Chapter

44 CARDIOPULMONARY
RESUSCITATION
David Shimabukuro and Linda L. Liu

BASIC LIFE SUPPORT

Responsiveness
Circulation
Airway
Breathing
C ardiopulmonary resuscitation (CPR) is a term that
was first used in the early 1960s by Safar and
Kouwenhoven to describe a combined technique of
Defibrillation mouth-to-mouth ventilation and closed cardiac chest
compressions in a pulseless patient. Over the past 40
ADULT ADVANCED CARDIOVASCULAR LIFE
years, significant advances in CPR and cardiovascular life
SUPPORT: ALGORITHMS
support have been made, especially in its application in
Pulseless Cardiac Arrest
the out-of-hospital setting. Today, the early descriptions
Bradycardia
of CPR would be considered basic life support (BLS),
Tachycardia
whereas adult advanced cardiovascular life support (ACLS)
ADULT ADVANCED CARDIOVASCULAR LIFE and pediatric advanced cardiovascular life support (PALS)
SUPPORT: DRUG THERAPY include the more sophisticated use of pharmacotherapy
Epinephrine and other definitive techniques. Out-of-hospital resusci-
Vasopressin tation has been well described in the literature. Yet, in-
Amiodarone hospital life support including resuscitation has only
occasionally been described.
PEDIATRIC ADVANCED LIFE SUPPORT
In 1986 the American Heart Association published the
Airway
first ACLS algorithms. In 2000, the International Liaison
Circulation
Committee on Resuscitation assembled the first interna-
External Compressions
tional conference to produce worldwide guidelines for
Defibrillation
emergency cardiovascular care and CPR. These expert
Drugs
panels meet every few years so that the guidelines and
POSTRESUSCITATION CARE algorithms for CPR and ACLS can be revised and updated
Mild Hypothermia based on newly published studies. The most recent guide-
Glucose Levels lines were released in October 2010 and will be covered
Normocapnia in this chapter.1,2
SPECIAL PERIOPERATIVE CONSIDERATIONS
Anaphylaxis
Gas Embolism BASIC LIFE SUPPORT
Local Anesthetic Toxicity
Neuraxial Anesthesia For any patient having cardiac arrest, the most important
QUESTIONS OF THE DAY steps are (1) immediate recognition of unresponsiveness,
(2) checking for lack of breathing or lack of normal
breathing (3) activating an emergency response system
and retrieving an automated external defibrillator (AED),
(4) checking for a pulse (no more than 10 seconds), and
(5) starting cycles of 30 chest compressions followed
by 2 breaths (Fig. 44-1).

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Section VI CONSULTANT ANESTHETIC PRACTICE

ADULT BLS HEALTHCARE PROVIDERS Figure 44-1

Resuscitation algorithm
for basic life support
1 (BLS). AED, automated
Unresponsive High-Quality CPR external defibrillator;
No breathing or no normal breathing • Rate at least 100/min ALS, advanced life support;
(i.e., only gasping) • Compression depth at
cm, centimeter; min,
least 2 inches (5 cm)
• Allow complete chest recoil minute. (From Berg RA,
2 after each compression Hemphill R, Abella BS, et
Activate emergency response system • Minimize interruptions in al. Part 5: Adult Basic Life
Get AED/defibrillator chest compressions Support: 2010 American
or send second rescuer (if available) to do this • Avoid excessive ventilation Heart Association
Guidelines and
Cardiopulmonary
3 3A
Definite Resuscitation and
Check pulse: pulse • Give 1 breath every Emergency Cardiovascular
DEFINITE pulse 5 to 6 seconds Care, Circulation 122:S689
within 10 seconds? • Recheck pulse every
2010.)
2 minutes
No pulse
4
Begin cycles of 30 COMPRESSIONS and 2 BREATHS

5
AED/defibrillator ARRIVES

6
Check rhythm
Shockable rhythm?

Shockable Not shockable

8
7 Give 1 shock Resume CPR immediately
Resume CPR immediately for 2 minutes
for 2 minutes Check rhythm every
2 minutes; continue until
ALS providers take over or
victim starts to move

Responsiveness the patient has no pulse, no signs of life, or the rescuer

is unsure, chest compressions should be started immedi-
Prior to approaching a victim, the rescuer should make
ately. The heel of the hand should be placed longitudi-
sure that the scene is safe; then the victim is assessed for
nally on the lower half of the sternum, between the
responsiveness by tapping or questioning (“Are you OK?”).
nipples (Fig. 44-2). The sternum should be depressed at
A quick check for presence of breathing or lack of normal
least 5 cm (2 inches) at a rate of at least 100 compressions
breathing should occur simultaneously. If distress is
per minute. Complete chest recoil is necessary to allow
present, then the emergency response system should be
for venous return and is important for effective CPR.
activated, and an AED should be quickly retrieved.
The pattern should be 30 compressions to 2 breaths
(30:2 equals 1 cycle of CPR), regardless of whether one
Circulation or two rescuers are present.

Because a pulse can be very difficult to assess, other clues

should be used, such as whether the patient is breathing
spontaneously or moving. The health care provider
should take no more than 10 seconds to check for a
definitive pulse either at the carotid or femoral artery. If
Airway
With the new 2010 BLS guidelines, the importance of
definitive airway management has taken a secondary
role. The old mnemonic ABCD (airway, breathing,

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 Chapter 44 Cardiopulmonary Resuscitation

Upstroke
1.5 – 2"
Downstroke

Fulcrum
(hip joint)

Figure 44-2 Proper hand and body position for performance of closed-chest (external) cardiac compressions in an adult. (From
Guidelines for cardiopulmonary resuscitation and emergency cardiac care. JAMA 1999;268:2171-2295, used with permission.)

circulation, and defibrillation) with “look, listen, and feel”

has been changed to CAB (compression, airway, breath-
ing). This change is due to evidence proving the impor-
tance of chest compressions and the need to quickly
restore blood flow to improve the likelihood of a return
of spontanenous circulation (ROSC). Airway maneuvers
should still be attempted, but they should occur quickly,
efficiently, and minimize interruptions in chest com-
pressions. Opening of the airway can be achieved by a
simple head tilt–chin lift technique (Fig. 44-3). A jaw
thrust maneuver can be used in patients with suspected
cervical spine injury. Simple airway devices, such as
nasal or oral airways, can be inserted to displace the tongue
from the posterior oropharynx.

