........................................................................

CHAPTER 1

V O L U M E

T H I R T Y

S E V E N

MANAGEMENT

OF
POSTANESTHESIA CARE
UNIT EMERGENCIES
MAGED ARGALIOUS, M.D., M.B.A.
ASSISTANT PROFESSOR OF ANESTHESIOLOGY
CLEVELAND CLINIC LERNER COLLEGE OF MEDICINE
DIRECTOR, POSTANESTHESIA CARE UNIT AND SAME DAY SURGERY
CLEVELAND CLINIC
CLEVELAND, OHIO

EDITOR: MEG A. ROSENBLATT, M.D.

ASSOCIATE EDITORS: JOHN F. BUTTERWORTH IV, M.D.
JEFFREY B. GROSS, M.D.

The American Society of Anesthesiologists, Inc.

........................................................................

The ASA Refresher Courses in Anesthesiology CME Program

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The American Society of Anesthesiologists, Inc.

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Management of Postanesthesia Care

Unit Emergencies
Maged Argalious, M.D., M.B.A.
Assistant Professor of Anesthesiology
Cleveland Clinic Lerner College of Medicine
Director, Postanesthesia Care Unit and Same Day Surgery
Cleveland Clinic
Cleveland, Ohio

In a recent study, the incidence of postanesthesia care unit (PACU) complications

in a university hospital setting was 24%.1 Postoperative nausea or vomiting was the
most common complication with an incidence of 10%. Other PACU complications in
order of decreasing frequency were as follows1,2:
 Requirement for upper airway support: 7% (nasal airway support: 47%,
pharyngeal airway support: 24%, prolonged airway support via endotracheal
tube (ETT): 0.02%)
 Hypoxemia (Spo2o 90%): 3%; hypotension: 3%; hypertension: 1%; arrhythmia:
0.1%; pulmonary edema: 0.1%; myocardial ischemia: 0.4%
Because airway and hemodynamic complications are the most frequently
encountered PACU emergencies, they are the focus of this Refresher Course. Table 1
lists PACU emergencies by organ system.

Airway Complications
Airway management is often challenging in the PACU or critical care unit. Factors
including surgery to the airway, intraoperative airway instrumentation or manipulation, previous neck dissection or radiation,3 prolonged surgery in the prone position,
large volumes of intraoperative fluids, and residual anesthetic effects contribute to
these difficulties. Even patients considered as having an easy airway in the
operating room can pose airway challenges in the PACU or critical care unit.

Airway Obstruction and Hypoxemia

The most common cause of postoperative airway obstruction is pharyngeal
obstruction by the tongue. Simple interventions such as rousing the patient with
gentle stimulation, jaw thrust, and, if necessary, insertion of a nasal or oral airway
may restore airway patency. Persistence of airway obstruction or signs of
laryngospasm mandate the application of positive pressure ventilation with oxygen
via a bag and mask. Small doses of succinylcholine (20 to 40 mg) may also be
necessary to relieve laryngospasm.
Copyright 2009 American Society of Anesthesiologists, Inc.

ARGALIOUS
TABLE 1. PACU Emergencies

Respiratory
Apnea
Hypoxemia
Hypercarbia
Airway obstruction (includes pharyngeal obstruction, stridor, laryngospasm, airway edema,
expanding neck hematoma)
Cardiovascular
Hypertension
Hypotension
Arrhythmias
Myocardial ischemia (acute coronary syndromes)
Pulmonary embolism
Cardiac tamponade
Neurologic
Postoperative vision loss
Acute paraplegia
Unexplained coma
Increased intracranial pressure
Status epilepticus
Endocrine/metabolic
Ionized hypocalcemia
Hyperkalemia
Adrenal insufficiency
Thyroid storm
Malignant hyperthermia
Alcohol withdrawal
Environmental
Gas leaks
Fires
Earthquakes
PACU postanesthesia care unit.

