responsible

for the injury.

An analysis of the ASA Closed Claims Project database focusing on MAC
likewise revealed that oversedation and respiratory arrest frequently led to
claims. Claims for burn injuries suffered in operating room fires were also found
in the database. Supplemental oxygen, draping, pooling of flammable antiseptic
preparatory solutions, and surgical cautery combine to produce the potential for
operating room fires (see Chapter 2).

EQUIPMENT PROBLEMS
“Equipment problems” is probably a misnomer; the ASA Closed Claims Project
review of 72 claims involving gas delivery systems found that equipment misuse
was three times more common than equipment malfunction. Anesthesia gas
delivery claims have decreased in recent years, accounting for just 1% of claims
in the new millennium. Provider equipment misuse was associated with severe
patient injuries.
Errors in drug administration also typically involve human error. It has been
suggested that as many as 20% of the drug doses given to hospitalized patients
are incorrect. Errors in drug administration account for 4% of cases in the ASA
Closed Claims Project. Errors resulting in claims were most frequently due to
either incorrect dosage or unintentional administration of the wrong drug
(syringe swap). In the latter category, accidental administration of epinephrine
proved particularly dangerous.
Another type of human error occurs when the most critical problem is ignored
because the anesthesia provider’s attention is inappropriately focused on a less
important problem or an incorrect solution (fixation error). Serious anesthetic
mishaps are often associated with distractions and other factors (Table 54–3).
The harmful impact of most equipment failures can be decreased or avoided
when the problem is identified during the mandatory preoperative anesthesia
workstation inspection and checkout. Many anesthetic fatalities occur only
after a series of coincidental circumstances, misjudgments, and technical errors
combine (mishap chain).

TABLE 54–3 Factors associated with human errors and equipment misuse.
Prevention
To minimize errors in drug administration, drug syringes and ampules in the
workspace should be restricted to those needed for the current specific case.
Drugs should be consistently diluted to the same concentration in the same way
for each use, and they should be clearly labeled. Computer systems for scanning
bar-coded drug labels are available that may help to reduce medication errors.
The conduct of all anesthetics should follow a predictable pattern by which the
anesthetist actively surveys the monitors, the surgical field, and the patient on a
recurrent basis. In particular, patient positioning should be frequently reassessed
to avoid the possibility of compression or stretch injuries. Increasingly, protocols
or algorithms, or both, are provided in anesthetizing locations to ensure
compliance with preprocedural checklists, to standardize responses to adverse
events, and to minimize errors related to transfer of patient care between
clinicians.

AIRWAY INJURY
The daily insertion of endotracheal tubes (particularly with stylets), laryngeal
mask airways, oral/nasal airways, gastric tubes, transesophageal echocardiogram
(TEE) probes, esophageal (bougie) dilators, and emergency airways all involve
the risk of airway damage. Common complaints, such as sore throat and
dysphagia, are usually self-limiting, but they may also be nonspecific symptoms
of more ominous complications.
The most common persisting airway injury is dental trauma. In a
retrospective study of 600,000 surgical cases, the incidence of injury requiring
dental intervention and repair was approximately 1 in 4500. In most cases,
laryngoscopy and endotracheal intubation were involved, and the upper incisors
were the most frequently injured. Major risk factors for dental trauma included
tracheal intubation, preexisting poor dentition, and patient characteristics
associated with difficult airway management (including limited neck motion,
previous head and neck surgery, craniofacial abnormalities, and a history of
difficult intubation).
Laryngeal injuries included vocal cord paralysis, granuloma, and arytenoid
dislocation. Most tracheal injuries were associated with emergency surgical
tracheotomy, but a few were related to endotracheal intubation. Some injuries
occurred during seemingly easy, routine intubations. Proposed mechanisms
include excessive tube movement in the trachea and excessive cuff inflation,
leading to pressure necrosis. Esophageal perforations contributed to death in 5 of
13 patients reviewed. Esophageal perforation often presents with delayed-onset
subcutaneous emphysema or pneumothorax, unexpected febrile state, and sepsis.
Pharyngoesophageal perforation is associated with difficult intubation, age over
60 years, and female gender. As in tracheal perforation, signs and symptoms are
often delayed in onset. Initial sore throat, cervical pain, and cough progress to
fever, dysphagia, and dyspnea, as mediastinitis, abscess, or pneumonia develop.
Mortality rates of up to 50% have been reported after esophageal perforation,
with better outcomes attributable to rapid detection and treatment.
Minimizing the risk of airway injury begins with the preoperative assessment.
Documentation of current dentition (including dental work) should be included.
The ASA algorithm for difficult airway management is a useful guide to have
immediately available in every anesthetizing location.

PERIPHERAL NERVE INJURY

The most commonly injured peripheral nerve is the ulnar nerve (Figure 54–6).
In a retrospective study of over 1 million patients, ulnar neuropathy (persisting
for more than 3 months) occurred in approximately 1 in 2700 patients. Of
interest, initial symptoms were most frequently noted more than 24 h after a
surgical procedure. Risk factors included male gender, hospital stay greater than
14 days, and very thin or obese body habitus. More than 50% of these patients
regained full sensory and motor function within 1 year. Anesthetic technique was
not implicated as a risk factor; 25% of patients with ulnar neuropathy underwent
monitored care or lower extremity regional technique. Many ulnar neuropathies
occurred despite notation of extra padding over the elbow area.

FIGURE 54–6 A: Pronation of the forearm can cause external compression of

the ulnar nerve in the cubital tunnel. B: Forearm supination avoids this problem.
(Modified with permission from Wadsworth TG. The cubital tunnel and the external compression
syndrome. Anesth Analg. 1974 Mar-April;53(2):303-308.)

The Role of Positioning

External pressure on a nerve may compromise its perfusion and disrupt its
cellular integrity, resulting in edema, ischemia, and necrosis. Pressure injuries
are particularly likely when nerves pass through closed compartments or take a
superficial course (eg, the peroneal nerve around the fibula). Postoperative lower
extremity neuropathies, particularly those involving the peroneal nerve, have
been associated with such factors as extreme degrees (high) and prolonged
(greater than 2 h) durations of the lithotomy position. Other risk factors for
postoperative lower extremity neuropathy include hypotension, thin body
habitus, older age, vascular disease, diabetes, and cigarette smoking. An axillary
(chest) “roll” is commonly used to reduce pressure on the inferior shoulder of
patients in the lateral decubitus position. This roll should be located caudad to
the axilla to prevent direct pressure on the brachial plexus and should be large
enough to relieve any pressure from the mattress on the lower shoulder.
The data are convincing that some postoperative peripheral nerve injuries are
not preventable. The risk of peripheral neuropathy should be included in
discussions leading to informed consent. When reasonable, patients with
contractures (or other causes of limited flexibility) can be positioned before
induction of anesthesia to check for feasibility and discomfort. Final positioning
should be evaluated prior to draping. In most circumstances, the head and neck
should be kept in a neutral position. Shoulder braces to support patients
maintained in a steep Trendelenburg position should be avoided if possible, and
shoulder abduction and lateral rotation should be minimized. The upper
extremities should not be extended greater than 90°. (There should be no
continuous external compression on the knee, ankle, or heel.) Although injuries
may still occur, additional padding may be helpful in vulnerable areas.
Documentation should include information on positioning, including the
presence of padding. Finally, patients who complain of sensory or motor
dysfunction in the postoperative period should be reassured that this is usually a
temporary condition. Motor and sensory function should be documented. When
symptoms persist for more than 24 h, the patient should be referred to a
neurologist, physiatrist, or hand surgeon who is knowledgeable about
perioperative nerve damage for evaluation. Physiological testing, such as nerve
conduction and electromyographic studies, can be useful to document whether
nerve damage is a new or chronic condition. In the latter case, fibrillations will
be observed in chronically denervated muscles. Fibrillations should not be
present in the first few days after an acute nerve injury.

Complications Related to Positioning

Changes of body position have physiological consequences that can be
exaggerated in disease states. General and regional anesthesia may limit the
cardiovascular response to such a change. Even positions that are safe for short
periods may eventually lead to complications in persons who are not able to
move in response to pain. Regional and general anesthesia abolish protective
reflexes and predispose patients to injury.
Many complications, including air embolism, blindness from sustained
pressure on the globe, and finger amputation following a crush injury, can be
caused by improper patient positioning (Table 54–4). These complications are
best prevented by evaluating the patient’s postural limitations during the
preanesthetic visit; padding pressure points, susceptible nerves, and any area of
the body that will possibly be in contact with the operating table or its
attachments; avoiding flexion or extension of a joint to its limit; having an
awake patient assume the position to ensure comfort; and understanding the
potential complications of each position. Monitors must often be disconnected
during patient repositioning, making this a time of greater risk for unrecognized
hemodynamic derangement or hypoventilation.

TABLE 54–4 Complications associated with patient positioning.

Compartment syndromes can result from hemorrhage into a closed space

following a vascular puncture or prolonged venous outflow obstruction,
particularly when associated with hypotension. In severe cases, this may lead to
muscle necrosis, myoglobinuria, and renal damage, unless the pressure within
the extremity compartment is relieved by surgical decompression (fasciotomy)
or in the abdominal compartment by laparotomy.

AWARENESS UNDER GENERAL ANESTHESIA

A continuing series of media reports have imprinted the fear of awareness under
general anesthesia into the psyche of the general population. Accounts of recall
and helplessness while paralyzed have made unconsciousness a primary concern
of patients undergoing general anesthesia. When unintended intraoperative
awareness does occur, patients may exhibit symptoms ranging from mild anxiety
to posttraumatic stress disorder (eg, sleep disturbances, nightmares, and social
difficulties).
Although the incidence is difficult to measure, approximately 2% of the
closed claims in the ASA Closed Claims Project database relate to awareness
under anesthesia. Analysis of the NHS Litigation Authority database from 1995
to 2007 revealed that 19 of 93 relevant claims were for “awake paralysis.”
Clearly, awareness is of great concern to patients and may lead to litigation.
Certain types of surgeries are most frequently associated with awareness,
including those for major trauma, obstetrics, and major cardiac procedures. In
some instances, awareness may result from the reduced depth of anesthesia that
can be tolerated by the patient. In early studies, recall rates for intraoperative
events during major trauma surgery have been reported to be as frequent as 43%;
the incidence of awareness during cardiac surgery and cesarean sections is 1.5%
and 0.4%, respectively. As of 1999, the ASA Closed Claims Project reported 79
awareness claims; approximately 20% of the claims were for awake paralysis,
and the remainder of the claims were for recall under general anesthesia. Most
claims for awake paralysis were thought to be due to errors in drug labeling and
administration, such as administering paralytics before inducing anesthesia.
Since the 1999 review, another 71 cases have appeared in the database. Claims
for recall were more likely in women undergoing general anesthesia without a
volatile agent. Patients with long-term substance abuse may have increased
anesthesia requirements that if not met can lead to awareness.
Other specific causes of awareness include inadequate inhalational anesthetic
delivery (eg, from vaporizer malfunction) and medication errors. Some patients
may complain of awareness, when, in fact, they received monitored anesthesia
care or regional anesthesia with moderate sedation; thus, anesthetists should
make sure that patients have reasonable expectations when regional or local
techniques are employed. Likewise, patients requesting regional or local
anesthesia because they want to “see it all” or “stay in control” often can become
irate when sedation dulls their memory of the perioperative experience. In all
cases, frank discussion between anesthesia staff and the patient is necessary to
avoid unrealistic expectations.
Some clinicians routinely discuss the possibility of intraoperative recall and
the steps that will be taken to minimize it as part of the informed consent for
general anesthesia. This makes particular sense for those procedures in which
recall is more likely. It is advisable to also remind patients who are undergoing
monitored anesthesia care with sedation that awareness is expected. Volatile
anesthetics should be administered at a level consistent with amnesia. If this is
not possible, benzodiazepines (or scopolamine, or both) can be used. Movement
of a patient may indicate inadequate anesthetic depth. Documentation should
include end-tidal concentrations of anesthetic gases (when available) and
dosages of amnesic drugs. Use of a bispectral index scale (BIS) monitor or
similar monitors may be helpful, although randomized clinical trials have failed
to demonstrate a reduced incidence of awareness with use of BIS when
compared with appropriate concentrations of volatile agents. Finally, if there is
evidence of intraoperative awareness during postoperative rounds, the
practitioner should obtain a detailed account of the experience, answer patient
questions, be very empathetic, and refer the patient for psychological counseling
if appropriate.

EYE INJURY
A wide range of conditions from simple corneal abrasion to blindness have been
reported. Corneal abrasion is by far the most common and transient eye injury.
The ASA Closed Claims Project identified a small number of claims for
abrasion, in which the cause was rarely identified (20%) and the incidence of
permanent injury was low (16%). It also identified a subset of claims for
blindness that resulted from patient movement during ophthalmological surgery.
These cases occurred in patients receiving either general anesthesia or monitored
anesthesia care.
Although the cause of corneal abrasion may not be obvious, securely closing
the eye lids with tape after loss of consciousness (but prior to intubation) and
avoiding direct contact between eyes and oxygen masks, drapes, lines, and
pillows (particularly during monitored anesthesia care, in transport, and in
nonsupine positions) can help to minimize the possibility of injury. Adequate
anesthetic depth (and, in most cases, paralysis) should be maintained to prevent
movement during ophthalmological surgery under general anesthesia. In patients
scheduled for MAC, the patient must understand that movement under
monitored care is hazardous and, thus, that only minimal sedation may be
administered to ensure that he or she can cooperate. Vigilance must be
maintained regarding patients’ propensity to want to rub their eyes following
emergence from anesthesia, especially in response to blurred vision secondary to
residual eye lubrication ointment.
Ischemic optic neuropathy (ION) is a devastating perioperative complication.
ION is now the most common cause of postoperative vision loss. Postoperative
vision loss is most commonly reported after cardiopulmonary bypass, radical
neck dissection, and spinal surgeries in the prone position. Both preoperative and
intraoperative factors may be contributory. Many of the case reports implicate
preexisting hypertension, diabetes, coronary artery disease, and smoking,
suggesting that preoperative vascular abnormalities may play a role.
Intraoperative deliberate hypotension and anemia have also been implicated (in
spine surgery), perhaps because of their potential to reduce oxygen delivery.
Finally, prolonged surgical time in positions that compromise venous outflow
(prone, head down, compressed abdomen) have also been found to be factors in
spine surgery. Symptoms are usually present immediately upon awakening from
anesthesia, but have been reported up to 12 days postoperatively. Such
symptoms range from decreased visual acuity to complete blindness. Analysis of
case records submitted to the ASA Postoperative Vision Loss Registry revealed
that vision loss was secondary to ION in 83 of 93 cases. Instrumentation of the
spine was associated with ION when surgery lasted more than 6 h and blood loss
was more than 1 L. ION can occur in patients whose eyes are free of pressure
secondary to the use of pin fixation, indicating that direct pressure on the eye is
not required to produce ION. Cortical blindness can likewise occur
perioperatively in association with profound hypoperfusion or embolic loads.
Recovery from cortical blindness is more likely than from other causes of
perioperative vision loss. Increased venous pressure in patients in the
Trendelenburg position may reduce blood flow to the optic nerve.
It is difficult to formulate recommendations to prevent this complication
because risk factors for ION are often unavoidable. Steps that might be taken
include (1) limiting the degree and duration of hypotension during controlled
(deliberate) hypotension, (2) administering a transfusion to severely anemic
patients who seem to be at risk of ION, and (3) discussing with the surgeon the
possibility of staged operations in high-risk patients to limit prolonged
procedures.
Of note, postoperative vision loss can be caused by other mechanisms as well,
including angle closure glaucoma or embolic phenomenon to the cortex or
retina. Immediate evaluation is advised.

CARDIOPULMONARY ARREST DURING SPINAL

ANESTHESIA
Sudden cardiac arrest during an otherwise routine administration of spinal
anesthetics is an uncommon complication. The initial published report was a
closed claims analysis of 14 patients who experienced cardiac arrest during
spinal anesthesia. The cases primarily involved young (average age 36 years),
relatively healthy (ASA physical status I–II) patients who were given appropriate
doses of local anesthetic that produced a high dermatomal level of block prior to
arrest (T4 level). Respiratory insufficiency with hypercarbia due to sedatives was
thought to be a potential contributing factor. The average time from induction of
spinal anesthesia to arrest was 36 min, and, in all cases, arrest was preceded by a
gradual decline in heart rate and blood pressure. Just prior to arrest, the most
common signs were bradycardia, hypotension, and cyanosis. Treatment
consisted of ventilatory support, ephedrine, atropine, cardiopulmonary
resuscitation (average duration 10.9 min), and epinephrine. Despite these
interventions, 10 patients remained comatose and 4 patients regained
consciousness with significant neurological deficits. A subsequent study
concluded that such arrests had little relationship to sedation, but were related to
extensive degrees of sympathetic blockade, with unopposed vagal tone and
profound bradycardia. Rapid appropriate treatment of bradycardia and
hypotension is essential to minimize the risk of profound bradycardia, complete
heart block, or cardiac arrest. Early treatment of bradycardia with atropine or
glycopyrrolate may prevent a downward spiral. Stepwise doses of ephedrine,
epinephrine, and other vasoactive drugs should be given to treat hypotension. If
cardiopulmonary arrest occurs, ventilatory support, cardiopulmonary
resuscitation, and full resuscitation doses of atropine and epinephrine should be
administered without delay.

HEARING LOSS
Perioperative hearing loss is usually transient and often goes unrecognized. The
incidence of low-frequency hearing loss following dural puncture may be as
high as 50%. It seems to be due to cerebrospinal fluid leak and, if persistent, can
be relieved with an epidural blood patch. Hearing loss following general
anesthesia can be due to a variety of causes and is much less predictable.
Mechanisms include middle ear barotrauma, vascular injury, and ototoxicity of
drugs (aminoglycosides, loop diuretics, nonsteroidal antiinflammatory drugs,
and antineoplastic agents).

