Authors:David Broussard, MDKelly Ural, MDSection Editors:Natalie F Holt, MD,

MPHJonathan B Mark, MDDeputy Editor:Nancy A Nussmeier, MD, FAHA

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer
review process is complete.

Literature review current through: Nov 2017. | This topic last

updated: Nov 20, 2017.

INTRODUCTION — Cardiovascular problems in the post-anesthesia care

unit (PACU) include hemodynamic instability due to hypotension,
hypertension, or arrhythmias, and complications such as myocardial
ischemia or decompensated heart failure. Cardiovascular issues are the
third most common problem requiring treatment in the immediate
postoperative period, after nausea and vomiting or respiratory problems
[1-3].

The likelihood of cardiovascular problems is related to:

●
Severity of preexisting cardiovascular comorbidities (eg, coronary artery
disease, chronic hypertension, congestive heart failure [CHF])

●
Invasiveness of the surgical procedure (eg, major vascular, thoracic,
abdominal, spine surgery)

●
Severity of perioperative stresses (eg, blood loss, fluid shifts, sepsis, pain,
hypothermia)

●
Effects of anesthetic agents and techniques

In this topic, we review the rapid diagnosis and treatment of cardiovascular

problems in the PACU after noncardiac surgery (eg, hypotension,
hypertension, cardiac arrhythmias, myocardial ischemia, and
decompensated heart failure). Postoperative complications after cardiac
surgery are discussed separately. (See "Postoperative complications
among patients undergoing cardiac surgery" and "Atrial fibrillation and
flutter after cardiac surgery".)

HYPOTENSION

Initial assessment and treatment — Hypotension may be absolute (eg,

systolic blood pressure [BP] <90 mmHg or mean BP <65 mmHg) or
relative (eg, systolic BP decrease >20 percent of baseline). These values
serve as a guide for treatment, although there is no widely accepted
definition of perioperative hypotension [4]. Hypotension in the post-
anesthesia care unit (PACU) is typically treated when the BP is reduced to
these values described, or if there is evidence of hypoperfusion (eg,
change in mental status or decreased urine output).

Before treating hypotension, the accuracy of BP measurements should be

assessed. Measurements using a noninvasive BP monitor may be
inaccurate due to inappropriate cuff size, patient movement, or shivering.
Measurements obtained from an intra-arterial catheter may be inaccurate
due to technical reasons such as incorrect zeroing or leveling of the
pressure transducer, or physiologic reasons such as peripheral arterial
stenosis.

Initial treatment includes intravenous (IV) isotonic crystalloid solution

administered in 250- to 500-mL increments. If necessary, IV vasopressor/
inotropic agents (eg, phenylephrine 40- to 100-mcg increments or
ephedrine 5- to 10-mg increments) are administered to increase BP.

For severe or refractory hypotension, small bolus doses of diluted IV

epinephrine 10 to 50 mcg, norepinephrine 4 to 16 mcg, or vasopressin 1 to
4 units may be administered, while a vasopressor/inotropic infusion is
prepared (table 1).

A quick assessment often points to an underlying etiology requiring

specific treatment:

●
Major surgical procedures pose a risk for hypovolemia due to large fluid
shifts or significant bleeding. (See 'Hypovolemia' below.)

●
Review of preoperative medications and anesthetic techniques and drugs
may suggest that an antihypertensive drug, residual anesthetic,
sympathectomy after neuraxial block, adrenal insufficiency, or an allergic
drug reaction is causing hypotension. (See 'Drug effects' below and
'Sympathectomy due to neuraxial block' below and 'Drug allergy and
anaphylaxis' below.)

●
Myocardial dysfunction due to myocardial ischemia or decompensated
heart failure (HF) is considered in patients at risk for these complications.
(See 'Myocardial dysfunction' below and 'Myocardial ischemia' below and
'Decompensated heart failure' below.)

●
Patients with profound hypotension or cardiovascular collapse may have a
condition requiring urgent intervention (eg, anaphylaxis, septic shock, local
anesthetic toxicity, tension pneumothorax, pulmonary embolus, pericardial
tamponade, dynamic left ventricular outflow tract obstruction). (See
'Hypotensive emergencies' below.)

Treatment of underlying causes — In addition to the initial treatment

noted above, specific treatment is often necessary after initial assessment
has determined the cause(s) of hypotension.

Hypovolemia — A combination of factors may result in hypovolemia (eg,

preoperative fasting resulting in dehydration, diuresis, intraoperative blood
loss or fluid shifts, ongoing fluid or blood loss in the postoperative period).

Inadequate fluid replacement — For patients who have had major

surgery or are likely to be dehydrated, we review the intraoperative records
to assess blood loss and other fluid losses (eg, preoperative fluid deficit,
urine output, fluid shifts), as well as adequacy of intraoperative fluid
replacement. If available, central venous pressure (CVP) is measured to
assess adequacy of intravascular volume, although it is poorly predictive
of fluid responsiveness in many patients [5,6]. (See "Intraoperative fluid
management", section on 'Causes of intravascular volume
derangements'.)

