Review

J Vet Intern Med 2008;22:9–25

C a r d i o p u l m o n a r y R e s u s c i t a t i o n i n S m a l l An i m a l M e d i c i n e :
A n U p da te
S.J. Plunkett and M. McMichael
In December 2005, the American Heart Association published new guidelines for cardiopulmonary cerebral resuscitation
(CPCR) in humans for the 1st time in 5 years. Many of the recommendations are based on research conducted in animal species
and may be applicable to small animal veterinary patients. One important change that may impact how CPCR is performed in
veterinary medicine is the recommendation to avoid administration of excessive ventilatory rates because this maneuver se-
verely decreases myocardial and cerebral perfusion, decreasing the chance of survival. The new guidelines also emphasize the
importance of providing well-executed, continuous, uninterrupted chest compressions. Interruption of chest compressions
should be avoided and, if necessary, should be minimized to o10 seconds. During defibrillation, immediate resumption of chest
compressions for 2 minutes after a single shock, before reassessment of the rhythm by ECG, is recommended. This recommen-
dation replaces previous recommendations for the delivery of 3 defibrillatory shocks in rapid succession. Allowing permissive
hypothermia postresuscitation has been found to be beneficial and may increase success rate. Medications utilized in cardio-
pulmonary resuscitation, including amiodarone, atropine, epinephrine, lidocaine, and vasopressin, along with the indications,
effects, routes of administration, and dosages, are discussed. The application of the new guidelines to veterinary medicine as
well as a review of cardiopulmonary resuscitation in small animals is provided.
Key words: Amiodarone; Cardiac arrest; Epinephrine; Lidocaine; Vasopressin.

n December 2005, the American Heart Association
I (AHA) published new guidelines for cardiopulmonary
cerebral resuscitation (CPCR) in humans for the 1st time
in 5 years.1 The International Liaison Committee on
Resuscitation, an international consortium of represen-
tatives from many resuscitation councils, reviewed the
current science, developed a worldwide evidence-based
guide for resuscitation practice, and collaborated to de-
velop the guidelines. The consensus statements were
published in December 2005 in the journal Circulation.1
These guidelines are available without charge online at
the website www.circulationaha.org.
Highlights of the new guidelines include a greater em-
phasis on chest compressions, avoidance of excessive
ventilation rates, and immediate resumption of compres-
sions after a single defibrillation. Many of the
recommendations are based on small animal research
and may be pertinent to the veterinary patient. The re-
vised recommendations particularly applicable to the pet
population as well as an overview of CPCR will be dis-
cussed in more detail in this article.
History of CPCR
The 1st scientific references to artificial ventilation ap-
peared in the 16th century.2 Andreas Vesalius, often
referred to as the father of resuscitation, described the
From the Emergency Animal Clinic, Phoenix, AZ (Plunkett); and
the Department of Small Animal Clinical Sciences, College of Veter-
inary Medicine and Biomedical Sciences, Texas A & M University,
College Station, TX (McMichael).
Corresponding author: Dr Signe Plunkett, Emergency Animal
Clinic, PLC, 2260 W. Glendale Avenue, Phoenix, AZ 85021; e-mail:
signedvm@cox.net.
Submitted April 2, 2007; Revised June 14, 2007; Accepted
October 2, 2007.
Copyright r 2008 by the American College of Veterinary Internal
Medicine
10.1111/j.1939-1676.2007.0033.x
use of bellows for apnea in 1530.2 Tossach documented
the administration of mouth-to-mouth ventilation in
1732.2 Various methods have been utilized to attempt to
save the life of the apparently deceased. Modern cardio-
pulmonary resuscitation had evolved by 1960 to include
endotracheal intubation, artificial ventilation, and cardi-
ac compressions. Since 1960, little improvement has been
made in the success rate of CPCR in humans.2,3
Approximately 330,000 people in the United States die
every year from sudden cardiac arrest, according to the
Center for Disease Control and Prevention.4 The surviv-
al rate for out-of-hospital sudden cardiac arrest in
people, defined by survival to discharge from the hospi-
tal, is o6.4% for the United States and Canada.5–10 In
dogs and cats that undergo cardiopulmonary arrest
(CPA) in the hospital, the reported survival rate to dis-
charge was approximately 4% for dogs and between
4 and 9.6% for cats.11,12
Recognition of CPA
In veterinary medicine, there are several elements
of CPCR that should be in place before CPA occurs to
optimize success, including essential supplies, oxygen,
and a crash cart with up-to-date medications to perform
CPCR. Communication with the client, including verifi-
cation of a telephone number where the client can be
reached, is essential. Clients frequently have false expec-
tations regarding the success of CPCR. Utilization of the
term ‘‘do not attempt resuscitation’’ (DNAR) with the
client may be beneficial, because it indicates that an at-
tempt will be made, rather than a guarantee of success.