ALLERGIC REACTIONS
Hypersensitivity (or allergic) reactions are exaggerated immunological responses
to antigenic stimulation in previously sensitized persons. The antigen, or
allergen, may be a protein, polypeptide, or smaller molecule. Moreover, the
allergen may be the substance itself, a metabolite, or a breakdown product.
Patients may be exposed to antigens through the respiratory tract,
gastrointestinal tract, eyes, skin and from previous intravenous, intramuscular, or
peritoneal exposure.
Anaphylaxis occurs when inflammatory agents are released from basophils
and mast cells as a result of an antigen interacting with immunoglobulin (Ig) E.
Anaphylactoid reactions manifest themselves in the same manner as
anaphylactic reactions, but are not the result of an interaction with IgE. Direct
activation of complement and IgG-mediated complement activation can result in
similar inflammatory mediator release and activity.
Depending on the antigen and the immune system components involved,
hypersensitivity reactions are classically divided into four types (Table 54–5). In
many cases, an allergen (eg, latex) may cause more than one type of
hypersensitivity reaction. Type I reactions involve antigens that cross-link IgE
antibodies, triggering the release of inflammatory mediators from mast cells. In
type II reactions, complement-fixing (C1-binding) IgG antibodies bind to
antigens on cell surfaces, activating the classic complement pathway and lysing
the cells. Examples of type II reactions include hemolytic transfusion reactions
and heparin-induced thrombocytopenia. Type III reactions occur when antigen–
antibody (IgG or IgM) immune complexes are deposited in tissues, activating
complement and generating chemotactic factors that attract neutrophils to the
area. The activated neutrophils cause tissue injury by releasing lysosomal
enzymes and toxic products. Type III reactions include serum sickness reactions
and acute hypersensitivity pneumonitis. Type IV reactions, often referred to as
delayed hypersensitivity reactions, are mediated by CD4+ T lymphocytes that
have been sensitized to a specific antigen by prior exposure. Examples of type
IV reactions are those associated with tuberculosis, histoplasmosis,
schistosomiasis, hypersensitivity pneumonitis, and some autoimmune disorders.

TABLE 54–5 Hypersensitivity reactions.

1. Immediate Hypersensitivity Reactions
Initial exposure of a susceptible person to an antigen induces CD4+ T cells to
lymphokines that activate and transform specific B lymphocytes into plasma
cells, producing allergen-specific IgE antibodies (Figure 54–7). The Fc portion
of these antibodies then associates with high affinity receptors on the cell surface
of tissue mast cells and circulating basophils. During subsequent reexposure to
the antigen, it binds the Fab portion of adjacent IgE antibodies on the mast cell
surface, inducing degranulation and release of inflammatory lipid mediators and
additional cytokines from the mast cell. The end result is the release of
histamine, tryptase, proteoglycans (heparin and chondroitin sulfate), and
carboxypeptidases. An elevated tryptase concentration in the setting of clinical
signs of hypersensitivity signals mast cell activation and is the diagnostic test of
choice for anaphylactic reactions. The combined effects of these mediators can
produce arteriolar vasodilation, increased vascular permeability, increased mucus
secretion, smooth muscle contraction, and other clinical manifestations of type I
reactions.
FIGURE 54–7 A: Induction of IgE-mediated allergic sensitivity to drugs and
other allergens. B: Response of IgE-sensitized cells to subsequent exposure to
allergens. Ig, immunoglobulin. (Reproduced with permission from Katzung BG, ed. Basic &
Clinical Pharmacology. 8th ed. New York, NY: McGraw-Hill; 2001.)

Type I hypersensitivity reactions are classified as atopic or nonatopic. Atopic

disorders typically affect the skin or respiratory tract and include allergic rhinitis,
atopic dermatitis, and allergic asthma. Nonatopic hypersensitivity disorders
include urticaria, angioedema, and anaphylaxis; when these reactions are mild,
they are confined to the skin (urticaria) or subcutaneous tissue (angioedema), but
when they are severe, they become generalized and a life-threatening medical
emergency (anaphylaxis). Urticarial lesions are characteristically well-
circumscribed skin wheals with raised erythematous borders and blanched
centers; they are intensely pruritic. Angioedema presents as deep, nonpitting
cutaneous edema from marked vasodilation and increased permeability of
subcutaneous blood vessels. When angioedema is extensive, it can be associated
with large fluid shifts; when it involves the pharyngeal or laryngeal mucosa, it
can rapidly compromise the airway.
Angioedema can lead to airway compromise and is frequently the cause for
anesthesiology airway management consultation in the emergency department.
Angioedema is secondary to increased capillary permeability secondary either to
activation of mast cells or through kinin mediation. Patients taking angiotensin-
converting enzyme (ACE) inhibitors may experience kinin-mediated
angioedema. Bradykinin is inactivated by ACE and consequently it may
accumulate when ACE is inhibited. Hereditary angioedema can occur in patients
with ineffective amounts of complement inhibitor (C1-INH). Treatment for
angioedema first focuses upon airway management as needed. Fresh frozen
plasma can be given to increase ACE if ACE inhibition is thought to be
contributing to angioedema. The bradykinin receptor antagonist icatibant can
likewise be administered if available. C1-INH replacement protein is also
available to inhibit kinin synthesis. The kallikrein inhibitor ecallantide can also
be used to decrease bradykinin production (Figure 54–8).

FIGURE 54–8 Treatment of acute attacks of angioedema based on underlying

etiology. ACE-I, angiotensin-converting enzyme inhibitor; ARB, angiotensin
receptor blocker; C1INHRP, C1 inhibitor replacement protein; FFP, fresh frozen
plasma; IV, intravenous; NSAID, nonsteroidal anti-inflammatory drug. (Reproduced
with permission from Barbara D, Ronan K, Maddox D, et al. Perioperative angioedema; background,
diagnosis and management. J Clin Anesth. 2013 Jun;25(4):335-343.)

2. Anaphylactic Reactions
Anaphylaxis is an exaggerated response to an allergen (eg, antibiotic) that is
mediated by a type I hypersensitivity reaction. The syndrome appears within
minutes of exposure to a specific antigen in a sensitized person and
characteristically presents as acute respiratory distress, circulatory shock, or
both. Death may occur from asphyxiation or irreversible circulatory shock. The
incidence of anaphylactic reactions during anesthesia has been estimated at a
rate of 1:3500 to 1:20,000 anesthetics. A study of 789 anaphylactic and
anaphylactoid reactions reported that the most common source antigens were
neuromuscular blockers (58%), latex (17%), and antibiotics (15%).
The most important mediators of anaphylaxis are histamine, leukotrienes,
basophil kallikrein (BK-A), and platelet-activating factor. They increase vascular
permeability and contract smooth muscle. H1-receptor activation contracts
bronchial smooth muscle, whereas H2-receptor activation causes vasodilation,
mucus secretion, tachycardia, and increased myocardial contractility. BK-A
cleaves bradykinin from kininogen; bradykinin increases vascular permeability
and vasodilation and contracts smooth muscle. Activation of Hageman factor
can initiate intravascular coagulation. Eosinophil chemotactic factor of
anaphylaxis, neutrophil chemotactic factor, and leukotriene B4 attract
inflammatory cells that mediate additional tissue injury. Angioedema of the
pharynx, larynx, and trachea produce upper airway obstruction, whereas
bronchospasm and mucosal edema result in lower airway obstruction.
Transudation of fluid into the skin (angioedema) and viscera produces
hypovolemia, whereas arteriolar vasodilation decreases systemic vascular
resistance. Coronary hypoperfusion and arterial hypoxemia promote arrhythmias
and myocardial ischemia. Leukotriene and prostaglandin mediators may also
cause coronary vasospasm. Prolonged circulatory shock leads to progressive
lactic acidosis and ischemic damage to vital organs. Table 54–6 summarizes
important manifestations of anaphylactic reactions.

TABLE 54–6 Clinical manifestations of anaphylaxis.

 Anaphylactoid reactions resemble anaphylaxis but do not depend on IgE
antibody interaction with antigen. A drug can directly release histamine from
mast cells (eg, urticaria following high-dose morphine sulfate) or activate
complement. Despite differing mechanisms, anaphylactic and anaphylactoid
reactions typically are clinically indistinguishable and equally life threatening.
Table 54–7 lists common causes of anaphylactic and anaphylactoid reactions.

TABLE 54–7 Causes of anaphylactic and anaphylactoid reactions.1

Serum tryptase measurement is helpful in confirming the diagnosis of an

anaphylactic reaction. Treatment must be immediate and tailored to the severity
of the reaction (Table 54–8).
TABLE 54–8 Treatment of anaphylactic and anaphylactoid reactions.

3. Allergic Reactions to Anesthetic Agents

True anaphylaxis due to anesthetic agents is rare; anaphylactoid reactions are
much more common. Risk factors associated with hypersensitivity to anesthetics
include female gender, atopic history, preexisting allergies, and previous
anesthetic exposures. An estimated 1 in 6500 patients has an allergic reaction to
a muscle relaxant. In many instances, the patient had no previous exposure to the
agent. Investigators suggest that over-the-counter drugs, cosmetics, and food
products, many of which contain tertiary or quaternary ammonium ions, can
sensitize susceptible individuals.
The incidence of anaphylaxis for thiopental and propofol is 1 in 30,000 and 1
in 60,000, respectively. Allergic reactions to etomidate, ketamine, and
benzodiazepines are exceedingly rare. True anaphylactic reactions due to opioids
are far less common than nonimmune histamine release. Similarly, anaphylactic
reactions to local anesthetics are much less common than vasovagal reactions,
toxic reactions to accidental intravenous injections, and side effects from
absorbed or intravenously injected epinephrine. IgE-mediated reactions to
certain ester-type local anesthetics (eg, procaine and benzocaine), however, are
well described secondary to reaction to the metabolite, para-aminobenzoic acid.
In contrast, true anaphylaxis due to amide-type local anesthetics is very rare; in
some instances, the preservative (paraben or methylparaben) was believed to be
responsible for an apparent anaphylactoid reaction to a local anesthetic.
Moreover, the cross-reactivity between amide-type local anesthetics seems to be
low. Volatile anesthetics are not likely to initiate anaphylaxis.

4. Latex Allergy
The severity of allergic reactions to latex-containing products ranges from mild
contact dermatitis to life-threatening anaphylaxis. Latex allergy associated with
anaphylaxis during anesthesia is now much rarer due to removal of latex-
containing products from the medical environment. Most serious reactions seem
to involve a direct IgE-mediated immune response to polypeptides in natural
latex, although some cases of contact dermatitis may be due to a type IV
sensitivity reaction to chemicals introduced in the manufacturing process.
Nonetheless, a relationship between the occurrence of contact dermatitis and the
probability of future anaphylaxis has been suggested. Chronic exposure to latex
and a history of atopy increases the risk of sensitization. Healthcare workers and
patients undergoing frequent procedures with latex items (eg, repeated urinary
bladder catheterization, barium enema examinations) should therefore be
considered at increased risk. Patients with spina bifida, spinal cord injury, and
congenital abnormalities of the genitourinary tract have a markedly increased
incidence of latex allergy. The incidence of latex anaphylaxis in children is
estimated to be 1 in 10,000. A history of allergic symptoms to latex should be
sought in all patients during the preanesthetic interview. Foods that cross-react
with latex include mango, kiwi, chestnut, avocado, passion fruit, and banana.
Interleukin (IL)-18 and IL-13 single nucleotide polymorphisms may affect the
sensitivity of individuals to latex and promote allergic responses.
Anaphylactic reactions to latex may be confused with reactions to other
substances (eg, drugs, blood products) because the onset of symptoms can be
delayed for more than 1 h after initial exposure. Treatment is the same as for
other forms of anaphylactic reactions. Preventing a reaction in sensitized patients
includes pharmacological prophylaxis and absolute avoidance of latex.
Preoperative administration of H1 and H2 histamine antagonists and steroids may
provide some protection, although their use is controversial. Although most
pieces of anesthetic equipment are now latex-free, some may still contain latex.
Manufacturers of latex-containing medical products must label their products
accordingly. Only devices specifically known not to contain latex (eg,
polyvinyl or neoprene gloves, silicone endotracheal tubes or laryngeal
masks, plastic face masks) can be used in latex-allergic patients.

5. Allergies to Antibiotics
Many true drug allergies in surgical patients are due to antibiotics, mainly β-
lactam antibiotics, such as penicillins and cephalosporins. Although 1% to 4% of
β-lactam administrations result in allergic reactions, only 0.004% to 0.015% of
these reactions result in anaphylaxis. Up to 2% of the general population is
allergic to penicillin, but only 0.01% of penicillin administrations result in
anaphylaxis. Cephalosporin cross-sensitivity in patients with penicillin allergy is
estimated to be 2% to 7%, but a history of an anaphylactic reaction to penicillin
increases the cross-reactivity rate up to 50%. Patients with a prior history of an
anaphylactic reaction to penicillin should therefore not receive a cephalosporin.
Although imipenem exhibits similar cross-sensitivity, aztreonam seems to be
antigenically distinct and reportedly does not cross-react with other β-lactams.
Sulfonamide allergy is also relatively common in surgical patients. Sulfa drugs
include sulfonamide antibiotics, furosemide, hydrochlorothiazide, and captopril.
Fortunately, the frequency of cross-reactivity among these agents is low.
Like cephalosporins, vancomycin is commonly used for antibiotic
prophylaxis in surgical patients. Vancomycin is associated with a reaction (the
“red man” or “red neck” syndrome) that consists of intense pruritus, flushing,
and erythema of the head and upper torso in addition to arterial hypotension.
Isolated systemic hypotension seems to be primarily mediated by histamine
release, because pretreatment with H1 and H2 antihistamines can prevent
hypotension, even with rapid rates of vancomycin administration. Vancomycin
can also produce true anaphylactic or anaphylactoid reactions. Protamine
commonly causes vasodilatory hypotension and less commonly presents as an
anaphylactoid reaction with pulmonary hypertension and systemic hypotension.
Immunological mechanisms are associated with other perioperative
pathologies. Transfusion-related lung injury may be secondary to the activity of
antibodies in the donor plasma, producing a hypersensitivity reaction that leads
to lung infiltrates and hypoxemia (see Chapter 51). IgG antibody formation
directed at heparin–PF4 complexes results in platelet activation, thrombosis, and
heparin-induced thrombocytopenia.

QUALITY MANAGEMENT
Risk management and continuous quality improvement programs at the
departmental level may reduce anesthetic morbidity and mortality rates, and
decrease perioperative costs, by addressing monitoring standards, equipment,
practice guidelines, continuing education, care variation and quality of care, and
staffing and “system” issues. Specific responsibilities of peer review committees
include identifying (and, ideally, preventing) potential problems, formulating and
periodically revising departmental policies, ensuring the availability of properly
functioning anesthetic equipment, enforcing standards required for clinical
privileges, and evaluating the appropriateness and quality of patient care. A
quality improvement system impartially and continuously reviews
complications, compliance with standards, and quality indicators (see Chapter
59).
Health care purchasers seek maximal health care value.

Consequently, anesthesia providers must consistently deliver high-quality results

while minimizing expenses. To achieve value, hospitals and providers alike have
looked to adopt principles of continuous improvement borrowed from industry.
Adapting the work of W. Edwards Deming, health care organizations often
employ the PDSA (Plan-Do-Study-Act) cycle to promote ongoing improvement,
to standardize results, and to reduce waste (see Figure 54–9). So-called lean
management strategies are used to achieve maximal health care value by
continually attempting to improve processes to minimize variability so to ensure
optimal results with minimal waste.

FIGURE 54–9 Plan-Do-Study-Act (PDSA) cycle for improvement. (Reproduced

with permission from Moriates C, Arora V, Shah N, eds. Understanding Value-Based Healthcare. New
York, NY: McGraw-Hill Education; 2015.)

OCCUPATIONAL HAZARDS IN
ANESTHESIOLOGY
Anesthesia providers spend much of their workday exposed to anesthetic gases,
low-dose ionizing radiation, electromagnetic fields, blood products, and
workplace stress. Each of these can contribute to negative health effects. A 2000
paper compared the mortality risks of anesthesiologists and internists. Death
from heart disease or cancer did not differ between the groups; however,
anesthesiologists had an increased rate of suicide and illicit drug-related death
(Table 54–9). Anesthesiologists also had a greater chance of death from external
causes, such as boating, bicycling, and aeronautical accidents compared with
internists. Nevertheless, both anesthesiologists and internists had lower mortality
than the general population, likely due to their higher socioeconomic status.
Anesthesiologists’ access to parenteral opioids possibly contributes to a 2.21
relative risk for drug-related deaths compared with that of internists.