If there is evidence of inadequate fluid replacement, we administer IV

isotonic crystalloid in 250- to 500-mL boluses and reassess volume status
and BP after each bolus.

Blood loss — For patients who had major surgery, we review estimated

intraoperative blood loss versus replacement and measure hemoglobin
(Hgb) level.

However, an individual Hgb value may not accurately reflect blood loss
during or immediately after an acute bleeding episode. Also, intraoperative
blood loss is commonly underestimated [7] and may continue into the
postoperative period due to circumstances that are case-specific (eg,
delayed blood loss after knee surgery with intraoperative use of a
tourniquet) or patient-specific (eg, preexisting coagulation disorders). For
these reasons, serial measurements may be more useful than a single
value.

For most patients, perioperative red blood cell (RBC) transfusions are
administered only if Hgb is <7 to 8 g/dL. Use of this transfusion threshold
is generally safe, reduces unnecessary transfusion, and may improve
clinical outcomes (table 2). (See "Intraoperative transfusion of blood
products in adults", section on 'Red blood cells'.)

Drug effects

Antihypertensive agents — Effects of chronically or recently administered

antihypertensive agents may cause hypotension. Intraoperative
administration of longer-acting IV agents (eg, hydralazine, metoprolol, or
labetalol) may result in postoperative hypotension once painful surgical
stimulation has ceased.

Treatment is administration of vasopressor/inotropic agents (see 'Initial

assessment and treatment' above). It is also necessary to treat
bradycardia (due to the negative chronotropic effects of an
antihypertensive drug) if this is contributing to hypotension. (See
'Bradycardia' below.)

Anesthetic agents — Residual effects of anesthetic agents or excessive

opioid doses may result in hypotension, particularly in patients who have
little pain after surgery. Such patients are typically somnolent or obtunded,
as well as hypotensive.

●
Benzodiazepines – If excessive benzodiazepine dosing is suspected, IV
flumazenil may be administered in 0.2-mg increments up to a
maximum dose of 3 mg within any one hour, which typically hastens
emergence from anesthesia, with resolution of hypotension [8]. (See
"Benzodiazepine poisoning and withdrawal", section on 'Antidote
(flumazenil)'.)

●
Opioids – If excessive opioid dosing is suspected, IV naloxone 40 mcg
may be administered every five minutes until the sedative and
respiratory depressant effects are reversed, typically with resolution of
hypotension. The half-life of naloxone is 1 to 1.5 hours, which may be
shorter than the half-life of the opioid being reversed. In these
instances, repeat doses of naloxone may be administered, or a
continuous infusion may be started at 0.5 to 1 mcg/kg/hour. (See
"Acute opioid intoxication in adults", section on 'Management'.)

Titration of such low doses of naloxone safely reverses opioid effects in

most patients. Rarely, sudden reversal of analgesic effects causes
extreme discomfort and a sympathetic surge resulting in hypertension,
tachycardia, and myocardial ischemia (see 'Myocardial ischemia'
below). Flash pulmonary edema has also been reported after a large
dose of naloxone [9].

Intraoperative administration of propofol, dexmedetomidine, and/or

inhalational anesthetic agents are unlikely to cause postoperative
hypotension because these agents are short-acting.

Sympathectomy due to neuraxial block — Sympathectomy due to high

neuraxial anesthetic block may result in hypotension. This is more likely
when the sensory block is above the T6 level and when local anesthetics
are infused through the epidural catheter. It is also more likely in patients
with preexisting hypertension [10].

If hypotension does not resolve after initial therapy with IV fluid boluses
and vasopressor/inotropic agents (see above), any ongoing neuraxial
infusion of local anesthetic is decreased or temporarily discontinued, or
the infusion is changed to contain only an opiate. Also, the location of the
epidural catheter is confirmed with aspiration to ensure that the tip has not
migrated to enter a blood vessel or the intrathecal space. If the epidural
catheter is malpositioned, it should be removed.

Allergic (hypersensitivity) reaction

Drug allergy and anaphylaxis — Postoperative hypotension may occur

due to exposure to latex or a medication administered during or after
surgery. Perioperative medications commonly causing allergic reactions
include antibiotics and protamine [11,12]. Allergic reactions typically
present as itching and as a rash or hives, but these minor symptoms may
not be noticed by a patient with residual postoperative sedation. (See
"Perioperative anaphylaxis: Clinical manifestations, etiology, and
management", section on 'Etiologies' and "Perioperative anaphylaxis:
Clinical manifestations, etiology, and management", section on 'Clinical
manifestations and diagnosis'.)

Treatment for anaphylaxis is initiated immediately if the rash is

accompanied by any evidence of hypotension, bronchospasm, oral or
facial edema, or inspiratory stridor. Management of perioperative
anaphylaxis is discussed in detail separately. (See "Anaphylaxis:
Emergency treatment".)