Promptly restoring airway patency reduces the likelihood of negative pressure

pulmonary edema and, more importantly, prevents O2 desaturation and hypoxemia.
Oxygen supplementation during patient transfer to the PACU is reasonable for all
patients. Hypoxic drive is inhibited by minimal residual concentrations of anesthetics.
Patients with stridor may require treatment with nebulized racemic epinephrine and
may benefit from a helium/oxygen mixture (70% helium, 30% oxygen), which
reduces airway resistance and work of breathing relative to oxygen or air. Quick
recognition of problems is necessary because stridor may advance to total airway
obstruction. Even in patients with suspected or identified tracheomalacia,
continuous positive airway pressure reverses the dynamic airway collapse and can
be used as a temporizing measure pending diagnosis by bronchoscopy and treatment
with tracheal stenting or tracheostomy.
Persistent hypoxemia after restoration of airway patency requires evaluation of
possible etiologies (Table 2). In negative-pressure pulmonary edema, inspiratory
efforts against an obstructed airway can cause alveolar--capillary membrane injury.
Such a capillary leak may lead to respiratory failure requiring mechanical ventilation
with positive end-expiratory pressure. The most common cause of hypoxemia in the
PACU is an increase in right to left shunting (most often from atelectasis). Other
common etiologies include pulmonary aspiration and pulmonary edema. An
unrecognized pneumothorax, perhaps caused by high inflation pressures during

MANAGEMENT OF PACU EMERGENCIES

TABLE 2. Causes of Hypoxemia

Mechanism
Decreased partial
pressure of
inspired oxygen
Hypoventilation

Ventilation-perfusion
mismatch
Shunt
Diffusion
impairment

Examples

Alveolar--Arterial
O2 Gradient

Response to
100% O2

Hypoxic gas mixture;

high altitude

Normal

Increased PaO2

Obesity --- hypoventilation

syndrome,
neuromuscular
disorders, sleep apnea
COPD, asthma, interstitial
lung disease

Normal

Increased PaO2

Increased

Increased PaO2

Increased

Minimal if any
increase in PaO2

Increased

Increased PaO2

Pulmonary edema, ARDS,

atelectasis, pneumonia,
pneumothorax
Pulmonary embolism

ARDS acute respiratory distress syndrome; COPD chronic obstructive pulmonary disease;
PaO2 partial oxygen tension in arterial blood.

attempts to ventilate the patient, may lead to hemodynamic compromise and render
resuscitation attempts useless.

Hypoventilation
Postoperative hypoventilation and apnea can be caused by residual neuromuscular blockade (as a result of overdose, inadequate reversal dosing, hypothermia, or
metabolic factors [e.g., hypokalemia] that interfere with adequate reversal).4 Opioidinduced respiratory depression is also a frequent cause of postoperative hypoventilation. Opioids not only shift the carbon dioxide response curve to the right (i.e., raise
the apneic threshold), but can also decrease the slope of the carbon dioxide
response curve (i.e., reduce the minute volume response to a high PaCO2). Although
the slope of the carbon dioxide response curve is unchanged by opioids in fully
awake patients, residual anesthetic effect can shift the carbon dioxide response
curve. Splinting resulting from incisional pain can also cause postoperative
hypoventilation.

Emergency Airway Management in Special Situations

Postoperative Expanding Neck Hematoma. In patients recovering from neck
surgery, who develop respiratory insufficiency, the possibility of an expanding neck
hematoma must be considered. In most instances, airway obstruction ensues quickly
as a result of encroachment and distortion of airway anatomy. If the neck hematoma
is visible but is not causing respiratory distress, apply pressure to the surgical site to
avoid further expansion. After notifying the surgeon, awake intubation (possibly
fiberoptic guided according to the American Society of Anesthesiologists difficult
airway algorithm5) may be prudent to stabilize the patient before drainage of the
hematoma.
In some cases, airway edema persists despite drainage of the hematoma. If
emergent intubation attempts are unsuccessful, the decision to proceed with a
surgical airway (emergency cricothyroidotomy or tracheostomy) depends on the

ARGALIOUS

ability (vs. inability) to ventilate the patient with a facemask or laryngeal mask
airway. If ventilation is unsuccessful or becomes inadequate despite drainage of the
neck hematoma, invasive airway access should proceed.5
Postoperative Airway Management After Cervical Spine Surgery. Patients
undergoing surgery for cervical spine disease have a greater incidence of difficult
intubation than matched control subjects.6 Airway complications are common after
anterior cervical spine surgery and range from acute airway obstruction (1.2%) to
chronic vocal cord dysfunction.7,8 Risk factors associated with airway obstruction
after cervical spine surgery include8,9









advanced age
obesity (greater than 100 kg)
exposure of three or more vertebral bodies or exposure of C2, C3, or C4
estimated blood loss greater than 300 ml
requirement for four or more red cell units
operative time more than 10 hours
combined anteroposterior cervical spine surgery
severe preoperative neurologic deficits