Breathing
Although several large out-of-hospital studies have
demonstrated that chest compression-alone CPR is not VI
inferior to traditional compression-ventilation CPR,
health care providers are still expected to provide assisted
ventilation.3 A lone rescuer, if not an expert in airway
management, should not use a bag-mask for ventilation,
but should use mouth-to-mouth or mouth-to-mask. Care Figure 44-3 The head tilt–jaw thrust maneuver provides a
should be taken to avoid rapid or forceful breaths. Deliv- patent upper airway by tensing the muscles attached to the
ered tidal volumes are given over 1 second and should tongue, thus pulling the tongue away from the posterior
produce visible chest rise. A lower than normal minute pharynx. Forward displacement of the mandible is accomplished
ventilation (cardiac output is much less than normal) by grasping the angles of the mandible and lifting with both
should be the goal because hyperventilation has been hands, which serves to displace the mandible forward while
proved to be detrimental for neurologic recovery. tilting the head backward.

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Section VI CONSULTANT ANESTHETIC PRACTICE
Defibrillation
A defibrillator should be attached to the patient as soon
as possible. Proper electrode pad placement on the chest
wall should be to the right of the upper sternal border
below the clavicle and to the left of the nipple with
the center in the midaxillary line (Fig. 44-4). Most elec-
trode pads now come with diagrams showing their
correct positioning. Alternative locations include anterior-
posterior, anterior-left infrascapular, and anterior-right
infrascapular. Right anterior axillary to left anterior
axillary is not recommended.
ENERGY USED FOR DEFIBRILLATION
The amount of energy (joules) delivered is dependent on
the type of defibrillator used. Two major defibrillator
types (monophasic and biphasic) are available. Monopha-
sic waveform defibrillators deliver a unidirectional
energy charge, whereas biphasic waveform defibrillators
deliver an in-series bidirectional energy charge. Based
on evidence from implantable defibrillators, bidirectional
energy delivery is probably more successful in terminat-
ing ventricular tachycardia (VT) and ventricular fibrilla-
tion (VF). In addition, biphasic waveform shocks require
less energy than traditional monophasic waveform
shocks (120 to 200 J versus 360 J, respectively) and
may therefore cause less myocardial damage.
Figure 44-4 Schematic depiction of the proper placement of
paddle electrodes in an adult.
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TIME TO DEFIBRILLATION
The time until defibrillation is critical to survival, espe-
cially because the most frequent initial cardiac rhythm
in adult patients is VT/VF. Survival rates after VF cardiac
arrest decrease by 7% to 10% with every passing minute.
If adequate chest compressions are provided, this
decrease in survival rate improves to 3% to 4% with
every minute of delay until defibrillation.4
ADULT ADVANCED CARDIOVASCULAR LIFE
SUPPORT: ALGORITHMS
Three ACLS algorithms relevant to the anesthesia pro-
vider in the operating room are (1) pulseless cardiac
arrest, (2) symptomatic bradycardia, and (3) symptomatic
tachycardia (Figs. 44-5 to 44-7).2
Pulseless Cardiac Arrest
Cardiac dysrhythmias that produce pulseless cardiac
arrest are (1) VF, (2) rapid VT, (3) pulseless electrical
activity (PEA), and (4) asystole (see Fig. 44-5). During
pulseless cardiac arrest, the primary goals are to provide
effective chest compressions and early defibrillation if
the rhythm is VF or VT. Drug administration is of second-
ary importance because the efficacy of pharmacologic
interventions has been difficult to measure or prove.
After initiating CPR and defibrillation, rescuers can then
establish intravenous access, obtain a more definitive
airway, and consider drug therapy, all while providing
continued chest compressions and ventilation.
AIRWAY MANAGEMENT
Bag-mask ventilation and ventilation through an
advanced airway (endotracheal tube, supraglottic air-
way) are acceptable methods of ventilation during
CPR. Because chest compressions are not performed
during tracheal intubation, the rescuer has to weigh
the need for compressions against the need for defini-
tive airway management. Perhaps insertion of an
advanced airway should be deferred until after the
patient fails to respond to several cycles of CPR and
defibrillation. However, this decision is not always
absolutely correct. For example, a patient in severe pul-
monary edema may benefit from endotracheal intuba-
tion sooner rather than later.
With the presence of a more definitive airway, the
adequacy of ventilation should be evaluated again. The
chest should rise bilaterally and breath sounds should
be auscultated. In addition, proper positioning of the
endotracheal tube should be confirmed with a second
test to decrease false positive and false negative findings.
Capnography to measure end-tidal carbon dioxide
(PETCO2) is the most ideal test and is highly recommended.
Alternative tests include pH paper (color change) and an
 ADULT CARDIAC ARREST
Shout for help/activate emergency response
CPR quality
• Push hard (≥2 inches
1 [5 cm]) and fast
Start CPR (≥100/mon) and allow
• Give oxygen complete chest recoil
• Minimize interruptions in
• Attach monitor/defibrillator compressions
• Avoid excessive ventilation
• Rotate compressor every
2 minutes
• If no advanced airway,
30:2 compression-
Rhythm ventilation ratio
• Quantitative waveform
shockable? capnography
Yes No – IF PETCO2 <10 mm Hg,
attempt to improve
CPR quality
2 9 • Intra-arterial pressure
VF/VT Asystole/PEA – If relaxation phase
(diastolic) pressure
<20 mm Hg, attempt
to improve CPR quality
3 Return of spontaneous
Shock circulation (ROSC)
• Pulse and blood pressure
• Abrupt sustained
increase in PETCO2
(typically ≥40 mm Hg)
4 • Spontaneous arterial
CPR 2 min pressure waves with
• IV/IO access intra-arterial monitoring