Transfusion reaction — Typical signs and symptoms of acute transfusion

reaction are fever, chills, pruritus, and urticaria. If a hemolytic or
anaphylactic transfusion reaction is suspected as the cause of
hypotension during a transfusion, the transfusion is stopped and IV fluids
and vasopressor/inotropic agents are administered. Standard treatment is
initiated for a mild allergic reaction or for a more severe anaphylactic
reaction, as appropriate (see 'Drug allergy and anaphylaxis' above). The
blood bank should be notified to determine the cause of the reaction. (See
"Approach to the patient with a suspected acute transfusion reaction".)

Adrenal insufficiency — Acute adrenal insufficiency may occur in a

patient who was receiving chronic glucocorticoid therapy but did not
receive adequate perioperative replacement therapy. While uncommon,
adrenal insufficiency is suspected in a patient on chronic therapy,
particularly if hypotension is refractory to standard treatment with fluids
and vasopressors. In such cases, IV hydrocortisone 100 mg or
dexamethasone 4 mg is administered, in addition to standard treatment
with IV fluids and vasopressor/inotropic agents. (See "Treatment of adrenal
insufficiency in adults", section on 'Adrenal crisis'.)

Myocardial dysfunction — Acute myocardial ischemia or perioperative

decompensation of preexisting HF may result in myocardial dysfunction
severe enough to cause hypotension. (See 'Myocardial ischemia' below
and 'Decompensated heart failure' below.)

Hypotensive emergencies — Conditions that cause profound

hypotension and/or hemodynamic collapse require immediate lifesaving
interventions. Support with vasopressor/inotropic agents is provided (table
1) while definitive treatment is underway (see 'Initial assessment and
treatment' above). Appropriate specialists are consulted to continue
management and/or intensive care after the patient is stabilized and
discharged from the PACU.

The cardinal features of these conditions are summarized below to provide

assistance in identifying a likely diagnosis.

●
Septic shock – Sepsis may be preexisting before surgery, or may develop
during or after surgery in patients with active infection. Sepsis should
be suspected in susceptible patients with tachycardia and profound
hypotension due to vasodilation (with high cardiac output if
intravascular volume is adequate). IV fluids and vasopressor
infusion(s) (eg, phenylephrine, norepinephrine, and/or vasopressin
(table 1)) are administered in the PACU to stabilize the patient. Also,
since early administration of antibiotics is critical for management of
patients with severe sepsis and septic shock, the surgeon and/or an
infectious disease specialist are consulted to ensure that antibiotic
coverage is appropriate and appropriate cultures are sent for testing.
(See "Evaluation and management of suspected sepsis and septic
shock in adults".)

●
Local anesthetic toxicity – Local anesthetic toxicity causes profound
hypotension and arrhythmias (eg, bradycardia, atrioventricular block,
ventricular arrhythmias). This may occur in the postoperative period
due to intravascular location of a misplaced epidural or peripheral
nerve catheter or, rarely, due to accidental IV administration of a local
anesthetic infusion intended for epidural or perineural administration.
Central nervous system symptoms (eg, ringing in the ears, metallic
taste, tingling of the lips, agitation, seizures) commonly precede signs
of cardiovascular toxicity. Treatment is discussed separately. (See
"Overview of peripheral nerve blocks", section on 'Local anesthetic
systemic toxicity'.)

●
Tension pneumothorax – Tension pneumothorax is suspected in patients
with hypotension, dyspnea, tachypnea, worsening oxygenation, chest
 pain, distended neck veins, tracheal deviation, or risk factors that
include attempted or actual central line insertion, surgery in the neck
or thorax, or chronic lung disease. Treatment of tension pneumothorax
is emergent needle decompression. (See "Evaluation of and initial
approach to the adult patient with undifferentiated hypotension and
shock", section on 'Tension pneumothorax'.)

●
Pulmonary embolus – Pulmonary embolus (PE) is suspected in
hypotensive patients with acute onset of shortness of breath,
tachycardia, and hypoxia. Specific details for management of patients
with hemodynamically unstable PE are discussed elsewhere
(algorithm 1). (See "Treatment, prognosis, and follow-up of acute
pulmonary embolism in adults", section on 'Hemodynamically
unstable'.)

●
Cardiac tamponade – Cardiac tamponade is suspected in patients with
dyspnea, tachycardia, hypotension, elevated jugular venous pressure,
distant heart sounds, pulsus paradoxus, and known risk factors (eg,
trauma, recent thoracic or pericardial procedure, prior pericardial
effusion). Urgent echocardiography is used to confirm the diagnosis
and guide immediate treatment. (See "Cardiac tamponade".)

●
Dynamic left ventricular outflow tract obstruction – Dynamic left
ventricular outflow tract (LVOT) obstruction associated with
hypotension and mitral regurgitation can be precipitated by
hypovolemia, vasodilation, tachycardia, and/or a high catecholamine
state in susceptible patients, usually those with hypertrophic
cardiomyopathy. Rapid diagnosis is possible with echocardiography.
Specific management of LVOT obstruction is described separately.
(See "Hypertrophic cardiomyopathy: Medical therapy", section on
'Acute hemodynamic collapse in the setting of LVOT obstruction'.)