TABLE 54–9 Relative rate ratios for drug and suicide deaths comparing
anesthesiologists with internists before and after January 1, 1987.1,2

1. Chronic Exposure to Anesthetic Gases

There is no clear evidence that exposure to trace amounts of anesthetics
presents a health hazard to operating room personnel. However, because
previous studies examining this issue have yielded flawed but conflicting results,
the U.S. Occupational Health and Safety Administration (OSHA) continues to
set maximum acceptable trace concentrations of less than 25 ppm for nitrous
oxide and 0.5 ppm for halogenated anesthetics (2 ppm if the halogenated agent is
used alone). Achieving these low levels depends on efficient scavenging
equipment, adequate operating room ventilation, and conscientious anesthetic
technique. Most people cannot detect the odor of volatile agents at a
concentration of less than 30 ppm. If there is no functioning scavenging system,
operating room anesthetic gas concentrations reach 3000 ppm for nitrous oxide
and 50 ppm for volatile agents.
2. Infectious Diseases
Hospital workers are exposed to many infectious diseases prevalent in the
community (eg, respiratory viral infections, rubella, and tuberculosis). Herpetic
whitlow is an infection of the finger with herpes simplex virus type 1 or 2 and
usually involves direct contact of previously traumatized skin with contaminated
oral secretions. Prevention involves wearing gloves when contacting oral
secretions.
Viral DNA has been identified in the smoke plume generated during laser
treatment of condylomata. The theoretical possibility of viral transmission from
this source can be minimized by using smoke evacuators, gloves, and
appropriate OSHA-approved masks.
More disturbing is the potential of acquiring serious blood-borne infections,
such as hepatitis B, hepatitis C, or HIV. Although parenteral transmission of
these diseases can occur following mucous membrane, cutaneous, or
percutaneous exposure to infected body fluids, accidental injury with a needle
contaminated with infected blood represents the most common occupational
mechanism. The risk of transmission can be estimated if three factors are known:
the prevalence of the infection within the patient population, the incidence of
exposure (eg, frequency of needlestick), and the rate of seroconversion after a
single exposure. The seroconversion rate after a specific exposure depends on
several factors, including the infectivity of the organism, the stage of the
patient’s disease (extent of viremia), the size of the inoculum, and the immune
status of the health care provider. Rates of seroconversion following a single
needlestick are estimated to range between 0.3% and 30%. Hollow
(hypodermic) needles pose a greater risk than do solid (surgical) needles because
of the potentially larger inoculum. The use of gloves, needleless systems, or
protected needle devices may decrease the incidence of some (but not all) types
of injury.
The initial management of needlesticks involves cleaning the wound and
notifying the appropriate authority within the health care facility. After an
exposure, anesthesia workers should report to their institution’s emergency or
employee health department for appropriate counseling on postexposure
prophylaxis options. All operating room staff should be made aware of the
institution’s employee health notification pathway for needlestick and other
injuries.
Fulminant hepatitis B (1% of acute infections) carries a 60% mortality rate.
Chronic active hepatitis (<5% of all cases) is associated with an increased
incidence of hepatic cirrhosis and hepatocellular carcinoma. Transmission of the
virus is primarily through contact with blood products or body fluids. The
diagnosis is confirmed by detection of hepatitis B surface antigen (HBsAg).
Uncomplicated recovery is signaled by the disappearance of HBsAg and the
appearance of antibody to the surface antigen (anti-HBs). A hepatitis B vaccine
is available and is strongly recommended prophylactically for anesthesia
personnel. The appearance of anti-HBs after a three-dose regimen indicates
successful immunization.
Hepatitis C is another important occupational hazard in anesthesiology. Many
of these infections lead to chronic hepatitis, which, although often
asymptomatic, can progress to liver failure and death. It is now possible to cure
hepatitis C with antiviral drug regimens.
Anesthesia personnel seem to be at low risk for the occupational contraction
of HIV. Universal contact precautions should be routinely employed to mitigate
the risk of transmission of infectious diseases to anesthesia workers.

3. Substance Abuse
Anesthesiology is a high-risk medical specialty for substance abuse. Probable
reasons for this include the stress of anesthetic practice and the easy availability
of drugs with addiction potential (potentially attracting people at risk of
addiction to the field). The likelihood of developing substance abuse is increased
by coexisting personal problems.
The voluntary use of nonprescribed mood-altering pharmaceuticals is a
disease. Untreated, substance abuse often leads to death from drug overdose—
intentional or unintentional. One of the greatest challenges in treating drug abuse
is identifying the afflicted individual, as denial is a consistent feature.
Unfortunately, changes evident to an outside observer are often both vague and
late: reduced involvement in social activities, subtle changes in appearance,
extreme mood swings, and altered work habits. Options related to routine and
for-cause workplace drug testing can be explored with a certified medical review
officer (MRO). Treatment begins with a careful, well-planned intervention.
Those inexperienced in this area would be well advised to consult with an
addictionologist or their employee health department, local medical society, or
licensing authority about how to proceed. The goal is to enroll the individual in a
formal rehabilitation program. The possibility that one may lose one’s medical
license and be unable to return to practice provides powerful motivation. Some
diversion programs report a success rate of approximately 70%; however, most
rehabilitation programs report a recurrence rate of at least 25%. Long-term
compliance often involves continued participation in support groups (eg,
Narcotics Anonymous), random urine testing, and oral naltrexone therapy (a
long-acting opioid antagonist). Effective prevention strategies are difficult to
formulate; “better” control of drug availability is unlikely to deter a determined
individual. It is unlikely that education about the severe consequences of
substance abuse will bring new information to the potential drug-abusing
physician. There remains controversy regarding the rate at which anesthesia staff
will experience recidivism. Many experts argue for a “one strike and you’re out”
policy for anesthesiology residents who abuse injectable drugs. The decision as
to whether a fully trained and certified physician who has been discovered to
abuse injectable drugs should return to anesthetic practice after completing a
rehabilitation program varies and depends on the rules and traditions of the
practice group, the medical center, the relevant medical licensing board, and the
perceived likelihood of recidivism. Physicians returning to practice following
successful completion of a program must be carefully monitored over the long
term, as relapses can occur years after apparent successful rehabilitation.
Alcohol abuse is a common problem among physicians and nurses, and
anesthesia personnel are no exception. Interventions for alcohol abuse, as is true
for injectable drug abuse, must be carefully orchestrated. Guidance from the
employee health program, local medical society, or licensing authority is highly
recommended.

4. Ionizing Radiation Exposure

The use of imaging equipment (eg, fluoroscopy) during surgery and
interventional radiological procedures exposes the anesthesiologist to the
potential risks of ionizing radiation. The three most important methods of
minimizing radiation doses are limiting total exposure time during procedures,
using proper barriers, and maximizing one’s distance from the source of
radiation. Anesthesiologists who routinely perform fluoroscopic image-guided
invasive procedures should consider wearing protective eyewear incorporating
radiation shielding. Lead glass partitions or lead aprons with thyroid shields are
mandatory for all personnel who are exposed to ionizing radiation. The inverse
square law states that the dosage of radiation varies inversely with the square of
the distance. Thus, the exposure at 4 m will be one-sixteenth that at 1 m. The
maximum recommended occupational whole-body exposure to radiation is 5
rem/y. This can be monitored with an exposure badge. The health impact of
exposure to electromagnetic radiation remains unclear.
CASE DISCUSSION

Unexplained Intraoperative Tachycardia & Hypertension

A 73-year-old man is scheduled for emergency relief of an intestinal
obstruction from a sigmoid volvulus. The patient had a myocardial
infarction 1 month earlier that was complicated by congestive heart
failure. His blood pressure is 160/90 mm Hg, pulse 110 beats/min,
respiratory rate 22 breaths/min, and temperature 38.8°C.
Why is this case an emergency?
Strangulation of the bowel begins with venous obstruction, but can
quickly progress to arterial occlusion, ischemia, infarction, and perforation.
Acute peritonitis could lead to severe dehydration, sepsis, shock, and
multiorgan failure.
What special monitoring is appropriate for this patient?
Because of the history of recent myocardial infarction and congestive
heart failure, an arterial line would be useful. TEE and pulse contour
analysis monitors of cardiac output could be used. Pulmonary arterial
flotation catheters have often been used in the past, but they are associated
with significant complications and their use does not improve patient
outcomes. Large fluid shifts should be anticipated. Furthermore,
information regarding myocardial oxygen supply (diastolic blood pressure)
and demand (systolic blood pressure, left ventricular wall stress, and heart
rate) should be continuously available.
What cardiovascular medications might be useful during
general anesthesia?
Severe tachycardia or extremes in arterial blood pressure should be
avoided. During the laparotomy, gradual increases in heart rate and blood
pressure are noted. ST-segment elevations appear on the electrocardiogram.
A nitroglycerin infusion is started. The heart rate is now 130 beats/min, and
the blood pressure is 220/140 mm Hg. The concentration of volatile
anesthetic is increased, and metoprolol is administered intravenously in 1-
mg increments. This results in a decline in heart rate to 115 beats/min, with
no change in blood pressure. Suddenly, the rhythm converts to ventricular
 tachycardia, with a profound drop in blood pressure. As amiodarone is
being administered and the defibrillation unit prepared, the rhythm
degenerates into ventricular fibrillation.
What can explain this series of events?
A differential diagnosis of pronounced tachycardia and hypertension
might include pheochromocytoma, malignant hyperthermia, or thyroid
storm. In this case, further inspection of the nitroglycerin infusion reveals a
labeling error: although the tubing was labeled “nitroglycerin,” the infusion
bag was labeled “epinephrine.”
How does this explain the paradoxic response to metoprolol?
Metoprolol is a β1-adrenergic antagonist. It inhibits epinephrine’s β1-
stimulation of heart rate, but does not antagonize α-induced
vasoconstriction. The net result is a decrease in heart rate, but a sustained
increase in blood pressure.
What is the cause of the ventricular tachycardia?
An overdose of epinephrine can cause life-threatening ventricular
arrhythmias. In addition, if a central venous catheter was malpositioned,
with its tip in the right ventricle, the catheter tip could have stimulated
ventricular arrhythmias.
What other factors may have contributed to this anesthetic
mishap?
Multiple factors will often combine to create an anesthetic misadventure.
Incorrect drug labels are but one example of errors that can result in patient
injury. Inadequate preparation, technical failures, knowledge deficits, and
practitioner fatigue or distraction can all contribute to adverse outcomes.
Careful adherence to hospital policies, checklists, patient identification
procedures, and surgical and regional block timeouts can all help to prevent
iatrogenic complications.

GUIDELINES
Institute for Healthcare Improvement. PDSA cycles.
http://www.ihi.org/resources/pages/tools/plandostudyactworksheet.aspx.
 Accessed October 18, 2017.
Practice advisory for the prevention of perioperative peripheral neuropathies: A
report by the American Society of Anesthesiologists Task Force on
prevention of peripheral neuropathies. Anesthesiology. 2011;114:1.

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 CHAPTER

55
Cardiopulmonary Resuscitation
N. Martin Giesecke, MD and George W. Williams, MD, FASA, FCCP

KEY CONCEPTS

Cardiopulmonary resuscitation and emergency cardiac care (CPR-

ECC) should be considered any time an individual cannot adequately
oxygenate or perfuse vital organs—not only following cardiac or
respiratory arrest.
Regardless of which transtracheal jet ventilation system is chosen, it
must be readily available, use low-compliance tubing, and have secure
connections.
Chest compressions should not be delayed; intubation may take place
during CPR or the pulse check.
Attempts at intubation should not interrupt ventilation for more than 10
s.
Chest compressions should begin prior to the delivery of breaths in the
pulseless patient.
Whether adult resuscitation is performed by a single rescuer or by two
rescuers, two breaths are administered every 30 compressions (30:2),
allowing 3 to 4 s for each two breaths. The cardiac compression rate
should be 100/min regardless of the number of rescuers.
Health care personnel working in hospitals and ambulatory care
facilities must be able to provide early defibrillation to patients with
ventricular fibrillation as soon as possible. Shock should be delivered
within 3 to 4 min of arrest.
If intravenous cannulation is difficult, an intraosseous infusion can
provide emergency vascular access in children and adults.
Lidocaine, epinephrine, atropine, naloxone, and vasopressin (but not
sodium bicarbonate) can be delivered via a catheter whose tip extends
 past the endotracheal tube. Dosages 2 to 2½ times higher than
recommended for intravenous use, diluted in 10 mL of normal saline or
distilled water, are recommended for adult patients.
Because carbon dioxide, but not bicarbonate, readily crosses cell
membranes and the blood–brain barrier, arterial hypercapnia causes
intracellular tissue acidosis.
A wide QRS complex following a pacing spike signals electrical
capture, but mechanical (ventricular) capture must be confirmed by an
improving pulse or blood pressure.

Cardiopulmonary resuscitation and emergency cardiac care (CPR-ECC)

should be considered any time an individual cannot adequately oxygenate or
perfuse vital organs—not only following cardiac or respiratory arrest.
This chapter presents an overview of the 2015 American Heart Association
(AHA) Guidelines Update for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care, which provides revised recommendations for establishing
and maintaining the “CABDs” of cardiopulmonary resuscitation: Circulation,
Airway, Breathing, and Defibrillation (Table 55–1, Figures 55–1 and 55–2).
The 2015 CPR-ECC guidelines have been updated with new evidence-based
recommendations. Points of particular importance for the layperson are that the
pulse should not be checked, and chest compression without ventilation may be
as effective as compression with ventilation for the first several minutes. If a
second lay rescuer is unavailable to perform mouth-to-mask ventilation, chest
compressions alone are preferred to the primary rescuer attempting to do both.
For the health care provider, defibrillation using biphasic electrical current works
best and endotracheal tube (ETT) placement should be confirmed with a
quantitative capnographic waveform analysis. More importantly, in the new
guidelines, emphasis has been placed on the quality and adequacy of
compressions, minimizing interruption time of compressions and preshock pause
(the time taken from the last compression to the delivery of shock).

TABLE 55–1 Emergency cardiac care (ECC).

FIGURE 55–1 Universal algorithm for adult emergency cardiac care. ACS,
acute coronary syndrome; BLS, basic life support; CPR, cardiopulmonary
resuscitation; IV, intravenous; OD, overdose; VF/VT, ventricular fibrillation and
pulseless ventricular tachycardia.

FIGURE 55–2 Comprehensive emergency cardiac care algorithm. BLS, basic

life support; CPR, cardiopulmonary resuscitation; IO, intraosseous; IV,
intravenous; PEA, pulseless electrical activity; VF/VT, ventricular fibrillation
and pulseless ventricular tachycardia.

The sequence of steps in resuscitation has been changed since the 2010
guidelines from ABC (airway and breathing first, before compression) to
CAB (compression first, with airway and breathing treated later). Based on
the 2015 guidelines, titrating resuscitative efforts to physiological parameters
does not improve outcome. Nonetheless, physiological monitoring methods to
optimize CPR quality and return of spontaneous circulation (ROSC) are still
useful. The rule of tens and multiples can be applied: less than 10 s to check
for pulse, less than 10 s to place and secure the airway, target chest
compression adequacy to maintain end-tidal pressure of carbon dioxide
(Petco2) greater than 10 mm Hg, and target chest compression to maintain
arterial diastolic blood pressure greater than 20 mm Hg and central venous
oxygen saturation (Scvo2) greater than 30%. The 2015 guidelines suggest that
a lack of a PETCO2 greater than 10 mm Hg after 20 min in an intubated patient
may be considered as a marker to end resuscitative efforts. An exception to this
determination applies to nonintubated patients, in whom a specific PETCO2 cutoff
should not be used to aid in the decision to end resuscitative efforts.
Changes in drug recommendations are notable for the exclusion of
routine administration of high-dose epinephrine (0.1–0.2 mg/kg) during
cardiac arrest. Additionally, vasopressin alone or in combination with
epinephrine, according to the guidelines, offers no advantage over normal-
dose epinephrine (1 mg every 3–5 min) in adult resuscitation following
cardiac arrest. Amiodarone may be considered for ventricular fibrillation
that is unresponsive to resuscitative efforts. Lidocaine is no longer
recommended for routine use after cardiac arrest; however, it may be
administered as an infusion following ROSC if the arrest occurred because
of ventricular fibrillation or pulseless ventricular tachycardia. Additionally,
β-blockers should not be used routinely in cardiac arrest (until after the
CPR period has passed).
While the use of extracorporeal membrane oxygenation (ECMO, also referred
to as extracorporeal cardiopulmonary resuscitation, ECPR) has been a topic of
great interest and is increasingly available, the routine use of ECPR for cardiac
arrest is not yet recommended. However, the guidelines suggest that when the
etiology of the cardiac arrest is potentially reversible, the use of ECPR may be
considered. The new guidelines also allow for the use of point-of-care
ultrasound, but do not require it. Ultrasound techniques should only be
performed by qualified personnel, and ultrasound interventions should not
disrupt normal resuscitative practices and protocols.
This chapter is not intended as a substitute for a formal course in either life
support without the use of special equipment (Basic Life Support [BLS]) or with
the use of special equipment and drugs (Advanced Cardiac Life Support
[ACLS]). Neonatal resuscitation is described in Chapter 41.
AIRWAY
Before CPR is initiated, unresponsiveness is established and the emergency
response system is activated. During low blood flow states such as cardiac
arrest, oxygen delivery to the heart and brain is limited by blood flow rather
than by arterial oxygen content; thus, current guidelines place greater
emphasis on immediate initiation of chest compressions than on rescuer
breaths.
The patient is positioned supine on a firm surface. After initiation of chest
compressions, the airway is evaluated. The airway is most commonly
obstructed by posterior displacement of the tongue or epiglottis. If there is
no evidence of cervical spine instability, a head-tilt chin-lift should be tried first
(Figure 55–3). One hand (palm) is placed on the patient’s forehead applying
pressure to tilt the head back while lifting the chin with the forefinger and index
finger of the opposite hand. The jaw-thrust may be more effective in opening the
airway and is executed by placing both hands on either side of the patient’s head,
grasping the angles of the jaw, and lifting. Basic airway management is
discussed in detail in Chapter 19, and the trauma patient is considered in Chapter
39.
FIGURE 55–3 Loss of consciousness is often accompanied by loss of
submandibular muscle tone (A). Occlusion of the airway by the tongue can be
relieved by a head-tilt chin-lift (B) or a jaw-thrust (C). In patients with possible
cervical spine injury, the angles of the jaw should be lifted anteriorly without
hyperextending the neck.

Any vomitus or foreign body visible in the mouth of an unconscious patient

should be removed. If the patient is conscious or if the foreign body cannot be
removed by a finger sweep, the Heimlich maneuver is recommended. This
subdiaphragmatic abdominal thrust elevates the diaphragm, expelling a blast of
air from the lungs that displaces the foreign body (Figure 55–4). Complications
of the Heimlich maneuver include rib fracture, trauma to internal viscera, and
regurgitation with aspiration. A combination of back blows and chest thrusts is
recommended to clear foreign body obstruction in infants (Table 55–2).

FIGURE 55–4 The Heimlich maneuver can be performed with the victim
standing (A) or lying down (B). The hands are positioned slightly above the
navel and well below the xiphoid process and then pressed into the abdomen
with a quick upward thrust. The maneuver may need to be repeated.

TABLE 55–2 Summary of recommended basic life support techniques.

