The goals of general anesthesia are analgesia, amnesia/hypnosis, suppression of autonomic and sensory reflexes, and skeletal muscle relaxation.⁹ Stages of anesthesia, defined by Guedel around World War I, were initially used to identify the patient’s physiologic state and monitor anesthetic depth. These stages are less relevant today due to technologic advances in monitoring and anesthetic agents with faster onset and elimination, limiting the usefulness of the classic signs and symptoms associated with the stages to assessment and care of the patient after surgery.¹⁰

Stage I, commonly called the stage of analgesia, begins with the initiation of an anesthetic agent and ends with the loss of consciousness. This stage has been described as the lightest level of anesthesia and represents mild sensory and mental depression. Patients can open their eyes on command, breathe normally, and maintain protective reflexes. The patient’s pain threshold is not appreciably lowered during this stage.

Stage II, also called the stage of delirium, begins with the loss of consciousness and ends with the onset of a regular pattern of breathing and the disappearance of the eyelid reflex. It is characterized by excitement, which can include uncontrolled movement and potentially dangerous responses to noxious stimuli. Other responses include vomiting, laryngospasm, tachycardia, and even cardiac arrest. If vomiting occurs, the patient is at risk for aspiration because of the loss of protective reflexes that is associated with this stage of anesthesia. With the use of newer and faster-acting anesthetic agents, this stage is passed through rapidly, decreasing the risk of complications. The use of propofol, etomidate, or short-acting barbiturates during the induction of anesthesia also facilitates rapid transition through stage II.

Stage III is the stage of surgical anesthesia. It lasts from the onset of a regular pattern of breathing to the cessation of breathing. This is the goal for anesthesia, because the response to surgical incision is absent. Patients experience a depression in all elements of nervous system function (i.e., sensory depression, loss of recall, reflex depression, and some skeletal muscle relaxation). Each anesthetic agent affects the patient’s clinical signs differently; therefore, monitoring the effects of anesthesia depends on the specific properties of each agent.

Stage IV is considered the stage of overdose and occurs when the patient receives too much anesthesia. In this stage, the patient shows signs of circulatory failure, and full cardiovascular and pulmonary support must be provided.

During general anesthesia, the goal is to keep the patient insensate, immobile, and safe. Recall or awareness during surgery can occur when the depth of anesthesia is inadequate (Box 42-2). Excessive anesthesia may stress the patient and increase emergence and recovery time. The level of anesthesia is monitored by continual assessment of the patient’s clinical presentation. Basic anesthetic monitoring standards adopted by the American Society of Anesthesiologists (ASA) mandate the use of pulse oximetry, capnography, an oxygen analyzer, disconnect alarms, body temperature measurements, and a visual display of an electrocardiogram (ECG) during the intraoperative period in all patients undergoing anesthesia.¹¹ The standard may be exceeded as warranted by the patient’s condition and additional monitors used. External monitoring devices used to assess levels of anesthesia include lower esophageal contractility, heart rate variability, surface electromyogram, spontaneous electroencephalographic activity monitors, and evoked potentials.

Box 42-2

Patient Safety Alert

Preventing and Managing the Impact of Anesthesia Awareness

Anesthesia awareness, also called unintended intraoperative awareness, occurs under general anesthesia when a patient becomes cognizant of some or all events during a procedure and has direct recall of those events. Because of the routine use of neuromuscular blocking agents (paralytics) during general anesthesia, the patient is often unable to communicate with the surgical team when this occurs.

The frequency of anesthesia awareness has been found in multiple studies to range between 0.1% and 0.2% of all patients undergoing general anesthesia.1–3 General anesthesia is administered to 21 million patients annually in the United States, so 20,000 to 40,000 cases of anesthesia awareness occur each year. Patients experiencing awareness report auditory recollections (48%), sensations of not being able to breathe (48%), and pain (28%).¹ More than 50% experience mental distress after surgery, including an indeterminate number with post-traumatic stress syndrome.^2,3 Some patients describe these occurrences as their “worst hospital experience,” and some determine to never again undergo surgery.

The incidence of awareness is reported to be greater in patients for whom the dose of general anesthetic must be smaller and carefully titrated to decrease significant side effects, such as a patient who is hemodynamically unstable. Procedures typically identified as falling into this category are some cardiac, obstetric, and major trauma cases.⁴ Factors contributing to the risk of anesthesia awareness include the increasing use of intravenous delivery of anesthesia, as opposed to inhalation, and the premature lightening of anesthesia at the end of procedures to facilitate operating room turnover.

Monitoring of patients under general anesthesia to prevent anesthesia awareness can be challenging. Despite a variety of available monitoring methods, awareness is difficult to recognize while it is occurring. Typical indicators of physiologic and motor response, such as high blood pressure, fast heart rate, movement, and hemodynamic changes, are often masked by the use of paralytic agents to achieve necessary muscle relaxation during the procedure, as well as the concurrent administration of other medications necessary to the patient’s management, such as beta-blockers or calcium channel blockers.

To overcome the limitations of current methods to detect anesthesia awareness, new methods are being developed that are less affected by the medications typically used during general anesthesia. These devices measure brain activity rather than physiologic responses. These electroencephalography devices (also called level-of-consciousness, sedation-level, or anesthesia-depth monitors) include the Bispectral Index (BIS), spectral edge frequency (SEF), and median frequency (MF) monitors. These devices may have a role in preventing and detecting anesthesia awareness in patients with the highest risk, thereby ameliorating the impact of anesthesia awareness. A body of evidence has not yet accumulated to precisely define the role of these devices in detecting and preventing anesthesia awareness; The Joint Commission expects additional studies on these subjects to emerge. In its review of the BIS monitor, the U.S. Food and Drug Administration determined that “Use of BIS monitoring to help guide anesthetic administration may be associated with the reduction of the incidence of awareness with recall in adults during general anesthesia and sedation.”

The anesthesia professional must often balance the psychologic risks of anesthesia awareness against the physiologic risks of excessive anesthesia for many critical medical conditions. The Joint Commission has asked the American Society of Anesthesiologists (ASA) and the American Association of Nurse Anesthetists (AANA) to address the adequacy of current monitoring practices regarding anesthesia levels, including those practices that involve little or no technologic support. The ASA recommends in its 2006 practice advisory that intraoperative monitoring include clinical (e.g., purposeful or reflex movement), conventional monitors (e.g., end-tidal anesthetic analyzer, HR, BP), and brain function monitoring on a case-by-case basis.⁵ Multimodal monitoring is suggested rather than reliance on any single monitor.

Reducing the Risk of Anesthesia Awareness

The ASA and the AANA provide guidelines for administering and monitoring anesthesia. Specific recommendations for the prevention of awareness were addressed in the February 2000 issue of Anesthesiology⁴:

• Consider premedication with amnesic medications (e.g., benzodiazepines, scopolamine), particularly when light anesthesia is anticipated.

• Administer more than a “sleep dose” of induction agents if they will be followed immediately by tracheal intubation. Avoid muscle paralysis unless absolutely necessary and, even then, avoid total paralysis (by using only the amount clinically required).

• Conduct periodic maintenance of the anesthesia machine and its vaporizers, and meticulously check the machine and its ventilator before administering anesthesia.

• Be alert to patients taking beta-blockers, calcium channel blockers, or other medications that can mask physiologic responses to inadequate anesthesia.

Managing the Impact of Anesthesia Awareness

Anesthesia awareness cannot always be prevented. Health care practitioners must be prepared to acknowledge and manage the occurrence of anesthesia awareness with compassion and diligence. The following practices are suggested when patients report awareness ⁴:

• Interview the patient after the procedure, taking a detailed account of his or her experience and including it in the patient’s chart.

• Apologize to the patient if anesthesia awareness occurred.

• Assure the patient of the credibility of his or her account, and sympathize with the patient’s suffering.

• Explain what happened and its reasons (e.g., the necessity to administer light anesthesia in the presence of significant cardiovascular instability).

• Offer the patient psychologic or psychiatric support, including referral to a psychiatrist or psychologist.

• Notify the patient’s surgeon, nurse, and other key personnel about the incident and the subsequent interview with the patient.

Surgical team members should also be educated about anesthesia awareness and its management.

Joint Commission Recommendations

Anesthesia awareness is underrecognized and undertreated in health care organizations. The Joint Commission recommends that health care organizations performing procedures under general anesthesia take the following steps to help prevent and manage anesthesia awareness:

1. Develop and implement an anesthesia awareness policy that addresses the following:

• Education of clinical staff about anesthesia awareness and how to manage patients who have experienced awareness.

• Identification of patients at proportionately higher risk for an awareness experience and discussion with such patients, before surgery, of the potential for anesthesia awareness.

• The effective application of available anesthesia monitoring techniques, including timely maintenance of anesthesia equipment.

• Appropriate postoperative follow-up of all patients who have undergone general anesthesia, including children.

• The identification, management, and, if appropriate, referral of patients who have experienced awareness.

2. Ensure access to necessary counseling or other support for patients who are experiencing post-traumatic stress syndrome or other mental distress.

References

1. Sebel PS, Bowdle TA, Ghoneim MM, et al. The incidence of awareness during anesthesia: a multicenter United States study. Anesth Analg. 2004;99(3):833.

2. Lennmarken C, Sandin R. Neuromonitoring for awareness during surgery. Lancet. 2004;363(9423):1747.

3. Osterman JE, Hopper J, Heran WJ, et al. Awareness under anesthesia and the development of posttraumatic stress disorder. Gen Hosp Psychiatry. 2001;23(4):198.

4. Ghoneim MM. Awareness during anesthesia. Anesthesiology. 2000;92(2):597.

5. Practice advisory for intraoperative awareness and brain function monitoring: A report by the American Society of Anesthesiologists Task Force on Intraoperative Awareness. Anesthesiology. 2006;104:847.

Bibliography

Ekman A, Lindholm ML, Lennmarken C, et al. Reduction in the incidence of awareness using BIS monitoring. Acta Anaesthesiol Scand. 2004;48(1):20.

Liska JM. Silenced screams: surviving anesthetic awareness during surgery—a true-life account. Park Ridge, IL: AANA Publishing, Council for Public Interest in Anesthesia; 2002.

Myles PS, Leslie K, McNeil J, et al. Bispectral index monitoring to prevent awareness during anaesthesia: the B-Aware randomised controlled trial. Lancet. 2004;363(9423):1757.

Modified from The Joint Commission. Sentinel event alert. Issue 32. October 6, 2004. http://www.jointcommission.org/SentinelEvents/SentinelEventAlert/sea_32.htm. Accessed September 2012.

Anesthetic Agents

Typically two or more anesthetic agents are used in combination to achieve the desired level of anesthesia. To anticipate the patient’s response, it is important for the nurse to have knowledge of the anesthetic agents that are used and their usual physiologic effects.² The characteristics of ideal anesthetic agents and adjuncts are listed in Box 42-3.

Inhalation Agents

Inhalation agents are used for induction and maintenance of anesthesia or, in combination with other anesthetic agents, to maintain surgical anesthesia. They can be classified as volatile or gaseous. Volatile agents are further classified as halogenated hydrocarbons or ethers, are liquid at room temperature, and have a boiling point of 20° C. Gaseous agents are gases at room temperature. Inhaled anesthetics are delivered through the respiratory tract and are absorbed into the circulation through the alveoli. The effects of inhalation agents depend on alveolar ventilation, the ventilation-perfusion ratio, co-administered gases, gas flow, and the physicochemical properties of the gas. Their exact mechanism of action is unknown, but all cause central nervous system (CNS) depression and a state of unconsciousness that is deep enough to allow surgery. Table 42-1 lists the inhalation anesthetics presently used and their chief characteristics, effects, and nursing implications.¹⁰

TABLE 42-1

INHALATION ANESTHETICS

MEDICATION	CHARACTERISTICS	EFFECTS	CONSIDERATIONS
Nitrous oxide	Light anesthetic; inorganic gas; nontoxic, nonirritating; carrier for other inhalation agents; always given with oxygen	Anesthetic and analgesic; minimal pulmonary, cardiac, or CNS effects; increases intracranial pressure; amnesia	Eliminated by ventilation; postoperative nausea and vomiting; diffusion hypoxia; mild myocardial depression
Isoflurane (Forane)	Pungent, ether-like odor; low potential for toxicity; volatile agent	Higher cardiovascular stability; potentiates muscle relaxants	Mild depression of spontaneous ventilation; may trigger malignant hypothermia; postoperative shivering; fewer dysrhythmias noted
Desflurane (Suprane)	Strong, pungent odor; rapid onset; volatile agent; requires warmed vaporizer for administration	Minimal metabolism; respiratory depression; cardiovascular depression; no lingering analgesia	Observe for breath holding; coughing and laryngospasm; may trigger malignant hypothermia; needs immediate postoperative analgesia
Sevoflurane (Ultane)	Nonirritating to airway; volatile agent; choice for pediatric anesthetic	Minimal airway irritation; rapid elimination; great precision and control over anesthetic depth; decreases SVR	May trigger malignant hypothermia; observe for breath holding; needs immediate postoperative analgesia

CNS, Central nervous system; SVR, systemic vascular resistance.