HYPERTENSION

Initial assessment and treatment — Hypertension occurring in the post-

anesthesia care unit (PACU) is typically treated if systolic blood pressure
(BP) is >180 mmHg or diastolic BP is >110 mmHg, particularly if
hypertension is persistent after treatment of presumed etiologies. (See
"Perioperative management of hypertension", section on 'Indications for
and approach to therapy'.)

Before treating hypertension, we review the patient's preoperative and

baseline BP, as well as the home medication list and timing of last doses of
antihypertensive medications. Treatment thresholds for patients who had
severe preoperative hypertension (ie, ≥180/≥120 mmHg) may vary, and are
discussed separately. (See "Management of severe asymptomatic
hypertension (hypertensive urgencies) in adults".)

If patients are due for a dose of their usual antihypertensive medication(s),

oral doses of those medications may be administered as initial treatment.
If response is inadequate or if oral administration of medications is not
feasible, then small doses of rapid-acting intravenous (IV) antihypertensive
agents are administered. Typically, labetalol 5 to 20 mg, metoprolol 1 to 5
mg, hydralazine 5 to 10 mg, or nicardipine 0.2-mg increments are titrated
to decrease systolic BP to a consistent value <160 mmHg. Since
metoprolol and labetalol have beta-blocking properties, these agents are
preferred if hypertension is associated with tachycardia [13,14].

Additional treatment of hypertension depends upon the specific etiology.

(See 'Treatment of underlying causes' below.)

Hypertensive emergencies — Emergency treatment of severe

hypertension is warranted if there is evidence of acute neurologic signs or
symptoms (eg, agitation, delirium, stupor, visual disturbances, seizures,
stroke), a cardiovascular emergency (eg, acute coronary syndrome, acute
decompensated heart failure [HF], aortic dissection), or renal injury (eg,
hematuria, rising creatinine). (See "Evaluation and treatment of
hypertensive emergencies in adults".)

Rarely, a pheochromocytoma may cause severe hypertension, typically

associated with tachycardia, arrhythmias, and/or cardiovascular collapse
[15,16]. Risks are particularly high when pheochromocytoma is previously
undiagnosed; mortality in this setting approaches 80 percent [17]. (See
"Anesthesia for the adult with pheochromocytoma".)

The IV drugs used for emergency treatment of severe hypertension are

discussed in detail elsewhere (table 3). (See "Drugs used for the treatment
of hypertensive emergencies".)

Treatment of underlying causes — In addition to the initial treatment

noted above, specific treatment is often necessary after initial assessment
has determined the cause(s) of hypertension.

Preexisting hypertension — Undiagnosed or poorly controlled

preexisting hypertension is the most common cause of perioperative
hypertension, particularly if the patient's chronically administered
antihypertensive medications were not continued up until the time of
surgery [18-22]. In particular, withdrawal syndromes with rebound
hypertension can occur with medications such as clonidine and beta
blockers. (See "Perioperative management of hypertension", section on
'Withdrawal syndromes' and "Perioperative management of hypertension",
section on 'Choice of drugs'.)

Noxious stimuli

●
Pain – Inadequately treated pain is a common cause of sympathetic
stimulation resulting in hypertension and tachycardia in the PACU,
particularly after major invasive surgical procedures. Details regarding
management of acute postoperative pain are discussed separately.
(See "Management of acute perioperative pain".)

●
Nausea and vomiting – Postoperative nausea and vomiting (PONV) is the
most common complication occurring in the PACU, and the
associated sympathetic stimulation may cause hypertension and/or
tachycardia [1]. Therapy is directed at treating this primary problem;
details are available elsewhere. (See "Overview of post-anesthetic
care for adult patients", section on 'Postoperative nausea and
vomiting' and "Postoperative nausea and vomiting".)

●
Hypoxia and/or hypercarbia – Respiratory problems causing hypoxia
and/or hypercarbia are the second most common complication
occurring in the PACU and may be accompanied by hypertension
and/or tachycardia due to sympathetic stimulation [1]. Details
regarding causes and management of respiratory problems in this
setting are available elsewhere. (See "Respiratory problems in the
post-anesthesia care unit (PACU)".)

●
Delirium and agitation – Emergence delirium with agitation,
hyperexcitation, or confusion occurs in up to 5 percent of adult
patients after general anesthesia and may be accompanied by
hypertension and/or tachycardia [23,24]. Treatment is discussed
separately. (See "Delayed emergence and emergence delirium in
adults", section on 'Emergence delirium'.)

●
Hypothermia with shivering – Hypothermia results in patient discomfort
and sympathetic stimulation with hypertension and/or tachycardia, as
well as markedly increased myocardial O2 consumption due to
shivering [25-27]. In patients with ischemic heart disease, these may
lead to myocardial ischemia and arrhythmias [28,29]. Concurrent
 priorities include treatment of hypothermia itself and treatment of
shivering (see "Overview of post-anesthetic care for adult patients",
section on 'Hypothermia or hyperthermia'). Severe or persistent
hypertension is addressed after initial treatment of hypothermia and
shivering. (See 'Initial assessment and treatment' above.)