 If after opening the airway there is no evidence of adequate breathing, the
rescuer should initiate assisted ventilation by inflating the victim’s lungs with
each breath using a bag-mask device (see Chapter 19). Breaths are delivered
slowly (inspiratory time of ½–1 s) at a rate of about 10 breaths/min, with smaller
tidal volumes [VT] so as to minimize adverse effect on cardiac preload.
Compressions (100–120/min) should not be suspended during two-person
CPR to permit ventilation unless ventilation is not possible during
compressions.
With positive-pressure ventilation, even with a small VT, gastric inflation
with subsequent regurgitation and aspiration is possible. Therefore, as soon as
feasible, the airway should be secured with an ETT, or, if that is not possible, an
alternative airway should be inserted. There is inadequate evidence to support
the optimal timing of the placement of an advanced airway (supraglottic device,
ETT); however, chest compressions should not be more than minimally
interrupted to place any advanced airway device. The benefit of an advanced
airway must be considered in light of the risk of potential interruption in
compressions. Advanced airways include the esophageal–tracheal Combitube
(ETC), laryngeal mask airway (LMA), pharyngotracheal lumen airway, King
laryngeal tube, and cuffed oropharyngeal airway. The ETC and LMA, along with
oral and nasopharyngeal airways, face masks, laryngoscopes, and ETTs, are
discussed in Chapter 19. Of these, the LMA is increasingly preferred for in-
hospital arrests. The choice of bag-mask ventilation versus placement of an
advanced airway is dependent upon the skills of the providers. Studies conflict
as to optimal use of advanced airway management techniques in comparison to
bag-mask ventilation.
Independent of which airway adjunct is used, the guidelines state that
rescuers must confirm ETT placement with a PETCO2 detector—an indicator, a
capnograph, or a capnometric device. The preferred choice for confirmation of
ETT placement is continuous capnographic waveform analysis. All confirmation
devices are considered adjuncts to clinical conformation techniques (eg,
auscultation). Once an artificial airway is successfully placed, it must be
carefully secured with a tie or tape (25% of airways are displaced during
transportation).
Some causes of airway obstruction may not be relieved by conventional
methods. Furthermore, endotracheal intubation may be technically impossible to
perform (eg, severe facial trauma), or repeated attempts may be unwise (eg,
cervical spine trauma). In these circumstances, cricothyrotomy or tracheotomy
may be necessary. Cricothyrotomy involves placing a large intravenous catheter
or a commercially available cannula into the trachea through the midline of the
cricothyroid membrane (Figure 55–5). Proper location is confirmed by
aspiration of air. A 12- or 14-gauge catheter requires a driving pressure of 50 psi
to generate sufficient gas flow for transtracheal jet ventilation. The catheter must
be adequately secured to the skin, as the jet ventilation pressure can otherwise
easily propel the catheter out of the trachea and, if the tip remains beneath the
skin, lead to massive subcutaneous emphysema.
FIGURE 55–5 Percutaneous cricothyrotomy with a 14-gauge over-the-needle
intravenous catheter. A: Locate the cricothyroid membrane. B: Puncture the
membrane at the midline while stabilizing the trachea with the other hand.
Proper location is confirmed by easy aspiration of air. C: Advance the catheter
and withdraw the needle. Attach syringe to catheter and aspirate again after the
catheter is advanced in order to confirm that the catheter remains in the tracheal
lumen.
 Various systems are available that connect a high-pressure source of oxygen
(eg, central wall oxygen, tank oxygen, or the anesthesia machine fresh gas
outlet) to the catheter (Figure 55–6). A hand-operated jet injector or the oxygen
flush valve of an anesthesia machine controls ventilation. The addition of a
pressure regulator minimizes the risk of barotrauma.

FIGURE 55–6 A, B: Two systems for transtracheal jet ventilation after

cricothyrotomy (see Figure 55–5). A jet ventilator and pressure regulator (as
shown in A) provide better control of the inspiratory cycle. Both systems use
low-compliance tubing and a high-pressure source of oxygen. C: The hub from a
7.0 ETT may be adapted to connect with a 14-gauge catheter and 3 mL syringe
in order to provide jet ventilation with oxygen when outside the operating room
or when jet ventilation is not available.

Regardless of which transtracheal jet ventilation system is chosen, it must be

readily available, use low-compliance tubing, and have secure connections.
Direct connection of a 12- or 14-gauge intravenous catheter to the anesthesia
circle system does not allow adequate ventilation because of the high
compliance of the corrugated breathing tubing and breathing bag. Similarly, one
cannot reliably deliver acceptable ventilation through a 12- or 14-gauge catheter
with a self-inflating resuscitation bag.
Adequacy of ventilation—particularly expiration—is judged by observation
of chest wall movement and auscultation of breath sounds. Acute complications
include pneumothorax, subcutaneous emphysema, mediastinal emphysema,
bleeding, esophageal puncture, aspiration, and respiratory acidosis. Long-term
complications include tracheomalacia, subglottic stenosis, and vocal cord
changes. Cricothyrotomy is not generally recommended in children younger than
10 years of age.
Tracheotomy can be performed in a more controlled fashion after
oxygenation has been restored by cricothyrotomy (see Chapter 19).

BREATHING
Assessment of spontaneous breathing should immediately follow the opening or
the establishment of the airway. Chest compressions and ventilation should
not be delayed for intubation if a patent airway is established by a jaw-thrust
maneuver; intubation may take place during CPR or the pulse check. Apnea is
confirmed by lack of chest movement, absence of breath sounds, and lack of
airflow. Regardless of the airway and breathing methods employed, a specific
regimen of ventilation has been proposed for the apneic patient and described
earlier in this chapter. Initially, two breaths are slowly administered (2 s per
breath in adults, 1–1½ s in infants and children). If these breaths cannot be
delivered, either the airway is still obstructed and the head and neck need
repositioning or a foreign body is present that must be removed.
Bag-mask rescue breathing should be instituted in the apneic patient when
these devices are immediately available. Supplemental oxygen, preferably
100%, should always be used if available. Successful rescue breathing, 400–700
mL Vt, 8–10 times per minute in an adult with a secured airway and a ratio
of 30 compressions to 2 ventilations if the airway is unsecured, is confirmed
by observing the chest rising and falling with each breath and hearing and
feeling the escape of air during expiration
Devices that avoid use of the provider’s mouth should be immediately
available everywhere in the hospital. Ventilation with a mask may be performed
in most patients by adjusting the airway or making the airtight seal more
effective (see Chapter 19). Use of cricoid pressure to prevent regurgitation
during cardiac arrest resuscitation may be considered; however, there are no data
to support its efficacy in this (or any other) circumstance and its routine use is
not recommended.
Endotracheal intubation by competent personnel should be attempted as soon
as practical. Attempts at endotracheal intubation should not interrupt
ventilation for more than 10 s. After intubation, the patient can be ventilated
with high oxygen concentrations. A rate of 8 to 10 breaths/min should be
maintained, as higher ventilatory rates may impede cardiac output during CPR in
a cardiac arrest situation.
The ratio of physiological dead space to tidal volume (VD/VT) reflects the
efficiency of CO2 elimination. VD/VT increases during CPR as a result of low
pulmonary blood flow and high alveolar pressures. Thus, minute ventilation may
need to be increased by 50% to 100% once circulation is restored as CO2 from
the periphery is brought back to the lungs.

CIRCULATION
Circulation takes precedence over airway interventions and breathing in the
cardiac arrest patient. As previously noted, chest compressions should
begin prior to the delivery of breaths. Subsequent actions to assess circulation
may then vary depending on whether the responder is a lay person or health care
provider. Although lay rescuers should assume that an unresponsive patient
is in cardiac arrest and need not check the pulse, health care providers
should assess for presence or absence of a pulse.
If the patient has an adequate pulse (carotid artery in an adult or child,
brachial or femoral artery in an infant) or blood pressure, breathing is continued
at 10 to 12 breaths/min for an adult or a child older than 8 years, and 20
breaths/min for an infant or a child younger than 8 years of age (Table 55–2). If
the patient is pulseless or severely hypotensive, the circulatory system must be
supported by a combination of external chest compressions, intravenous drug
administration, and defibrillation when appropriate. Initiation of chest
compressions is mandated by the inadequacy of peripheral perfusion, and drug
choices and defibrillation energy levels often depend on electrocardiographic
diagnosis of arrhythmias.

External Chest Compression

Chest compressions force blood to flow either by increasing intrathoracic
pressure (thoracic pump) or by directly compressing the heart (cardiac pump).
During CPR of short duration, the blood flow is created more by the cardiac
pump mechanism; as CPR continues, the heart becomes less compliant and the
thoracic pump mechanism becomes more important. As important as the rate and
force of compression are for maintaining blood flow, effective perfusion of the
heart and brain is best achieved when chest compression consumes 50% of the
duty cycle, with the remaining 50% devoted to the relaxation phase (allowing
blood return into the chest and heart).
To perform chest compressions in the unresponsive or pulseless patient, the
xiphoid process is located and the heel of the rescuer’s hand is placed over the
lower half of the sternum. The other hand is placed over the hand on the sternum
with the fingers either interlaced or extended, but off the chest. The rescuer’s
shoulders should be positioned directly over the hands with the elbows locked
into position and arms extended, so that the weight of the upper body is used for
compressions. With a straight downward thrust, the sternum is depressed
approximately 2 in. (5 cm) in adults, 1 to 1½ in. (2–4 cm) in children, and then
allowed to return to its normal position. For an infant, compressions ½ to 1 in.
(1½–2½ cm) in depth are made with the middle and ring fingers on the sternum
one finger-breadth below the nipple line. Compression and release times should
be equal.
Whether adult resuscitation is performed by a single rescuer or by two
rescuers, two breaths are administered every 30 compressions (30:2),
allowing 3 to 4 s for the two breaths. The cardiac compression rate should be
100/min regardless of the number of rescuers. A slightly higher compression rate
of more than 100/min is suggested for infants, with two breaths delivered every
30 compressions.

Assessing the Adequacy of Chest Compressions

Adequacy of cardiac output can be estimated by monitoring PETCO2 (>10 mm
Hg), SCVO2 (>30%), or arterial pulsations (with arterial diastolic relaxation
pressure >20 mm Hg). Arterial pulsations during chest compressions are not a
good measure of adequate chest compression; however, spontaneous arterial
pulsations are an indicator of ROSC. Physiological parameters, such as PETCO2,
SCVO2, and diastolic arterial pressure, may aid in assessing the adequacy of chest
compressions but cannot be used exclusively to determine if CPR should be
discontinued.

1. Petco2—In an intubated patient, a PETCO2 greater than 10 mm Hg indicates

good-quality chest compressions; a PETCO2 less than 10 mm Hg has been shown
to be a predictor of poor outcomes of CPR (decreased chance of ROSC) in CPR
of more than 20 min duration. A transient increase in PETCO2 may be seen with
administration of sodium bicarbonate; however, an abrupt and sustained rise of
PETCO2 is an indicator of ROSC.

2. Coronary perfusion pressure (CPP)—This is the difference between the

aortic diastolic pressure and the right atrial diastolic pressure. Arterial diastolic
pressure in the radial, brachial, or femoral artery is a good indicator of CPP.
Arterial diastolic pressure greater than 20 mm Hg is an indicator of adequate
chest compressions.

3. SCVO2—An SCVO2 less than 30% in the jugular vein is associated with poor
outcomes. If the SCVO2 is less than 30%, attempts to improve the quality of CPR,
either by improving the quality of compressions or through administration of
medications, should be considered.

DEFIBRILLATION
Ventricular fibrillation is found most commonly in adults who experience
nontraumatic cardiac arrest. The time from collapse to defibrillation is the
most important determinant of survival. The chances for survival decline 7%
to 10% for every minute without defibrillation (Figure 55–7). Therefore,
patients who have cardiac arrest should be defibrillated at the earliest possible
moment. Health care personnel working in hospitals and ambulatory care
facilities must be able to provide early defibrillation to collapsed patients with
ventricular fibrillation as soon as possible. Shock should be delivered within 3 to
4 min of arrest.
FIGURE 55–7 Success of defibrillation versus time. The chance of successful
defibrillation of a patient in ventricular fibrillation decreases 7% to 10% per
minute.

There is no definite relationship between the energy requirement for

successful defibrillation and body size. A shock with too low an energy level
will not successfully defibrillate; conversely, too high an energy level may result
in myocardial injury. Defibrillators deliver energy in either monophasic or
biphasic waveforms. Biphasic waveforms are recommended for cardioversion as
they achieve the same degree of success but with less energy and theoretically
less myocardial damage; newly manufactured defibrillators use biphasic
waveforms.
In many institutions, automated external defibrillators (AEDs) are available.
Such devices are increasingly being used throughout communities by police,
firefighters, security personnel, sports marshals, ski patrol members, and airline
flight attendants, among others. They are placed in any public location where
20,000 or more people pass by every day. AEDs are technologically advanced,
microprocessor-based devices that are capable of electrocardiographic analysis
with very high specificity and sensitivity in differentiating shockable from
nonshockable rhythms. All AEDs manufactured today deliver some type of
biphasic waveform shock. Compared with monophasic shocks, biphasic shocks
deliver energy in two directions with equivalent efficacy at lower energy levels
and possibly with less myocardial injury. These devices deliver impedance-
compensating shocks employing either biphasic truncated exponential (BTE) or
rectilinear (RBW) morphology. Biphasic shocks delivering low energy for
defibrillation (120–200 joule [J]) have been found to be as or more effective than
200 to 360 J monophasic damped sine (MDS) waveform shocks. When using
AEDs, one electrode pad is placed beside the upper right sternal border, just
below the clavicle, and the other pad is placed just lateral to the left nipple, with
the top of the pad a few inches below the axilla.
A decrease in time delay between the last compression and the delivery of a
shock (the preshock pause) has received special emphasis in the new guidelines.
Stacking shocks (delivering two or more shocks in immediate succession
without intervening compressions) increases the time to next compression, and it
has been noted that the first shock is usually associated with a 90% efficacy.
Thus, stacked shocks have been replaced by a recommendation for a single
shock, followed by immediate resumption of chest compressions.
For cardioversion of atrial fibrillation (Table 55–3), 120–200 J can be used
initially with escalation if needed. For atrial flutter or paroxysmal
supraventricular tachycardia (PSVT), an initial energy level of 50 to 100 J is
often adequate. All monophasic shocks should start with 200 J. Manufacturer
instructions typically provide the recommended starting shock energy level
specific to the device.

TABLE 55–3 Energy requirements for cardioversion using biphasic

truncated exponential (BTE) or rectilinear morphology.1

Ventricular tachycardia, particularly monomorphic ventricular tachycardia,

responds well to shocks at initial energy levels of 100 J. For polymorphic
ventricular tachycardia or for ventricular fibrillation, initial energy can be set at
120 to 200 J, depending upon the type of biphasic waveform being used.
Stepwise increases in energy levels can be used if the first shock fails, although
some AEDs operate with a fixed-energy protocol of 150 J with very high success
in terminating ventricular fibrillation (Table 55–3).
Cardioversion should be synchronized with the QRS complex and is
recommended for hemodynamically stable, wide-complex tachycardia requiring
cardioversion, PSVT, atrial fibrillation, and atrial flutter. Polymorphic
ventricular tachycardia should be treated as ventricular fibrillation with
unsynchronized shocks.

Invasive Cardiopulmonary Resuscitation

Thoracotomy and open-chest cardiac massage are not part of routine CPR
because of the frequent incidence of complications. Nonetheless, these invasive
techniques can be helpful in specific life-threatening circumstances that preclude
effective closed-chest massage. Possible indications include cardiac arrest
associated with penetrating or blunt chest trauma, penetrating abdominal trauma,
severe chest deformity, pericardial tamponade, or pulmonary embolism.
Extracorporeal membrane oxygenation is increasing employed when the cause
of arrest (eg, local anesthetic systemic toxicity) is reversible.

Intravenous Access
Even though establishing reliable intravenous access is a high priority, it
should not take precedence over initial chest compressions, airway
management, or defibrillation. A preexisting internal jugular or subclavian
catheter is ideal for venous access during resuscitation. If there is no central line
access, an attempt should be made to establish peripheral intravenous access in
either the antecubital or the external jugular vein. Peripheral intravenous sites are
associated with a significant delay of 1 to 2 min between drug administration
and delivery to the heart, as peripheral blood flow is drastically reduced during
CPR. Administration of drugs given through a peripheral intravenous line should
be followed by an intravenous flush (eg, a 20-mL fluid bolus in adults) or
elevation of the extremity for 10 to 20 s, or both. Establishing central vein access
can potentially cause interruption of CPR but should be considered if an
inadequate response is seen to peripherally-administered drugs.
If intravenous cannulation is difficult, an intraosseous infusion can provide
emergency vascular access in children and adults. A rigid 18-gauge spinal needle
with a stylet or a small bone marrow trephine needle can be inserted into the
distal femur or proximal tibia. If the tibia is chosen, a needle is inserted 2 to 3
cm below the tibial tuberosity at a 45° angle away from the epiphyseal plate
(Figure 55–8). Once the needle is advanced through the cortex, it should stand
upright without support. Correct placement is confirmed by the ability to aspirate
marrow through the needle and deliver a smooth infusion of fluid. A network of
venous sinusoids within the medullary cavity of long bones drains into the
systemic circulation by way of nutrient or emissary veins. This route is very
effective for administration of drugs, crystalloids, colloids, and blood and can
achieve flow rates exceeding 100 mL/h under gravity. Much higher flow rates
are possible if the fluid is placed under pressure (eg, 300 mm Hg) with an
infusion bag. The onset of drug action may be slightly delayed compared with
intravenous or tracheal administration. The intraosseous route may require a
higher dose of some drugs (eg, epinephrine) than recommended for intravenous
administration. The use of intraosseous infusion for induction and maintenance
of general anesthesia, antibiotic therapy, seizure control, and inotropic support
has been described. (Note that most studies have evaluated the placement of
intraosseous access in patients with intact hemodynamics or hypovolemic states,
not in cardiac arrest situations.) Because of the risks of osteomyelitis and
compartment syndrome, however, intraosseous infusions should be replaced by a
conventional intravenous route as soon as possible. In addition, because of the
theoretical risk of bone marrow or fat emboli, intraosseous infusions should be
avoided if possible in patients with right-to-left shunts, pulmonary hypertension,
or severe pulmonary insufficiency. Some resuscitation drugs are fairly well
absorbed following administration through an ETT. Lidocaine, epinephrine,
atropine, naloxone, and vasopressin (but not sodium bicarbonate) can be
delivered via a catheter whose tip extends past the ETT. Notably, the American
Heart Association recommends endotracheal dosing only when IV and
intraosseous dosing cannot be accomplished. Dosages 2 to 2½ times higher than
recommended for intravenous use, diluted in 10 mL of normal saline or distilled
water, are recommended for adult patients.
FIGURE 55–8 Intraosseous infusions provide emergency access to the venous
circulation in pediatric patients by way of the large medullary venous channels.
The needle is directed away from the epiphyseal plate to minimize the risk of
injury.