Shock energy
• Biphasic: manufacturer
recomendation
Rhythm No (120–200 J); if unknown,
use maximum available.
shockable? Second and subsequent
10
CPR 2 min doses should be equiva-
Yes lent, and higher doses
• IV/IO access may be considered.
5 • Epinephrine every 3–5 min • Monophasic: 360 J
Shock • Consider advanced airway,
Drug therapy
capnography • Epinephrine IV/IO dose:
1 mg every 3–5 minutes
• Vasopressin IV/IO dose:
40 units can replace
6 CPR 2 min first or second dose of
Rhythm Yes epinephrine
• Epinephrine every 3–5 min
• Consider advanced airway, shockable? • Amiodarone IV/IO dose:
First dose: 300 mg bolus
capnography No Second dose: 150 mg

11 Advanced airway
CPR 2 min • Supraglottic advanced
airway or endotracheal
• Treat reversible causes intubation
Rhythm No • Waveform capnography
shockable? to confirm and monitor
ET tube placement
Yes • 8–10 breaths per minute
with continuous chest
7 Rhythm compressions
shockable?
Shock
No Yes Reversible causes
– Hypovolemia
– Hypoxia
VI
12 – Hydrogen ion (acidosis)
– Hypo-/hyperkalemia
8 • If no signs of return of Go to 5 or 7 – Hypothermia
CPR 2 min spontaneous circulation – Tension pneumothorax
• Amiodarone (ROSC), go to 10 or 11 – Tamponade, cardiac
• Treat reversible causes – Toxins
• IF ROSC, go to – Thrombosis, pulmonary
Post-Cardiac Arrest Care – Thrombosis, coronary

Figure 44-5 Resuscitation algorithm for pulseless arrest. cm, centimeter; ET, endotracheal; IO, intraosseus; IV, intravenous; J, joules;
mg, milligram; min, minute; mm Hg, milliliters of mercury; PEA, pulseless electrical activity; PETCO2, partial pressure of end-tidal
carbon dioxide; VF, ventricular fibrillation; VT, ventricular tachycardia. (From Neumar RW, Otto CW, Link MS, et al. Part 8: Adult
Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines and Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care, Circulation 122:S736, 2010.)

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Section VI CONSULTANT ANESTHETIC PRACTICE

ADULT BRADYCARDIA Figure 44-6 Resuscitation

(WITH PULSE) algorithm for bradycardia
with a pulse. ECG,
1 electrocardiogram; IV,
Assess appropriateness for clinical condition. intravenous; kg, kilogram;
Heart rate typically <50/min if bradyarrhythmia. mcg, microgram; mg,
milligram; min, minute.
(From Neumar RW, Otto
2 CW, Link MS, et al. Part 8:
Identify and treat underlying cause Adult Advanced
• Maintain patent airway; assist breathing as necessary Cardiovascular Life
• Oxygen (if hypoxemic) Support; 2010 American
• Cardiac monitor to identify rhythm; monitor blood pressure and oximetry Heart Association
• IV access
Guidelines and
• 12-lead ECG if available; don’t delay therapy
Cardiopulmonary
Resuscitation and
3 Emergency Cardiovascular
Persistent bradyarrhythmia Care, Circulation 122:S749,
causing: 2010.)
4
No • Hypotension?
Monitor and observe • Acutely altered mental status?
• Signs of shock?
• Ischemic chest discomfort?
• Acute heart failure?
Yes
5
Atropine
If atropine ineffective: Doses/details
• Transcutaneous pacing
OR Atropine IV dose:
• Dopamine infusion First dose: 0.5 mg bolus
OR Repeat every 3–5 minutes
• Epinephrine infusion Maximum: 3 mg

Dopamine IV infusion:
6 2–10 mcg/kg per minute
Consider:
• Expert consultation Epinephrine IV infusion:
• Transvenous pacing 2–10 mcg per minute

esophageal detector device (EDD). An EDD involves using
a bulb suction that is attached to the end of the endotra-
cheal tube once the bulb is compressed. If the endotra-
cheal tube is in the trachea, the bulb quickly inflates
with air in the lungs because the tracheal rings are stiff
and do not collapse around the tube. If the endotracheal
tube is in the esophagus, the esophageal walls, which
are pliable, collapse around the end of the endotracheal
tube, and the bulb remains in the compressed state. Once
the endotracheal tube is confirmed to be in the trachea, it
should be secured in place. One breath should be deliv-
ered every 6 to 8 seconds without synchronization with
compressions. Failed resuscitation may reflect poor chest
compressions or migration of the endotracheal tube out
of the trachea. Continuous monitoring of PETCO2 can be
extremely beneficial during the resuscitation. Although
values have not been correlated with ROSC, it does guide
the rescuers in adequacy of pulmonary blood flow. If
continuous end-tidal carbon dioxide monitoring is not
available, tube placement should be checked periodically,
especially during prolonged resuscitation.
MEDICATIONS
Establishing intravenous access is important, but it
should not interfere with CPR and defibrillation. A large
peripheral venous catheter is sufficient in most resuscita-
tions of pulseless patients. Drugs should be administered
rapidly and followed with a 20-mL fluid bolus if given
peripherally. If intravenous access cannot be obtained
or is lost, certain drugs (epinephrine, lidocaine, vasopres-
sin, atropine, naloxone) can be given via the endotra-
cheal tube. The endotracheal tube dose is 2 to 10 times
the recommended intravenous dose, and the drug should
be diluted in 5 to 10 mL of sterile water before instillation
down the endotracheal tube. A preferable alternative
to the intravenous route is the intraosseus route. Kits
are now commercially available to rapidly place these
lines. No dose changes are required from the IV route.