●
Bladder distention – A distended bladder is a common and often
overlooked cause of sympathetic stimulation and hypertension in the
PACU, particularly in patients with recent anorectal surgery, neuraxial
block, excess intraoperative fluid administration, or a history of urinary
retention [30,31]. Patients with >600 mL of urine noted on bladder
ultrasound are treated with one-time catheterization. (See "Overview
of post-anesthetic care for adult patients", section on 'Inability to
void'.)

Hypervolemia — Volume overload due to intraoperative fluid or blood

administration may result in postoperative hypertension. Initial therapy is
administration of an IV diuretic, typically furosemide 20 to 40 mg, in
addition to treatment of hypertension. Vasodilator therapy (eg, IV
nitroglycerin or nitroprusside infusions) (table 3) may be necessary to lower
BP if hypervolemic hypertension is severe or associated with acute
decompensated HF. (See "Treatment of acute decompensated heart
failure: Components of therapy", section on 'Diuretics' and "Treatment of
acute decompensated heart failure: Components of therapy", section on
'Vasodilator therapy'.)

Use of alcohol, opioids, and other drugs — Patients chronically using

alcohol or opioids may develop hypertension and/or tachycardia in the
PACU due to sympathetic stimulation associated with withdrawal. Severe
hypertension may develop in patients who have recently used any drug
that causes a hyperadrenergic response (eg, cocaine, amphetamine,
phencyclidine, or a monoamine oxidase inhibitor).

●
Alcohol withdrawal – Symptoms of alcohol withdrawal (eg, hypertension,
tachycardia, tremulousness, sweating, nausea, anxiety) may manifest
as early as 6 to 24 hours after the last drink and can progress to
delirium tremens with worsening hypertension in 48 to 96 hours.
Benzodiazepines (eg, IV lorazepam) are administered to treat
withdrawal symptoms. Management of alcohol withdrawal is
discussed separately. (See "Management of moderate and severe
alcohol withdrawal syndromes".)

●
Opioid withdrawal – Symptoms of opioid withdrawal (eg, hypertension,
tachycardia, mydriasis, piloerection, nausea, dysphoria) typically begin
6 to 12 hours after the last opioid dose. Management of opioid
withdrawal is discussed separately. (See "Opioid withdrawal in the
emergency setting" and "Management of acute perioperative pain",
section on 'Opioid-dependent patients'.)

●
Recent cocaine, amphetamine, or phencyclidine use – Recent use of
drugs that produce a hyperadrenergic state (eg, cocaine,
amphetamine, phencyclidine, or a monoamine oxidase inhibitor) can
cause sympathetic overactivity and hypertension, tachycardia, and
cardiac arrhythmias. In these patients, administration of a
sympathomimetic agent may precipitate severe hypertension or a
cardiovascular or neurologic emergency requiring immediate
treatment. (See 'Hypertensive emergencies' above.)

Further details regarding management of cardiovascular complications of

these drugs may be found elsewhere:

•
(See "Cocaine: Acute intoxication", section on 'Cardiovascular
complications'.)

•
(See "Acute amphetamine and synthetic cathinone ("bath salt")
intoxication", section on 'Hypertension'.)

•
(See "Phencyclidine (PCP) intoxication in adults", section on 'Treatment of
complications'.)

CARDIAC ARRHYTHMIAS — Most arrhythmias noted in the post-

anesthesia care unit (PACU) are transient and clinically insignificant.
However, the appearance of a new arrhythmia may indicate myocardial
ischemia in a patient with preexisting cardiovascular disease [21]. (See
'Myocardial ischemia' below.)

Proper lead placement for the electrocardiogram (ECG) should be

confirmed, and a 12-lead ECG is obtained as soon as feasible in a patient
with a new arrhythmia. Contributing causes should be identified and
treated (eg, hypoxemia, hypoventilation, acidemia, anemia, electrolyte
abnormalities). In particular, hypokalemia should be identified and
corrected immediately. (See "Clinical manifestations and treatment of
hypokalemia in adults", section on 'Intravenous potassium repletion'.)

A severe bradyarrhythmia or tachyarrhythmia may cause hemodynamic

instability or cardiac arrest. Management of arrhythmias in unstable
patients is summarized below and discussed in detail separately [32]. (See
"Advanced cardiac life support (ACLS) in adults", section on 'Management
of specific arrhythmias'.)

Bradycardia

Initial treatment — Severe bradycardia (heart rate [HR] <40 beats/minute

[bpm]) in an unstable patient (eg, hypotension, altered mental status) is
initially treated with intravenous (IV) atropine 0.5 mg; this dose is repeated
every three to five minutes up to a total of 3 mg (algorithm 2). Further
management of bradycardia is discussed separately. (See "Advanced
cardiac life support (ACLS) in adults", section on 'Bradycardia'.)

Severe bradycardia (HR <40 bpm) in a patient who is stable or has less
severe symptoms may be initially treated with IV glycopyrrolate in 0.2-mg
increments up to 1 mg and/or ephedrine in 5 to 10 mg increments, since
atropine may cause undesirable tachycardia (eg, in patients with ischemic
heart disease) or altered mental status (eg, in elderly patients).