Arrhythmia Recognition
Successful pharmacological and electrical treatment of cardiac arrest (Figure
55–9) depends on definitive identification of the underlying arrhythmia.
Interpreting rhythm strips in the midst of a resuscitation situation is frequently
complicated by artifacts and variations in monitoring techniques (eg, lead
systems, equipment).
FIGURE 55–9 Adult cardiac arrest algorithm—2015 update. Algorithm for
treating ventricular fibrillation and pulseless ventricular tachycardia (VF/VT).
Pulseless ventricular tachycardia should be treated in the same way as
ventricular fibrillation. Note: This figure and Figures 55–1 and 55–2 emphasize
the concept that rescuers and health care providers must assume that all
unmonitored adult cardiac arrests are due to VF/VT. In each figure, the flow of
the algorithm assumes that the arrhythmia is continuing. CPR, cardiopulmonary
resuscitation; IV/IO, intravenous or intraosseous; PEA, pulseless electrical
activity. (Reprinted with permission from Advanced Cardiovascular Life Support Provider Manual
©2016 American Heart Association, Inc.)

Drug Administration
Many of the drugs administered during CPR have been described elsewhere in
this text. Table 55–4 summarizes the cardiovascular actions, indications, and
dosages of drugs commonly used during resuscitation.

TABLE 55–4 Cardiovascular effects, indications, and dosages of

resuscitation drugs.1,2
 Atropine is not included as a drug for pulseless electrical activity/asystole
in the new CPR-ECC guidelines; however, its use is retained for
symptomatic bradycardia. Infusions of chronotropic drugs (eg, dopamine,
epinephrine, isoproterenol) can be considered as an alternative to pacing if
atropine is ineffective in the setting of symptomatic bradycardia. Calcium
chloride, sodium bicarbonate, and bretylium are conspicuously absent from
this table. Calcium (2–4 mg/kg of the chloride salt) is helpful in the treatment of
documented hypocalcemia, hyperkalemia, hypermagnesemia, or a calcium
channel blocker overdose. When used, 10% calcium chloride can be given at 2
to 4 mg/kg every 10 min. Sodium bicarbonate (0.5–1 mEq/kg) is not
recommended in the guidelines and should be considered only in specific
situations such as preexisting metabolic acidosis or hyperkalemia, or in the
treatment of tricyclic antidepressant or barbiturate overdose. Sodium
bicarbonate elevates plasma pH by combining with hydrogen ions to form
carbonic acid, which readily dissociates into carbon dioxide and water. Because
carbon dioxide, but not bicarbonate, readily crosses cell membranes and the
blood–brain barrier, arterial hypercapnia causes intracellular tissue acidosis.
Although successful defibrillation is not related to arterial pH, increased
intramyocardial carbon dioxide may reduce the possibility of successful cardiac
resuscitation. Furthermore, bicarbonate administration can lead to detrimental
alterations in osmolality and the oxygen–hemoglobin dissociation curve.
Therefore, effective alveolar hyperventilation and adequate tissue perfusion
are the treatments of choice for the respiratory and metabolic acidosis that
accompany resuscitation.
 Intravenous fluid therapy with either colloid or balanced salt solutions is
indicated in patients with intravascular volume depletion (eg, acute blood loss,
diabetic ketoacidosis, thermal burns). Dextrose-containing solutions may lead to
a hyperosmotic diuresis and may worsen neurological outcome. They should be
avoided unless hypoglycemia is suspected. Likewise, administration of free
water (eg, D5W) may lead to cerebral edema.

Emergency Pacemaker Therapy

Transcutaneous cardiac pacing (TCP) is a noninvasive method of rapidly
treating arrhythmias caused by conduction disorders or abnormal impulse. TCP
is not routinely recommended in cardiac arrest. TCP use may be considered to
treat asystole, bradycardia caused by heart block, or tachycardia from a reentrant
mechanism. If there is concern about the use of atropine in high-grade block,
TCP is always appropriate. If the patient is unstable with marked bradycardia,
TCP should be implemented immediately while awaiting treatment response to
drugs. A pacemaker unit has become a built-in feature of some defibrillator
models. Disposable pacing electrodes are usually positioned on the patient in an
anterior–posterior manner. The placement of the negative electrode corresponds
to a V2 electrocardiograph position, whereas the positive electrode is placed on
the left posterior chest beneath the scapula and lateral to the spine. Note that this
positioning does not interfere with paddle placement during defibrillation.
Failure to capture may be due to electrode misplacement, poor electrode-to-skin
contact, or increased transthoracic impedance (eg, barrel-shaped chest,
pericardial effusion). Current output is slowly increased until the pacing stimuli
obtain electrical and mechanical capture. A wide QRS complex following a
pacing spike signals electrical capture, but mechanical (ventricular) capture
must be confirmed by an improving pulse or blood pressure. Conscious patients
may require sedation to tolerate the discomfort of skeletal muscle contractions.
Transcutaneous pacing can provide effective temporizing therapy until
transvenous pacing or other definitive treatment can be initiated. TCP has many
advantages over transvenous pacing because it can be used by almost all acute
care providers and can be initiated quickly at the bedside.

Precordial Thump
The precordial thump is to be considered only in witnessed, monitored, pulseless
ventricular tachycardia when a defibrillator is not immediately available. It
provides only 5 to 10 joules of mechanical energy to the heart. Recent studies
suggest the precordial thump rarely results in ROSC and usually results in either
no change in rhythm or deterioration into ventricular fibrillation or asystole. The
latter situation may represent the phenomenon known as commotio cordis, where
blunt impact to the chest without structural trauma results in ventricular
arrhythmias or asystole.

RECOMMENDED RESUSCITATION PROTOCOLS

A resuscitation team leader integrates the assessment of the patient, including
electrocardiographic diagnosis, with the electrical and pharmacological therapy
(Table 55–5). This person must have a firm grasp of the guidelines for cardiac
arrest presented in the CPR-ECC algorithms (Figures 55–9 to 55–13).

TABLE 55–1 Steps for synchronized cardioversion.1,2

FIGURE 55–10 Pulseless electrical activity (PEA) algorithm. ACS, acute
coronary care; IV/IO, intravenous or intraosseous; OD, overdose; PETCO2, end-
tidal carbon dioxide; VF/VT, ventricular fibrillation and pulseless ventricular
tachycardia.
FIGURE 55–11 Asystole: The silent heart algorithm. DP, diastolic pressure;
IV/IO, intravenous or intraosseous; PETCO2, end-tidal carbon dioxide; SCVO2,
central venous oxygen saturation; VF/VT, ventricular fibrillation and pulseless
ventricular tachycardia.
FIGURE 55–12 Adult bradycardia with a pulse algorithm. AV, atrioventricular;
ECG, electgrocardiogram; IV, intravenous. (Reprinted with permission from Advanced
Cardiovascular Life Support Provider Manual ©2016 American Heart Association, Inc.)
FIGURE 55–13 Adult tachycardia with a pulse algorithm. CHF, congestive
heart failure; ECG, electrocardiogram; IV, intravenous; VT, ventricular
tachycardia; WPW, Wolff-Parkinson-White syndrome. (Reprinted with permission from
Advanced Cardiovascular Life Support Provider Manual ©2016 American Heart Association, Inc.)

CASE DISCUSSION

Intraoperative Hypotension & Cardiac Arrest

A 16-year-old boy is rushed to the operating room for emergency
laparotomy and thoracotomy after suffering multiple abdominal and
thoracic stab wounds. In the field, paramedics intubated the patient,
started two large-bore intravenous lines, began fluid resuscitation, and
inflated a pneumatic antishock garment. Upon arrival in the operating
room, the patient’s blood pressure is unobtainable, heart rate is 128
beats/min (sinus tachycardia), and respirations are being controlled by
a bag-valve device.
What should be done immediately?
Cardiopulmonary resuscitation must be initiated immediately: external
chest compressions should be started as soon as the arterial blood pressure
is found to be inadequate for vital organ perfusion. Because the patient is
already intubated, the location of the endotracheal tube should be confirmed
with chest auscultation and quantitative waveform capnography (if
available, to assist in both confirmation of tube placement as well as to
assess the adequacy of CPR) and 100% oxygen should be delivered.
Which CPR sequence best fits this situation?
Pulselessness in the presence of sinus rhythm suggests severe
hypovolemia, cardiac tamponade, ventricular rupture, dissecting aortic
aneurysm, tension pneumothorax, profound hypoxemia and acidosis, or
pulmonary embolism. Epinephrine, 1 mg, should be administered
intravenously.
What is the most likely cause of this patient’s profound
hypotension?
The presence of multiple stab wounds strongly suggests hypovolemia.
Point-of-care abdominal ultrasonography can rapidly identify a collapsed
vena cava, which is pathognomonic of hypovolemia. Warmed fluids should
be rapidly administered. Additional venous access can be sought as other
members of the operating room team administer fluid through blood pumps
or other rapid infusion devices. Five percent albumin or lactated Ringer’s
solution is acceptable until blood products are available. Activation of a
massive transfusion protocol is indicated.
What are the signs of tension pneumothorax and pericardial
tamponade?
The signs of tension pneumothorax—the presence of air under pressure
in the pleural space—include increasing peak inspiratory pressures,
tachycardia and hypotension (decreased venous return), hypoxia
(atelectasis), distended neck veins, unequal breath sounds, tracheal
deviation, and mediastinal shift away from the pneumothorax. Point-of-care
ultrasonography can also be used for identification of tension
pneumothorax (and for diagnosis of pericardial tamponade), but should not
interrupt chest compressions.
 Pericardial tamponade—cardiac compression from pericardial contents
—should be suspected in any patient with narrow pulse pressure, pulsus
paradoxus (>10 mm Hg drop in systolic blood pressure with inspiration),
elevated central venous pressure with neck vein distention, distant heart
sounds, tachycardia, hypotension, and equalization of central venous, atrial,
and ventricular end-diastolic pressures. Many of these signs may be masked
by concurrent hypovolemic shock.
Fluid administration and properly performed external cardiac
compressions do not result in satisfactory carotid or femoral
pulsations. What else should be done?
Because external chest compressions are often ineffective in trauma
patients, an emergency thoracotomy should be performed as soon as
possible to clamp the thoracic aorta, relieve a tension pneumothorax or
pericardial tamponade, identify possible intrathoracic hemorrhage, and
perform open-chest cardiac compressions. Cross-clamping of the thoracic
aorta increases brain and heart perfusion and decreases subdiaphragmatic
hemorrhage. Lack of response to cross-clamping is a good predictor of
demise.
What is the function of the pneumatic antishock garment, and
how should it be removed?
Inflation of the bladders within a pneumatic antishock garment increases
arterial blood pressure by elevating peripheral vascular resistance.
Functionally, the suit has the same effect as thoracic aorta cross-clamping
by decreasing blood flow and hemorrhage in the lower half of the body.
Complications of inflating the abdominal section of the pneumatic
antishock garment include kidney dysfunction, altered lung volumes, and
visceral injury during external chest compressions. The suit should be
deflated only after restoration of hemodynamic parameters. Even then,
deflation should be gradual, as it may be accompanied by marked
hypotension and by metabolic acidosis caused by reperfusion of ischemic
tissues.

GUIDELINES
Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult advanced
 cardiovascular life support: 2015 American Heart Association guidelines
update for cardiopulmonary resuscitation and emergency cardiovascular care.
Circulation. 2015;132(suppl 2):S444

SUGGESTED READINGS
ATLS Subcommittee; American College of Surgeons Committee on Trauma;
International ATLS Working Group. Advanced trauma life support (ATLS):
The ninth edition. J Trauma Acute Care Surg. 2013;74:1363.
Brooks SC, Anderson ML, Bruder E, et al. Part 6: Alternative techniques and
ancillary devices for cardiopulmonary resuscitation. 2015 American Heart
Association guidelines update for cardiopulmonary resuscitation and
emergency cardiovascular care. Circulation. 2015;132(suppl 2):S436.
de Caen AR, Berg MD, Chameides L, et al. Part 12: Pediatric advanced life
support. 2015 American Heart Association guidelines update for
cardiopulmonary resuscitation and emergency cardiovascular care.
Circulation. 2015;132(suppl 2):S526.
Hazinski MF, Shuster M, Donnino MW, et al. Highlights of the 2015 American
Heart Association Guidelines Update for CPR and ECC. Dallas, TX:
American Heart Association; 2015:1-33.
Kleinman ME, Brennan EE, Goldberger ZD, et al. Part 5: Adult basic life
support and cardiopulmonary resuscitation quality. 2015 American Heart
Association guidelines update for cardiopulmonary resuscitation and
emergency cardiovascular care. Circulation. 2015;132(suppl 2):S414.
Lavonas EJ, Drenan IR, Gabrielli A, et al. Part 10: Special circumstances of
resuscitation. 2015 American Heart Association guidelines update for
cardiopulmonary resuscitation and emergency cardiovascular care.
Circulation. 2015(suppl 2);132:S501.
Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult advanced
cardiovascular life support: 2015 American Heart Association guidelines
update for cardiopulmonary resuscitation and emergency cardiovascular care.
Circulation. 2015(suppl 2);132:S444.
Maron BJ, Poliac LC, Kaplan JA, et al. Blunt impact to the chest leading to
sudden death from cardiac arrest during sports activities. N Engl J Med.
1995;333:337.
Nehme Z, Andrew E, Bernard SA, et al. Treatment of monitored out-of-hospital
ventricular fibrillation and pulseless ventricular tachycardia utilising the
precordial thump. Resuscitation. 2013;84:1691.
Neumar RW, Shuster M, Callaway CW, et al. Part 1: Executive summary. 2015
American Heart Association guidelines update for cardiopulmonary
resuscitation and emergency cardiovascular care. Circulation. 2015(suppl
2);132:S315.
 CHAPTER

56
Postanesthesia Care

KEY CONCEPTS

Patients emerging from anesthesia should not leave the operating room
until they have a patent airway, have adequate ventilation and
oxygenation, and are hemodynamically stable; qualified anesthesia
personnel must attend the transfer to the postanesthesia care unit
(PACU).
Before the recovering patient is fully responsive, pain is often
manifested as postoperative restlessness or agitation. Significant
systemic disturbances (eg, hypoxemia, respiratory or metabolic
acidosis, hypotension), bladder distention, or a surgical complication
(eg, occult intraabdominal hemorrhage) must also be considered in the
differential diagnosis of postoperative restlessness or agitation.
Postoperative nausea and vomiting (PONV; see Chapter 17) is the most
common significant complication following general anesthesia,
occurring in approximately 30% or more of all patients.
Intense shivering causes precipitous rises in oxygen consumption, CO2
production, and cardiac output. These physiological effects may be
poorly tolerated by patients with cardiac or pulmonary impairment.
Respiratory problems are the most frequently encountered serious
complications in the PACU. The overwhelming majority are related to
airway obstruction, hypoventilation, hypoxemia, or a combination of
these problems.
Hypoventilation in the PACU is most commonly due to the residual
depressant effects of anesthetic agents on respiratory drive, often made
worse by preexisting obstructive sleep apnea.
Hypoventilation with obtundation, circulatory depression, and severe
acidosis (arterial blood pH < 7.15) is an indication for immediate and
 decisive ventilatory and hemodynamic intervention, including airway
and inotropic support as needed.
Following naloxone administration, patients should be observed closely
for recurrence of opioid-induced respiratory depression
(“renarcotization”), as naloxone has a shorter duration of action than
many opioids.
Increased intrapulmonary shunting from a decreased functional residual
capacity relative to closing capacity is the most common cause of
hypoxemia following general anesthesia.
The possibility of a postoperative pneumothorax should always be
considered following central line placement, supraclavicular or
intercostal blocks, abdominal or chest trauma (including rib fractures),
neck dissection, thyroidectomy (especially if thyroid dissection extends
into the thorax), tracheostomy, nephrectomy, or other retroperitoneal or
intraabdominal procedures (including laparoscopy), especially if the
diaphragm may have been penetrated or disrupted.
Hypovolemia is the most common cause of hypotension in the PACU
and can result from inadequate fluid replacement, wound draining, or
hemorrhage.
Noxious stimulation from incisional pain, endotracheal intubation,
bladder distention, or preoperative discontinuation of antihypertensive
medication is usually responsible for postoperative hypertension.

Historically, emphasis on specialized nursing care during the immediate

postoperative period was prompted by the realization that many preventable
early postoperative deaths occurred immediately after anesthesia and surgery.
The World War II experience of providing surgical care to large numbers of
battle casualties contributed to the postwar trend of centralization of immediate
postoperative care in recovery rooms, where skilled nurses could pay close
attention to several acute postoperative patients simultaneously. Recently, the
practice of caring for selected postoperative patients overnight in a
postanesthesia care unit (PACU), or the equivalent, has been a response to
increasingly complex surgical procedures performed on higher-acuity patients,
when there is a shortage of surgical intensive care beds.
Another recent transformation in postanesthesia care is related to the shift
from inpatient to outpatient surgery. Now, more than 70% of surgical procedures
in the United States are performed on an outpatient basis. Two phases of
recovery may be recognized for outpatient surgery. Phase 1 is the immediate
care for patients during emergence and awakening from anesthesia that
continues until standard PACU discharge criteria are met (see Discharge Criteria,
later in the chapter). Phase 2 is a lower-level care that continues until the patient
is ready to go home. “Fast-tracking” of appropriately managed outpatients may
allow them to safely bypass phase 1 recovery and go directly to the phase 2 level
of care.
In many institutions, the PACU also functions as a more intensely monitored
location for perioperative and chronic pain patients undergoing procedures such
as single-shot nerve blocks and placement of epidural and peripheral nerve
catheters, and for patients undergoing other invasive procedures such as central
line placement, electroconvulsive therapy, thoracentesis, paracentesis, or
cardioversion. The PACU must be appropriately staffed and equipped to manage
such patients and their potential complications. For example, in areas where
regional and epidural blocks are administered, Intralipid should be stocked in
anticipation of treating systemic local anesthetic toxicity.
This chapter reviews the essential components of a modern PACU, the
general care of patients acutely recovering from anesthesia and surgery, and the
respiratory and circulatory complications most commonly encountered in the
PACU.