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 Chapter 44 Cardiopulmonary Resuscitation

ADULT TACHYCARDIA Doses/details

(WITH PULSE)
Synchronized cardioversion
1 Initial recommended doses:
Assess appropriateness for clinical condition. • Narrow regular: 50–100 J
Heart rate typically ≥150/min if tachyarrhythmia. • Narrow irregular: 120–200 J
biphasic or 200 J monophasic
• Wide regular: 100 J
2 • Wide irregular: defibrillation dose
Identify and treat underlying cause (NOT synchronized)
• Maintain patent airway; assist breathing as necessary
• Oxygen (if hypoxemic) Adenosine IV dose:
• Cardiac monitor to identify rhythm; monitor blood First dose: 6 mg rapid IV push;
pressure and oximetry follow with NS flush.
Second dose: 12 mg if required.
___________________________
3
Persistent tachyarrhythmia 4 Antiarrhythmic infusions for
causing: stable wide-QRS tachycardia
Synchronized cardioversion
• Hypotension? Yes • Consider sedation
• Acutely altered mental status? Procainamide IV dose:
• If regular narrow complex,
• Signs of shock? 20–50 mg/min until arrhythmia
consider adenosine
• Ischemic chest discomfort? suppressed, hypotension ensues,
• Acute heart failure? 6 QRS duration increases >50%, or
maximum dose 17 mg/kg given.
No • IV access and 12-lead ECG Maintenance infusion: 1–4 mg/min.
5 if available Avoid if prolonged QT or CHF.
Wide QRS? Yes • Consider adenosine only if
≥0.12 second regular and monomorphic Amiodarone IV dose:
• Consider antiarrhythmic infusion First dose: 150 mg over 10 minutes.
No • Consider expert consultation Repeat as needed if VT recurs.
7 Follow by maintenance infusion of
• IV access and 12-lead ECG if available 1 mg/min for first 6 hours.
• Vagal maneuvers
• Adenosine (if regular) Sotalol IV dose:
• β-blocker or calcium channel blocker 100 mg (1.5 mg/kg) over 5 minutes.
• Consider expert consultation Avoid if prolonged QT.

Figure 44-7 Resuscitation algorithm for tachycardia with a pulse. CHF, congestive heart failure; ECG, electrocardiogram; IV,
intravenous; J, joules; kg, kilogram; min, minute; mg, milligram; NS, normal saline; VT, ventricular tachycardia. (From Neumar RW, Otto
CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines and
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, Circulation 122:S751, 2010.)

VENTRICULAR FIBRILLATION/VENTRICULAR (Table 44-1). Epinephrine, 1 mg IV, may be administered

TACHYCARDIA
If the cardiac arrest was witnessed, the health care provider
should immediately place the defibrillator pads on the
patient’s chest, determine the rhythm, and deliver a shock
if VF or VT is present (see Fig. 44-5). In unwitnessed arrests,
rescuers may give five cycles of CPR before checking the
rhythm and attempting defibrillation. CPR should be
resumed immediately after delivery of the shock and
continued for five cycles or about 2 minutes, followed by
reevaluation of the cardiac rhythm. If the patient remains
in VF/VT, the defibrillator should be charged to the appro-
priate energy level (360 J for monophasic or 120 to
200 J for biphasic) while CPR is still being performed.
If VF or VT persists after one to two sets of CPR-
defibrillation cycles, a vasopressor should be given
every 3 to 5 minutes. One dose of vasopressin, 40 units
IV, may replace either the first or second dose of epineph-
rine. Drug administration should be timed to minimize
interruptions in chest compressions. If VF/VT persists after VI
another set of CPR-defibrillation and vasopressor adminis-
tration, an antiarrhythmic medication, amiodarone, is
recommended for VF/VT. Lidocaine can be considered if
amiodarone is not available, but a survival benefit for lido-
caine over amiodarone is not clear. Magnesium sulfate can
be considered if torsades de pointes is suspected.
ASYSTOLE AND PULSELESS ELECTRICAL ACTIVITY
Asystole is usually an agonal rhythm, whereas PEA is
often caused by a reversible condition and can be treated
if the inciting cause is identified (Table 44-2). These two

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Section VI CONSULTANT ANESTHETIC PRACTICE

Table 44-1 Drugs Used During Adult Cardiopulmonary Resuscitation

Drug Name Dose Indication
Adenosine 6 mg IV For stable narrow QRS tachycardia or
May repeat 12 mg IV monomorphic VT (contraindicated with
(cut dose in half if using central line) preexcitation syndrome)
Amiodarone 300 mg IV For pulseless VT/VF
May repeat 150 mg IV
150 mg IV over a 10-minute period For stable VT or uncertain wide QRS
Maintenance infusion of 1 mg/min for 6 hours, then 0.5 mg/min tachycardia and narrow QRS
Maximum total dose of 2.2 g/24 hr tachycardias
Atropine* 0.5 mg IV For bradycardia
May repeat to total dose of 3 mg
Diltiazem 15 to 20 mg (0.25 mg/kg) IV over a 2-minute period For stable narrow QRS tachycardia
May repeat 20 to 25 mg (0.35 mg/kg) in 15 minutes (contraindicated with preexcitation
Maintenance infusion of 5- to 15- mg/hr, syndrome)
titrated to heart rate
Dopamine 2 to 10 mg/kg/min by infusion For bradycardia instead of a pacer, while
awaiting a pacer, or if a pacer is
ineffective or not tolerated
Epinephrine* 1 mg IV For pulseless cardiac arrest
Repeat every 3 to 5 minutes
2 to 10 mg/min by infusion For bradycardia instead of a pacer, while
awaiting a pacer, or if a pacer is
ineffective or not tolerated
Esmolol 0.5 mg/kg IV load, followed by an infusion at For stable narrow QRS tachycardias
0.05 mg/kg/min (contraindicated with preexcitation
May repeat the 0.5-mg/kg bolus and increase the infusion to syndrome)
0.1 mg/kg/min
Maximum infusion of 0.3 mg/kg/min
Lidocaine* 1 to 1.5 mg/kg IV For pulseless VT/VF when amiodarone is
May repeat 0.5 to 0.75 mg/kg IV NOT available
Maximum total of 3 doses or 3 mg/kg
Magnesium 1 to 2 g IV For torsades de pointes
Metoprolol 5 mg IV For stable narrow QRS tachycardias
May repeat every 5 minutes (contraindicated with preexcitation
Maximum total dose of 15 mg syndrome)
Procainamide 20 to 50 mg/min IV (max 17 mg/kg) until arrhythmia suppressed For stable wide QRS tachycardia
Maintenance infusion of 1 to 4 mg/min
Sotalol 100 mg (1.5 mg/kg) IV over 5 minutes For stable wide QRS tachycardia
Vasopressin* 40 U IV For pulseless cardiac arrest to replace
the first or second dose of epinephrine
Verapamil 2.5 to 5 mg IV over a 2-minute period For stable narrow QRS tachycardia
May repeat 5 to 10 mg over a 15- to 30-minute period (contraindicated with preexcitation
Maximum total dose of 20 mg syndrome)
*Also effectively delivered by tracheal mucosal absorption when administered through an endotracheal tube.
g, gram; hr, hour; IV, intravenous; kg, kilogram; mcg, microgram; mg, milligram; min, minute; U, unit; VF, ventricular fibrillation; VT, ventricular
tachycardia.