Intravenous Anesthetics

Because inhalation anesthetics can produce adverse effects such as vasodilation, hypotension, dysrhythmias, and myocardial depression, other medications and methods of delivery have been sought to provide general anesthesia. Intravenous anesthetics are commonly used in the perioperative period. Intravenous anesthetics are grouped by their primary pharmacologic action as nonopioid or opioid intravenous agents.12–14 The nonopioid agents are further divided into the barbiturates, nonbarbiturates, and sedatives. These medications can be administered by intermittent intravenous push dosing to induce anesthesia or by continuous intravenous drip to maintain anesthesia.

Nonopioid Intravenous Anesthetics

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter. The nonopioid medications appear to interact with GABA in the brain. Activation of the GABA receptors inhibits the postsynaptic neurons and results in a loss of consciousness. Barbiturates bind to GABA postsynaptic receptors, inhibiting neuronal activity and causing a loss of consciousness. Sedatives such as benzodiazepines potentiate the action of GABA, leading to inhibition of neuronal activity. Nonbarbiturate induction agents, such as etomidate, antagonize the muscarinic receptors in the CNS and work as opioid agonists, resulting in a hypnotic state and loss of consciousness. Table 42-2 presents the nonopioid intravenous anesthetics and their effects and nursing considerations.¹²

TABLE 42-2

NONOPIOID INTRAVENOUS ANESTHETICS

MEDICATION	CHARACTERISTICS	EFFECTS	CONSIDERATIONS
Barbiturates
Sodium thiopental* (Pentothal)	Good patient acceptance; quick onset; very brief duration; no analgesia	CNS depression; spontaneous ventilation arrested; loss of laryngeal reflexes; causes histamine release (vasodilation, hypotension, and flushing)	IV administration painful; may cause myoclonus, coughing, and hiccoughs; increased risk of aspiration
Methohexital (Brevital)	Similar to thiopental but three times as potent; no analgesia; hepatic metabolism; ultra-fast onset of action	Similar to thiopental; lowers seizure threshold (epileptiform)	Similar to thiopental
Nonbarbiturates
Etomidate (Amidate)	Agent of choice in patients with cardiovascular dysfunction	Heart rate and cardiac output remain constant; minimal negative inotropic effects; suppression of adrenal function up to 5-8 hours after a single dose	May cause nausea and vomiting; burns when given IV; may cause myoclonus, laryngospasm, cough, and hiccoughs; no analgesic effects
Propofol (Diprivan)	No analgesic effect; avoid in patients with coronary stenosis, ischemia, or hypovolemia; antiemetic properties; hepatic metabolism	Minimal residual CNS effects; myocardial depressant; may decrease blood pressure 20%-25%	Rapid emergence may hasten pain awareness; low incidence of postoperative side effects; pain on administration; dose reduction in older adults, patients with cardiac disease and hypovolemia; long-term or high-dose infusions can result in hypertriglyceridemia; contraindicated in patients allergic to soybean oil, egg lecithin, or glycerol
Dissociative Anesthetic
Ketamine (Ketalar)	Profound analgesia and unconsciousness; provides amnesia; may be used alone, may be given IV, IM, or PO	Produces cardiovascular and respiratory stimulation; may increase blood pressure and heart rate 10%-50%; increases intracranial pressure	Monitor for and prevent emergent reactions; minimize stimulation of the patient during emergence; titrate pain medications; benzodiazepines or dexmedetomidine may help reduce agitation during emergence
Butyrophenones
Haloperidol (Haldol)	Limited use in anesthesia because of long duration; antipsychotic; antiemetic	—	High incidence of extrapyramidal reactions Potential for torsade de pointes due to prolongation of QT interval
Droperidol (Inapsine)	Major tranquilizer; works with CNS as dopamine antagonist; hepatic metabolism; used in low doses for antiemetic prophylaxis	Prevents and treats nausea and vomiting; in higher doses acts as neuroleptic, causing amnesia or indifference to surroundings; adrenergic blocker, causing extrapyramidal muscle movements, hypotension, and peripheral vasodilation	Postanesthetic dysphoria (internalized overwhelming fear); effects last longer than those of opioids (rare in low doses); prolongs QT interval
Benzodiazepines
Diazepam (Valium)	Rapid onset; long half-life; anterograde amnesic; effective anxiolysis; renal excretion	—	Titrate opioid medications and monitor for respiratory depression; used orally as premedicant
Midazolam (Versed)	Rapid onset; short duration; potent amnesic; effective anxiolysis; hepatic metabolism	—	Reduce dose in older adults, debilitated, use cautiously in patients with myocardial ischemia, COPD, and hepatic disease; titrate opioid medications; monitor for respiratory depression
Lorazepam (Ativan)	Slow onset of action; long duration; anticonvulsant action; hepatic metabolism; renal excretion; no active metabolites	Pronounced sedation; minimal cardiovascular effects	Poor IV compatibility; titrate opioid medications and monitor for respiratory depression; watch for orthostatic hypotension

CNS, Central nervous system; COPD, chronic obstructive pulmonary disease; IM, intramuscular; IV, intravenous; PO, per os (orally).

^*Unavailable in United States since January 2011.

Benzodiazepine Antagonists

Flumazenil (Romazicon) reverses the sedative, amnesic, respiratory depressant, and muscle-relaxant effects of benzodiazepines.¹⁴ This medication is specific for the benzodiazepine receptors and does not reverse the effects of barbiturates or opiates. It should be used with caution in patients who have a history of seizures or chronic benzodiazepine use, as it can precipitate seizures. Because flumazenil has a shorter duration of action than most of the benzodiazepines, the risk of resedation can occur after the initial dose starts to wear off, especially when high doses of benzodiazepines are administered. The patient must be monitored for resedation and other residual effects. If the patient develops signs of resedation, flumazenil is repeated at 20-minute intervals. Flumazenil has proved to be a valuable asset in the care of the patient who has received an excessive dose of a benzodiazepine such as midazolam or lorazepam. Consequently, flumazenil is very useful intraoperatively, postoperatively, and in the critical care unit.

Opioid Intravenous Anesthetics

Intravenous opioid anesthetics play an important role in clinical anesthesia care. These medications enhance the effectiveness of inhalation agents by providing the analgesic portion of the anesthetic process. Intravenous opioids blunt the sympathetic response to painful stimuli during anesthesia. The use of opioids allows for reduction in the concentration of the inhalation agent to be administered, increasing safety. Opioids bind to specific receptors and produce a morphine-like or opioid agonist effect. Opioids are used to manage acute and chronic pain and are administered for general anesthesia, sedation, and pain relief during regional anesthesia; they are important in all phases of the perioperative experience. Table 42-3 presents a summary of clinical uses and nursing implications for the most frequently used opioids.¹³

TABLE 42-3

OPIOID ADJUNCTIVE AGENTS *

CLINICAL USES	IMPLICATIONS	CONSIDERATIONS
Preoperative sedation	Monitor for hypotension	Keep naloxone (Narcan) available
Induction of anesthesia	Monitor for bradycardia	Keep resuscitation equipment available
Maintenance of anesthesia	Monitor for respiratory depression	Respiratory depressant effect may outlast analgesia
Postoperative pain management	May cause nausea and vomiting

^*Agents include alfentanil (Alfenta), fentanyl (Sublimaze), ketorolac (Toradol), morphine, sufentanil (Sufenta), remifentanil (Ultiva), and hydromorphone (Dilaudid).

Opioid Antagonists

Opioid antagonists are used to reverse the effects of opioids, particularly respiratory depression, restoring spontaneous ventilation in patients who are breathing inadequately. The medication of choice in perianesthesia care is naloxone (Narcan). Naloxone competes with and displaces the opioid on the receptor site; it therefore reverses respiratory depressant and analgesic effects of opioids. Naloxone is diluted and then titrated to the patient’s response, minimizing the risk of rapid reversal and subsequent adverse effects. The onset of action is 1 to 2 minutes and the duration of action is 1 to 4 hours. If adequate reversal has not been achieved after 3 to 5 minutes, naloxone administration is repeated until reversal is complete.¹⁵

If long-acting opioids are used, the patient must be monitored for respiratory insufficiency, because the depressant effects of the opioids may return. Often, a low-dose, continuous intravenous drip of naloxone proves effective. Close monitoring of vital signs is critical. Monitor the patient for increased blood pressure, which may occur in response to pain following large doses of naloxone. In addition, tachycardia, nausea, vomiting, or diaphoresis may occur if the reversal is too rapid. Naloxone must be used with caution in patients with cardiac irritability and in patients who are physically dependent on opioids, because reversal may precipitate an acute withdrawal syndrome.

Neuromuscular Blocking Agents

Neuromuscular blocking agents (NMBAs), or muscle relaxants, interrupt the transmission of impulses from the nerve to the muscle, causing a decrease in muscle activity. Decreasing muscle activity allows the surgeon to operate in a quiet field and decreases the need for deep anesthesia. These medications have contributed greatly to clinical anesthesia care. Use of NMBAs is not limited to the operating room; they are used to facilitate endotracheal intubation, to terminate laryngospasm, to eliminate chest wall rigidity that may occur after the rapid injection of potent opioids, and to facilitate mechanical ventilation by producing total paralysis of the respiratory muscles.¹⁵

NMBAs cause paralysis of the respiratory muscles, and the patient receiving these agents requires ventilatory support with a handheld bag-valve-mask device or a mechanical ventilator. NMBAs do not have analgesic, amnesic, anxiolytic, or sedative effects. The paralyzed patient is not able to communicate his or her needs; NMBAs must be used in combination with other medications to prevent pain and provide sedation.

Skeletal muscle contraction occurs when acetylcholine is released from the motor neuron and binds to receptor sites on the muscle fiber (i.e., neuromuscular junction), resulting in depolarization. Skeletal muscle relaxation occurs when the release of acetylcholine ceases and any residual acetylcholine is destroyed by the enzyme acetylcholinesterase, resulting in repolarization. NMBAs interfere with the relationship between acetylcholine and the receptor. There are two general categories of skeletal muscle relaxants: nondepolarizing and depolarizing.

Depolarizing agents compete with acetylcholine at the neuromuscular junction, causing the muscle to depolarize and inhibiting repolarization. The muscle stays in a prolonged depolarized state, and movement is inhibited. The principal depolarizing skeletal muscle agent is succinylcholine (Anectine). After succinylcholine attaches to the receptor, a brief period of depolarization occurs, which is manifested by transient muscular fasciculations. Succinylcholine has a rapid onset, 60 to 90 seconds, and a short duration of action, 5 to 10 minutes. It is frequently used to facilitate intubation. Succinylcholine cannot be pharmacologically reversed.

Nondepolarizing NMBAs are typically longer-acting agents than depolarizing agents. Nondepolarizing agents do not cause initial muscle contraction or depolarization. They compete with and block the uptake of acetylcholine at the muscle receptor site and prevent repolarization. Sustained muscle relaxation occurs, and voluntary control of skeletal muscle contraction is weakened or lost.