THE POSTANESTHESIA CARE UNIT

At the conclusion of any procedure requiring anesthesia, after anesthetic agents
are discontinued, monitors are disconnected and the emerging patient is taken to
the PACU by one or more qualified anesthesia providers, often assisted by other
personnel. During transport, supplemental oxygen is given by nasal cannulae or
mask and the patient is monitored with pulse oximetry. Following general
anesthesia, if an endotracheal tube or laryngeal mask airway (LMA) was
utilized, the endotracheal tube or LMA will usually be removed prior to
transport. Patients are also routinely observed in the PACU following regional
anesthesia and monitored anesthesia care (local anesthesia with sedation). Most
facilities have protocols that require patients to be admitted to the PACU
following any type of anesthesia, except by specific order of the attending
anesthesiologist. After a brief “hand off” report to the PACU nurse, the patient
will remain in the PACU until the major effects of anesthesia have worn off and
any anesthesia- or surgery-related complications of significance have been
adequately addressed. This period is characterized by a frequent incidence of
potentially life-threatening respiratory and circulatory complications.
 The delivery of anesthesia services in areas remote from the main operating
room, such as gastrointestinal and pulmonary endoscopy, interventional
radiology, and magnetic resonance imaging suites, is common. Patients
recovering from anesthesia delivered in these areas must receive the same
standard of care as surgical patients recovering from anesthesia. Some
institutions have “satellite” PACUs to serve each of these remote areas
individually and others send patients from their various procedural areas to one
centralized PACU; however, the standard of postanesthesia care must be the
same for all PACUs within a given institution.

Design
The PACU should be located near the operating rooms and remote procedure
areas. A central location in the operating room area itself is desirable, as it
ensures that the patient can be urgently transported back to surgery, if needed, or
that members of the operating room team can quickly respond to urgent or
emergent patient care issues in the PACU. Proximity to radiographic, laboratory,
and other intensive care facilities on the same floor is also advantageous.
Prolonged transfers subject critically ill patients to increased jeopardy from
urgent problems that may arise along the way.
An open-ward design facilitates observation of multiple patients
simultaneously. However, individually enclosed patient care spaces are required
for patients needing isolation for infection control. Many institutions
constructing new PACUs choose to fully enclose all the PACU patient beds for
infection control and privacy. A ratio of 1.5 PACU beds per operating room is
customary, although this ratio will vary depending on the respective operating
room suite’s case type and volume, average case duration, and patient acuity.
Each patient space should be well lit and large enough to allow easy access to
patients for intravenous infusion pumps, ventilators, and radiographic
equipment. Construction guidelines typically specify a minimum of 7 ft between
beds and 120 sq ft per patient. Multiple electrical outlets, including at least one
with backup emergency power, and at least one outlet each for oxygen and
suction, should be present at each bed space.

Equipment
Inadequate monitoring in the PACU can lead to serious morbidity or mortality.
Pulse oximetry (SpO2), electrocardiogram (ECG), and automated noninvasive
blood pressure (NIBP) monitors are mandatory for each patient. Although ECG,
SpO2, and NIBP must be utilized for every patient in the initial phase of recovery
from anesthesia (phase 1), decreased monitoring may be adequate thereafter.
Appropriate equipment must be available for those patients with intraarterial,
central venous, pulmonary artery, or intracranial pressure monitoring.
Capnography is often useful for both intubated and extubated patients alike.
Mercury or electronic thermometers must be used if an abnormality in
temperature is suspected. A forced-air warming device, heating lamp, or a
warming/cooling blanket should be available.
The PACU must have its own supplies of basic and emergency equipment,
separate from that of the operating room, including airway equipment and
supplies, such as oxygen cannulas, a selection of masks, oral and nasal airways,
laryngoscopes, endotracheal tubes, LMAs, a cricothyrotomy kit, and self-
inflating bags for ventilation. Respiratory therapy equipment for aerosol
bronchodilator treatments, continuous positive airway pressure (CPAP), and
ventilators should be in close proximity to the recovery room. A difficult airway
equipment and supplies cart with a bronchoscope and a video laryngoscope must
be immediately available.
A readily available supply of catheters for venous, arterial, and central venous
cannulation is mandatory in an inpatient setting. A defibrillation device with
transcutaneous pacing capabilities, and an emergency cart with drugs and
supplies for advanced life support (see Chapter 55) and infusion pumps, must be
present and periodically inspected according to accreditation standards.
Transvenous pacing catheters; pulse generators; and tracheostomy, chest tube,
and vascular cut-down trays are typically present, depending on the surgical
patient population. Point-of-care ultrasonography equipment is increasingly
available for central line and perineural catheter placement, assessment of
hemodynamic status, endotracheal tube placement, gastric and bladder volume,
and detection of pleural effusion, pneumothorax, and other pulmonary
pathology.

Staffing
Inadequate staffing is often cited as a major contributing factor in PACU
mishaps. The PACU should be staffed by nurses specifically trained in the care
of patients emerging from anesthesia. They should have expertise in airway
management and advanced cardiac life support, as well as in problems
commonly encountered in surgical patients relating to wound care, drainage
catheters, and postoperative hemorrhage.
 Patients in the PACU should be under the medical direction of a physician,
usually an anesthesiologist, who must be immediately available to respond to
urgent or emergent patient care problems. High-volume tertiary care surgical
institutions often have an anesthesiologist assigned full time to the PACU. The
management of the patient in the PACU should reflect a coordinated effort
involving qualified anesthesia providers, surgeons, nurses, respiratory therapists,
and appropriate consultants. The anesthesia team emphasizes management of
analgesia, airway, cardiac, pulmonary, and metabolic problems, whereas the
surgical team generally manages any problems directly related to the surgical
procedure itself. A ratio of one recovery nurse for two patients is generally
satisfactory; however, staffing for nursing care should be tailored to the unique
requirements of each patient and each facility. If the operating room schedule
regularly includes pediatric patients or frequent short procedures, a ratio of one
nurse to one patient is often needed. A charge nurse should be assigned to ensure
optimal staffing resource management at all times, including the appropriate
response to urgent or emergent patient care problems.

Care of the Patient

EMERGENCE FROM GENERAL ANESTHESIA
Emergence from general anesthesia should ideally be characterized by a smooth
and gradual awakening in a controlled environment. However, problems such as
airway obstruction, shivering, agitation, delirium, pain, nausea and vomiting,
hypothermia, and autonomic lability are frequently encountered. Patients
receiving spinal or epidural anesthesia may experience decreases in blood
pressure during transport or recovery; the sympatholytic effects of major
conduction blocks may prevent compensatory reflex vasoconstriction when
patients are moved or when they sit up.
Following an inhalational-based anesthetic, the speed of emergence is directly
proportional to alveolar ventilation, but inversely proportional to the agent’s
blood solubility (see Chapter 8). Hypoventilation delays emergence from
inhalational anesthesia. As the duration of anesthesia increases, emergence also
becomes increasingly dependent on total tissue uptake, which is a function of
agent solubility, the average concentration used, and the duration of exposure to
the anesthetic. Emergence from an intravenous anesthetic is a function of drug
pharmacokinetics. Recovery from most intravenous agents is dependent
primarily on redistribution rather than metabolism and elimination. As the total
administered dose increases, however, cumulative effects become clinically
apparent in the form of prolonged emergence; the termination of action becomes
increasingly dependent on the metabolism or elimination. This is the basis for
the concept of a context-sensitive half-time (see Chapter 7). Advanced age or
kidney or liver disease can prolong emergence (see Chapter 9). Short- and
ultrashort-acting anesthetic agents, such as propofol and remifentanil,
significantly shorten emergence and time to discharge. Use of a bispectral index
(BIS) monitor (see Chapter 6) may reduce total drug dosage and shorten
recovery and time to discharge. The speed of emergence can also be influenced
by preoperative medications. Premedication with agents that outlast the
procedure (eg, lorazepam) may be expected to prolong emergence. The short
duration of action of midazolam makes it a suitable premedication agent for
short procedures.

Delayed Emergence
The most frequent cause of delayed emergence (when the patient fails to regain
consciousness within an expected period of time after general anesthesia) is
residual drug effect. Delayed emergence may occur as a result of absolute or
relative drug overdose. The effects of preoperative sleep deprivation or drug
ingestion (alcohol, sedatives) can be additive to those of anesthetic agents in
producing prolonged emergence. Intravenous naloxone (in 80 mcg increments in
adults) and flumazenil (in 0.2 mg increments in adults) will readily reverse the
effects of an opioid and benzodiazepine, respectively. Intravenous physostigmine
(1–2 mg) may partially reverse the effect of other agents. A nerve stimulator can
be used to exclude persisting neuromuscular blockade in poorly responsive
patients on a mechanical ventilator who have inadequate spontaneous tidal
volumes.
Less common causes of delayed emergence include hypothermia, marked
metabolic disturbances, and perioperative stroke. A core temperature of less than
33°C has an anesthetic effect and greatly potentiates the actions of central
nervous system depressants. Forced-air warming devices are most effective in
raising body temperature. Hypoxemia and hypercarbia are readily excluded by
pulse oximetry, capnography, and blood gas analysis. Hypercalcemia,
hypermagnesemia, hyponatremia, and hypoglycemia and hyperglycemia are rare
causes of delayed emergence that require laboratory measurements for diagnosis.
Perioperative stroke is rare, except after neurological, cardiac, and
cerebrovascular surgery (see Chapter 28); diagnosis is facilitated by neurological
evaluation and radiological imaging.
TRANSPORT FROM THE OPERATING ROOM TO
THE PACU
This seemingly short period may be complicated by the lack of adequate
monitoring, medication access, or airway and resuscitative equipment.
Patients emerging from anesthesia should not leave the operating room until they
have a patent airway, have adequate ventilation and oxygenation, and are
hemodynamically stable; qualified anesthesia personnel must attend the transfer.
Transient hypoxemia (SpO2 <90%) may develop in as many as 30% to 50% of
otherwise “normal” patients during transport while breathing room air;
supplemental oxygen may therefore be advisable for all transported patients,
especially if the PACU is not in immediate proximity to the operating room.
Unstable patients should remain intubated and should be transported with a
portable monitor (ECG, SpO2, and blood pressure) and a supply of emergency
drugs. Since the transfer of intubated patients will always include the risk of
inadvertent endotracheal tube dislodgement, appropriate airway equipment and
supplies should be included in the transfer process, especially if the transfer
travel distance is lengthy or includes an elevator ride.
All patients should be taken to the PACU on a bed or gurney that can be
placed in either the head-down (Trendelenburg) or back-up position. The head-
down position is useful for management of hypovolemic patients, whereas the
back-up position is useful for patients with underlying pulmonary dysfunction
(see Chapters 20 and 23). Patients at increased risk of vomiting or upper airway
bleeding (eg, following tonsillectomy) should be transported in the lateral
position, which also helps prevent airway obstruction and facilitates drainage of
secretions.

ROUTINE RECOVERY
General Anesthesia
Airway patency, vital signs, oxygenation, and level of consciousness must be
assessed immediately upon PACU arrival. Subsequent blood pressure, heart rate,
and respiratory rate measurements are routinely made at least every 5 min for 15
min or until stable, and every 15 min thereafter. Pulse oximetry and ECG are
monitored continuously in all patients. In awake PACU patients, neuromuscular
function should be assessed clinically (eg, head-lift and grip strength). At least
one temperature measurement must also be obtained. Additional monitoring
includes assessment of pain; the presence or absence of nausea or vomiting; and
adequacy of hydration and output, including urine flow, drainage, and bleeding.
After initial vital signs have been recorded, the anesthesia provider should give a
report to the PACU nurse that includes (1) relevant preoperative history
(including mental status and any communication problems, such as language
barriers, deafness, blindness, or mental disability); (2) pertinent intraoperative
events (type of anesthesia, the surgical procedure, blood loss, fluid replacement,
antibiotic and other relevant medication administration, and any complications);
(3) any expected postoperative problems; (4) any anticipated need for PACU
medication administration, such as antibiotics; and (5) postanesthesia orders.
Postoperative orders should address analgesia and nausea/vomiting therapy;
epidural or perineural catheter care, including the need for acute pain service
involvement; administration of fluids or blood products; postoperative
ventilation; chest radiographs for follow-up of central venous catheterization,
etc.
All patients recovering from general anesthesia must receive supplemental
oxygen and pulse oximetry monitoring during emergence because transient
hypoxemia can develop even in healthy patients. A decision regarding
continuation of supplemental oxygen therapy at the time of PACU discharge can
be made based on SpO2 readings on room air. Arterial blood gas measurements
may be obtained to confirm abnormal oximetry readings, but are usually not
necessary. Oxygen therapy should be carefully controlled in patients with a
history of, or potential for, CO2 retention. Patients should generally be nursed in
the back-up position to optimize oxygenation. However, elevating the head of
the bed before the patient is responsive can lead to airway obstruction. In such
cases, a preexisting oral or nasal airway should be left in place until the patient is
awake and able to maintain airway. Deep breathing and coughing should be
encouraged periodically.

Regional Anesthesia
Patients who are heavily sedated or hemodynamically unstable following
regional anesthesia should also receive supplemental oxygen in the PACU.
Sensory and motor levels should be periodically recorded following regional
anesthesia to document regression of the block. Precautions in the form of
padding or repeated warning may be necessary to prevent self-injury from
uncoordinated arm movements following brachial plexus blocks. Blood pressure
should be closely monitored following spinal and epidural anesthesia. Bladder
catheterization may be necessary in patients who have had spinal or epidural
anesthesia.

Pain Control
Moderate to severe postoperative pain is most commonly treated with oral or
parenteral opioids. However, perioperative opioid administration is associated
with side effects (nausea and vomiting, respiratory depression, pruritis, ileus, and
urinary retention) which may have significant adverse effects on postoperative
convalescence. In response to this problem, a variety of opioid-sparing strategies
have been embraced over the past two decades to decrease opioid requirements
and opioid-related side effects, while maintaining satisfactory analgesia (see
Chapter 47). Preoperative oral administration of nonsteroidal antiinflammatory
drugs (NSAIDs), acetaminophen, and gabapentin or pregabalin may significantly
reduce postoperative opioid requirements, and these medications may be
readministered postoperatively when the patient can resume oral medication.
Additional analgesic modalities utilizing local anesthetics, such as intraoperative
wound infiltration, field blocks, postoperative wound catheter infusions, single-
shot and continuous catheter peripheral nerve blocks, and continuous epidural
infusions, also reduce postoperative opioid analgesic requirements, and thus also
reduce opioid-related side effects.
Mild to moderate postoperative pain can be treated orally with
acetaminophen, ibuprofen, hydrocodone, or oxycodone. Alternatively, ketorolac
(15–30 mg in adults), an equivalent dose of diclofenac or ibuprofen, or
acetaminophen (paracetamol) (15 mg/kg, or 1 g if patient >50 kg) may be
administered intravenously.
In situations where moderate to severe postoperative pain is present, or oral
analgesia is not possible, parenteral or intraspinal opioids, single-shot or
continuous nerve blocks, wound infiltration, field blocks, intravenous lidocaine
infusion, and continuous epidural analgesia are used, often in combination
techniques (see Section IV). Parenteral opioids are most safely administered by
titration of small doses. Considerable variability in opioid requirements should
be expected, and adequate analgesia must be balanced against the risk of
excessive sedation and respiratory depression. Intravenous opioids of
intermediate to long duration, such as hydromorphone, 0.25 to 0.5 mg (0.015–
0.02 mg/kg in children), or morphine, 2 to 4 mg (0.025–0.05 mg/kg in children),
are most commonly used. Intravenous meperidine is most often used in small
doses to treat postoperative shivering. Opioid requirements are often markedly
increased in patients with opioid tolerance, especially in patients with
psychological dependence. Consultation with a pain specialist is often extremely
helpful in these situations. If liposomal bupivacaine (Exparel) wound infiltration
is used, appropriate written and verbal communication must be employed to
preempt use of additional local anesthetics that could lead to systemic local
anesthetic toxicity.
Analgesic effects of intravenous opioids usually peak within minutes of
administration, although maximal respiratory depression, particularly with
morphine and hydromorphone, may not occur until 20 to 30 min later. Patient-
controlled analgesia can be instituted for inpatients when they are fully awake.
Intramuscular administration of opioids is discouraged because delayed and
variable onset (10–20 min or longer) and delayed respiratory depression (up to 1
h).
When an epidural catheter is used, epidural bolus administration of fentanyl
(50–100 mcg) or sufentanil (20–30 mcg) with 5 to 10 mL of 0.1% bupivacaine
can provide excellent pain relief in adults. Epidural morphine (3–5 mg) may also
be used, but delayed respiratory depression with epidural administration of this
opioid mandates close monitoring for 24 h afterward (see Chapter 48).

