate ventilation, the cause of the upper airway obstruction should be identified and treated. The sedating effects of opioids and benzodiazepines can be reversed with persistent stimulation or small, titrated doses of naloxone or flumazenil, respectively (see Chapter 8 ). Residual effects of neuromuscular blocking drugs can be reversed pharmacologically or by correcting contributing factors such as hypothermia (see Chapter 11 ).

Ventilating the lungs of a patient with severe upper airway obstruction as a result of edema or hematoma may not be possible via a mask. In the case of hematoma after thyroid or carotid surgery, 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, ready access to difficult airway equipment should be arranged and, if possible, surgical backup for performance of an emergency tracheostomy. If the patient is able to move air by spontaneous ventilation, an awake endotracheal intubation technique is preferred because visualization of the cords by direct laryngoscopy may not be possible.

Monitoring Airway Patency During Transport

Upper airway patency and the effectiveness of the patient’s respiratory efforts must be monitored during transportation from the operating room to the PACU. Hypoventilation in a patient receiving supplemental oxygen will not be reliably detected by monitoring with pulse oximetry during transport. Adequate ventilation must be confirmed by watching for the appropriate rise and fall of the chest wall with inspiration, listening for breath sounds, or simply feeling for exhaled breath with the palm of one’s hand over the patient’s nose and mouth. As indicated previously, this can be a critically dangerous time in the immediate postoperative period.

Hypoxemia in the Postanesthesia Care Unit

Atelectasis and alveolar hypoventilation are the most common causes of transient postoperative arterial hypoxemia in the immediate postoperative period. Filling the patient’s lungs with oxygen at the conclusion of anesthesia, as well as the administration of supplemental oxygen, should blunt any effect of diffusion hypoxia as a contributor to arterial hypoxemia. Review of the patient’s history, operative course, and clinical signs and symptoms will direct the workup to determine possible causes of persistent hypoxia ( Box 39.3 ) (also see Chapter 5 ).

Box 39.3

Causes of Postoperative Hypoxemia

  • Right-to-left shunt

    • Pulmonary: atelectasis

    • Intracardiac: congenital heart disease

  • Mismatching of ventilation to perfusion

  • Congestive heart failure

  • Pulmonary edema—fluid overload, postobstructive

  • Alveolar hypoventilation—residual effects of anesthetics and neuromuscular blocking drugs

  • Diffusion hypoxia—unlikely if patient is receiving supplemental oxygen

  • Aspiration of gastric contents

  • Pulmonary embolus

  • Pneumothorax

  • Posthyperventilation hypoxia

  • Increased oxygen consumption (e.g., shivering)

  • Acute respiratory distress syndrome (ARDS)

  • Sepsis

  • Transfusion-related acute lung injury

  • Advanced age

  • Obesity

Alveolar Hypoventilation

Postoperative ventilatory failure can result from a depressed drive to breathe or generalized weakness from either residual neuromuscular blockade or underlying neuromuscular disease. Restrictive pulmonary conditions such as preexisting chest wall deformity, postoperative abdominal binding, or abdominal distention can also contribute to inadequate ventilation ( Box 39.4 ).

Box 39.4

Factors Leading to Postoperative Hypoventilation

  • Drug-induced central nervous system depression (volatile anesthetics, opioids)

  • Residual effects of neuromuscular blocking drugs

  • Suboptimal ventilatory muscle mechanics

  • Increased production of carbon dioxide

  • Coexisting chronic obstructive pulmonary disease

Review of the alveolar gas equation demonstrates that hypoventilation alone is sufficient to cause arterial hypoxemia in a patient breathing room air ( Fig. 39.1 ). At sea level, a normocapnic patient breathing room air will have an alveolar oxygen partial pressure of 100 mm Hg. Thus, a healthy patient without a significant alveolar-arterial (A-a) gradient will have a Pa o 2 near 100 mm Hg. In the same patient, an increase in Pa co 2 from 40 to 80 mm Hg (alveolar hypoventilation) results in an alveolar oxygen partial pressure (P ao 2 ) of 50 mm Hg. This exercise demonstrates that even a patient with normal lungs will become hypoxic if allowed to significantly hypoventilate while breathing room air.

Fig. 39.1

Hypoventilation as a cause of arterial hypoxemia.