Table 42-4 presents a pharmacologic overview of the commonly used skeletal muscle relaxants.¹⁶ A number of factors can potentiate or antagonize the effects of nondepolarizing NMBAs; these factors are listed in Box 42-4.¹⁷

Box 42-4 Factors Influencing Neuromuscular Blockade

• Antibiotics (gentamicin, tobramycin, amikacin, kanamycin, neomycin, polymyxin B, clindamycin, tetracyclines, piperacillin, streptomycin)

• Antidysrhythmics (procainamide, lidocaine, quinidine)

• Beta-adrenergic blockers

• Calcium channel blockers

• Diuretics (furosemide, thiazides)

• Hepatobiliary disease

• Renal failure

• Neuromuscular diseases

• Sympathomimetic agents

• Corticosteroids

• Azathioprine

TABLE 42-4

NEUROMUSCULAR BLOCKING AGENTS *

	IMPLICATIONS
CHARACTERISTICS	DEPOLARIZING	NONDEPOLARIZING
Compete with acetylcholine at the myoneural junction	Nonreversible	Reversible with time and anticholinesterases
	Use cautiously in patients with neuromuscular disease, such as myasthenia gravis or muscular dystrophy; contraindicated for pediatric use except in emergencies	Use cautiously in patients with hepatic or renal disease, obesity, asthma, or COPD
Shorter-acting agents are most appropriate for anesthesia	Adverse effects include bradycardia, tachycardia, ventricular dysrhythmias, asystole, hypertension, hyperkalemia	Adverse effects include tachycardia, hypertension, hypotension, bronchospasm, and flushing
Provide surgical relaxation Facilitate intubation	Increases intraocular, intracranial, and intragastric pressure
Assist in ventilatory support	Precipitates muscle fasciculations and pain
	Prolongs respiratory depression
	Histamine release causes hypotension
	Use cautiously in patients with head injury, cerebral edema, trauma, burns, electrolyte imbalances, and renal or hepatic disease
	Monitor for clinical signs of malignant hyperthermia

^*Long-acting agents include pancuronium (Pavulon); intermediate-acting agents include atracurium (Tracrium), vecuronium (Norcuron), and cisatracurium (Nimbex); short-acting agents include rocuronium (Zemuron) and succinylcholine (Anectine), which is a depolarizing agent.

Neuromuscular Blocking Agent Antagonists

The pharmacologic actions of nondepolarizing NMBAs can be reversed by anticholinesterase medications such as neostigmine (Prostigmin). These medications increase the amount of acetylcholine available at the receptor sites by preventing its destruction by acetylcholinesterase. This promotes more effective competition of acetylcholine with the nondepolarizing skeletal muscle relaxant that is occupying the receptor sites. Because of the increased availability and mobilization of the acetylcholine, the concentration gradient favors acetylcholine and the removal of the nondepolarizing agent from the receptors, resulting in the return of normal skeletal muscle depolarization and contraction.¹⁸ These medications also produce undesired side effects by increasing the level of acetylcholine at receptor sites in the heart, the lungs, the eyes, and gastrointestinal tract, which can lead to bradycardia, bronchospasm, miosis, and increased peristalsis and secretion. To prevent or minimize these effects, anticholinergic agents such as atropine or glycopyrrolate (Robinul) are given with the anticholinesterase agent. Table 42-5 outlines the common NMBA reversal agents used in anesthesia and their nursing implications.¹⁸

TABLE 42-5

NMBA REVERSAL AGENTS

MEDICATION	CHARACTERISTICS	EFFECTS	CONSIDERATIONS
Anticholinesterase
Neostigmine (Prostigmin)	Binds with cholinesterase and inactivates it Preserves endogenous anticholinesterase More effective in antagonizing intense blocks than pyridostigmine or edrophonium

Antidote for nondepolarizing NMBAs

Prevents postoperative distention and urinary retention

Muscarinic effects cause bradycardia, bronchoconstriction, peripheral vasodilation, and coronary vasoconstriction

Does not cross blood–brain barrier

Lasts 30-90 min

May be given with atropine and glycopyrrolate to decrease muscarinic effects; most commonly given with glycopyrrolate

Use cautiously in patients with asthma or coronary artery disease

Pyridostigmine (Regonol)

Analogue of neostigmine with fewer adverse effects

Only 20% as potent as neostigmine

Rapid onset of action (5-15 min)

Antidote for nondepolarizing NMBAs

Muscarinic effects less severe than those of neostigmine

Longer half-life

Lasts 120 min

May be given with atropine and glycopyrrolate

Use cautiously in patients with asthma, peptic ulcer, epilepsy, or pregnancy

Edrophonium (Tensilon)

Cholinergic

Short-acting anticholinesterase

Parasympathetic effects:

GI: salivation, dysphasia, nausea, vomiting, increased peristalsis

CV: bradycardia, cardiac dysrhythmias, hypotension

RESP: increased pharyngeal and tracheobronchial secretions

EENT: lacrimation, miosis, diplopia

Must be given with atropine

Very rapid onset but brief duration of action

Use cautiously in presence of asthma, peptic ulcer, or bradycardia

Anticholinergic Atropine

Anticholinergic

Antimuscarinic

Chronotropic stimulator in event of bradycardia

Preanesthetic medication to prevent or reduce respiratory tract secretions

Restoration of cardiac rate during anesthesia

Antidote for cholinesterase inhibitors

Causes decreased sweating and predisposition to heat prostration

Crosses blood–brain barrier

Ensures adequate hydration

Provides temperature control to prevent hyperpyrexia

Glycopyrrolate (Robinul)

Similar to atropine

Longer duration

Less incidence of dysrhythmias

Slow increase in heart rate

Protection against peripheral muscarinic effects of neostigmine and pyridostigmine

Does not cross blood–brain barrier

Contraindicated in presence of glaucoma, peptic ulcer, or COPD

COPD, Chronic obstructive pulmonary disease; CV, cardiovascular; EENT, eyes, ears, nose, and throat; GI, gastrointestinal; NMBA, neuromuscular blocking agent; RESP, respiratory.

Perianesthesia Assessment and Care

The goal of management in the immediate postoperative period is the recognition and immediate treatment of any problems, to eliminate or lessen complications that may occur. This requires the collaborative effort of the nurse, the anesthesiologist, and the surgeon. Physical assessment of the postanesthesia patient begins immediately on admission to the unit. This initial assessment focuses on airway, ventilation, and circulation (heart rate, rhythm, and blood pressure). Following the brief initial assessment, the nurse admitting the patient receives a verbal report from the anesthesia care provider and surgeon. The report includes information about the patient’s general condition, significant past history or co-morbidities, the operation performed, the type of anesthesia administered, estimated blood loss, total intake and output during surgery, and any problems or complications encountered in the operating room.¹⁹

Assessment of the cardiopulmonary system is the immediate priority. The patient’s airway is assessed to ensure that it is patent, with or without adjuncts, and the patient’s breathing pattern is evaluated to ensure that it is unlabored. The patient’s blood pressure, pulse, rate of respiration, oxygen saturation level, and temperature are measured and recorded. All dressings and drains are quickly inspected for integrity and gross bleeding. After these initial observations have been made, it is essential to systematically assess the patient’s total condition.

Respiratory Function

Because patients have experienced some interference with their respiratory system, postanesthesia maintenance of adequate gas exchange is a crucial aspect of care in the immediate postoperative period. Oxygen administration may be used in the immediate postoperative phase. Any change in respiratory function must be detected early so that appropriate measures can be taken to ensure adequate oxygenation and ventilation. Respiratory function is evaluated by using physical assessment skills: inspection, palpation, percussion, and auscultation. Several pre-existing conditions can increase the probability that ventilatory support will be needed in the postoperative period. These include pre-existing pulmonary disease, thoracic or upper abdominal surgery, history of smoking, recent significant opioid administration, and low oxygen saturation before surgery.

Pulse oximetry, a noninvasive technique, measures oxygen saturation of functional hemoglobin. Pulse oximetry can be used to identify hypoxemia, and its use should be standard on all postoperative patients. If the patient is intubated and mechanically ventilated, capnography can be used to assess for adequate ventilation. Arterial blood gas measurements are appropriate to definitively confirm abnormal pulse oximetry or capnography values. Normal pulse oximetry values are 97% to 99%; however, preanesthetic baseline values must be noted. Some patients normally have lower saturation values on room air for a variety of reasons, and attempting to maintain higher oxygen saturation levels may result in prolonged oxygen therapy.²⁰

For spontaneously breathing patients, supplemental oxygen may be needed, typically using nasal cannula (prongs) or simple facemask. Surgery and anesthesia often interrupt the normal functioning of the nose, so humidification or nebulization with oxygen delivery may be needed. Humidifiers convert water from the liquid to the gaseous state, whereas nebulizers produce tiny water particles. This is especially helpful at higher flow rates.²¹

Patients may require mechanical ventilation following anesthesia. Various modes, such as positive end-expiratory pressure (PEEP), continuous positive airway pressure (CPAP), and synchronized intermittent mandatory ventilation (SIMV), are used to improve the respiratory status of the patient.²¹

Stir-Up Regimen

A significant aspect of perianesthesia nursing management is the stir-up regimen.²² The regimen is aimed at the prevention of complications, primarily atelectasis and venous stasis. The stir-up regimen consists of five major activities—deep-breathing exercises, coughing, positioning, mobilization, and pain management.

Deep-Breathing Exercises.

The major factor contributing to postoperative pulmonary complications is low lung volumes resulting from a shallow, monotonous, sighless breathing pattern caused by general anesthesia, opioids, and pain. The patient must be stimulated to take three or four deep breaths every 5 to 10 minutes. Full lung expansion is important, and every effort must be made to enhance the patient’s ability to accomplish it.

The sustained maximal inspiration (SMI) maneuver is a method to enhance the lung volumes of postoperative patients.²² The SMI maneuver consists of having the patient inhale as close to lung capacity as possible and, at the peak of inspiration, hold that volume for 3 to 5 seconds before exhaling it. This maneuver is more effective than simple deep breathing in preventing reduced lung volumes in the immediate postanesthesia periods. If the patient’s vital capacity is inadequate or if anesthesia respiratory depression is prolonged, deep breathing and the SMI maneuver may be augmented with a manual resuscitation bag connected to an oxygen source or with an intermittent positive-pressure breathing apparatus.

Incentive spirometry is used to assist with preventing and treating atelectasis, promoting normal lung expansion, and improving oxygenation. Incentive spirometry devices allow patients visual feedback and observation of inspiratory volume. Instruction and practice before surgery provide patients with the opportunity to master the device and establish their baseline levels before anesthetic and surgical interventions.

Coughing.

A purposeful cough is the most effective method to clear the air passages of obstructive secretions.²² For the patient recovering from anesthesia, the cascade cough is the most effective coughing maneuver. Instruct the patient to take a rapid, deep inhalation. This will increase the volume of air in the lungs and dilate the airways, allowing air to pass behind the retained secretions. On exhalation, have the patient perform multiple coughs. With each cough the length of the airways increases, enhancing the effectiveness of the cough.

Coughing is most effective with the patient sitting upright. Splinting of incisions and adequate analgesia facilitate coughing. If the patient is unable to sit upright, place the patient in a side-lying position with hips and knees flexed, or in a semi-Fowler’s position with the head and arms supported with pillows and the knees flexed. This positioning decreases abdominal tension and allows maximal movement of the diaphragm, improving the effectiveness of the cough.

Between cascade cough maneuvers, the patient is encouraged to inhale and close the glottis. This dilates the airways, increases intrathoracic pressure, and compresses the smaller airways, pushing the secretions toward the larger airways where they can be expectorated in succeeding cough maneuvers.

When a large amount of secretions accumulates in the patient’s lungs and cannot be handled effectively by coughing, suctioning must be instituted. Suctioning is not without complications and should be done only when necessary and not routinely^.

In most patients, the nurse uses physical assessment skills to evaluate cardiovascular function.²⁹ The patient’s overall condition is observed, especially skin color and turgor. Peripheral cyanosis, edema, jugular venous distention, shortness of breath, and many other findings may be indicative of cardiovascular problems. All operative and access sites are checked for bleeding, and the amount of blood lost during surgery and the patient’s most recent hemoglobin level are noted.