cardiac rhythms have been combined as the second part of
the pulseless arrest algorithm because of similarities
in their management (see Fig. 44-5). Neither will benefit
from defibrillation, so the focus should be on performing
effective CPR with minimal interruptions, identifying
reversible causes, and establishing an advanced airway.
A vasopressor may be administered after initiation of
CPR. Epinephrine, 1 mg IV, may be given every 3 to 5
minutes. Alternatively, a single dose of vasopressin, 40
units IV, may replace either the first or second dose of

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Table 44-2 Major Causes of Cardiovascular Collapse in
the Perioperative Period
8 Hs 8 Ts
Hypovolemia Toxins (anaphylaxis/
anesthesia)
Hypoxia Tamponade
Hydrogen ion (acidosis) Tension pneumothorax
Hyperkalemia/ Thrombosis in coronary artery
hypokalemia
Hypoglycemia Thrombus in pulmonary artery
Hypothermia Trauma
Malignant QT interval prolongation
hyperthermia
Hypervagal response Pulmonary hypertension
Adapted from the 5 Hs and 5 Ts proposed by the American Heart
Association (AHA).
epinephrine. Atropine has been removed from the algorithm
because studies show that routine use of atropine is unlikely
to provide any benefit. Cardiac rhythm checks should be
performed after every five cycles or 2 minutes of CPR. If an
organized cardiac rhythm is present, the rescuer should check
for a pulse. If there is no pulse, CPR should be continued. If a
pulse is present, the rescuer should identify the rhythm and
treat accordingly. Given the poor survival and neurologic
recovery rates of patients in asystole, the length and effort
of resuscitation should be carefully considered.
Bradycardia
Bradycardia is defined as a heart rate slower than 60 beats/
min (see Fig. 44-6). Some patients, especially young ath-
letes, may have a resting heart rate slower than 60 beats/
min yet continue to exhibit signs of adequate perfusion.
Asymptomatic patients do not require treatment. Interven-
tion by pharmacologic treatment or electrical pacing
should be based on signs and symptoms of inadequate
perfusion. Symptoms cannot be obtained under anesthe-
sia, so the anesthesia provider should use discretion in
determining whether end-organ perfusion is compromised
by the slow heart rate. Initial treatment of symptomatic
bradycardia should focus on support of airway, breathing,
and circulation. Supplemental oxygen should be delivered,
and continuous cardiac rhythm, systemic blood pressure,
and pulse oximetry should be monitored. Further therapies
include atropine (0.5 mg IV every 3 to 5 minutes; no more
than 3 mg), an infusion of b-adrenergic agonists (dopamine,
epinephrine), or transcutaneous pacing.
Tachycardia
Regardless of the underlying origin of the tachycardia,
unstable or symptomatic patients should be immediately
shocked via synchronized cardioversion (see Fig. 44-7).
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Chapter 44 Cardiopulmonary Resuscitation
A trial of adenosine before cardioversion can be consid-
ered in select cases of unstable regular narrow-complex
tachycardia. In stable patients with fast ventricular rates,
determining whether the underlying rhythm has a narrow
or wide QRS complex (>0.12 second) on the electro-
cardiogram is important. Patients with asymptomatic
tachycardias, especially those with wide-complex tachy-
cardias, should be evaluated by a consultant to help
determine whether the rhythm is ventricular or atrial in
origin. Treatment should be guided by the consultant’s
opinion, which often can include the use of antidysrhyth-
mic medication or atrioventricular (AV) nodal blocking
drugs. If the rhythm is an irregular narrow-complex
tachycardia, the underlying rhythm is probably atrial
fibrillation, and heart rate control should be attempted
with AV nodal blocking drugs. If the rhythm is a regular
narrow-complex tachycardia, conversion back to sinus
rhythm should be attempted by vagal maneuvers or the
administration of adenosine, or both. Cardiac rhythm
conversion signifies probable reentry supraventricular
tachycardia, and recurrence can be treated with adeno-
sine or longer-acting AV nodal blocking drugs. If cardiac
rhythm conversion does not occur, the underlying
rhythm is possibly atrial flutter or junctional tachycardia.
In this case, effort should be made to achieve rate control
with the use of AV nodal blocking drugs.
ADULT ADVANCED CARDIOVASCULAR LIFE
SUPPORT: DRUG THERAPY (Also See
Chapter 7)
Epinephrine, vasopressin, and amiodarone are among the
most commonly used drugs in the ACLS algorithms
(see Table 44-1) and deserve special attention.
Epinephrine
Epinephrine is a combined direct a- and b-adrenergic
receptor agonist. It increases myocardial oxygen con-
sumption by increasing heart rate and afterload. In mul-
tiple animal studies, epinephrine has shown to be of
benefit in establishing return of spontaneous circulation.
Epinephrine can increase diastolic pressure and thereby
restore coronary perfusion pressure and blood flow back
to the myocardium.
VI
Vasopressin
Vasopressin is a naturally occurring antidiuretic hormone
with a half-life of 10 to 20 minutes. It is a nonadrenergic
peripheral vasoconstrictor that acts by direct stimulation
of smooth muscle vasopressin-1 receptors and leads to
intense vasoconstriction of the vasculature in the skin,
skeletal muscles, intestine, and fat. Vasopressin has also
been found in animals to selectively vasodilate the
cerebral, coronary, and pulmonary vascular beds. Like
epinephrine, vasopressin is believed to increase diastolic
723
Section VI CONSULTANT ANESTHETIC PRACTICE
pressure and therefore increase coronary perfusion pres-
sure with restoration of blood flow to the myocardium.
Given its relatively long half-life, it is recommended that
vasopressin be given only once during the resuscitation
of a pulseless patient.
There are no significant differences in rates of hospital
admission or survival between patients with out-of-
hospital arrest who receive vasopressin or epinephrine.
When compared with epinephrine in patients with asystole,
vasopressin is associated with more frequent hospital
admission and hospital discharge rates, but not neurologi-
cally intact survival.5 A recent study has shown no
improvement in hospital admissions with the addition of
vasopressin to epinephrine during asystole.6 Because the
effects of vasopressin and epinephrine in patients with car-
diac arrest are not significantly different, one dose of vaso-
pressin may substitute for either the first or second dose of
epinephrine in the treatment of pulseless cardiac arrest.
Amiodarone
Amiodarone was initially developed as an antianginal
drug in the 1950s but was abandoned because of its side
effects. Because it has effects on cardiac sodium and potas-
sium channels, as well as a- and b-receptors, amiodarone
has been reinvestigated for its antiarrhythmic effects. In
this regard, amiodarone prolongs repolarization and
refractoriness in the sinoatrial node, the atrial and ventri-
cular myocardium, the AV node, and the His-Purkinje car-
diac conduction system. Amiodarone can exacerbate or
induce arrhythmias, especially torsades de pointes. This
drug may interact with volatile anesthetics to produce
heart block, profound vasodilation, myocardial depres-
sion, and severe hypotension. It has many drug interac-
tions, and can prolong the effects of oral anticoagulants,
phenytoin, digoxin, and diltiazem. Despite its multiple
disadvantages, amiodarone has been shown in adults with
out-of-hospital VF/VT arrest to improve survival to
hospital admission when compared with placebo and lido-
caine.7,8 The recommended dose of amiodarone for VF/VT
is 300 mg IV. An additional dose of 150 mg IV may be
given for persistent VF/VT.
PEDIATRIC ADVANCED LIFE SUPPORT
(Also See Chapter 34)
Resuscitation of infants and children follows the same basic
principles as those for adults. It is important to remember
that most pediatric cardiac events are a result of arterial
hypoxemia and respiratory compromise, and thus, airway
management and breathing are critical to successful pediat-
ric resuscitation. In contrast, adults tend to experience car-
diac arrest as a result of VT or VF secondary to myocardial
ischemia. Defibrillation is the more important early inter-
vention in these cases. Regardless, pediatric BLS follows
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the same algorithm as for adults: C-A-B. Naturally, there
are several specific differences between adult and pediatric
patients because children are much smaller. For the health
care provider, infants are considered to be younger than
1 year, whereas children are considered to be between 1 year
old and adolescence. Adult BLS resuscitation guidelines can
be used for adolescent children (Table 44-3).
Airway
The airway of pediatric patients is slightly different
from that of an adult, but head tilt–chin lift is still the tech-
nique of choice to open the airway. Children tend to have a
larger tongue and epiglottis in relation to the mouth and
larynx. In addition, they have a larger head in relation to
the body. Over extension or excessive flexion of the head
can lead to difficulty visualizing the glottic opening during
direct laryngoscopy. Straight laryngoscope blades may be
preferred over curved blades to lift the epiglottis anteriorly
and away from the glottic opening in young children.
Circulation
Pulse checks and closed chest compressions are performed
slightly differently, depending on whether the patient is
a child or an infant. In children, the pulse is palpated at
the carotid or femoral artery, similar to adults. In infants,
the pulse is checked at the brachial or femoral artery.
External Compressions
In a child, the heel of one or both hands should be placed
on the lower half of the sternum, between the nipples,
while keeping the fingers off the rib cage and staying
above the xiphoid process. In an infant, chest compressions
are delivered via the two-finger technique. Two fingers of
one hand are placed over the lower half of the sternum
approximately one fingerwidth below the intermammary
line while keeping above the xiphoid process. For both
infants and children, the sternum should be depressed at
least one third to one half the anterior-posterior diameter
of the chest at a rate of at least 100 compressions per
minute. The pattern should be 30 compressions to 2 breaths
(30:2) if there is a single rescuer and 15 compressions to
2 breaths (15:2) if there are two rescuers.
Defibrillation
In children, defibrillation should be performed when a
pulseless rhythm (VT, VF) is present. An initial energy
of 2 to 4 J/kg should be attempted, regardless of the
waveform type. Subsequent defibrillations should be at
least 4 J/kg, but should not exceed 10 J/kg. Biphasic
automated external defibrillators can be used in children
older than 1 year outside the hospital setting. American
Heart Association guidelines recommend the use of a
 Chapter 44 Cardiopulmonary Resuscitation