Mild sinus bradycardia (ie, HR 40 to 60 bpm) that remains stable in an

asymptomatic patient does not require treatment. (See "Sinus
bradycardia".)

Assessment and treatment of underlying causes — For bradycardia

occurring in the PACU, we review the following potential causes and
institute appropriate specific therapy:

●
Medications

•
Negative chronotropic agents – A beta blocker or other negative
chronotropic agent (eg, calcium channel blockers, digoxin,
amiodarone) is the most common cause of postoperative
bradycardia. In patients with ischemic heart disease, these drugs
are administered (chronically or recently) to maintain HR in the
range of 50 to 80 bpm. For these patients, baseline (admission)
HR is noted, and bradycardia is treated only if it is severe (HR <40
bpm) or if symptoms develop. (See "Anesthesia for noncardiac
surgery in patients with ischemic heart disease", section on
'Prevention of ischemia'.)

•
Anticholinesterase agents – Bradycardia in the PACU may be caused by
the muscarinic effects of an acetylcholinesterase inhibitor (eg,
neostigmine or edrophonium) used for reversal of nondepolarizing
neuromuscular blocking agents (NMBAs) near the end of surgery.
The anesthesia record is reviewed to determine if the patient
received an acetylcholinesterase inhibitor administered with an
adequate dose of anticholinergic agent (eg, glycopyrrolate or
atropine). If underdosing of the anticholinergic agent is
suspected, an additional dose of IV glycopyrrolate 0.2 mg or
atropine 0.4 mg is administered and may be repeated. (See
"Clinical use of neuromuscular blocking agents in anesthesia".)

•
Neuraxial anesthesia – Neuraxial anesthesia with a T1 to T4 anesthetic
level may cause bradycardia and hypotension [33-36]. Although
atropine may be administered, bradycardia caused by blockade
of the cardiac accelerator fibers responds best to beta-adrenergic
agonists (eg, ephedrine 5 to 10 mg or, if severe, epinephrine 10 to
20 mcg, titrated to effect, then followed by an epinephrine
infusion if the bradycardia is persistent (table 1)). Also, the
epidural infusion is reduced or temporarily discontinued.

●
Adverse perioperative events

•
Hypoxia – Hypoxia inactivates pacemaker channels, leading to a reduction
in the pacemaker rate of the sinoatrial node and consequent
bradycardia. (See "Respiratory problems in the post-anesthesia
care unit (PACU)".)

•
Myocardial ischemia – Sinus bradycardia occurs in 15 to 25 percent of
patients having an acute myocardial infarction, particularly if
ischemia involves the right coronary artery. (See "Supraventricular
arrhythmias after myocardial infarction", section on 'Sinus
bradycardia' and 'Myocardial ischemia' below.)

•
Bowel or bladder distention after abdominal surgery – Visceral
distention of the bowel or bladder may initiate a vagal reflex,
causing bradycardia.

Atrial tachyarrhythmias — For atrial tachyarrhythmias causing

hemodynamic instability (eg, hypotension, myocardial ischemia, pulmonary
edema), urgent cardioversion is recommended, unless it is certain that the
rhythm is sinus tachycardia (algorithm 3).

●
Sinus tachycardia – Sinus tachycardia with HR >100 bpm is common in
the PACU due to:

•
Pain – hypertension typically also present (see 'Noxious stimuli' above).

•
Hypovolemia – hypotension typically also present (see 'Hypovolemia'
above).

•
Anemia – hypotension typically also present (see 'Blood loss' above).

For most patients with mild sinus tachycardia (ie, HR 100 to 120 bpm),
treatment of the underlying causes is adequate.

For patients with known or possible ischemic heart disease or those with
HR >120 bpm, sinus tachycardia is treated with an IV beta
blocker (eg, bolus doses of esmolol 10 to 25 mg or metoprolol 1
to 5 mg) to decrease HR to ≤80 bpm, provided that blood
pressure (BP) is adequate and there are no contraindications.

●
Atrial fibrillation – Atrial fibrillation (AF) is a narrow complex irregular
arrhythmia (waveform 1 and waveform 2). Risk factors include
preexisting AF or ischemic heart disease, while specific factors in the
PACU include increased sympathetic activity due to operative stress,
hypoxia, pain, acute anemia, or myocardial irritability caused by
procedures performed near the heart (eg, pulmonary or esophageal
surgery) [37,38]. Treatment of AF depends upon hemodynamic
stability (algorithm 3). (See "Advanced cardiac life support (ACLS) in
adults", section on 'Tachycardia'.)

●
Regular supraventricular tachycardia – Treatment of regular
supraventricular tachycardia (SVT) with either narrow (<120
milliseconds) or wide (≥120 milliseconds) QRS complex depends on
hemodynamic stability (algorithm 3). For stable patients with regular,
 narrow complex SVT, vagal maneuvers are attempted, followed by
administration of adenosine 6 mg rapid IV push. If cardioversion does
not occur, adenosine 12 mg rapid IV push is administered, and this 12
mg dose may be repeated once. Expert consultation is recommended
for all patients with wide complex tachycardia as soon as possible
[32,39]. (See "Advanced cardiac life support (ACLS) in adults", section
on 'Regular narrow complex' and "Advanced cardiac life support
(ACLS) in adults", section on 'Regular wide complex'.)