The patient’s blood pressure must be assessed and correlated to the preoperative assessment, intraoperative course, and anesthetic course. The major component of systolic pressure is stroke volume, and the major component of diastolic pressure is systemic vascular resistance (SVR). Changes in the patient’s systolic or diastolic pressure or narrowing of the pulse pressure may indicate cardiovascular comprominse.²⁹ Peripheral pulses are assessed bilaterally. The rate, character, and any irregularities are documented and reported to the physician if clinically indicated.²⁹ Electrocardiographic (ECG) monitoring is also essential in the immediate postoperative recovery period. Dysrhythmias of any type may occur at any time and in any patient during the postoperative period.^29,30

Two components of CO are heart rate and stroke volume. If CO is compromised, one of the first compensatory responses is an increase in heart rate, followed by peripheral vasoconstriction. Medications such as beta-blockers and angiotensin-converting enzyme inhibitors, as well as anesthetic agents, can impair the patient’s ability to initiate that response. The nurse must be aware of the patient’s preoperative medications and the impact they may have in the initial phase of recovery. Hemodynamic monitoring is commonly used with higher-acuity patients in the postanesthesia recovery period. Hemodynamic monitoring is usually accomplished by a pulmonary artery catheter and arterial blood pressure monitoring.

Central Nervous System Function

Assessment of the CNS in the immediate postanesthesia period typically involves gross evaluation of behavior, level of consciousness, intellectual performance, and emotional status. Anesthetic agents are usually reversed before the patient leaves the operating room, and the nurse should anticipate that the patient will be responsive. However, even if anesthesia is not reversed, most patients can respond within 60 to 90 minutes from time of admission to the unit.³¹ Perioperative stroke can occur in up to 7% of patients following noncardiac and non-neurosurgical procedures.³² As a result of this risk, the nurse caring for the postanesthesia patient following general anesthesia should complete a neurologic assessment that includes stroke assessment (facial symmetry, vocalization to assess for slurred speech, strength, and movement of extremities), and pupillary check. In addition, Glasgow coma scale assessment may be completed. For patients who have undergone neurosurgical procedures, a more detailed assessment of the CNS is necessary.

Occasionally, a patient becomes agitated and thrashes about; this behavior when extreme is referred to as emergence delirium. It occurs more often in children, older adults, and patients with histories of drug dependency or psychiatric disorder.³⁰ Emergence delirium also tends to occur more commonly in patients who have undergone breast and abdominal procedures and procedures of longer duration.³³

Thermal Balance

Measurement of the patient’s body temperature in the immediate postanesthesia recovery period is particularly important. Factors influencing the body temperature include type of anesthesia, preoperative medication, age of patient, site and temperature of intravenous fluids, body surface exposure, temperature of irrigation solutions, temperature of the ambient air, and vasoconstriction (from blood loss or anesthetic agents). Hypothermia (temperature less than 36° C) and hyperthermia (temperature greater than 38° C) are associated with physiologic alterations that may interfere with recovery.³⁴

The body maintains its temperature in a narrow range, between 36° C and 38° C. This is accomplished by a balance of heat production and heat loss that is controlled by the thermoregulation mechanisms in the CNS. These mechanisms receive input from various thermoreceptors located in the skin, nose, oral cavity, thoracic viscera, and spinal cord. They then send sensory information in hierarchic order to the spinal cord, the reticular formation, and the primary control center in the hypothalamic region of the brain.³⁵

The central temperature controls maintain body temperature through physiologic and behavioral responses. The physiologic thermoregulatory responses consist of sweating, shivering, and alterations in peripheral vasomotor tone. These responses fine-control the regulatory process of body temperature; heat is conserved by vasoconstriction and lost by vasodilation and sweating. The physiologic responses also can lower the metabolic rate to decrease heat production or increase muscle tone and shivering to increase heat production. Behavioral thermoregulation is accomplished by subjective feelings of discomfort or comfort. For example, in a hot environment a person seeks air conditioning, and in a cold environment a person seeks heat. Behavioral thermoregulation is a stronger response mechanism, but it cannot fine-tune body temperature as the physiologic responses can.³⁵

Fluid and Electrolyte Balance

Evaluation of a patient’s fluid and electrolyte status involves total body assessment. Imbalances readily occur in the postoperative patient because of a number of factors, including restriction of food and fluids preoperatively, fluid loss during surgery, and stress. The normal body response to stress, surgery, trauma, and anesthesia is to release the antidiuretic hormone responsible for the retention of water and sodium. Postanesthesia patients often have abnormal avenues of fluid loss after surgery.

Each patient must be evaluated to determine his or her baseline requirements and the fluid needed to replace abnormal losses. Most patients in the immediate postanesthesia recovery period receive intravenous fluids. It is important to know what fluids, if any, are to follow and whether the infusion is to be discontinued. All intravenous sites are checked regularly for signs of extravasation, phlebitis, and infection.

Oral intake is prohibited after anesthesia until the patient regains laryngeal and pharyngeal reflexes. These reflexes are demonstrated by the patient’s ability to gag and swallow effectively. The management of postoperative nausea and vomiting (PONV) remains critical.

Normal output in the average adult results from urinary output and insensible losses, including evaporation of water from the skin and exhalation during respiration.³⁶

A lower-than-normal urinary output can be expected in the immediate postanesthesia recovery period as a result of the body’s normal reaction to stress and anesthetics. External losses from vomiting, nasogastric tubes, T-tubes, and wound drainage are assessed and monitored. Accurate measurement and recording of all intake and output is vital in the assessment of the patient’s fluid and electrolyte status.³⁶

In the surgical patient, intravenous access to the circulatory system is necessary for the administration of anesthesia, resuscitation medications, blood and blood products, and fluid and electrolyte solutions. Postoperative parenteral fluid requirements vary with the patient’s preoperative status and with the surgical procedure. Disease processes, tissue injuries, and operative procedures greatly influence the physiology of fluids and electrolytes in the body.

In deciding the type of fluid to use in the postanesthesia recovery period, the clinician can differentiate between crystalloids and colloids, between maintenance and replacement fluids, and among fluids of differing tonicity. Because of the large variety of fluid solutions, some general guidelines are recommended in clinical practice.³⁶ Crystalloids are typically used as maintenance fluids to compensate for insensible fluid losses and as replacement fluids to correct body fluid deficits (i.e., treatment of specific fluid and electrolyte disturbances). Maintenance fluid requirements are calculated according to body weight and are used to replace insensible losses from the lungs, skin, urine, and feces. Adults typically require 1.5 to 2 mL/kg/hour. When crystalloids are used to replace blood loss, the replacement factor is 3 mL of crystalloid for each 1 mL of blood loss.³⁷ Isotonic solutions, 0.9% normal saline, or lactated Ringer solution are usually administered in the immediate postoperative period. Colloids typically are used for fluid replacement associated with severe hypotension or shock resuscitation. In general, they do not leave the intravascular space and therefore require lower infusion volumes to achieve volume replacement.

The goal of fluid therapy in the immediate postanesthesia recovery period is the restoration of blood volume and tissue perfusion. Recovery after surgery is a dynamic process, and fluid reassessment is conducted periodically. Fluid challenges may be necessary in the hypovolemic patient or in the patient with clinical manifestations of hypoperfusion. The decision of whether to use crystalloids or colloids for fluid resuscitation is complex, controversial, and often determined by physician preference. Either can meet the replacement needs of the patient and achieve the desired outcome when administered appropriately. As with any therapeutic intervention, complications can occur with fluid administration, and the patient should be monitored closely.

Blood and blood components are reserved for specific patient situations.³⁷ Red blood cells are indicated to increase oxygen-carrying capacity in patients with anemia. Platelets are used to treat bleeding associated with deficiencies in platelet number or function. Fresh-frozen plasma is transfused to increase clotting factor levels in patients with demonstrated deficiencies. A good understanding of the fluid types available, a systematic approach to evaluating fluid depletion, and awareness of the indications for blood component therapy allow the nurse to make appropriate decisions when implementing fluid therapy in the immediate postanesthesia period.

Psychosocial Status

Assessment of the patient’s psychosocial and emotional well-being is an important component of perianesthesia care. As with any other assessment, this must be made in the context of the whole patient. Almost all patients experience a degree of anxiety about anesthesia and the surgical procedure and a fear of postoperative pain.³⁸ The physical manifestations include increased heart rate and blood pressure; pale, cool skin; increased respiratory rate; increased muscle tone; restlessness; agitation; and dilated pupils.

Other Nursing Considerations

In the postanesthesia care unit (PACU), assessment and nursing care are based on the complexity and acuity of the patient’s condition.³⁹ Concerns surround the use of the PACU as an overflow unit for critically ill patients.⁴⁰ Issues surrounding these concerns are competencies of staff; adequacy of equipment, medications, supplies, and technology; and appropriate nurse staffing. Refer to Box 42-5 for guidelines for the overflow of critical care patients into the PACU.⁴⁰

Box 42-5

A Joint Position Statement on ICU Overflow Patients

Developed by ASPAN, AACN, and ASA’s Anesthesia Care Team Committee and Committee on Critical Care Medicine and Trauma Medicine

Issue

A phase I postanesthesia care unit (PACU) is a critical care area providing postanesthesia nursing care for patients immediately after operative and invasive procedures, before discharge to the phase II ambulatory setting, the inpatient surgical unit, and the intensive care unit.

Perianesthesia nurses have identified concerns regarding the increasing use of the phase I PACU for the care of surgical and nonsurgical intensive care unit (ICU) patients when ICU beds are not available in the facility.

Purpose

As professional societies involved in the provision of care for operative and invasive procedures and critically ill patients, the American Society of PeriAnesthesia Nurses (ASPAN), the American Association of Critical-Care Nurses (AACN), and the American Society of Anesthesiologists (ASA) collaborated to develop criteria for the purposes of maintaining quality care in the PACU, ensuring quality care for the ICU patient, and promoting the safe practice of perianesthesia nursing and critical care nursing.

ASPAN exists to promote quality and cost-effective care for patients, their families, and the community through public and professional education, research, and standards of practice. ASPAN has the responsibility for defining the practice of perianesthesia nursing. An integral part of this responsibility involves identifying the educational requirements and competencies essential to perianesthesia practice and recommending acceptable staffing requirements for the perianesthesia environment.

AACN was established to provide the highest quality resources to maximize nurses’ contributions to care for critically ill patients and their families. AACN provides and inspires leadership to develop standards and guidelines that establish work and care environments that are respectful, healing, and humane.

ASA was established to raise and maintain the standard of the medical practice of anesthesiology and improve the care of the patient during anesthesia and recovery, and ASA is involved in the provision of critical care medicine in the ICU.

Background

In response to concerns expressed by perianesthesia nurses around the country, the ASPAN Standards and Guidelines Committee conducted a review of current literature and perianesthesia nursing practice to identify issues related to the care of critically ill surgical and nonsurgical patients in phase I PACUs during times when all other ICU beds are full. The review identified the following trends:

1. Staffing requirements identified for phase I PACUs may be exceeded during times when PACUs are being utilized for ICU overflow patients.¹

2. The phase I PACU nurse may be required to provide care to a surgical or nonsurgical ICU patient despite a lack of proper training and the required valid care competencies.¹

3. Phase I PACUs may be unable to receive patients normally admitted from the operating room when staff are caring for ICU overflow patients.¹

4. Because the need to send ICU overflow patients to the phase I PACU does not occur regularly, the PACU and hospital management may not be properly prepared to deal with the admission and discharge of phase I PACU and ICU patients.¹

Statement

When it is necessary to admit ICU overflow patients or to prolong the stay of the surgical ICU patient in the phase I PACU, ASPAN, AACN, and ASA recommend that the following criteria be met:

1. It must be recognized that the primary responsibility for the phase I PACU is to provide the optimal standard of care to the postanesthesia patient and to effectively maintain the flow of the surgery schedule.

2. Appropriate staffing requirements should be met to maintain safe, competent nursing care of the postanesthesia patient and the ICU patient.² Staffing criteria for the ICU patient should be consistent with ICU guidelines and based on individual patient acuity and needs.³

3. Phase I PACUs are by their nature critical care units, and PACU staff should meet the competencies required for the care of the critically ill patient. These competencies include, but are not limited to, ventilator management, hemodynamic monitoring, and medication administration, as appropriate to the patient population.