The decision to attempt CPCR should be based on the
client’s desires. The decision to terminate CPCR should
be based on the patient’s disease process, the original
prognosis, and the client’s desires. In most cases, contin-
ued CPCR efforts are ended by 20 minutes after arrest.13
All hospitalized patients should be assigned to 1 of
3 groups, depending on the extent of CPCR to be
10 Plunkett and McMichael
provided: patients with DNAR orders, external CPCR,
and those patients for whom everything possible should
be attempted, including open chest CPCR.
The most successful CPCR is the one avoided. In small
animal practice, there are many predisposing causes for
CPA, including sepsis, cardiac failure, pulmonary disease,
neoplasia, coagulopathies, anesthesia, toxicities, multisys-
tem trauma, traumatic brain injury, and systemic in-
flammatory response syndrome.12–16 Anticipation of CPA
and vigilant monitoring for deterioration in critical patients
are essential. Frequent reevaluation and repetition of criti-
cal diagnostic tests and procedures may be necessary.
Before CPA, several changes may be observed, in-
cluding obtundation, hypothermia, bradycardia, hypo-
tension, and dilated, unresponsive pupils. Changes in
respiratory depth, rate, or rhythm may occur, progress-
ing to gasping and finally agonal breaths at death.17–20
Mucous membrane color and capillary refill time should
not be used to assess the patient for CPA because they
may remain normal for several minutes after arrest. The
definitive clinical signs of CPA include loss of conscious-
ness, absence of spontaneous ventilation, absence of heart
sounds on auscultation, and absence of palpable pulses.16
Basic Life Support
Performing chest compressions, providing ventilatory
breaths, and administering a defibrillatory shock for ven-
tricular fibrillation are the only aspects of CPCR proven
to be effective treatment for CPA.1 Only manual chest
compressions with manual ventilation and the use of a
defibrillator for the treatment of ventricular fibrillation
or pulseless ventricular tachycardia have consistently im-
proved long-term survival from CPA.1 All veterinary
team members should be trained and efficient in provid-
ing CPCR.
Airway
Establishment of an airway is performed, ideally by
placement of a well-fitting, low-pressure, high-volume,
cuffed endotracheal tube. If the ideal endotracheal tube
is not available or does not fit, other options include
placement of any hollow tube that fits into the trachea
via the orotracheal route or via an emergency tracheos-
tomy. The surgical approach for a tracheostomy is
documented elsewhere.21,22 A laryngoscope should be
utilized to place the endotracheal tube and avoid vagal-
induced bradycardia from excessive manipulation of the
epiglottis.23,24 Suctioning of blood or fluid from the cau-
dal oropharynx may be necessary in some patients.
Proper placement should be confirmed by visualization,
appropriate chest wall excursions during ventilation,
and palpation of the tube in the trachea rather than
palpation of ‘‘two tracheas,’’ which indicates the end-
otracheal tube is in the esophagus.
End-tidal carbon dioxide (ETCO2) monitoring has
been helpful to confirm endotracheal tube placement in
anesthetized animals.25–27 A positive reading for exhaled
CO2 is usually a reliable indicator of proper tube place-
ment within the trachea in animals with normal
circulation. However, in the patient with CPA, ETCO2
initially may read near zero because of lack of perfusion
and therefore may not be a reliable indicator of proper
tube placement in these patients.25,28,29
Breathing
The veterinary patient is given 2 breaths 1–2 seconds in
duration, with positive pressure ventilation using 100%
inspired oxygen, and then evaluated for spontaneous
ventilation.30 If the patient resumes spontaneous ventila-
tion, a full CPA situation may have been avoided. If the
patient has only respiratory arrest, acupuncture of the
Jen Chung (GV26) point should be considered. This
technique is performed by twirling a 25-G, 5/8-in. needle
inserted to the bone in the nasal philtrum at the ventral
aspect of the nares.16,31 This technique has been effective
at increasing the ventilation rate in dogs.16,31 Reversal
agents are administered for medications that may cause
apnea. Doxapram administration is contraindicated be-
cause it decreases cerebral blood flow and increases
cerebral oxygen consumption and requirement.32–34
If spontaneous ventilation does not return in the vet-
erinary patient, ventilations are begun at a rate of 10–12
breaths per minute (bpm) at airway pressures of
20 cmH2O.25,35 All breaths should be given over 1 sec-
ond with sufficient volume to cause a visual rise in the
chest wall, and then allow normal relaxation of the chest
wall.36 The ventilations delivered to the patient should be
neither too large nor too forcefully administered, or
barotrauma of the lungs may occur.14,37 An ambu bag