Table 44-3 Comparative Resuscitation Techniques between Adults, Children, and Infants (Summary of Key BLS
Components for Adults, Children, and Infants*)
Recommendations
Component Adults Children Infants
Unresponsive (for all ages)
Recognition No breathing or no normal
No breathing or only gasping
breathing (i.e., only gasping)
No pulse palpated within 10 seconds for all ages (HCP only)
CPR sequence C-A-B
Compression rate At least 100/min
Compression depth At least 2 inches (5 cm) At least 1/3 AP diameter At least 1/3 AP diameter
About 2 inches (5 cm) About 11/2 inches (4 cm)
Chest wall recoil Allow complete recoil between compressions
HCPs rotate compressors every 2 minutes
Compression interruptions Minimize interruptions in chest compressions
Attempt to limit interruptions to <10 seconds
Airway Head tilt – chin lift (HCP suspected trauma: jaw thrust)
Compression-to-ventilation 30:2 (Single rescuer)
ratio (until advanced airway 30:2 (1 or 2 rescuers)
placed) 15:2 (2 HCP rescuers)
Ventilations: when rescuer
untrained or trained and not Compressions only
proficient
Ventilations with advanced 1 breath every 6–8 seconds (8–10 breaths/min)
airway (HCP) Asynchronous with chest compressions
About 1 second per breath
Visible chest rise
Defibrillation Attach and use AED as soon as available. Minimize interruptions in chest compressions before
and after shock; resume CPR beginning with compressions immediately after each shock.