4. Management should develop and implement a comprehensive resource utilization plan with ongoing assessment that supports the staffing needs for PACU and ICU patients when the need for overflow admission arises.³

5. Management should have a multidisciplinary plan to address appropriate utilization of ICU beds. Admission and discharge criteria should be used to evaluate the necessity for critical care and to determine the priority for admissions.³

Expected Actions

ASPAN, AACN, and the ASA committees (Anesthesia Care Team, Critical Care Medicine, and Trauma Medicine) recognize the complexity of caring for patients in a dynamic health care environment where reduced availability of resources and expanding roles for the registered nurse have an impact on patient care. We encourage all members to actively pursue the education and development of competencies required for the care of the critically ill patient in the perianesthesia environment. We also encourage members to actively identify strategies for collaboration and problem solving to address complex staffing issues.

This information and position is to be shared with all individuals, organizations, and institutions involved in the care of the critically ill patient in the perianesthesia environment.

Approval Statement

This statement was recommended by a vote of the ASPAN Board of Directors on April 14, 2000 in Kansas City, Missouri, and approved by a vote of the ASPAN Representative Assembly on April 16, 2000 in Kansas City, Missouri.

This position statement was reviewed and updated at the October 2009 meeting of the Standards and Guidelines Committee in Batesville, Indiana.

References

1. Johannes, MS. A new dimension of the PACU: The dilemma of the ICU overflow patient. J Post Anesth Nurs. 1994; 9:297.

2. American Society of PeriAnesthesia Nurses. Resource 2: patient classification/recommended staffing guidelines in the Standards of Perianesthesia Nursing Practice. Thorofare, NJ: ASPAN; 1998.

3. Medina, J. Staffing Blueprint: Constructing Your Staffing Solutions. Alisa Viejo, CA: AACN; 1999.

Bibliography

2005. AACN standards for establishing and sustaining healthy work environments: a journey to excellence. Am J Crit Care. 2005; 3(14):187.

Hegeedus, M. Taking the fear out of postanesthesia care in the intensive care unit. Dimens Crit Care Nurs. 2003; 6(22):237.

Kiekkas, P, et al. Workload of postanesthesia care unit nurses and intensive care overflow. Brit J Nurs. 2005; 8(14):434.

Odom-Forren, J. The PACU as Critical Care Unit. J PeriAnesth Nurs. 2003; 6(18):431.

Schweizer, A, et al. Opening of a new postanesthesia care unit: impact on critical care utilization and complications following major vascular and thoracic surgery. J Clin Anesth. 2002; 14:486.

Sullivan, E. Teamwork and collaboration. J PeriAnesth Nurs. 2002; 17:334.

Weissman, C, The enhanced postoperative care system. J Clin Anesth. 2005(17):314.

From American Society of Perianesthesia Nurses. A joint position statement on ICU overflow patients developed by ASPAN, AACN, and ASA’s Anesthesia Care Team Committee and Committee on Critical Care Medicine and Trauma Medicine. http://www.aspan.org/Portals/6/docs/ClinicalPractice/PositionStatement/1012/Pos_Stmt_5_Joint_ICUOverflow.pdf. Accessed September 2012.

General Comfort Management

Postanesthesia care includes general comfort and safety measures.²² Whenever patients are recovering, at least two nurses (one of whom is a registered nurse competent in Phase I perianesthesia nursing) must always be present in the same room or unit for safety.⁴¹ Patients should not be left alone, especially when unconscious and emerging from anesthesia. Side rails should be in the up position and locked when care is not being provided. Wheel locks prevent sliding of the bed.

General physical measures such as cleaning and comfort measures are important to the total well-being of postanesthesia patients and are often overlooked. Following the initial assessment and when safe, the skin should be cleansed of preparation solutions and electrodes or sensors that are not in use should be removed. Repositioning in an alternative position from the operative position may prevent future complaints of discomfort for patients who have undergone lengthy operative procedures. While repositioning, patient movement and deep breathing may help prevent atelectasis, promote circulation, and prevent pressure ulcers from developing on skin surfaces.

Oral care is comforting to the patient who has had no oral intake and has received drying medications. Ice chips and small sips of water or juice may be offered to patients who can tolerate fluids. A non–petroleum-based ointment is applied to the lips after oral care to prevent drying and cracking.

Patients often complain of being cold when returning from the operating suite. This is a result of the effects of anesthesia and premedications and the cool atmosphere of the operating suite. The normothermic patient may shiver or complain of feeling cold, so warm blankets may provide psychologic comfort. Blankets of any type must not, however, obscure the intravenous lines, arterial lines, or other monitoring apparatus from the direct view of the attending nurse. The patient’s temperature must be monitored closely to avoid overheating.

In addition to the physical comfort measures, psychologic comfort should be provided. Reorientation, especially to time and place, is important to the postanesthesia patient, as is constant reassurance that the procedure has been completed and the patient is now recovering. The nurse’s presence at the bedside or gentle touch may also be comforting to the patient.

Management of Postanesthesia Problems and Emergencies

In the immediate postoperative period, significant physiologic changes occur as the patient emerges from the effects of anesthesia. Factors that influence the development of problems are listed in Box 42-6.⁴²

Respiratory Complications and Emergencies

Respiratory complications occur with some regularity in the postanesthesia period. All general anesthetic agents and opioid analgesic medications have respiratory depressant effects. Acute pain also impairs the ability to breathe deeply. Most respiratory complications are related to upper airway obstruction, although other problems can occur, including acute respiratory failure, aspiration, pulmonary edema, and respiratory arrest.³⁰

Airway Obstruction

Relaxed nasal or oropharyngeal muscles, rigid neck muscles, or secretions in the upper respiratory tract can cause obstruction of the airway. Soft tissue obstruction occurs when the pharynx is blocked and air cannot flow in and out. The most common cause of soft tissue obstruction is the tongue. Clinical manifestations of an airway obstruction include snoring, stridor, flaring of the nostrils, retractions at the intercostal spaces and the suprasternal notch, abnormal use of accessory muscles, asynchronous movements of the chest and abdomen, increased pulse rate, decreased oxygen saturation level, and decreased breath sounds.⁴³

Management of an airway obstruction begins with immediate recognition. Stimulation may be all that is necessary to relieve the obstruction and obtain a patent airway. With the nonreactive patient, the head tilt–chin lift maneuver or elevation of the mandible at its angles (jaw thrust) can be used to displace the tongue and open the airway. If patency of the airway cannot be achieved by either of these methods, an oropharyngeal or nasopharyngeal airway is inserted. A nasopharyngeal airway is usually better tolerated, although it can occasionally cause nasal bleeding. Oropharyngeal airways should be used only for an unconscious patients, because they can cause gagging, vomiting, and laryngospasm in the awake patient. The patient can also be turned on his or her side to a lateral position, which facilitates displacement of the tongue and drainage of secretions. If the obstruction is still unrelieved, positive-pressure mask ventilation, intubation, tracheotomy, or cricothyrotomy may be required.4,30,43

Laryngeal Edema

Laryngeal edema is defined as swelling of the laryngeal tissue. This edema can cause various degrees of airway obstruction. Manifestations include stridor, retraction, hoarseness, and a crouplike cough. Apprehension and restlessness may be present in the awake patient.

Management consists of placing the patient in the upright position; using cool, humidified oxygen; and administering nebulized racemic epinephrine. If the laryngeal edema is a result of an allergic reaction, the reaction must be managed with epinephrine, bronchodilators, and antihistamines. Reintubation is performed only if the patient’s symptoms cannot be controlled by an inhalation treatment within 30 minutes, if hypercarbia persists, or if the patient appears to be in respiratory distress. If reintubation is done, the endotracheal tube must be at least one size smaller than the previous tube used, and an air leak must be present around the cuff.30,43

Laryngospasm

Laryngospasm is caused by reflex contractions of the pharyngeal muscles, which results in spasms of the vocal cords and the inability of the patient to take a breath. The spasms may result in partial or complete airway obstruction. Involvement of the intrinsic laryngeal muscles causes a reflex closure of the glottis, which results in an incomplete obstruction. Involvement of the extrinsic muscles causes a reflex closure of the larynx, which results in a complete airway obstruction. Signs and symptoms of laryngospasm include dyspnea, hypoxia, hypoventilation, absence of breath sounds, and hypercarbia. Crowing sounds may be heard if the spasm is incomplete. The chest does not expand normally, and a rocking motion of the chest wall that stimulates abdominal breathing may be present. The patient panics if awake.

Several factors can help identify the patient at risk for a laryngospasm. Preoperatively, risks include a history of asthma, chronic obstructive pulmonary disease (COPD), or smoking. Intraoperatively, risks include the use of an endotracheal tube, anesthetic agents, “light” anesthesia, multiple attempts at intubation, and surgical airway manipulation. After surgery, risks include coughing, “bucking” on the endotracheal tube, repeated suctioning, and excessive secretions in the nasopharyngeal area. Laryngospasm may also be precipitated by irritants and foreign bodies.

Laryngospasm is an emergency that requires an immediate response; otherwise, the patient may rapidly deteriorate. Management is initiated by removing the stimulus, along with any irritants such as secretions, blood, or an artificial airway that is too long. The patient’s head must be hyperextended and positive-pressure mask ventilation instituted on 100% oxygen. The anesthesiologist is notified immediately. If complete obstruction is unrelieved by positive-pressure ventilations, a small dose of succinylcholine (10 to 20 mg) may be needed to relax the vocal cords to allow for ventilation. Positive-pressure mask ventilation is continued until full muscle function has resumed. Endotracheal intubation is required if the laryngospasm persists or if refractory hypoxemia develops, even though it may cause further irritation of the airways. Medications that may be used in the treatment of laryngospasm include lidocaine, steroids, and atropine.

After the spasm, the patient continues to receive supplemental oxygen until stable. It is also important at that time for the nurse to reassure the patient that the spasm has resolved. The patient’s feelings of being unable to breathe during laryngospasm are intense, and emotional support from the nurse is imperative.30,44

Bronchospasm

Bronchospasm is a lower airway obstruction that is characterized by spasmodic contractions of the bronchial tubes. Bronchial airway constriction is a result of an increase in smooth muscle tone in the airways, and bronchospasms develop when the smooth muscles constrict and obstruct the airway. Inflammation has also been recognized as a fundamental component of bronchospasms.

Bronchiolar constriction may be centrally generated, as in asthma, or it may be a local response to airway irritation. Manifestations include wheezing; noisy, shallow respirations; chest retractions; and use of accessory muscles. The patient can exhibit shortness of breath, coughing, and a prolonged expiratory phase of respiration. Hypertension and tachycardia may be present. The patient’s level of consciousness may range from lethargy to extreme anxiety.

Patients who smoke and those with chronic bronchitis have essentially irritable airways that react to stimulation. A preoperative history of asthma, a recent upper respiratory infection, severe emphysema, pulmonary fibrosis, and radiation pneumonitis are indicators of a greater risk of bronchospasm. Stimuli that may produce a bronchospasm postoperatively include secretions, vomitus, and blood. Patients who have had laryngoscopy, bronchoscopy, or other surgical stimulation are also at increased risk of bronchospasm. Some medications are also thought to predispose the patient to bronchoconstriction resulting from cholinomimetic stimulation; these medications include physostigmine, neostigmine, edrophonium, and barbiturates. Other histamine-releasing medications, such as tubocurarine, morphine, metocurine, and atracurium, may potentially foster bronchospasm.