Agitation
Before the recovering patient is fully responsive, pain is often manifested
as postoperative restlessness or agitation. Significant systemic disturbances
(eg, hypoxemia, respiratory or metabolic acidosis, hypotension), bladder
distention, or a surgical complication (eg, occult intraabdominal
hemorrhage) must also be considered in the differential diagnosis of
postoperative restlessness or agitation. Marked agitation may necessitate arm
and leg restraints to avoid self-injury, particularly in children. When serious
physiological disturbances have been excluded in children, cuddling and kind
words from a sympathetic attendant or, preferably, the parents, often calms the
pediatric patient. Other contributory factors include marked preoperative anxiety
and fear, as well as adverse drug effects (large doses of central anticholinergic
agents, phenothiazines, or ketamine). Physostigmine, 1 to 2 mg intravenously
(0.05 mg/kg in children), is most effective in treating delirium due to atropine
and scopolamine. If serious systemic disturbances and pain are excluded,
persistent agitation may require sedation with intermittent intravenous doses of
midazolam, 0.5 to 1 mg (0.05 mg/kg in children).

Nausea & Vomiting

 Postoperative nausea and vomiting (PONV; see Chapter 17) is the most
common significant complication following general anesthesia, occurring in
approximately 30% or more of all patients. Moreover, PONV occurs at home
within 24 h of an uneventful discharge (postdischarge nausea and vomiting) in a
significant number of ambulatory surgery patients. The etiology of PONV is
usually multifactorial and associated with anesthetic and analgesic agents, the
type of surgical procedure, and intrinsic patient factors, such as a history of
motion sickness. It is also important to recognize that nausea is a common
complaint reported at the onset of hypotension, particularly following spinal or
epidural anesthesia.
Table 56–1 lists commonly recognized risk factors for PONV. An increased
incidence of nausea and vomiting is reported following opioid administration
and following intraperitoneal (especially laparoscopic), breast, or strabismus
surgery. The greatest incidence seems to be in young women. Increased vagal
tone manifested as sudden bradycardia commonly precedes, or coincides with,
emesis. Propofol anesthesia decreases the incidence of PONV, and a
preoperative history of smoking lessens the likelihood of PONV. Selective 5-
hydroxytryptamine (serotonin) receptor 3 (5-HT3) antagonists, such as
ondansetron, 4 mg (0.1 mg/kg in children), granisetron, 0.01–0.04 mg/kg, and
dolasetron, 12.5 mg (0.035 mg/kg in children), are effective in preventing
PONV, and, to a lesser extent, in treating established PONV. It should be noted
that unlike ondansetron, which is usually effective immediately, dolasetron
requires 15 min for onset of action. An orally disintegrating tablet preparation of
ondansetron (8 mg) may be useful for treatment of, and prophylaxis against,
postdischarge nausea and vomiting. Metoclopramide, 0.15 mg/kg intravenously,
is a less effective alternative to 5-HT3 antagonists. 5-HT3 antagonists are not
associated with the acute extrapyramidal (dystonic) manifestations and
dysphoric reactions that may be encountered with metoclopramide or
phenothiazine-type antiemetics. Transdermal scopolamine is effective, but can
be associated with side effects including sedation, dysphoria, blurred vision, dry
mouth, urinary retention, or exacerbation of glaucoma, particularly in elderly
patients. Intravenous dexamethasone, 4 to 10 mg (0.10 mg/kg in children), when
utilized as an antiemetic, has the additional advantages of providing a varying
degree of analgesia and a sense of patient well-being. Moreover, it seems to be
effective for up to 24 h, and, thus, may be useful for postdischarge nausea and
vomiting. Oral aprepitant (Emend), 40 mg, may be administered within 3 h prior
to anesthesia induction. Intravenous droperidol, 0.625 to 1.25 mg (0.05–0.075
mg/kg in children), when given intraoperatively, significantly decreases the
likelihood of PONV. Unfortunately, droperidol carries a U.S. Food and Drug
Administration “black box” warning, indicating that large (5–15 mg) doses can
prolong the QT interval and have been associated with fatal cardiac arrhythmias.
Nonpharmacological prophylaxis against PONV includes ensuring adequate
hydration (20 mL/kg) after fasting, and stimulation of the P6 acupuncture point
(wrist). The latter may include application of pressure, electrical current, or
injections.

TABLE 56–1 Risk factors for postoperative nausea and vomiting.

Controversy exists regarding routine PONV prophylaxis for all patients.

Because of the cost of treatment of established PONV, it may be cost-effective to
provide prophylaxis to all patients in certain populations (eg, outpatients).
Clearly, patients with multiple risk factors should receive prophylaxis. In
addition, the use of two or three agents that act on differing receptors is more
effective than single-agent prophylaxis.

Shivering & Hypothermia

Shivering can occur in the PACU as a result of intraoperative hypothermia or the
effects of anesthetic agents, or both, and it is also common in the immediate
postpartum period. The most important cause of hypothermia is a redistribution
of heat from the body core to the peripheral compartments (see Chapter 52). A
relatively cool ambient operating room temperature, prolonged exposure of a
large wound, and use of large amounts of unwarmed intravenous fluids or high
flows of unhumidified gases can also be contributory. Nearly all anesthetics,
particularly volatile agents and spinal and epidural anesthesia, decrease the
normal vasoconstrictive response to hypothermia by decreasing sympathetic
tone. Although anesthetic agents also decrease the shivering threshold, shivering
commonly observed during or after emergence from general anesthesia often
represents the body’s effort to increase heat production and raise body
temperature, and may be associated with intense vasoconstriction. Emergence
from even brief general anesthesia is sometimes also associated with shivering,
and although the shivering can be one of several nonspecific neurological signs
(eg, posturing, clonus, or Babinski’s sign) that are sometimes observed during
emergence, it is most often due to hypothermia. Regardless of the mechanism, its
incidence seems to be related to the duration of surgery and the use of a volatile
agent. Shivering may occasionally be sufficiently intense to cause hyperthermia
(38–39°C) and significant metabolic acidosis, both of which promptly resolve
when the shivering stops. Other causes of shivering should be excluded, such as
bacteremia and sepsis, drug allergy, or transfusion reaction.
Hypothermia should be treated with a forced-air warming device, or (less
satisfactorily) with warming lights or heating blankets, to raise body temperature
to normal. Intense shivering causes precipitous rises in oxygen consumption,
CO2 production, and cardiac output. These physiological effects may be poorly
tolerated by patients with cardiac or pulmonary impairment. Hypothermia has
been associated with an increased incidence of myocardial ischemia,
arrhythmias, coagulopathy with increased transfusion requirements, and
prolonged muscle relaxant effects. Small intravenous doses of meperidine (10–
25 mg) can dramatically reduce or even stop shivering. Intubated, mechanically
ventilated, and sedated patients can be given a muscle relaxant until
normothermia is reestablished by active rewarming.
Discharge Criteria
A. PACU
Standards for discharging patients from the PACU are established by the
department of anesthesiology and the hospital medical staff. They may allow
PACU nurses to determine when patients may be transferred without the
presence of a qualified anesthesia provider if all PACU discharge criteria have
been met. Criteria can vary according to whether the patient is going to be
discharged to an intensive care unit, a regular ward, phase 2 recovery, or directly
home.
Before PACU discharge, patients should have been observed for respiratory
depression for at least 20 to 30 min after the last dose of parenteral opioid. Other
minimum discharge criteria for patients recovering from general anesthesia
usually include the following:

1. Easy arousability
2. Full orientation
3. The ability to maintain and protect the airway
4. Stable vital signs for at least 15 to 30 min
5. The ability to call for help, if necessary
6. No obvious surgical complications (such as active bleeding)

Postoperative pain and nausea and vomiting must be controlled, and

normothermia should be reestablished prior to PACU discharge. PACU patient
scoring systems are widely used. Most assess SpO2 (or color), consciousness,
circulation, respiration, and motor activity (Table 56–2). The majority of
patients can meet discharge criteria within 60 min from the time of PACU
arrival. Patients to be transferred to other intensive care areas need not meet all
requirements.

TABLE 56–2 Postanesthetic Aldrete recovery score.1,2

 In addition to the preceding criteria, patients receiving regional anesthesia
should also be assessed for regression of both sensory and motor blockade.
Complete resolution of the block prior to PACU dismissal avoids inadvertent
injuries due to motor weakness or sensory deficits; however, many institutions
have protocols that allow earlier discharge to appropriately monitored areas, and
patients may be discharged with peripheral nerve blocks from single-shot or
continuous perineural catheter infusions for the purpose of regional analgesia.
Documenting regression of a block is important. Failure of a spinal or epidural
block to resolve 6 h after the last dose of local anesthetic raises the possibility of
spinal subdural or epidural hematoma, which should be excluded by prompt
radiological imaging and neurologic evaluation.
A major goal of most anesthetics should be rapid, comfortable emergence
with minimal risk of PONV and postoperative pain in order to minimize the time
needed in recovery and facilitate transfer to the next stage of recovery.
Outpatients who meet the discharge criteria when they exit the operating room
may be “fast-tracked,” bypassing the PACU and proceeding directly to the phase
2 recovery area. Similarly, inpatients who meet the same criteria may be
transferred directly from the operating room to their ward, if appropriate staffing
and monitoring are present.

B. Outpatients
In addition to emergence and awakening, recovery from anesthesia following
outpatient procedures includes two additional stages: home readiness (phase 2
recovery) and complete psychomotor recovery. A scoring system has been
developed to help assess home readiness discharge (Table 56–3). Recovery of
proprioception, sympathetic tone, bladder function, and motor strength are
additional criteria following regional anesthesia. For example, intact
proprioception of the big toe, minimal orthostatic blood pressure or heart rate
changes, and normal plantar flexion of the foot are important signals of recovery
following spinal anesthesia. Urination and drinking or eating before discharge
are usually no longer required; exceptions include patients with a history of
urinary retention and those with diabetes.

TABLE 56–3 Postanesthesia discharge scoring system (PADS).1,2

 All outpatients must be discharged home in the company of a responsible
adult who will stay with them overnight. Patients and their adult accompaniment
must be provided with written postoperative instructions covering both routine
follow-up care and urgent/emergent assistance. The assessment of home
readiness is the responsibility of a qualified anesthesia provider who is
preferably already familiar with the patient, although authority to discharge a
patient home can be delegated to a nurse if approved discharge criteria are
applied.
Home readiness does not imply that the patient has the ability to make
important decisions, to drive, or to return to work. These activities require
complete psychomotor recovery, which is often not achieved until 24 to 72 h
postoperatively. All outpatient centers must use some system of postoperative
follow-up, preferably phone contact or smartphone/web app the day after
discharge.

Management of Complications

RESPIRATORY COMPLICATIONS
Respiratory problems are the most frequently encountered serious
complications in the PACU. The overwhelming majority are related to airway
obstruction, hypoventilation, hypoxemia, or a combination of these problems.
Because hypoxemia is the final common pathway to serious morbidity and
mortality, routine monitoring of pulse oximetry in the PACU leads to earlier
recognition of these complications and fewer adverse outcomes.

Airway Obstruction
Airway obstruction in unconscious patients is most commonly due to the
tongue falling back against the posterior pharynx and is often seen in
patients with obstructive sleep apnea (see Chapter 19). Other causes include
laryngospasm, glottic edema, aspirated vomitus, a retained throat pack,
secretions or blood in the airway, or external pressure on the trachea (eg,
from a neck hematoma). Partial airway obstruction usually presents as
sonorous respiration. Near-total or total obstruction causes cessation of airflow
and an absence of breath sounds and may be accompanied by paradoxic
(rocking) movement of the chest. The abdomen and chest should normally rise
together during inspiration; however, with airway obstruction, the chest descends
as the abdomen rises during each inspiration (paradoxic chest movement).
Patients with airway obstruction should receive supplemental oxygen while
corrective measures are undertaken. A combined jaw-thrust and head-tilt
maneuver pulls the tongue forward and opens the airway, and insertion of an oral
or nasal airway often alleviates the problem. Nasal airways may be better
tolerated than oral airways by patients emerging from anesthesia, especially
when lidocaine-containing lubricant is used, and may decrease the likelihood of
trauma to the teeth if the patient bites down. Nasal airways may be easier to
insert, with less risk of significant nasal bleeding, if a nasal spray
vasoconstrictor, such as phenylephrine, is first administered. They should be
inserted with caution, if at all, in patients with coagulopathy.
Laryngospasm should be considered if the aforementioned maneuvers fail to
reestablish a patent airway. Laryngospasm is usually characterized by high-
pitched crowing noises during ventilation, but may be silent with complete
glottic closure. Spasm of the vocal cords is more apt to occur following airway
trauma, repeated instrumentation, or stimulation from secretions, blood, or other
foreign material in the airway. The jaw-thrust maneuver, particularly when
combined with gentle positive airway pressure via a tight-fitting face mask,
usually breaks laryngospasm. Insertion of an oral or nasal airway is also helpful
in ensuring a patent airway down to the level of the vocal cords. Secretions,
blood, or other foreign material in the hypopharynx should be suctioned to
prevent recurrence. Refractory laryngospasm should be treated with a small dose
of intravenous succinylcholine (10–20 mg in adults) and positive-pressure
ventilation with 100% oxygen. Endotracheal intubation may occasionally be
necessary to reestablish ventilation; emergent cricothyrotomy or transtracheal jet
ventilation is indicated if intubation is unsuccessful in such instances.
Glottic edema following airway instrumentation is an important cause of
airway obstruction in infants and young children because of the relatively small
airway lumen. Significant pharyngeal and glottic edema and irritability, with
friable, oozing oropharyngeal mucosa, is common in patients undergoing head
and neck radiation therapy. Intravenous corticosteroids (dexamethasone, 0.5
mg/kg, 10-mg dose maximum) or aerosolized racemic epinephrine (0.5 mL of a
2.25% solution with 3 mL of normal saline) may be useful in such cases.
Postoperative wound hematomas following thyroid, carotid artery, and other
neck procedures can quickly compromise the airway, and opening the wound
immediately relieves tracheal compression in most cases. Rarely, a gauze “throat
pack” may be unintentionally left in the hypopharynx following oral surgery and
can cause immediate or delayed complete airway obstruction.
Decannulation of a fresh tracheostomy is hazardous because recannulation
may be very difficult or impossible when the wound has not yet healed into a
well-formed track. When a tracheostomy has been performed within the
previous 4 weeks, intentional replacement of a tracheostomy cannula should
only be performed with a surgeon at the bedside and with a tracheostomy
instrument set, along with other appropriate difficult airway equipment,
immediately available.
Hypoventilation
Hypoventilation, which is generally defined as a PaCO2 greater than 45 mm Hg,
is common following general anesthesia. In most instances, such hypoventilation
is mild and not recognized. Significant hypoventilation may present clinical
signs when the PaCO2 is greater than 60 mm Hg or arterial blood pH is less than
7.25, including excessive somnolence, airway obstruction, slow respiratory rate,
tachypnea with shallow breathing, or labored breathing. Mild to moderate
respiratory acidosis may cause tachycardia, hypertension, and cardiac irritability
via sympathetic stimulation, but more severe acidosis produces circulatory
depression (see Chapter 50). If significant hypoventilation is suspected,
assessment and management is facilitated by capnography or arterial blood gas
measurement, or both.
Hypoventilation in the PACU is most commonly due to the residual
depressant effects of anesthetics on respiratory drive, often made worse by
preexisting obstructive sleep apnea. Opioid-induced respiratory depression
characteristically produces a slow respiratory rate, often with large tidal
volumes. The patient is somnolent, but often responsive to verbal and physical
stimulus and able to breathe on command. Delayed occurrence of respiratory
depression has been reported with all opioids. Proposed mechanisms include
variations in the intensity of stimulation during recovery and delayed release of
the opioid from peripheral tissue compartments as the patient rewarms or begins
to move.
Causes of residual muscle weakness in the PACU include inadequate muscle
relaxant reversal, drug interactions that potentiate muscle relaxants, altered
muscle relaxant pharmacokinetics (due to hypothermia, altered volumes of
distribution, and renal or hepatic dysfunction), and metabolic factors such as
hypokalemia, hyper- or hypomagnesemia, or respiratory acidosis. Regardless of
the cause, generalized weakness, uncoordinated movements (“fish out of
water”), shallow tidal volumes, and tachypnea are usually apparent. The
diagnosis of inadequate neuromuscular blockade reversal can be made with a
nerve stimulator in unconscious patients; head lift and grip strength can be
assessed in awake and cooperative patients. Splinting due to incisional pain,
diaphragmatic dysfunction following upper abdominal or thoracic surgery,
abdominal distention, and tight abdominal dressings are other factors that can
contribute to hypoventilation. Increased CO2 production from shivering,
hyperthermia, or sepsis can also increase PaCO2, even in normal patients
recovering from general anesthesia. Marked hypoventilation and respiratory
acidosis can result when these factors are superimposed on an impaired
ventilatory reserve due to preexisting pulmonary, neuromuscular, or neurological
disease.

Treatment of Hypoventilation
Treatment should generally be directed at the underlying cause, but marked
hypoventilation always requires assisted or controlled ventilation until causal
factors are identified and corrected. Hypoventilation with obtundation,
circulatory depression, and severe acidosis (arterial blood pH <7.15) is an
indication for immediate and decisive ventilatory and hemodynamic
intervention, including airway and inotropic support as needed. If
intravenous naloxone is used to reverse opioid-induced respiratory depression,
titration in small increments (80 mcg in adults) usually avoids complications and
minimizes reversal of analgesia. Antagonism of opioid-induced depression with
large doses of naloxone often results in sudden pain and marked increase in
sympathetic tone. The latter can precipitate a hypertensive crisis, pulmonary
edema, and myocardial ischemia or infarction. Following naloxone
administration, patients should be observed closely for recurrence of opioid-
induced respiratory depression (“renarcotization”), as naloxone has a shorter
duration of action than many opioids. If residual muscle paralysis is present,
sugammadex (if rocuronium or vecuronium has been administered) or an
additional cholinesterase inhibitor may be administered. Inadequate reversal in
spite of a full dose of sugammadex or a cholinesterase inhibitor necessitates
controlled ventilation under close observation until adequate recovery of muscle
strength occurs. Hypoventilation due to pain and splinting following upper
abdominal or thoracic procedures should be treated with multimodal analgesia,
including intravenous or intraspinal opioid administration, intravenous
acetaminophen, or NSAIDs, or with regional anesthesia techniques.