Normally, minute ventilation increases by approximately 2 L/min for every 1 mm Hg increase in arterial P co 2 . This linear ventilatory response to carbon dioxide can be significantly depressed in the immediate postoperative period by the residual effects of drugs (e.g., inhaled anesthetics, opioids, sedative-hypnotics) administered during anesthesia.

Arterial hypoxemia secondary to hypercapnia alone can be reversed by the administration of supplemental oxygen or by restoring the Pa co 2 to normal, or both ( Fig. 39.2 ). In the PACU, Pa co 2 can be returned to normal by external stimulation of the patient to wakefulness, pharmacologic reversal of opioid or benzodiazepine effect, or controlled mechanical ventilation. Fig. 39.2 demonstrates why pulse oximetry is an unreliable marker of hypoventilation in a patient receiving supplemental oxygen.

Fig. 39.2

Alveolar P co 2 as a function of alveolar ventilation at rest. The percentages indicate the inspired oxygen concentration required to restore alveolar P o 2 to normal.

Adapted from Lumb AB, ed. Nunn’s Applied Respiratory Physiology . 6th ed. Philadelphia: Elsevier/Butterworth-Heinemann; 2005, used with permission.

Decreased Alveolar Partial Pressure of Oxygen

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 P ao 2 and P aco 2 . In a patient breathing room air, the resulting decrease in P ao 2 can produce arterial hypoxemia. In the absence of supplemental oxygen administration, diffusion hypoxia can persist for 5 to 10 minutes after a nitrous oxide anesthetic and thus contribute to arterial hypoxemia in the initial moments as the patient is admitted to the PACU.

When providing supplemental oxygen to a patient during transport to the PACU, care should be taken to avoid the relative decrease in the fraction of inspired oxygen (F io 2) that can result from an unrecognized disconnection of the oxygen source or from an empty oxygen tank.

Ventilation-to-Perfusion Mismatch and Shunt

Hypoxic pulmonary vasoconstriction (HPV) is an 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. The HPV response is inhibited by many conditions and medications, including pneumonia, sepsis, and vasodilators. In the PACU, the residual effects of inhaled anesthetics and vasodilators such as nitroprusside and dobutamine will blunt HPV and contribute to arterial hypoxemia.

Unlike a ventilation-to-perfusion 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 positive airway pressure via a face mask can be effective in treating atelectasis.

Increased Venous Admixture

Increased venous admixture typically refers to low cardiac output states. It is due to mixing of desaturated venous blood with oxygenated arterial blood. Normally, only 2% to 5% of cardiac output is shunted through the lungs, and this small amount of shunted blood with a normal mixed venous saturation has a minimal effect on Pa o 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 Pa o 2 .

Decreased Diffusion Capacity

A decreased diffusion capacity is caused by underlying lung disease such as emphysema, interstitial lung disease, pulmonary fibrosis, or primary pulmonary hypertension. The differential diagnosis of arterial hypoxemia in the PACU must include the contribution of any preexisting pulmonary condition.

Pulmonary Edema in the Postanesthesia Care Unit

Pulmonary edema in the immediate postoperative period is often cardiogenic in nature, the result of increased intravascular volume or cardiac dysfunction. Noncardiogenic edema may occur in the PACU as a result of pulmonary aspiration of gastric contents or sepsis. Rarely, postoperative pulmonary edema is the result of airway obstruction (postobstructive pulmonary edema) or transfusion of blood products (transfusion-related acute lung injury) (also see Chapter 24 ).

Postobstructive Pulmonary Edema

Postobstructive pulmonary edema (POPE), also referred to as negative-pressure pulmonary edema, and the resulting arterial hypoxemia are rare but significant consequences of upper airway obstruction and may follow tracheal extubation at the conclusion of anesthesia and surgery. POPE is characterized by a transudative edema produced by one of two mechanisms: the exaggerated negative pressure generated by inspiration against acute airway obstruction (type I) or following relief of a chronic partial airway obstruction (type II). The pathophysiology of type I POPE involves exaggerated negative intrathoracic pressure, which increases venous return, afterload, and pulmonary venous pressures, and promotes the transudation of fluid. Muscular healthy patients are at increased risk because of their ability to generate significant inspiratory force.

Laryngospasm is the most common cause of upper airway obstruction leading to type I POPE, but it may result from any condition that occludes the upper airway including epiglottitis, bilateral vocal cord paralysis, goiter, and occlusion of the ETT. Arterial hypoxemia with respiratory distress is usually manifested within 90 minutes after relief of airway obstruction and is frequently accompanied by tachypnea, tachycardia, rales, rhonchi, and evidence of bilateral pulmonary edema on the chest radiograph. The diagnosis depends on clinical suspicion once other causes of pulmonary edema are ruled out. Treatment is supportive and includes supplemental oxygen, diuresis, and, in severe cases, positive-pressure ventilation utilizing CPAP or mechanical ventilation.