Bronchospasm is treated initially by removal of any possible irritants or medications. The first line of therapy consists of inhaled bronchodilators. These inhalants cause fewer cardiovascular side effects than systemically administered medications. Common inhalant medications used are albuterol, metaproterenol, and beclomethasone. Systemic bronchodilators and anti-inflammatory agents may also be required at times. Epinephrine is occasionally needed as a continuous infusion. Intravenous methylprednisolone manages the inflammatory aspect of bronchospasm. Cholinergics have been given by nebulizer to decrease secretions.30,44

Noncardiogenic Pulmonary Edema

Pulmonary edema may be defined simply as increased total lung water. Fluid can accumulate in the interstitial spaces or in the alveoli as the result of cardiogenic or pulmonary capillary processes. Noncardiogenic pulmonary edema, also known as postobstructive pulmonary edema, in the postanesthesia recovery period can result from pulmonary aspiration, blood transfusion reaction, allergic medication reaction, upper airway obstruction, or sepsis.⁴⁵ The most common causative factor seems to be an upper airway obstruction, usually laryngospasm. Often, a short episode of airway obstruction occurred in the operating room. Noncardiogenic pulmonary edema has also been reported after the administration of naloxone to patients who have received general anesthesia. Reversal of the analgesics causes a rise in the level of adrenal catecholamines, which can lead to pulmonary hypertension and probably increased pulmonary vascular permeability.

During laryngospasm, the patient is inhaling against a closed glottis. This generates an increase in negative intrathoracic pressure. A tremendous subatmospheric transpulmonary pressure gradient is created that causes transudation, or leakage of fluid, from the pulmonary capillaries into the interstitium.

Management consists of maintenance of an unobstructed airway and supplemental oxygen to correct hypoxemia. Those patients who cannot maintain adequate oxygenation with a mask may require the use of CPAP or even mechanical ventilation with PEEP. The use of PEEP or CPAP improves hypoxemia by restoring the functional residual capacity (FRC). Vigorous pulmonary toilet and the use of hemodynamic monitoring may be required if the patient’s blood pressure is labile and fluid balance is difficult to maintain. Morphine can be titrated to relieve anxiety. Corticosteroid therapy can be used to decrease laryngeal edema and stabilize the pulmonary membrane. Noncardiogenic pulmonary edema occurs rapidly and requires early assessment and immediate intervention.

Aspiration

Aspiration can be defined as the passage of regurgitated gastric contents or other foreign materials into the trachea and down to the smaller air units. It can occur during the period of reduced protective airway reflexes. The most common and most severe form of aspiration is the aspiration of gastric contents. The gastric acid in gastric contents damages the alveolar and capillary endothelial cells. Fluid rich with protein leaks into the interstitium and alveoli. This results in atelectasis and consolidation. Pulmonary compliance and FRC are decreased, and airway resistance and intrapulmonary shunting are increased, with hypoxemia resulting.

If aspiration is suspected, management begins with lowering the patient’s head, if possible. The patient is positioned to the side or the head is turned to the side to permit gravity to pull secretions from the trachea. Management centers on promoting tissue oxygenation by maintaining arterial oxygenation by means of CPAP and supplemental oxygen. Positive-pressure ventilation by mask can be applied if the patient is awake and can protect his or her airway or by an endotracheal tube if the patient cannot tolerate the mask or requires higher levels of airway pressure.30,44

Hypoxemia

Administration of oxygen by facemask or nasal cannula to recovering patients may be needed to prevent hypoxemia in the postoperative patient, based on oxygen saturation levels that may be assessed by noninvasively by pulse oximetry. Respiratory depressant effects of residual agents may result in a shallow breathing pattern with an increased ratio of dead space to tidal volume. This is even more evident in patients after upper abdominal surgery, and the reduction in the effective ventilation can have serious effects on oxygenation.⁴²

The most common cause of hypoxemia is ventilation perfusion mismatching. Atelectasis often occurs as a result of bronchial obstruction by secretions or blood. Reduction in FRC is caused by the effects of anesthesia and, in the case of upper abdominal surgery, by the surgical procedure. When FRC falls below closing capacity, dependent alveoli occlude, leading to increased mismatching. Impairment of hypoxic pulmonary vasoconstriction by inhalation agents and some vasoactive medications potentiates this effect.³⁰

Hypoventilation

Central respiratory depression is caused by all anesthetic agents. This may lead to significant hypoventilation and hypercarbia. Impaired respiratory muscle function, particularly after upper abdominal surgery, may contribute to the problem of carbon dioxide elimination. Incomplete reversal of neuromuscular blockade must also be considered. Other contributory factors may include tight dressings and body casts, obesity, and gastric dilation. Increased carbon dioxide production may occur as a result of shivering or sepsis. This leads to hypercarbia in patients who are unable to increase ventilation enough to compensate.

Hypercarbia resulting from postoperative hypoventilation may cause hypertension and tachycardia, increasing the risk of myocardial ischemia in susceptible individuals. Hypoventilation, by itself or in combination with the other factors previously discussed, can cause hypoxemia. Very high levels of carbon dioxide may have sedative effects. Evaluation of suspected hypoventilation requires measurement of arterial blood gases. Capnographic monitoring may be especially useful in patients at high risk for hypoxemia.³⁰

Careful titration of opioid antagonists, such as naloxone, may be effective in improving ventilation without compromising pain relief. Planning ahead to provide adequate postoperative analgesia is essential for maintaining ventilation, particularly in patients undergoing abdominal or thoracic procedures. Placing obese patients in a semi-Fowler’s position and relieving the effects of tight dressings and casts can also be important. Hypoventilation that cannot be improved sufficiently by noninvasive means requires intubation and mechanical ventilation until the patient can maintain adequate ventilation.⁴⁴

Cardiovascular Problems and Emergencies

In the immediate postoperative period, cardiovascular complications causing an alteration in CO can occur. These include anesthetic effects on cardiac function, myocardial dysfunction, dysrhythmias, hypertension, and hypotension. These conditions may occur individually or in combination.30,46

Effects of Anesthesia on Cardiac Function

In the immediate postoperative period, the residual effects of anesthetic agents and their adjuncts must be considered in the evaluation of a patient who has cardiac dysfunction. Volatile anesthetic agents such as sevoflurane and isoflurane can cause a dose-related reduction in myocardial function. The actions of these agents may be observed for several hours after the conclusion of surgery.⁴ Nitrous oxide is an inhalation agent that demonstrates insignificant cardiac depression. However, the combined action of opioids given during emergence from nitrous oxide can result in marked cardiovascular depression.³

Therapy directed toward mitigating the myocardial depressant effects of inhalation anesthetic agents primarily focuses on increasing preload. Elevation of the legs and a crystalloid fluid bolus are commonly sufficient treatment, but ephedrine or other positive inotropic agents may be needed.²⁴

Individually, most opioids and benzodiazepines only moderately depress cardiac function. Opioids reduce the sympathetic response and enhance vagal and parasympathetic tone. This results in vasodilation and a decrease in SVR. Benzodiazepines also cause vasodilation and a decrease in the SVR. Used in combination, these medications can have a significant effect on the cardiovascular system. Specifically, the overall reaction may include a lowered SVR, heart rate, ventricular contractility, catecholamine level, baroreceptor reflex, CO, and blood pressure. Aggressive administration of crystalloid solutions may be required to counteract these effects. High-dose opioids combined with vecuronium produce a negative inotropic and chronotropic effect. Patients may require short-term vascular support until these medications dissipate.30,47

Barbiturates depress the activity of the vasomotor center, causing peripheral vasodilation and hypotension. These actions are dose related and are more marked in the presence of underlying cardiovascular disease. Ketamine has a direct myocardial depressant effect that is usually counterbalanced by its indirect effect on the autonomic nervous system to increase heart rate and blood pressure. In patients who are unable to mount a sympathetic response to stress, ketamine causes a net decrease in CO. Propofol causes a dose-dependent decrease in blood pressure primarily because of a decrease in SVR. This must be considered when caring for patients who are hypovolemic or have minimal cardiac reserves.44,48

Local anesthetic agents can cause cardiovascular toxicity if inadvertently injected into the systemic circulation or if an excessive dosage of the agent is used. Decreased myocardial contractility, reduced SVR, and diminished CO have resulted from these agents. Cardiovascular compromise appears to occur in a dose-related fashion. Management of the cardiovascular complications associated with local anesthetic agents includes measures to increase preload, namely elevation of legs and fluid administration. In refractory cases, ephedrine may also be needed.4,30

Myocardial Dysfunction

During the immediate postoperative period, the causes of myocardial depression include pathologic processes and aberrant physiologic states, in addition to anesthetic side effects. These processes may occur alone or in combination and may be particularly hazardous in the presence of underlying cardiac disease.

Myocardial ischemia results from an imbalance of oxygen supply and demand. Commonly, ischemia results from a decrease in myocardial blood flow caused by atherosclerosis, vasospasm, or hypotension. In the postoperative period, the stress of surgery and the actions of certain anesthetic agents can increase myocardial ischemia.30,46

Dysrhythmias

In the immediate postanesthetic period, patients are predisposed to a variety of cardiac dysrhythmias. The most common dysrhythmias are sinus tachycardia, sinus bradycardia, premature ventricular contractions, supraventricular tachydysrhythmias, and ventricular tachycardia. A variety of causes can result in dysrhythmias, including circulatory instability, pre-existing heart disease, an increase in vagal tone, medications, pain, electrolytic disturbances, and hypoxemia.⁴⁹

Accurate interpretation and identification of the dysrhythmia are essential, because therapeutic intervention is based on diagnosis. Appropriate skin preparation and lead placement are extremely important to ensure a clear, readable tracing that is free from artifact. Additional 12-lead ECG capabilities should be used if an interpretation cannot be made from tracings obtained with bedside monitoring.

The hemodynamic effects of the dysrhythmia also should be thoroughly assessed. The clinical presentation of the dysrhythmia determines the severity of underlying cardiac disease and the type of treatment. Tachydysrhythmias shorten diastolic filling time and interfere with coronary artery perfusion. These two effects, coupled with an increase in myocardial oxygen consumption, may produce cardiac decompensation. Bradycardia can produce a clinically significant decrease in CO if stroke volume is limited by underlying cardiac disease or if the venous return is reduced. The cause of the rhythm disturbance should be considered.⁴⁸

General anesthesia lowers the dysrhythmia threshold of the myocardium. Inhalation agents sensitize the myocardium to catecholamines and depress sinoatrial (SA) and atrioventricular (AV) nodal function. Junctional rhythms and premature ventricular contractions are the most common dysrhythmias. Ketamine produces sympathetic stimulation, resulting in tachycardia and hypertension. Succinylcholine stimulates the cholinergic receptors, enhancing vagal tone, and it can produce sinus bradycardia or junctional escape rhythms. Opioids may cause bradycardia because of direct stimulation of the vagus nerve.

Endogenous catecholamine levels in postoperative patients are elevated because of the pain and stress of surgery. Increased catecholamine levels increase sinus and AV node rates, as well as atrial and ventricular irritability. The direct result is tachydysrhythmias and atrial or ventricular premature contractions.30,46,48

Postoperative Hypertension

Hypertension is not an unusual occurrence in the immediate postoperative period. The diagnosis of hypertension must be considered in the context of an elevated blood pressure in relation to the patient’s preoperative and intraoperative blood pressure range. Most commonly, postoperative hypertension is related to fluid overload, heightened sympathetic nervous system activity, or pre-existing hypertension. Postoperative hypertension, even as a transient episode, can have significant cardiovascular and intracranial consequences, so aggressive diagnosis and treatment are indicated.

Increased sympathetic tone in the immediate postoperative period may result from the stress of surgery, postoperative pain, anxiety, or restlessness during emergence from anesthesia, bladder or bowel distention, or hypothermia. Stimulation of the autonomic nervous system can occur because of hypoxia or hypercarbia. These factors can occur alone or in combination.

Pain is one of the most common sources of increased sympathetic tone. Administering adequate amounts of analgesics, repositioning the patient for comfort, providing reassurance, and limiting environmental stimuli can contribute to alleviating postoperative pain and to lowering blood pressure. Hypothermia and shivering also contribute to postoperative hypertension and are easily treated with warm blankets, active warming devices, and warm intravenous fluids. Bladder distention contributes to postoperative hypertension and must be alleviated. Placement of a urinary catheter may be needed. Hypoxia and hypercarbia must also be treated.