AED, automated external defibrillator; AP, anterior-posterior; CPR, cardiopulmonary resuscitation; HCP, healthcare provider.
*Excluding the newly born, in whom the etiology of an arrest is nearly always asphyxial.
(From Hazinski MR, ed. Highlights of the 2010 American Heart Association Guidelines for CPR and ECC, 2010, p 8)

pediatric dose attenuator system that will decrease the
amount of delivered energy. If one is not available, a
standard external defibrillator can be substituted.
Drugs
Most drug dosages are calculated by using current known
weight or ideal body weight based on height. Most pedi-
atric units have resuscitation carts divided by weight to
facilitate drug administration in an emergency so that
calculations do not need to be performed and valuable
time is not wasted.
POSTRESUSCITATION CARE
After successful resuscitation with return of spontaneous
circulation, patients should be admitted to the intensive
care unit (if not already there) for further definitive and
supportive treatment (Fig. 44-8).9 Postcardiac arrest care
should be focused to optimize cardiopulmonary function
to ensure organ perfusion is adequate. It should be consis-
tent, integrated, and multidisciplinary. When possible,
therapies are administered concurrently. Specifically, percu-
taneous coronary interventions (PCI) should not be delayed
to institute hypothermia, and the institution of hypothermia VI
should not delay PCI. Often, vasopressors and inotropes
need to be administered during the immediate postresuscita-
tion period because of the presence of myocardial stunning
and hemodynamic instability. Central venous access for
drug administration may be necessary, along with an intra-
arterial catheter to facilitate hemodynamic monitoring.
In addition to cardiac recovery, neurologic recovery is of
vital importance. This is especially true during the immedi-
ate postresuscitation phase. Hypothermia protocols should
be established to facilitate institution. Consequently, due
to the widespread use of mild hypothermia, traditional

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Section VI CONSULTANT ANESTHETIC PRACTICE

ADULT IMMEDIATE POST-CARDIAC ARREST CARE

1
Doses/details
Return of spontaneous circulation (ROSC)
Ventilation/oxygenation
2 Avoid excessive ventilation.
Start at 10–12 breaths/min
Optimize ventilation and oxygenation and titrate to target PETCO2
• Maintain oxygen saturation ≥94% of 35–40 mm Hg.
• Consider advanced airway and waveform capnography When feasible, titrate FIO2
• Do not hyperventilate to minimum necessary to
achieve SpO2 ≥94%.
3
IV bolus
Treat hypotension (SBP <90 mm Hg) 1–2 L normal saline
• IV/IO bolus or lactated Ringer’s.
• Vasopressor infusion If inducing hypothermia,
• Consider treatable causes may use 4°C fluid.
• 12-lead ECG
Epinephrine IV infusion:
4 0.1–0.5 mcg/kg per minute
5 (in 70-kg adult: 7–35 mcg
No Follow
Consider induced hypothermia per minute)
commands?
Yes Dopamine IV infusion:
6 5–10 mcg/kg per minute
7
Yes STEMI
Coronary reperfusion OR Norepinephrine
high suspicion of AMI IV infusion:
0.1–0.5 mcg/kg per minute
No (in 70-kg adult: 7–35 mcg
8 per minute)
Advanced critical care
Reversible causes:
– Hypovolemia
– Hypoxia
– Hydrogen ion (acidosis)
– Hypo-/hyperkalemia
– Hypothermia
– Tension pneumothorax
– Tamponade, cardiac
– Toxins
– Thrombosis, pulmonary
– Thrombosis, coronary

Figure 44-8 Algorithm for postcardiac arrest care. AMI, acute myocardial infarction; C, centigrade; ECG, electrocardiogram; FIO2, fraction
of inspired oxygen; IO, intraosseous; IV, intravenous; kg, kilogram; L, liters; mcg; microgram; min, minute; mm Hg, millimeters of mercury;
PETCO2, partial pressure of end-tidal carbon dioxide; SBP, systolic blood pressure; SpO2, pulse oximeter oxygen saturation; STEMI, ST-
elevation myocardial infarction. (From Peberdy M, Callaway CW, Neumar RW, et al. Part 9: Post Cardiac Arrext Care: 2010 American Heart
Association Guidelines and Cardiopulmonary Resuscitation and Emergency Cardiovascular Care, Circulation 122:S769, 2010.)

means to determine neurologic prognosis in patients who
have been cooled have not been validated and should be
interpreted accordingly.
Mild Hypothermia
Temperature should be monitored closely, and hyper-
thermia should be avoided at all times. Mild hypothermia
for the first 24 to 48 hours may be beneficial to the neuro-
logic recovery of patients after out-of-hospital VF/VT
arrest.10,11 Recommendations are to cool comatose (defined
as inability to follow verbal commands) patients who are
successfully resuscitated from out-of-hospital VF/VT arrest
to 32 C to 34 C for the first 12 to 24 hours. Hypothermia
has not been well studied in patients with an initial rhythm
of asystole or PEA. However, given recent technologic
advances in cooling patients quickly and easily, mild hypo-
thermia has been expanded to all comatose patients follow-
ing return of spontaneous circulation regardless of the
initial pulseless rhythm and whether it occurred out of hos-
pital or in hospital.12 Warming is allowed to occur passively
unless it is beyond the 48-hour window.