Transfusion-Related Acute Lung Injury

The differential diagnosis of pulmonary edema in the PACU should include transfusion-related acute lung injury (TRALI) in any patient who received blood, coagulation factor, or platelet transfusions intraoperatively and is described in Chapter 24 . Treatment is generally supportive and includes supplemental oxygen and diuresis. Rarely, TRALI results in a prolonged course of acute respiratory distress syndrome (ARDS). Historically, the lack of specific diagnostic criteria has led to the underdiagnosis and underreporting of TRALI. In a 2007-2008 study, implementation of TRALI risk mitigation policies that utilized a predominantly male plasma supply indicated a significant reduction in the incidence of TRALI (see Chapter 24 for more details).

Oxygen Supplementation

The delivery of supplemental oxygen in the immediate postoperative period is usually routine for the prevention of possible hypoxemia. Still, the “optimal” perioperative oxygenation procedure remains controversial. Whether increased oxygenation delivery results in a reduction in the incidence of postoperative nausea and vomiting (PONV) and promotion of surgical wound healing is not clear.

Oxygen Delivery

The choice of oxygen delivery systems in the PACU is determined by the degree of hypoxemia, the surgical procedure, and patient compliance. Patients who have undergone head and neck surgery may not be candidates for administration of oxygen via a face mask owing to the risk of pressure necrosis of incision sites and microvascular flaps, whereas nasal packing prohibits the use of nasal cannulas in others.

Delivery of oxygen by traditional nasal cannula should be limited to 6 L/min flow to minimize discomfort and complications that result from inadequate humidification. As a general rule each 1 L/min of oxygen flow through nasal cannula increases F io 2 by 0.04, with 6 L/min resulting in approximately 0.44 F io 2 .

Until recently maximum oxygen delivery to patients whose tracheas have been extubated required a nonrebreather mask or high-flow nebulizer. Delivery of oxygen via mask can be inefficient when mask fit is inadequate or large minute ventilation is required, which results in significant entrainment of room air. Alternatively, oxygen can be delivered up to 40 L/min by high-flow nasal cannulas. These high-flow nasal cannula delivery systems humidify and warm the gas to 99.9% relative humidity and 37° C. Unlike nonrebreather masks, these devices deliver oxygen directly to the nasopharynx throughout the respiratory cycle. The efficacy of these systems may be enhanced by a CPAP effect produced by the high gas flow.

Continuous Positive Airway Pressure and Noninvasive Positive-Pressure Ventilation

Approximately 8% to 10% of patients who undergo abdominal surgery require endotracheal intubation and mechanical ventilation for hypoxemia postoperatively. Application of CPAP in the PACU reduces the incidence of reintubation of the trachea, pneumonia, infection, and sepsis. Even with the application of CPAP in the PACU, many patients will require additional ventilatory support. Ventilatory failure in the immediate postoperative period may result from many conditions including excessive intravascular volume, splinting due to pain, diaphragmatic dysfunction, muscular weakness, and pharmacologically depressed respiratory drive.

Although the use of noninvasive positive-pressure ventilation (NPPV) in both chronic and acute respiratory failure is well established, there is limited experience with its application in the PACU. NPPV can be used in the PACU for patients with increased risk for pulmonary complications and as a rescue technique for patients in postoperative respiratory distress. NPPV is often avoided in the immediate postoperative period because of the potential for gastric distention, aspiration of gastric contents, and wound dehiscence, especially in patients who have undergone gastric or esophageal surgery. Thus, the decision to use noninvasive modes of ventilation in the PACU must be guided by careful consideration of both patient and surgical factors. Contraindications include hemodynamic instability or life-threatening arrhythmias, altered mental status, increased risk of aspiration of gastric contents, inability to use a nasal or face mask (head and neck procedures), and refractory hypoxemia. In the appropriate patient population, particularly for prophylactic use in patients following bariatric surgery and for patients in postoperative respiratory distress, NPPV is effective in avoiding endotracheal intubation in the PACU.

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Oct 21, 2019 | Posted by in ANESTHESIA | Comments Off on Postanesthesia Recovery
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