Pharmacologic treatment of postoperative hypertension includes the use of vasodilators, adrenergic inhibitors, and calcium channel blockers. The use of these agents is necessary when hypertension persists despite conservative measures previously mentioned.30,46

Postoperative Hypotension

Maintenance of blood pressure depends on adequate preload, myocardial contractility, and afterload. The most common cause of hypotension is intravascular volume depletion caused by inadequate replacement of blood loss, third space fluid loss, insensible loss, and urinary output. Pulmonary embolism may also reduce preload by blocking flow of blood to the left side of the heart. Reduced myocardial contractility may be a result of the effects of anesthetic medications, myocardial ischemia, or dysrhythmias. Reduced afterload in the form of low SVR may occur as a result of sepsis, hyperthermia, sympathectomy, or large arteriovenous shunts, as seen in chronic liver failure.

Prolonged hypotension can lead to serious ischemic organ damage. Prompt treatment is essential. If the underlying cause is not immediately apparent, the first treatment is an attempt to increase preload by elevating the patient’s legs and infusing fluids. Examination of the ECG monitor for dysrhythmias or evidence of ischemia may help guide therapy. The lungs are examined for evidence of pulmonary edema or tension pneumothorax. Vasopressors may be administered to maintain perfusion while additional monitoring modalities are evaluated and established. Insertion of a central venous catheter allows measurement of right ventricular filling pressure and may be used to guide fluid administration in patients with normal myocardial function. In the presence of left ventricular dysfunction or when the cause remains unclear, a pulmonary artery catheter may be inserted to guide therapy through evaluation of left-sided filling pressure, CO, and SVR. The use of additional fluids, inotropic agents, or vasoconstrictor or vasodilator medications is determined by these measurements.⁴⁹

Thermoregulatory Problems and Emergencies

Patients recovering from anesthesia usually experience some form of thermoregulatory imbalance (i.e., a core body temperature that is outside the normothermic range of 36° C to 38° C). Hypothermia and hyperthermia can occur in the postoperative patient. Management of these alterations is important, because they are associated with other physiologic alterations that may interfere with recovery.

Hypothermia

Hypothermia is a common occurrence intraoperatively and postoperatively, because the conditions associated with surgery and anesthesia typically inhibit the body’s heat-generating mechanisms and favor its heat-loss mechanisms.⁵⁰ Hypothermia occurs when systemic heat loss lowers core body temperature below 36° C. Causes include wound and skin exposure, respiratory gas exchange, fluid and blood administration, use of mechanical warming or cooling devices, chemical reactions, alterations in body temperature regulation, and disease states. Clinical manifestations of hypothermia include bluish tint to the skin (peripheral cyanosis); shivering and an increase in metabolic rate (early sign); dysrhythmias; and a decrease in metabolic rate (late sign), oxygen consumption, muscle tone, heart rate, and level of consciousness.³⁵

Hypothermia has several adverse effects, including discomfort, vasoconstriction, and shivering. It depresses the myocardium and increases susceptibility to ventricular dysrhythmias. Significant hypothermia slows metabolic processes, leading to reduced medication biotransformation and impaired renal transport. This may prolong medication effects and delay emergence.35,50

Shivering

Shivering may be a result of the compensatory response to hypothermia or the effects of anesthetic agents, and it can produce an increase in the metabolic rate. Under these conditions, increased oxygen consumption and greater carbon dioxide production can increase the ventilatory requirements. If these requirements are not met, the Paco₂ increases and the Pao₂ can decrease, especially if any significant intrapulmonary shunting coexists. The demand for blood flow by the diaphragm can increase sharply, requiring CO and myocardial workload to increase and causing an increase in myocardial oxygen consumption. This can result in myocardial ischemia, particularly in older adult patients and patients with coronary artery disease.35,50

Vasoconstriction, a particularly deleterious consequence of postoperative hypothermia, may be responsible for unexplained hypertension in the postanesthesia period. Because vasoconstriction can increase SVR and myocardial workload, the potential for myocardial ischemia exists. Vasoconstriction can mask hypovolemia, and sudden reductions in blood pressure can occur as the patient warms and vasodilates.⁵¹ Delayed medication clearance as a consequence of hypothermia is particularly significant in older adult patients who may already have impaired medication-clearing mechanisms and a decreased metabolic rate. For example, the maximal rate of renal excretion of a medication can decline by 10% for every 0.6° C drop in body temperature. Older adult hypothermic patients are more likely to have residual paralysis because of muscle relaxants that are difficult to reverse pharmacologically.⁵²

Management of the hypothermic patient is directed toward the restoration of normothermia. Rewarming prevents the thermoregulatory responses to cold, such as shivering. Management depends on the degree of temperature loss. If the patient’s body temperature is between 36° C and 37° C, the patient can simply be covered with warmed blankets, and heat lamps can be used to keep the patient adequately warm. If the patient’s body temperature is less than 36° C, rapid rewarming is required to decrease the possible complications of hypothermia and the postanesthesia recovery time. Convective warming devices provide a safe and effective means of rewarming the patient.³⁴ In patients with a normal metabolic rate, a setting of “low” or “medium” increases the mean body temperature by about 1° C per hour. A “high” setting increases the mean body temperature by about 1.5° C per hour.⁴ Other methods of rewarming are thermal mattresses, fluid and blood warming, and environmental warming. Supplemental oxygen may be needed to meet the increased metabolic demand in shivering patients. Patients who are shivering may respond to a small dose of meperidine (Demerol).⁵¹

Hyperthermia

By definition, hyperthermia occurs at any core body temperature above normal. Severe, clinically significant hyperthermia results when core temperature exceeds 40° C. Although it is not as common perioperatively as hypothermia, hyperthermia is nevertheless a serious complication of surgery. Postoperative temperature elevations may be caused by accidental overwarming of the patient during surgery, infection, sepsis, or transfusion reactions. Because an elevated temperature increases oxygen demand and, subsequently, the ventilatory and cardiac workload, a hyperthermia patient with poor cardiac reserve suffers serious consequences.⁵³

Postoperative fever must be distinguished from other hyperthermic syndromes. A fundamental difference exists between fever and specific hyperthermic states. In non–fever-related hyperthermic states, body temperature rises above normal despite the body’s heat-dissipating mechanisms (e.g., vasodilation, sweating). Excessive heat gain from internal or external factors exceeds the body’s cooling capabilities, with a consequent rise in body temperature.2,4

In contrast, fever results from a resetting to a higher temperature from the normal set point. Until the body reaches its new set point temperature, heat-generating mechanisms (i.e., vasoconstriction and shivering) are activated. After the new set point temperature is reached, there is an equilibrium between heat generation and heat loss. Unlike hyperthermia, with fever there is no physiologic activity to bring body temperature back to normal. Factors that can contribute to raising core body temperature and fever during the perioperative period are listed in Box 42-7.⁵⁰

Box 42-7 Factors Influencing Temperature And Fever

CAUSES OF ELEVATED CORE TEMPERATURE	CAUSES OF POSTOPERATIVE FEVER
• Blood transfusion • Medication-induced fever • Overuse of techniques to prevent hypothermia • Hypothalamic injury • Malignant hyperthermia • Warm environment • Use of anticholinergics • Endocrine disorders • Neurogenic hyperthermia

• Atelectasis

• Wound infection

• Abscess formation

• Fat emboli after bone trauma

• Medication reactions

• Malignancy

• Silent aspiration

• Dehydration

• Blood transfusion reaction

• Central nervous system damage

• Urinary tract infections

• Phlebitis, deep vein thrombosis

• Pulmonary emboli

Primary therapy for hyperthermia includes cooling and decreasing thermogenesis. Cooling by evaporative or direct external methods has proved effective. This includes ice packs, a cool environment, and cooling blankets. Gastric and bladder lavage have also proved effective. Although physical cooling is an appropriate therapy for other hyperthermias, attempts to cool a febrile patient may be resisted by the thermoregulatory system. Consequently, the first course of action is to restore normothermia with the use of antipyretic medications. Antipyretics are useful because they have the ability to prevent prostaglandin synthesis in the hypothalamus. Measures to manage the febrile patient include using antipyretics (as indicated), providing a sponge bath with tepid water, keeping the environment cool, using a cooling blanket for sustained fever, and monitoring fluid and electrolyte balance as fluid needs increase during fever. The possibility of malignant hyperthermia (MH) must always be considered.⁵³

Malignant Hyperthermia

Malignant hyperthermia is a genetically determined condition. MH is precipitated by certain general inhalation anesthetics, depolarizing skeletal muscle relaxants, local anesthetics, and stress in susceptible patients. The incidence of MH ranges from 1 in 15,000 in children to 1 in 50,000 in adults. The onset of MH usually occurs during induction of anesthesia but may occur within the first few hours of recovery from anesthesia.³ Because successful management of MH depends on early assessment and prompt intervention, the nurse must be knowledgeable about the pathophysiology and treatment of this syndrome.

Identification before anesthesia of patients who may be susceptible to MH is of major therapeutic importance.⁵⁴ Patient history or genealogy going back two generations may be positive. Physical examination may reveal myopathies such as cryptorchidism, pectus carinatum, kyphosis, lordosis, ptosis, or hypoplastic mandible. Electromyographic changes are seen in fewer than half of MH-susceptible patients.

The most definitive test for detecting MH susceptibility is a biopsy of skeletal muscle.⁵⁴ Samples are obtained from the quadriceps muscles and are subjected to isometric contractor testing. The skeletal muscle of the MH-susceptible patient has an increased isometric tension when exposed to caffeine or halothane. Genetic testing for the presence of a ryanodine mutation that predicts MH susceptibility may ultimately replace the invasive diagnostic tests.³

When a susceptible patient is exposed to a triggering agent for MH, such as isoflurane, the clinical features are produced by an excess of calcium ions in the myoplasm. With an elevated calcium ion concentration in the myoplasm, skeletal muscle contraction is intense and prolonged, leading to a hypermetabolic state of acid and heat production. More specifically, heat is produced by the accelerated and continued synthesis and use of adenosine triphosphate (ATP) during glycolysis. The metabolic byproduct of glycolysis, lactic acid, is transported to the liver and then back to the metabolically active muscle, where the cycle repeats. Respiratory acidosis and metabolic acidosis develop because of this hypermetabolic state, and symptoms such as tachycardia, tachypnea, ventricular dysrhythmias, and unstable blood pressure appear. Because of intense vasoconstriction, the skin is mottled and cyanotic.⁵⁵ Box 42-8 lists the clinical manifestations of MH.

Box 42-8

Signs and Symptoms of Malignant Hyperthermia

• Muscle rigidity

• Increased CO₂ production (hypercapnia)

• Rhabdomyolysis

• Marked temperature elevation (hyperthermia)

• Tachycardia

• Tachypnea

• Metabolic acidosis

• Respiratory acidosis

• Hyperkalemia

• Myoglobinuria

• Elevated creatine phosphokinase

• Ventricular dysrhythmias

• Unstable blood pressure

Modified from Odom-Forren J. Drain’s Perianesthesia Nursing: a Critical Care Approach. 6th ed. St. Louis: Elsevier; 2013.

Elevated body temperature can actually be a late sign of MH. For this reason, the nurse must not prolong the assessment of the patient on the assumption that the patient’s temperature must be significantly elevated before intervention is attempted. After the patient’s temperature begins to rise, it may increase at a rate of 1° C every 3 to 5 minutes and may approach levels as high as 46° C.³⁰

Muscle rigidity occurs in about 75% of the patients who experience MH. This is especially true in MH-susceptible patients after the administration of succinylcholine. Muscle rigidity may be so severe that the nurse cannot open the patient’s mouth to insert an airway. The onset of skeletal muscle rigidity after the administration of succinylcholine could be a sign of impending development of MH.53,55

Various environmental and pharmacologic agents can stimulate an acute episode of MH (Box 42-9).⁵⁴ Fatigue, emotional upset, or very hot and humid weather can trigger a waking febrile episode. The anesthetic agents that may trigger MH seem to affect the sarcoplasmic reticulum. Because of their widespread use, volatile anesthetic agents (e.g., isoflurane) and succinylcholine are the most common triggering agents. In MH-susceptible patients and in patients who have had an episode of MH in the operating room, all possible triggering agents must be stringently avoided. As another precaution, because emotional upsets trigger MH, nurses must provide a stress-free environment for the MH-susceptible patient.

Box 42-9

Environmental and Pharmacologic Triggers of Malignant Hyperthermia

Environmental Stimuli

• Extremely hot and humid weather

• Strenuous and prolonged exercise

Modified from Odom-Forren J. Drain’s Perianesthesia Nursing: a Critical Care Approach. 6th ed. St. Louis: Elsevier; 2013.