Hypoxemia
Mild hypoxemia is common in patients recovering from anesthesia when
supplemental oxygen is not given. Mild to moderate hypoxemia (PaO2 50–60
mm Hg) in young healthy patients may be well tolerated initially, but with
increasing duration or severity, the initial sympathetic stimulation often seen is
replaced with progressive acidosis and circulatory depression. Cyanosis may not
be detected if the hemoglobin concentration is reduced. Hypoxemia may also be
suspected from restlessness, agitation, tachycardia, or atrial or ventricular
dysrhythmias. Obtundation, bradycardia, hypotension, and cardiac arrest are late
signs. Pulse oximetry facilitates early detection of hypoxemia and must be
routinely utilized in the PACU. Arterial blood gas measurements may be
performed to confirm the diagnosis and guide therapy.
Hypoxemia in the PACU is usually caused by hypoventilation with or
without obstruction, increased right-to-left intrapulmonary shunting, or
both. A decrease in cardiac output or an increase in oxygen consumption (as
with shivering) will accentuate hypoxemia. Diffusion hypoxia (see Chapter 8) is
an uncommon cause of hypoxemia when recovering patients are given
supplemental oxygen. Hypoxemia due exclusively to hypoventilation without
obstruction is also unusual in patients receiving supplemental oxygen, unless
marked hypercapnia or a concomitant increase in intrapulmonary shunting is
present. Increased intrapulmonary shunting from a decreased functional
residual capacity (FRC) relative to closing capacity is the most common
cause of hypoxemia following general anesthesia. The greatest reductions in
FRC occur following upper abdominal and thoracic surgery. The loss of lung
volume is often attributed to microatelectasis, as atelectasis is often not
identified on a chest radiograph. A semi-upright position helps maintain FRC.
Marked right-to-left intrapulmonary shunting is usually
caused by atelectasis from prolonged intraoperative hypoventilation with low
tidal volumes, unintentional endobronchial intubation, lobar collapse from
bronchial obstruction by secretions or blood, pulmonary aspiration, pulmonary
edema, large pleural effusion, or pneumothorax. Postoperative pulmonary edema
may present with wheezing or less commonly with pink frothy fluid in the
airway. Pulmonary edema may be due to left ventricular failure (cardiogenic),
acute respiratory distress syndrome, or relief of prolonged airway obstruction
(negative-pressure pulmonary edema). In contrast to wheezing associated with
pulmonary edema, wheezing due to primary obstructive lung disease, which also
often results in large increases in intrapulmonary shunting, is not associated with
edema fluid in the airway or infiltrates on the chest radiograph. The possibility
of a postoperative pneumothorax should always be considered following central
line placement, supraclavicular or intercostal blocks, abdominal or chest trauma
(including rib fractures), neck dissection, thyroidectomy (especially if the
thyroid dissection extends into the thorax), tracheostomy, nephrectomy, or other
retroperitoneal or intraabdominal procedures (including laparoscopy), especially
if the diaphragm may have been penetrated or disrupted. Patients with subpleural
blebs or large bullae can also develop pneumothorax during positive-pressure
ventilation.
Treatment of Hypoxemia
Oxygen therapy, with or without positive airway pressure, and relief of any
existing airway obstruction with airway maneuvers, an oral or nasal airway, or
oropharyngeal suctioning, provide the cornerstones of treatment for hypoxemia.
Routine administration of 30% to 60% oxygen is usually enough to prevent
hypoxemia with even moderate hypoventilation and hypercapnia. Importantly,
clinical signs of hypoventilation and hypercapnia may be masked by routine
oxygen administration. Patients with underlying pulmonary or cardiac disease
may require higher concentrations of oxygen; oxygen therapy should be guided
by SpO2 or arterial blood gas measurements. Oxygen concentration must be
closely controlled in patients with chronic CO2 retention to avoid precipitating
acute respiratory failure. Patients with severe or persistent hypoxemia should be
given 100% oxygen via a nonrebreathing mask, LMA, or endotracheal tube until
the cause is established and appropriate therapy is instituted; controlled or
assisted mechanical ventilation may also be necessary. The chest radiograph
(preferably with the patient positioned sitting upright) is valuable in assessing
lung volume and heart size and in demonstrating pneumothorax, atelectasis,
pulmonary infiltrates. However, in cases of pulmonary aspiration, infiltrates are
usually initially absent. If pneumothorax is suspected, a chest radiograph taken
at end-expiration helps highlight the pneumothorax by providing the greatest
contrast between lung tissue and adjacent air in the pleural space. In the
intubated patient with hypoxemia, a chest radiograph should be used to verify
proper endotracheal tube position. Transthoracic ultrasonography is also a
valuable tool for rapid, accurate assessment of endotracheal tube placement and
diagnosis of lobar consolidation, pleural effusion, and pneumothorax.
Additional treatment of hypoxemia should be directed at the underlying
cause. A chest tube or Heimlich valve should be inserted for any symptomatic
pneumothorax or one that is greater than 15% to 20%. An asymptomatic
pneumothorax may be aspirated or followed by observation. Bronchospasm
should be treated with aerosolized bronchodilator therapy and potential or partial
obstruction secondary to glottic or pharyngeal edema can be treated with
racemic epinephrine or corticosteroids, or both. Diuretics should be given for
fluid overload. Persistent hypoxemia in spite of 50% oxygen generally is an
indication for positive end-expiratory pressure ventilation or continuous positive
airway pressure. Therapeutic bronchoscopy is often useful in reexpanding lobar
atelectasis caused by bronchial plugs or particulate aspiration. In the setting of
an intubated patient, secretions or debris must be removed by suction and also by
lavage, if necessary, and a malpositioned endotracheal tube must be
appropriately repositioned.

CIRCULATORY COMPLICATIONS
The most common circulatory disturbances in the PACU are hypotension,
hypertension, and arrhythmias. The possibility that the circulatory abnormality is
secondary to an underlying respiratory disturbance should always be considered
before any other intervention, especially in children.

Hypotension
Hypotension is usually due to hypovolemia, left ventricular dysfunction, or
excessive arterial vasodilatation. Hypovolemia is the most common cause of
hypotension in the PACU, and can result from inadequate fluid replacement,
wound drainage, or hemorrhage. Vasoconstriction from hypothermia may mask
hypovolemia until the patient’s temperature begins to rise again; subsequent
peripheral vasodilation during rewarming unmasks the hypovolemia and results
in hypotension. Spinal and epidural anesthesia produce hypotension from a
combination of arterial vasodilation and venous pooling of blood. Venodilators
such as nitroglycerine (or spinal anesthesia) produce venous pooling and reduce
the effective circulating blood volume, despite an otherwise normal intravascular
volume (see Chapter 45). Hypotension associated with sepsis and allergic
reactions is usually the result of both hypovolemia and vasodilation.
Hypotension from a tension pneumothorax or cardiac tamponade is the result of
impaired venous return to the right atrium. Removal of more than 500 to 1000
mL of ascites fluid during surgical procedure or paracentesis may result in
subsequent hypotension as additional fluid migrates from the intravascular space
into the abdomen.
Left ventricular dysfunction in previously healthy persons is unusual unless
associated with severe metabolic disturbances (hypoxemia, acidosis, or sepsis).
Hypotension due to ventricular dysfunction is primarily encountered in patients
with underlying coronary artery or valvular heart disease or congestive heart
failure and is usually precipitated by fluid overload, myocardial ischemia, acute
increases in afterload, or arrhythmias.

Treatment of Hypotension
Mild hypotension during recovery from anesthesia is common and typically does
not require intensive treatment. Significant hypotension is often defined as a
20% to 30% reduction in blood pressure below the patient’s baseline level and
usually requires correction. Treatment depends on the ability to assess
intravascular volume. An increase in blood pressure following a fluid bolus
(250–500 mL crystalloid or 100–250 mL colloid) generally confirms
hypovolemia. With severe hypotension, a vasopressor or inotrope (dopamine or
epinephrine) may be necessary to increase arterial blood pressure until the
intravascular volume deficit can be at least partially corrected. Signs of cardiac
dysfunction should be sought in patients with known heart disease or cardiac risk
factors. Failure of a patient with severe hypotension to promptly respond to
initial treatment mandates echocardiographic examination or invasive
hemodynamic monitoring (see Chapter 5). Manipulations of cardiac preload,
contractility, and afterload are at times all required to restore the blood pressure
to acceptable levels. The presence of a tension pneumothorax, as suggested by
hypotension with unilaterally decreased breath sounds, hyperresonance, and
tracheal deviation, is an indication for immediate pleural aspiration, even before
ultrasound or radiographic confirmation. Similarly, hypotension due to cardiac
tamponade, usually following chest trauma or thoracic surgery, often necessitates
immediate pericardiocentesis or surgical exploration.

Hypertension
Postoperative hypertension is common in the PACU and typically occurs within
the first 30 min after admission. Noxious stimulation from incisional pain,
endotracheal intubation, bladder distention, or preoperative discontinuation of
antihypertensive medication, is usually responsible. Postoperative hypertension
may also reflect the neuroendocrine stress response to surgery or increased
sympathetic tone secondary to hypoxemia, hypercapnia, or metabolic acidosis.
Patients with a history of hypertension are more likely to develop hypertension
in the PACU. Fluid overload or intracranial hypertension may also occasionally
present as postoperative hypertension.

Treatment of Hypertension
Mild hypertension generally does not require treatment, but a reversible cause
should be sought. Marked hypertension can precipitate postoperative bleeding,
myocardial ischemia, heart failure, or intracranial hemorrhage. Although
decisions to treat postoperative hypertension should be individualized, in
general, elevations in blood pressure greater than 20% to 30% of the patient’s
baseline, or those associated with adverse effects such as myocardial ischemia,
heart failure, or bleeding, should be treated. After pain and potential bladder
distention have been addressed, mild to moderate elevations can be treated with
intravenous labetalol; an angiotensin-converting enzyme inhibitor, such as
enalapril; or a calcium channel blocker, such as nicardipine. Hydralazine and
sublingual nifedipine (when administered to patients not receiving β-blockers)
may cause tachycardia and myocardial ischemia and infarction. Marked
hypertension in patients with limited cardiac reserve requires direct intraarterial
pressure monitoring and should be treated with an intravenous infusion of
nitroprusside, nitroglycerin, nicardipine, clevidipine, or fenoldopam. The
endpoint for treatment should be consistent with the patient’s own normal blood
pressure.

Arrhythmias
Respiratory disturbances, particularly hypoxemia, hypercarbia, and acidosis, will
commonly be associated with cardiac arrhythmias. Residual effects from
anesthetic agents, increased sympathetic nervous system activity, other
metabolic abnormalities, and preexisting cardiac or pulmonary disease also
predispose patients to arrhythmias in the PACU.
Bradycardia often represents the residual effects of cholinesterase inhibitors,
opioids, or β-adrenergic blockers. Tachycardia in the PACU is most commonly
caused by pain, hypovolemia, or fever, but may also be due to the effects of an
anticholinergic agent, a β-agonist such as albuterol, or reflex tachycardia from
hydralazine. Anesthetic-induced depression of baroreceptor function makes heart
rate an unreliable monitor of intravascular volume in the PACU.
Premature atrial and ventricular beats may be the result of hypokalemia,
hypomagnesemia, increased sympathetic tone, or, less commonly, myocardial
ischemia. The latter can be diagnosed with a 12-lead ECG. Premature atrial or
ventricular beats noted in the PACU without discernable cause will often also be
found on the patient’s preoperative ECG, if one is available. Supraventricular
tachyarrhythmias, including paroxysmal supraventricular tachycardia, atrial
flutter, and atrial fibrillation, are typically encountered in patients with a history
of these arrhythmias and are more commonly encountered following thoracic
surgery. The management of arrhythmias is discussed in Chapters 21 and 55.

CASE DISCUSSION
Fever & Tachycardia in a Young Adult Male
A 19-year-old man sustained a closed fracture of the femur in a motor
vehicle accident. He was placed in traction for 3 days prior to surgery.
During that time, a persistent low-grade fever (37.5–38.7°C orally),
mild hypertension (150–170/70–90 mm Hg), and tachycardia (100–126
beats/min) were noted. His hematocrit remained at 30%. Broad-
spectrum antibiotic coverage was initiated.
He is scheduled for open reduction and internal fixation of the
fracture. When the patient is brought into the operating room, vital
signs are as follows: blood pressure 160/95 mm Hg, pulse 150
beats/min, respirations 20 breaths/min, and oral temperature 38.1°C.
He is sweating and is anxious. On close examination, he is noted to have
a slightly enlarged thyroid gland.
Should the surgical team proceed with the operation?
The proposed operation is elective; therefore, significant abnormalities
should be diagnosed and properly treated preoperatively, if possible, to
prepare the patient optimally for surgery. If the patient had an open fracture,
the risk of infection would clearly mandate immediate operation. Even with
a closed femoral fracture, cancellations or delays should be avoided
because nonoperative treatment potentiates the risks associated with bed
rest, including atelectasis, pneumonia, deep venous thrombosis, and
potentially lethal pulmonary thromboembolism. In deciding whether to
proceed with the surgery, the anesthesia provider must ask the following
questions:
1. What are the most likely causes of the abnormalities based on the
clinical presentation?
2. What, if any, additional investigations or consultations might be
helpful?
3. How would these or other commonly associated abnormalities affect
anesthetic management?
4. Are the potential anesthetic interactions serious enough to delay surgery
until a suspected cause is conclusively excluded? The tachycardia of
150 beats/min and the low-grade fever therefore require further
evaluation prior to surgery.
What are the likely causes of the tachycardia and fever in this
patient?
These two abnormalities may reflect one process or separate entities
(Tables 56–4 and 56–5). Moreover, although multiple factors can often be
simultaneously identified, their relative contribution is often not readily
apparent. Fever commonly follows major trauma; contributory factors can
include the inflammatory reaction to the tissue trauma, superimposed
infection (most commonly wound, pulmonary, or urinary), antibiotic
therapy (drug reaction), or thrombophlebitis. Infection must be seriously
considered in this patient because of the risk of bacteria seeding and
infecting the metal fixation device placed during surgery. Although
tachycardia is commonly associated with a low-grade fever, it is usually not
of this magnitude in a 19-year-old patient. Moderate to severe pain, anxiety,
hypovolemia, or anemia may be other contributory factors. Pulmonary
embolism should also be considered in any patient with long bone fracture,
particularly when hypoxemia, tachypnea, or mental status changes are
present. Lastly, the possibly enlarged thyroid gland, sweating, and anxious
appearance, together with both fever and tachycardia, suggest
thyrotoxicosis.

TABLE 56–4 Perioperative causes of tachycardia.

TABLE 56–5 Perioperative causes of fever.
What (if any) additional measures may be helpful in evaluating
the fever and tachycardia?
Arterial blood gas measurements, echocardiography and a chest
radiograph would be helpful in the identification of pulmonary embolism. A
repeat hematocrit or hemoglobin concentration measurement would exclude
worsening anemia; significant tachycardia may be expected when the
hematocrit is below 25% to 27% (hemoglobin <8 g/dL) in most patients.
The response to an intravenous fluid challenge with 250 to 500 mL of a
colloid or crystalloid solution may be helpful; a decrease in heart rate after
the fluid bolus would be strongly suggestive of hypovolemia. Similarly,
response of the heart rate to sedation and additional opioid analgesia would
be helpful in excluding anxiety and pain, respectively, as causes. Although
a tentative diagnosis of hyperthyroidism can be made based on clinical
grounds, confirmation requires measurement of serum thyroid hormones.
Signs of infection—such as increased inflammation or purulence in a
wound, purulent sputum, an infiltrate on the chest film, pyuria, or
leukocytosis with premature white cells on a blood smear (“shift to the
left”)—should prompt cultures and a delay of surgery until the results are
obtained and correct antibiotic coverage is confirmed.
The patient is transferred to the PACU for further evaluation. A 12-lead
ECG confirms sinus tachycardia of 150 beats/min. A chest film is normal.
Arterial blood gas measurements on room air are normal (pH 7.44, PaCO2
41 mm Hg, PaO2 87 mm Hg, and HCO3− 27 mEq/L). The hemoglobin
concentration is found to be 11 g/dL. Blood for thyroid function tests is sent
to the laboratory. The patient is sedated intravenously with midazolam (2
mg) and fentanyl (50 mcg) and is given 500 mL of 5% albumin. He seems
to be relaxed and pain free, but the heart rate decreases only to 144
beats/min. The decision is made to proceed with surgery using continuous
lumbar epidural anesthesia with 2% lidocaine. Esmolol is administered
slowly until his pulse decreases to 120 beats/min, and a continuous esmolol
infusion is administered at a rate of 300 mcg/kg/min.
The procedure is completed in 3 h. Although the patient did not
complain of any pain during the procedure and was given only minimal
additional sedation (midazolam, 2 mg), he is delirious upon admission to
the PACU. The esmolol infusion is continuing at a rate of 500 mcg/kg/min.
Estimated blood loss was 500 mL, and fluid replacement consisted of 2
units of packed red blood cell, 500 mL of 5% albumin solution, and 2000
mL of lactated Ringer’s injection. Vital signs are as follows: blood pressure
105/40 mm Hg, pulse 124 beats/min, respirations 30 breaths/min, and rectal
temperature 38.8°C. Arterial blood gas measurements are reported as
follows: pH 7.37, PaCO2 37 mm Hg, PaO2 91 mm Hg, and HCO3− 22
mEq/L.
What is the most likely diagnosis?
The patient appears to be in a hypermetabolic state manifested by
excessive adrenergic activity, fever, and a worsening mental status. The
absence of major metabolic acidosis and lack of exposure to a known
triggering agent exclude malignant hyperthermia (see Chapter 52). Other
possibilities include a transfusion reaction, sepsis, or an undiagnosed
pheochromocytoma. The sequence of events makes the first two unlikely,
and the decreasing prominence of hypertension (now replaced with relative
hypotension) and increasing fever also make the latter unlikely. The clinical
presentation now suggests thyroid storm. He has also received a very large
dose of esmolol for several hours and this may be contributing to the
relatively low blood pressure despite aggressive fluid administration.