Further details regarding management of atrial tachyarrhythmias can be

found elsewhere:

●
(See "Advanced cardiac life support (ACLS) in adults", section on
'Tachycardia'.)

●
(See "Overview of the acute management of tachyarrhythmias".)

●
(See "Reentry and the development of cardiac arrhythmias".)

●
(See "Approach to the management of wide QRS complex tachycardias".)

Ventricular tachyarrhythmias

●
Premature ventricular contractions – Premature ventricular contractions
(PVCs) are relatively common in the PACU due to increased
sympathetic stimulation; they typically resolve without treatment.

●
Ventricular fibrillation, flutter, or monomorphic ventricular tachycardia
– Ventricular fibrillation, flutter, or monomorphic ventricular
tachycardia (waveform 3 and waveform 4 and waveform 5) requires
initiation of cardiopulmonary resuscitation (CPR) and immediate
defibrillation as the first steps in the advanced cardiac life support
(ACLS) guidelines (algorithm 4). (See "Advanced cardiac life support
(ACLS) in adults", section on 'Ventricular fibrillation and pulseless
ventricular tachycardia'.)

●
Polymorphic ventricular tachycardia (torsades de pointes) – Torsades
de pointes is an irregular polymorphic ventricular tachycardia
associated with a prolonged QT interval (waveform 6). If the patient
loses consciousness or the rhythm degenerates into ventricular
 fibrillation, ACLS with CPR is initiated and immediate defibrillation is
performed. (See "Advanced cardiac life support (ACLS) in adults",
section on 'Irregular wide complex'.)

The management of the stable conscious patient having recurrent

episodes of torsades de pointes is discussed separately. (See
"Overview of the acute management of tachyarrhythmias", section on
'Polymorphic ventricular tachycardia'.)

CARDIOVASCULAR COMPLICATIONS — Myocardial ischemia or

decompensated heart failure (HF) may occur in the post-anesthesia care
unit (PACU) with or without associated hemodynamic instability (eg,
hypotension, hypertension, arrhythmias).

Myocardial ischemia — Patients at high risk for perioperative myocardial

ischemia or infarction include those having in-hospital surgery with one or
more additional risk factors in the revised cardiac risk score (table 4). (See
"Perioperative myocardial infarction after noncardiac surgery".)

The highest-risk patients are those having urgent or emergent surgery with:

●
Recent myocardial infarction or unstable angina [22]. (See "Evaluation of
cardiac risk prior to noncardiac surgery", section on 'Very high-risk
patients'.)

●
Recent percutaneous coronary intervention (PCI), particularly if dual
antiplatelet therapy was prematurely discontinued for surgery. (See
"Noncardiac surgery after percutaneous coronary intervention".)

In high-risk patients, continuous electrocardiography (ECG) monitoring for

myocardial ischemia includes multiple leads (eg, II and V5) and
computerized ST-segment analysis, if available in the PACU. Other
recommendations for screening for myocardial ischemia in high-risk
patients are discussed separately. (See "Perioperative myocardial
infarction after noncardiac surgery", section on 'Screening'.)

Optimal myocardial oxygen (O2) supply and minimal O2 demand are

achieved by maintaining a low to normal heart rate, normal to high blood
pressure (BP), and adequate arterial oxygen content, as well as avoiding
hypothermia and fluid overload (table 5). (See "Anesthesia for noncardiac
surgery in patients with ischemic heart disease", section on 'Prevention of
ischemia'.)

In patients with symptoms or signs suggestive of myocardial ischemia, we

recommend obtaining a 12-lead ECG and troponin measurements. If
available, bedside transthoracic echocardiography can be used to quickly
detect regional wall motion abnormalities. Also, a cardiologist is consulted
since urgent subspecialist interventions will be necessary if an acute
coronary syndrome is developing (table 6). The diagnosis and
management of perioperative myocardial infarction are discussed
separately. (See "Perioperative myocardial infarction after noncardiac
surgery" and "Role of echocardiography in acute myocardial infarction".)

Decompensated heart failure — Patients at increased risk for

development of acute HF in the immediate postoperative period include
those with a history of chronic left or right HF, as well as those with
diastolic HF (also called HF with preserved ejection fraction). This is due to
intraoperative factors such as fluid overload resulting from fluid shifts
during major surgery, anemia, myocardial ischemia, severe hypertension,
stress-induced (Takotsubo) cardiomyopathy, or prolonged unfavorable
surgical positioning (eg, supine positioning of a patient who cannot
tolerate this position while awake). (See "Perioperative management of
heart failure in patients undergoing noncardiac surgery", section on
'Postoperative management'.)

Acute HF typically manifests as respiratory distress with or without overt

pulmonary edema. Respiratory distress may be accompanied by
hypertension due to hypervolemia or hypotension due to cardiogenic
shock or excess vasodilator use. (See "Approach to acute decompensated
heart failure in adults".)