The cornerstone of successful management of MH is early detection. If the patient develops acute MH, all inhalation anesthetics are stopped, the patient is hyperventilated with 100% oxygen, and dantrolene is given. To be administered, dantrolene must be diluted with sterile water. Cooling measures, such as administering cold intravenous fluids, packing the patient in ice, and irrigating body cavities (e.g., stomach, bladder) with cold fluids, are initiated as needed based on the patient’s temperature. Accurate intake and output records are essential because large amounts of fluids and diuretics are given. Laboratory tests, such as complete blood cell counts (CBC) and coagulation studies, are closely scrutinized for signs of bleeding or the onset of disseminated intravascular clotting. Ongoing ECG and temperature monitoring are also essential. It is recommended that all emergency medications be available on a special cart in the operating room or in the PACU.

Neurologic Problems and Emergencies

Almost all patients exhibit some level of arousal within 15 minutes after anesthesia is completed.³ Although many factors are known to prolong anesthetic effects, most reports of delayed emergence and emergence delirium are anecdotal.

Delayed Emergence

Delayed awakening after general anesthesia occurs occasionally, and is defined as a failure to regain consciousness within 20 to 30 minutes after the anesthetic ends.⁵⁶ It can usually be attributed to prolonged action of anesthetic medications, metabolic causes, or neurologic injury.³⁰ In most cases, prolonged sedation is the result of residual general anesthetic. Hypoventilation resulting from a high concentration of inhaled anesthetic limits exhalation of the agent and prolongs its retention. Opioids used as adjunct therapy may contribute to hypercarbia and sedation as well. Hypothermia, advanced age, hepatic dysfunction, and renal disease may contribute to prolonged recovery from anesthetics by heightening sensitivity or delaying elimination, or both. The use of premedication may also prolong recovery, especially if opioids or benzodiazepines, particularly lorazepam, are used.⁵⁷

In addition to experiencing a slowing elimination of potent inhalation anesthetic, the hypoventilating patient may develop hypoxia and hypercapnia. The hypercapnia may cause significant narcosis and may potentiate the depressive effects of the anesthetics. In the diabetic patient, fasting or excessive insulin may cause electrolyte abnormalities, leading to unconsciousness, or even coma.⁵⁶

Severe electrolyte disturbances are most commonly seen after excessive water absorption during transurethral prostate surgery. The subsequent dilution hyponatremia may manifest as sedation, coma, or hemiparesis. Dilution hyponatremia may also be seen after the inappropriate release of antidiuretic hormone. Hypocalcemia after parathyroid surgery may result in delayed awakening. High magnesium levels after prolonged administration of magnesium sulfate to the eclamptic or pre-eclamptic patient may also result in prolonged postoperative sedation and in muscle weakness after cesarean section under general anesthesia.³⁶

Neurologic injury and subsequent unconsciousness may be the result of an unsuspected cerebral vascular accident. Intracranial hemorrhage may result from hypertensive responses to anesthetic agents or surgical manipulations, especially in the patient receiving anticoagulant therapy. Paradoxic air emboli may cross a patent foramen ovale in the presence of a right-to-left shunt. Direct emboli from cardiac valves, intracardiac thrombi, and atherosclerotic vessels may also be a threat. Fat emboli can occur after massive long-bone or tissue damage and may not appear until during or after surgical manipulation or reduction of the fracture. Deliberate, induced hypotension in normal patients is not usually associated with neurologic damage. However, uncontrolled intraoperative hypotension may result in ischemia, especially in the patient with hypertension or carotid occlusive disease.⁵⁷

The successful management of delayed arousal depends on careful consideration of the differential diagnosis. A thorough review of the patient’s preoperative medical condition and the intraoperative course (surgical and anesthetic) usually points to a cause. If the cause of the sedation is not immediately obvious, the first consideration must be assessing the patient’s oxygenation and ensuring adequate gas exchange. Pulse oximetry, end-tidal carbon dioxide measurement, and arterial blood gas analysis can give an estimate of any ventilatory depression and rule out ongoing hypoxia and hypercarbia factors.57,58

If the cause is thought to be residual inhalation anesthetic, maintenance of adequate ventilation should be sufficient treatment. Residual opioids can be reversed by naloxone, and anticholinergic CNS depression can be reversed by physostigmine. The benzodiazepine antagonist flumazenil has been shown to directly antagonize the CNS sedative and amnesic effects of the benzodiazepines.⁴

Body temperature is measured, and warming is instituted if hypothermia exists. Serum electrolytes and magnesium and calcium levels are checked if ion disturbance is suspected. Blood for a serum glucose assay may also be drawn, but the simple fingerstick glucose determination is faster and accurate enough to exclude hypoglycemia from consideration if the result is normal. Other laboratory tests may be useful if hepatic or renal disease is being considered. Unless perioperative events point specifically to it, neurologic injury is usually a diagnosis of exclusion. If other causes of prolonged arousal have been excluded, a thorough neurologic consultation is obtained.⁵⁷

Emergence Delirium

Most patients emerge from general anesthesia in a calm, tranquil manner. Some patients, however, emerge in a state of excitement, a condition characterized by restlessness, disorientation, crying, moaning, or irrational talking. In the extreme form of excitement, which is referred to as emergence delirium, the patient screams, shouts, and thrashes about wildly. This condition is seen most frequently after tonsillectomy, thyroid surgery, circumcision, hysterectomy, and perineal and abdominal wall procedures.30,58

Hypoxia with resulting air hunger and hypercarbia may appear as restlessness, disorientation, slurred speech, and agitation. Hyponatremia, hypochloremia, and acid–base changes can all be seen during the immediate postoperative period and can be the cause of mental confusion. Pain is a common cause of restlessness and is frequently seen postoperatively. Urinary bladder and gastric distention, which can cause considerable discomfort, are easily overlooked.30,58

Medication reactions are commonly implicated as the cause of postoperative agitation. Such reactions are less common than they once were, because the use of offending medications is less prevalent. The most frequently implicated medications are the anticholinergics, most notably scopolamine and atropine. They have been shown to have CNS-toxic effects that can include psychotic behavior, delirium, and motor disturbance. Ketamine is also associated with a high incidence of unpleasant agitation. Neuroleptic medications such as droperidol, especially in rarely used high doses, may be associated with development of dyskinesia and involuntary muscle activity and with postoperative confusion.⁵⁷

The patient’s state of apprehension or anxiety can have a marked effect on emergence agitation; it is especially notable in apprehensive patients and, conversely, in those who are seemingly unconcerned about forthcoming major surgery. Factors such as fear of disfigurement (e.g., caused by cancer surgery) and feelings of suffocation also increase the likelihood of emergence excitement. Young patients tend to have an increased incidence of postoperative excitation, as do patients undergoing emergency procedures. Several psychiatric factors have been shown to increase the incidence of postoperative delirium, including a history of alcoholism, insomnia, depression, or debility.30,58

If emergence delirium occurs, the patient’s status is thoroughly evaluated. Management includes determining a cause, initiating specific therapy, and protecting patients from injuring themselves. When the nurse encounters a restless, confused postoperative patient, the first measure is to ensure that the agitation is not the result of hypoxia. Presuming pain to be the cause of agitation in a hypoxic patient and treating the excitement with opioids or sedatives can have disastrous consequences. Hypoxia must be quickly excluded from the differential diagnosis by pulse oximetry or arterial blood gas determination, or both.2,59

Hyponatremia may be suspected in the confused patient after prostate surgery, especially if the surgery was prolonged. A serum electrolyte determination can confirm the diagnosis. The treatment usually consists of fluid restriction and, rarely, hypertonic saline administration. Severe acid–base disturbances can be diagnosed and therapy directed by arterial blood gas determination. If pain appears to be the diagnosis after exclusion of hypoxia, intravenous opioids may be administered in small increments. The CNS effects of the anticholinergics are usually dramatically reversed by the administration of physostigmine. The incidence of hallucinations with ketamine may be decreased by benzodiazepine administration. Gastric distention may be relieved by nasogastric aspiration, and urinary bladder distention is easily treated with catheterization.⁴

When dealing with perioperative anxiety, the best treatment is prevention. Some patients need reassurance that they will not experience intraoperative awareness and will receive pain medication, if needed, on awakening.

Occasionally, the nurse is faced with a restless postoperative patient who does not seem to be getting relief from opioid administration. Small intravenous doses of a short-acting benzodiazepine such as midazolam may be warranted. The anxiolytics are administered in reduced doses, because their respiratory depressant effects are cumulative with those of existing opioids, sedatives, and residual general anesthetics. If overt psychotic behavior is apparent despite adequate treatment, psychiatric consultation should be obtained.⁵⁸

The patient’s respiratory function and airway patency are checked first, because restlessness is a well-known manifestation of hypoxia. Other causes of emergence delirium include a full bladder, cramped or sore muscles and joints from prolonged abnormal positioning on the operating table, pain, incomplete reversal of NMBAs, withdrawal from alcohol and other medications, acid–base disturbances, and electrolyte abnormalities. The restless patient requires constant, careful observation. Gentle physical restraint may be required to prevent injury. Several nurses or other personnel may be needed. If hypoxia, pain, and a full bladder are ruled out, a change in positioning may have a quieting effect.²

Nausea and Vomiting

Nausea and vomiting, although usually not life-threatening, are probably the most unpleasant and lasting memories many patients have of their anesthesia.⁶⁰ Although the incidence has decreased in recent years, nausea and vomiting still result in significant postoperative morbidity and patient discomfort. Nausea is described as a subjective, unpleasant mental experience that usually leads to vomiting. Retching is the rhythmic muscular activity that usually precedes vomiting. Vomiting is defined as the forceful expulsion of gastrointestinal contents through the mouth.⁶¹

Decidedly unpleasant, vomiting can also be significant.⁶² The physical exertion may increase postoperative bleeding and disrupt delicate suture lines. Tearing or rupture of the esophagus is probably rare but must be a concern in patients with a history of esophageal pathology. Aspiration of emesis is a life-threatening complication in a patient whose airway-protective reflexes are blunted by residual anesthetic or sedative medications or damaged by surgical activity. If the vomiting is protracted, dangerous hypokalemia, hypochloremia, hyponatremia, and dehydration may develop. Nausea and vomiting are also the leading causes of unexpected hospitalization after surgery.^61,63

Risk factors most strongly associated with postoperative nausea and vomiting include female gender, history of PONV, history of motion sickness (subjective as reported by patient), nonsmoker, postoperative use/administration of opioids, use of volatile anesthetics, and use of nitrous oxide.⁶⁴ Age, duration of surgery, and type of surgery are supported as risk factors by weak or conflicting evidence.

The most effective treatment of postoperative nausea and vomiting is prevention.⁶² Several maneuvers merit mention as being fairly simple to perform and effective in their usefulness. Avoidance of gastric insufflation is paramount. Swallowing of blood should be prevented during oral, pharyngeal, or nasal surgery. If distention is suspected, it should be decompressed intraoperatively.^4,52 A nasogastric tube is placed to empty fluid and gases from the stomach, but its presence may trigger gagging and subsequent vomiting. An oral airway may elicit the same response in a partially conscious patient and is removed at the first signs of gagging to prevent vomiting and subsequent aspiration.⁶⁵

Many medications have been shown to possess antiemetic qualities, and prophylactic antiemetics and combination medications have been shown to be effective in decreasing or preventing postoperative nausea and vomiting. Available antiemetics include anticholinergics, phenothiazines, antihistamines, butyrophenones, and antidopaminergics. Complementary therapies, including acupuncture and aromatherapy with peppermint oil, have also been shown to be effective in relieving symptoms.⁶⁶ It is important to remember the supportive care of the nauseated and vomiting patient. If vomiting is severe, electrolyte replacement must be considered. Prolonged vomiting may result in hypovolemia. Intravenous fluids may need to be increased to compensate for fluid losses. Decreased opioid doses may be needed to reduce the risk of nausea and vomiting; adding nonopioids, such as nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen, may allow for adequate analgesia with less risk of nausea.⁶⁷