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Glucose Levels
Increased blood glucose concentrations after resuscitation
from cardiac arrest are associated with poor neurologic out-
come. However, studies have not shown that tight control
of serum glucose improves neurologic outcome. Regard-
less, glucose levels after resuscitation should be monitored
closely to avoid hypoglycemia and hyperglycemia.
Normocapnia
Hyperventilation does not protect the brain or other vital
organs after resuscitation from cardiac arrest. In fact, iatro-
genic hyperventilation can lead to increased airway
pressure, intrinsic positive end-expiratory pressure (“auto-
PEEP”), increased intrathoracic pressure, and increased
intracranial pressure. In patients with brain injury, hyper-
ventilation may worsen the neurologic outcome. There are
no data to support targeting a specific partial pressure of
arterial carbon dioxide PaCO2 after resuscitation, so venti-
lation to normocapnic levels is recommended.
SPECIAL PERIOPERATIVE
CONSIDERATIONS
Anesthesia providers sometimes encounter unique situa-
tions and experiences that are rarely seen by other medical
practitioners. Cardiac arrest during anesthesia is distinct
from cardiac arrest in other settings in that our patients
have a different pathophysiology. Cardiac arrests under
anesthesia are usually witnessed, and frequently antici-
pated. The traditional guidelines don’t often translate well
into the perioperative setting. Because of that, the Ameri-
can Society of Anesthesiologists (ASA) Committee on Crit-
ical Care Medicine published a monograph specific to
advanced life support for anesthesia. They expanded
the traditional 5 Hs and 5 Ts as established by the American
Heart Association (AHA) to the 8 Hs and 8 Ts. Included in
the list is hypoglycemia, malignant hyperthermia, hyperva-
gal response, trauma, QT interval prolongation, and pulmo-
nary hypertension (see Table 44-2). Four unique
circumstances to the general anesthesia providers are
detailed in the next paragraphs.13
Anaphylaxis
Minor drug reactions such as a rash are not an uncom-
mon occurrence in the operating room. Major reactions,
like anaphylactic shock, occur much less often, but will
happen at least once to every anesthesiologist. Common
agents associated with anaphylaxis are latex, beta-lactam
antibiotics, succinylcholine, nondepolarizing muscle
relaxants (i.e., rocuronium; also see Chapter 12), and
intravenous contrast material. The treatment of anaphy-
laxis involves giving epinephrine to interrupt the cascade
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Chapter 44 Cardiopulmonary Resuscitation
Table 44-4 Treatment of Anaphylaxis
Stop or remove inciting agent or drug
Oxygen at FIO2 1.0
Intravenous fluids
CPR/ACLS if pulseless
Epinephrine, intravenous
▪Bolus: 10 to 100 mg—if not pulseless
▪Bolus: 1-3 mg—if pulseless
▪Infusion: 4-10 mg/min
Vasopressin, intravenous
▪
Bolus: 0.5 to 2 units—if not pulseless
▪
Bolus: 40 units—if pulseless
H1 blocker, intravenous: diphenhydramine 50 mg
H2 blocker, intravenous: famotidine 20 mg
Steroid, intravenous: hydrocortisone 50 to 150 mg
ACLS, adult advanced cardiovascular life support; CPR,
cardiopulmonary resuscitation; H1, H2, histamine receptor types.
of profound vasodilation and significant vascular leak. If
possible, the offending drug should be removed or
stopped. Epinephrine and vasopressin can be used to
support blood pressure, while steroids and antihistamines
are administered to further attenuate the response. Intra-
venous fluid administration is essential secondary to the
vascular leak. CPR and ACLS should be immediately
instituted if there is no pulse. In the event of complete
cardiovascular collapse, much larger doses of epineph-
rine may be required (Table 44-4).
Gas Embolism (Also See Chapter 30)
Although a very rare event, the incidence of gas embolism
has the potential to increase in parallel with the worldwide
increase in laparoscopic surgical procedures, posterior
spine surgery, and endobronchial laser procedures. The
initial management should be to stop the cause (i.e., halt
insufflation), occlude open veins, and flood the surgical
field with saline. Patients should be placed in Trendelen-
burg position with left side down to keep the gas in the
apex of the ventricle and allow for filling. Complete VI
circulatory collapse should be treated with CPR and ACLS.
Local Anesthetic Toxicity (Also See Chapter 11)
Local anesthetics affect sodium channels throughout the
body, including the brain and the heart. In general, toxicity
occurs in a dose-dependent fashion with cardiovascular
collapse occurring at the end of the spectrum. In nona-
nesthetized patients, central nervous system symptoms
are vital to recognize as they tend to precede cardiac
manifestations. Cardiac rhythms can range from premature
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Section VI CONSULTANT ANESTHETIC PRACTICE

occur in younger, otherwise healthy patients under-

Table 44-5 Treatment of Local Anesthetic Toxicity
going routine surgical procedures with neuraxial anes-
Stop local anesthetic thesia. Proposed mechanisms causing the arrest include
CPR/ACLS if pulseless a shift in autonomic balance toward the parasympa-
thetic system, a decrease in venous return from pooling
20% Intralipid IV:
in the splanchnic circulation, and activation of barore-
▪Load: 1.5 mL/kg
ceptors that stimulate a paradoxical Bezold-Jarisch
▪Infusion: 0.25 mL/kg/hr
response. A high spinal anesthesia seems to be the big-
Sodium bicarbonate to maintain pH >7.25 in a prolonged gest culprit. Regardless, treatment follows standard
resuscitation CPR and ACLS recommendations.
Consider transcutaneous or transvenous pacing for
bradycardic rhythms
Continue CPR for at least 60 min
QUESTIONS OF THE DAY
ACLS, adult advanced cardiovascular life support; CPR,
cardiopulmonary resuscitation.
1. What is the impact of time to defibrillation on the
ventricular contractions to asystole. If possible, the adminis- survival from ventricular fibrillation?
tration of the local anesthetic should be stopped. Intralipid 2. What ACLS medications can be administered by
should be given for cardiovascular toxicity.14 There have endotracheal tube? How should they be prepared and
been reports of good neurologic recovery in these patients delivered?
despite the prolonged resuscitation (Table 44-5). 3. What is the proper hand placement for external
cardiac compression in children and infants? What is
the proper depth and frequency of compression?
Neuraxial Anesthesia (Also See Chapter 17) 4. Which postcardiac arrest patients with neurologic
Cardiovascular collapse from neuraxial anesthesia has injury are most likely to benefit from therapeutic
been described, but is a poorly understood.15 It seems to hypothermia?

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2. Neumar RW, Otto CW, Link MS, et al:
Part 8: Adult Advanced Cardiovascular
Life Support: 2010 American Heart
Association Guidelines for
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