Airway complications may also occur after cervical spine surgery in the prone
position, most commonly macroglossia and laryngeal edema. Decreased venous
return from the face and upper neck is likely because of etiologic factors.10 A plan for
reintubation should be in place before any extubation attempts. The presence of
external stabilization devices complicates airway management. Removal of the
anterior part of a cervical collar during reintubation attempts improves airway
visualization but should be accompanied by manual inline stabilization in patients
with an unstable cervical spine. Manual inline stabilization reduces cervical spine
motion during intubation attempts in patients with an unstable cervical spine.11
Komatsu et al.12 reported a reasonable success rate of intubation with the use of an
intubating laryngeal mask airway in patients with rigid neck collars. A recent study
on postoperative patients after anterior cervical spine surgery showed a reduced
incidence of airway complication with routine postoperative fiberoptic evaluation of
the airway for evidence of airway edema.13 Patients tracheas were only extubated if
there was no reactive swelling or pharyngeal edema. Close communication among
surgeons, anesthesiologists, and respiratory therapists helps in reducing emergency
airway complications.

Role of Airway Exchange Catheters in the Postanesthesia Care Unit

Although the presence of an airway exchange catheter does not guarantee
success at subsequent reintubation, a high success rate has been reported.14,15 In
addition, oxygen insufflation through an airway exchange catheter (AEC) can
maintain oxygenation until definitive measures are taken to secure the airway (e.g.,
tracheal intubation, cricothyroidotomy, tracheostomy).
Numerous AECs are available, but these devices must be used correctly because
airway complications can develop (e.g., perforation of the tracheobronchial tree,
failure to pass the ETT over the AEC, barotrauma) when the wrong size, type, or
technique is used.16--22 Suggestions for success include the following:
 AECs with a very small outer diameter should be avoided because they are
prone to kinking, making railroading of the new ETT difficult

MANAGEMENT OF PACU EMERGENCIES

 Match the marking of the AEC with the centimeter markings on the ETT to
avoid excessive advancement of the AEC, which can irritate the carina and
cause bronchial trauma and bleeding
 Use an AEC with an inner hollow lumen that allows oxygen insufflation,
whether by jet ventilation or a bag valve device. Two adapters Rapi-Fits
adaptors (Cook Medical, Bloomington, IN) usually accompany the AEC for this
purpose
 If resistance is encountered during the advancement of the ETT over the AEC,
oral laryngoscopy (if feasible) can aid tube advancement. Rotation of the ETT in
90-degree increments also helps to pass the ETT tip past the arytenoids. ETTs
with flexible tips (Parker Flex-Tip) serve the same purpose in that the tube tip is
prevented from becoming caught against the arytenoids
 Avoid using force in advancing the AEC and the ETT because it may traumatize
airway structures19
 Applying a silicone-based spray or a lubricant gel on the outside of the AEC can
facilitate tube advancement
 The position of the new ETT should be confirmed before the AEC is withdrawn.
This can be done by end-tidal capnography through a flexible bronchoscope
adapter16
 Longer AECs are available for double-lumen tubes and can be used with the
same precautions

Role of the Cuff Leak Test

A cuff leak test can be performed on a spontaneously breathing patient by
deflating the ETT cuff, blocking the ETT opening, and listening for a leak around the
cuff while the patient inspires. Becuase this method cannot quantify the volume of a
leak, a cuff leak test is more effective in detecting postextubation stridor while a
patient is being mechanically ventilated. With the patient on controlled ventilation
assist/control mode, an inspiratory VT and six subsequent expiratory VT values are
recorded after oropharyngeal suctioning and ETT cuff deflation. Six cycles are
recorded because it was found that the exhaled VT values decreased decrementally
during the first few breaths before reaching a plateau. The leak is measured as the
difference between the preset inspiratory VT and the average of the three lowest of
the subsequent six expiratory VT values.23 A leak of less than 110 ml is considered
a positive result of the cuff leak test and indicates that the patient is at risk for
postextubation stridor secondary to laryngeal edema. Cuff leak tests have been
criticized because of their poor sensitivity in detecting postextubation stridor and
their low positive predictive value.24--26

Acute Postoperative Hypertension

Despite advances in chronic hypertension management, acute postoperative
hypertension (APH) occurs with a reported incidence of 4 to 35%.27 APH may lead
to serious neurologic (hemorrhagic stroke, cerebra ischemia, encephalopathy),
cardiovascular (myocardial ischemia, cardiac arrhythmia, congestive heart failure,
pulmonary edema), renal (acute kidney injury, acute tubular necrosis), and surgical
site complications (bleeding, failure of vascular anastomosis) and requires prompt