Treatment for acute decompensated HF incudes (table 7):

●
Administration of supplemental O2.

●
For persistent respiratory distress, respiratory acidosis, and/or hypoxia
despite oxygen therapy, initiation of noninvasive ventilation (NIV) or
endotracheal intubation and mechanical ventilation, as indicated. (See
"Noninvasive ventilation in acute respiratory failure in adults", section on
'Cardiogenic pulmonary edema'.)

●
Administration of intravenous (IV) diuretics to relieve pulmonary congestion
or fluid overload [40].

●
Initiation of vasodilator therapy in the following settings: early IV
nitroglycerin as a component of therapy in patients with refractory HF (eg,
inadequate response to diuretics and/or low cardiac output), or IV
nitroprusside as arterial vasodilator therapy to reduce afterload in patients
with severe hypertension (table 3).

●
Initiation of an inotropic infusion (eg, milrinone or dobutamine) in patients
with known systolic HF and signs of cardiogenic shock, in combination
with a vasopressor (eg, norepinephrine) if necessary to maintain systemic
BP.

If symptoms do not rapidly resolve in the PACU, a cardiologist or other

specialist (eg, an intensivist) is consulted to arrange further management
and transfer to an intensive care unit (ICU). Details regarding management
of acute decompensated HF are available elsewhere. (See "Treatment of
acute decompensated heart failure: Components of therapy".)

SUMMARY AND RECOMMENDATIONS

●
Hypotension in the post-anesthesia care unit (PACU) is treated when
systolic blood pressure (BP) is <90 mmHg or has decreased >20 percent
of baseline, or if the patient develops symptoms or other evidence of
hypoperfusion (eg, change in mental status or decreased urine output).
(See 'Initial assessment and treatment' above.)

•
Initial treatment includes intravenous (IV) isotonic crystalloid solution
administered in 250- to 500-mL increments and, if necessary, IV
vasopressor/inotropic agents (eg, phenylephrine 40 to 100 mcg or
ephedrine 5 to 10 mg increments). Severe or refractory hypotension is
treated with IV bolus doses of epinephrine 10 to 50 mcg, norepinephrine 4
to 16 mcg, or vasopressin 1 to 4 units, while a vasopressor/inotropic
infusion is prepared (table 1). (See 'Initial assessment and treatment'
above.)

•
Additional treatment of hypotension depends upon the specific etiology
(eg, hypovolemia due to inadequate fluid replacement or blood loss, drug
effects due to antihypertensive or anesthetic agents, allergic reaction,
adrenal insufficiency, myocardial dysfunction). (See 'Treatment of
underlying causes' above.)

•
Severe hypotension or hemodynamic collapse requiring immediate
lifesaving intervention may occur due to anaphylactic shock, septic shock,
local anesthetic toxicity, tension pneumothorax, pulmonary embolus,
cardiac tamponade, or dynamic left ventricular outflow tract obstruction.
Support with vasopressor/inotropic agents is necessary while definitive
treatment is underway (table 1). (See 'Hypotensive emergencies' above.)

●
Hypertension is typically treated when systolic BP is >180 mmHg or
diastolic BP is >110 mmHg, particularly if it persists after treatment of
presumed etiologies. (See 'Initial assessment and treatment' above.)

•
Initial treatment is with small bolus doses of rapid-acting antihypertensive
agents such as labetalol 5 to 20 mg, titrated to decrease systolic BP to a
stable value <160 mmHg. Metoprolol or labetalol are preferred for treating
hypertension associated with tachycardia due to their beta-blocking
properties. For severe or refractory hypertension, a vasodilator infusion is
prepared (table 3). (See 'Initial assessment and treatment' above.)

•
Additional treatment of hypertension depends upon the specific etiology
(eg, poorly controlled preexisting hypertension; sympathetic stimulation
due to pain or other noxious stimuli; hypervolemia; alcohol or opioid
withdrawal; recent use of cocaine, amphetamine, or phencyclidine). (See
'Treatment of underlying causes' above.)

•
Emergency treatment of severe hypertension is warranted if there is
evidence of acute neurologic signs or symptoms (eg, agitation, delirium,
stupor, visual disturbances, seizures, stroke) or a cardiovascular
emergency (eg, acute coronary syndrome, acute decompensated heart
failure [HF], aortic dissection) (table 3). (See "Drugs used for the treatment
of hypertensive emergencies".)

●
Severe bradycardia or tachyarrhythmias causing hemodynamic instability
require emergency treatment. (See "Advanced cardiac life support (ACLS)
in adults", section on 'Management of specific arrhythmias'.)

•
Underlying causes should be identified and treated. (See 'Cardiac
arrhythmias' above and 'Assessment and treatment of underlying causes'
above.)

●
Myocardial ischemia or decompensated HF may occur in the PACU with or
without associated hemodynamic instability (eg, hypotension,
hypertension, arrhythmias). (See "Perioperative myocardial infarction after
noncardiac surgery" and "Perioperative management of heart failure in
patients undergoing noncardiac surgery".)

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