ARGALIOUS

intervention and management.27,28 Although there is no precise quantification of

APH in the literature, APH typically refers to stages II and III hypertension according
to the Joint National Committee classification of hypertension29 (Table 3). APH can
also be defined as a 20% or more increase in systolic blood pressure, diastolic blood
pressure, or mean arterial pressure above baseline.
The final common pathway leading to hypertension seems to be the activation of
the sympathetic nervous system as evidenced by increased plasma catecholamine
concentrations in patients with APH. Patients undergoing carotid endarterectomy,
cardiac surgery, aortic surgery, radical neck dissection, and intracranial neurosurgery
have the greatest frequency of APH. APH is especially undesirable in patients in
whom postoperative bleeding into a closed space can have life-threatening
consequences (e.g., craniotomy, carotid endarterectomy).30,31
In the nonoperative setting, hypertensive emergency has been differentiated from
hypertensive urgency by the presence of end organ damage.32 In the postoperative
setting, both clinical entities require prompt intervention to prevent the occurrence
or progression of end organ damage and surgical site complications.
Identifying baseline blood pressure helps define a target blood pressure to avoid
the deleterious consequences of overaggressive treatment. Prospective studies
showing clinical benefits of aggressive blood pressure control in the postoperative
period are lacking.28 Whether to titrate to a target mean arterial pressure or systolic
blood pressure is still controversial. There are, however, recent reports of the
deleterious effects of pulse pressure hypertension on postoperative outcomes,
supporting a focus on systolic blood pressure.33
Algorithm for Management of Acute Postoperative Hypertension.
1. Appropriate outpatient treatment of chronic hypertension before elective
surgical procedures (Table 3, definition of hypertension)
2. Avoid discontinuation of oral antihypertensive medications on the day of
surgery
3. Identify a baseline blood pressure preoperatively that acts as a reference point
for postoperative management
4. Exclude factors associated with APH (e.g. pain, anxiety, hypothermia, hypoxemia,
hypercarpnia, bladder distension, presence of an ETT on emergence from
anesthesia, antihypertensive withdrawal, increased intracranial pressure,
hypervolemia)
5. Evaluate for APH and initiate therapy with intravenous short-acting antihypertensive agents after excluding other factors that can cause/exacerbate
APH (pain, anxiety)
6. Short-acting intravenous agents are preferable for the initial management
of APH (nitroglycerine, nitroprusside, nicardipine, fenoldopam, clevidipine)
because their effect can be reversed by the discontinuation of therapy (Table 4).

TABLE 3. Classification of Blood Pressure

Normal
Prehypertension
Stage 1 hypertension
Stage 2 hypertension
Reprinted from Chobanian et al.29

o 120 and o 80 mmHg

120--139 or 80--89 mmHg
140--159 or 90--99 mmHg
4 160 or 4 100 mmHg

MANAGEMENT OF PACU EMERGENCIES

TABLE 4. Recommended Antihypertensive Agents for Acute Postoperative Hypertension

With End Organ Damage
Acute pulmonary edema/systolic heart
failure
Acute pulmonary edema with isolated
diastolic heart failure
Acute myocardia ischemia
Hypertensive encephalopathy
Acute aortic dissection
Preeclampsia, eclampsia
Acute renal failure/microangiopathic
anemia
Sympathetic crisis/cocaine overdose

APH
Acute ischemic stroke/intracerebral bleed

Nicardipine, fenoldopam, or nitroprusside

in combination with nitroglycerin and
loop diuretic
Esmolol, metoprolol, labetalol, or verapamil
in combination with low-dose
nitroglycerin and a loop diuretic
Standard treatment (b-blockers, ASA,
consideration for reperfusion) for ACS
combination with nitroglycerin
Nicardipine, nitroprusside, or fenoldopam
possibly including b-blockers
Reduce dP/dt with b-blockers before
initiating vasodilators
Labetalol, nitroglycerine, or nicardipine
Nicardipine or fenoldopam
Verapamil, diltiazem, or nicardipine in
combination with a benzodiazepine
Sympathetic crisis from
pheochromocytoma can be treated with
phentolamine and (if needed) b-blockers
Vasodilators and/or b-blockers, depending
on vital signs and setting
Nicardipine, labetalol, or fenoldopam

Reprinted with permission from Marik and Varon.28

ACS acute coronary syndrome; APH acute postoperative hypertension; ASA American Society of
Anesthesiologists.

Esmolol may be appropriate for patients who will also benefit from
b-blockade
7. Avoid abrupt reduction of blood pressure (greater than 20%), especially in
patients at no immediate risk (hypertensive urgencies)
8. Resume oral antihypertensive therapy as soon as possible postoperatively to
reduce the occurrence of rebound hypertension, especially in patients taking
centrally acting a-2 agonists or b-blockers. Initiate additional agents as needed.

Postoperative Hypotension and Shock States

Postoperative hypotension is defined as a decrease of 20% from baseline
preoperative blood pressure, a systolic blood pressure less than 80 mmHg, or a
diastolic blood pressure less than 50 mmHg, whereas shock refers to multisystem
organ hypoperfusion and inadequate oxygen delivery to tissues. Assessment of
hypotension is commonly approached in terms of evaluation of cardiac rate, rhythm,
contractility, and peripheral resistance and adequacy of intravascular volume.34,35
Hypotension in the PACU is often a sign of hypovolemia and often responds to
intravenous fluid boluses. In patients with persistent hypotension despite a fluid
challenge, additional fluids may precipitate acute pulmonary edema, especially in
patients with reduced left ventricular function. Other causes of hypotension and
shock (including cardiogenic secondary to acute pulmonary edema or myocardial

ARGALIOUS
TABLE 5. Causes of Hypotension in the Postanesthesia Care Unit

Hypovolemia
Inadequate fluid replacement (for dehydration or third space losses)
Hemorrhage (external or internal)
Temporary: high neuraxial block
Mechanical (obstructive): pneumothorax, pericardial effusion, abdominal tamponade,
excessive PEEP, superior vena cava syndrome, or atrial occlusion
Cardiogenic
Chronic heart failure
Acute pulmonary edema
Acute myocardial infarction
Pulmonary embolism
Distributive
Septic shock, anaphylaxis
PEEP positive end-expiratory pressure.

infarction, tension pneumothorax, or distributive shock resulting from septic shock

or anaphylaxis) should be excluded (Table 5).
Several studies have documented the value of early goal-directed therapy in
patients with shock. Rapid diagnosis and intervention improve outcomes.34--37
Several simple tools are used in the initial management of shock, including chest
radiograph, electrocardiogram, serum chemistries, and blood gas analysis. Measurement of central venous pressure and pulmonary artery pressure may be used to
classify the mechanisms of shock, but multiple studies fail to show a good correlation
between the so-called filling pressures and clinical reality. In addition, measurement of central venous oxygen saturation from a central vein or mixed venous
oxygen saturation from a pulmonary artery catheter may be useful in diagnosing and
monitoring the impact of therapeutic interventions in patients with shock.

Volume Responsiveness
One of the most frequently encountered management dilemmas in the PACU
is deciding whether additional intravenous fluid should be administered to a
postoperative patient with acute circulatory failure. Most postoperative patients will
have a positive fluid balance. A fluid challenge may result in acute pulmonary edema,
especially in patients with increased capillary permeability.
Static markers of cardiac preload, especially central venous pressure or pulmonary
artery occlusion pressure, but also left ventricular end-diastolic area and early/late
diastolic wave ratio do not identify fluid responders from nonresponders.37 These
static markers, especially those derived from echocardiography, can identify whether
a cardiac chamber is full or empty; they do not reliably predict the hemodynamic
response to a subsequent fluid bolus administration. The reason why cardiac preload
is not synonymous with fluid responsiveness is shown in Figure 1.
The physiologic benefit of a fluid bolus is based on the Frank--Starling relationship
whereby an increase in cardiac preload results in an increased stroke volume and
subsequently an increased cardiac output. This concept assumes that a patients
preload is on the steep portion of the Frank--Starling curve. However, there are
several curves that rely on stroke volume and cardiac preload, depending on the
ventricular function. A given value of cardiac preload can be associated with an
increase in stroke volume and the presence of preload reserve in patients with good

MANAGEMENT OF PACU EMERGENCIES

FIG. 1. Frank--Starling curve and its relationship to fluid responsiveness. Reprinted with
permission from Monnet et al.37

ventricular function, whereas the same value of preload will not be associated with
an increase in stroke volume (no preload reserve) in patients with poor ventricular
function. Thus, it is the actual interaction among the three parameters --- preload,
stroke volume, and cardiac contractility --- which determines fluid responsiveness.

Functional Change in Preload in Mechanically Ventilated Patients

Although inducing an actual change in cardiac preload can be simply and quickly
accomplished by a fluid bolus, an alternative method to predicting volume
responsiveness is to challenge the Frank--Starling curve by inducing a functional
change in cardiac preload and monitoring the response in stroke volume, cardiac
output, or their surrogates.38--41
In mechanically ventilated patients, this functional change in preload is already
occurring as a result of mechanical ventilation-induced changes in cardiac preload
and can be monitored by observing the magnitude of change in hemodynamic
signals in relation to cyclic changes in airway pressure. For the purposes of this
discussion, we are assuming that the ventilator is delivering appropriate tidal
volumes to the patient. Arterial pressure rises during inspiration and falls during
expiration as a result of changes in intrathoracic pressure secondary to positive
pressure ventilation. In patients with preload reserve, mechanical ventilation will
result in greater cyclic changes in the right ventricle and subsequently the left
ventricle stroke volume and can therefore predict volume responsiveness.38,40
Respiratory variations in hemodynamic signals do not predict volume responsiveness
in spontaneously breathing patients, in patients with cardiac arrhythmias, and are
inaccurate in patients with isolated right ventricle dysfunction or pulmonary
hypertension.37

Functional Change in Preload in Spontaneously Breathing Patients

In spontaneously breathing patients, the functional change in preload is
accomplished by the passive leg-raising test. It consists of lifting the legs passively
45 degrees from the horizontal (supine) position (or tilting the bed to the same

10

ARGALIOUS
TABLE 6. Steps for Assessment of Fluid Responsiveness

A. Induce a change in cardiac preload

1. Actual change: administer a fluid bolus
2. Functional change
 In mechanically ventilated patients, use existing respiratory variations in
hemodynamic signals
 In spontaneously breathing patients, use passive leg-raising test
B. Observe the change
1. Change in arterial pulse pressure38
 Delta pulse pressure*
 A value of 13% or higher predicts fluid responsiveness
 Delta down
 A value of 5 mmHg or higher predicts fluid responsiveness
2. Stroke volume variation39,41
Difference between maximal and minimal stroke volume divided by their mean during
one respiratory cycle
A value 4 10% change predicts fluid responsiveness
3. Change in cardiac output40
A value 4 15% change predicts fluid responsiveness
C. Use one of the following monitoring tools (varying sensitivities) capable of measuring
changes in stroke volume or its surrogates36,37,43 (data must be displayed in a beatto-beat manner)
1. Pulse oximetry plethysmography
2. Noninvasive finger arterial pulse
3. Invasive arterial monitoring with pulse contour analysis: uses data from the arterial
pressure waveform for continuous monitoring of stroke volume and cardiac output. It
relies on calculating the area under the systolic portion of the arterial pressure waveform,
which, divided by aortic impedance, allows estimation of left ventricular stroke volume
4. Esophageal Doppler measurements of descending aortic blood flow
5. Transthoracic or transesophageal echocardiography measurement of variations in stroke
volume, cardiac output, velocity time integral, mitral inflow velocities, superior/inferior
vena caval diameter
* Difference between maximal and minimal pulse pressure during one respiratory cycle divided by their
mean. Systolic arterial pressure at the end of a 5-second respiratory pause and its minimal value during
the course of one mechanical breath.

extent) and observing the change occurring in hemodynamic effects (change

in stroke volume, cardiac output, or arterial pulse pressure) as a result of the
gravitational transfer of blood from the lower extremities toward the intrathoracic
compartment.42 This test has the advantage of being simple, reversible, and
applicable in spontaneously breathing patients (most patients in PACU). However, it
is impractical to raise the legs of patients with abdominal, pelvic, or lower extremity
surgery because of surgical site pain associated with the movement of the lower
extremities. Table 6 lists the steps for assessment of fluid responsiveness.

Conclusions
Prompt recognition, diagnosis, and treatment of various PACU emergencies and
also the knowledge of potential complications unique to certain surgical procedures
are essential for improving postoperative morbidity and mortality outcomes. The role
of anesthesiologists as perioperative physicians is emphasized in the management
of PACU emergencies and requires familiarity with a variety of diagnostic and
monitoring tools.

MANAGEMENT OF PACU EMERGENCIES

11

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