or rebreathing bag on an anesthetic machine with the in-
halant anesthetic turned off should be used.36
In patients with pre-existing hypoxia or severe pulmo-
nary disease, higher ventilation rates, 12–15 bpm, may be
beneficial.22,37 Previous recommendations for veterinary
patients were to provide a ventilatory rate of 20–
24 bpm.22,30 Lower ventilation rates are an essential part
of the new guidelines.1 In humans, a ventilatory rate of
8–12 bpm is recommended for adults and 12–20 bpm
for pediatric patients and neonates.1,35,38 Delivery of an
excessive ventilatory rate should be avoided, because an
excessive rate has been shown to lower coronary perfusion
pressure and decrease the success rate of CPCR
in human and in animal models.38–40 Excessive ventilatory
rates cause decreased coronary perfusion pressure, de-
creased cardiac preload, decreased cardiac output,
decreased right ventricular function, increased intratho-
racic pressure, and decreased venous return to the heart.38
Although ventilatory rates are currently controversial,
a recent study published in the medical literature found
that providing chest compressions alone in resuscitation
for out-of-hospital witnessed cardiac arrest resulted in a
higher survival rate than no CPCR at all.41 In instances
in which 1 person is available or during transport, it may
be appropriate to administer chest compressions only
while awaiting assistance.41
Circulation
Standard manual CPCR was developed to pump
blood from the chest to the vital organs during chest
 Cardiopulmonary Resuscitation in Small Animals
compression and enhance venous return into the chest
during relaxation of the chest wall. The goal is to maxi-
mize cerebral and myocardial perfusion.42–45 The differ-
ence between mean arterial pressure and intracranial
pressure is cerebral perfusion pressure. Maintenance of
cerebral blood flow and function depends on adequate ce-
rebral perfusion pressure.46,47 The difference between
aortic diastolic pressure and right atrial pressure deter-
mines myocardial perfusion. Studies in humans and
animals have shown that successful return of spontaneous
circulation (ROSC) corresponds with maintenance of
sufficiently high myocardial perfusion pressures.46,48
Compression of the chest wall causes an increase in
intrathoracic pressure and direct compression of the
heart. The degree of recoiling of the chest wall has a tre-
mendous impact on the amount of blood flow back to the
chest. With each chest wall decompression, venous re-
turn of blood to the right heart increases and intracranial
pressure decreases transiently.42,49–52 The decrease in in-
tracranial pressure is the result of direct transfer of
pressure through the thoracic spine to the cerebrospinal
fluid and increased venous drainage of the nonvalvular
veins of the paraspinal plexuses, resulting in increased
venous return to the heart via the jugular veins.50,53–55
External Chest Compressions
The new guidelines for people emphasize the impor-
tance of continuous, uninterrupted chest compressions.1
Every effort should be made to minimize the number
and the duration of interruptions to o10 seconds, be-
cause interruptions allow a decrease in intrathoracic
pressure, intravascular pressure, and coronary perfusion
pressure.1,56–60 According to recent studies in humans,
interruptions for attempted defibrillation, securing and
checking the airway, placement of IV catheters, drug ad-
ministration, ECG evaluation, and CPCR assessment
resulted in cessation of chest compressions 40–50% of the
time and were associated with increased mortality.56,57,59–61
Rapid auscultation of the chest for audible heart
sounds is performed while simultaneously palpating for
the presence of a peripheral pulse. If heart sounds and
pulses are absent, continuous external chest compres-
sions are begun. The thoracic pump theory, the
mechanism thought to be in effect in humans and medi-
um to large dogs, suggests that the application of
pressure to the chest wall in a rhythmic manner creates
blood flow by increasing intrathoracic pressure that is
transmitted to arteries and veins, with a pressure gradient
causing forward blood flow, and also by compressing the
heart directly.22,62 The cardiac pump theory is the meth-
od thought to be responsible for forward blood
movement from external chest compressions in cats and
in dogs o15 kg. According to the cardiac pump theory,
arterial flow is thought to be caused by direct compres-
sion of the ventricles.22 External chest compressions that
are correctly performed in humans can generate systolic
arterial pressure peaks of 60–80 mmHg and cardiac out-
put between 25 and 40% of prearrest values.46,63
The patient should be placed on a firm surface in right
lateral recumbency. Ideally, the person administering
11
chest compressions (the compressor) should be above
the patient’s chest.64,65 Placement of the compressor’s
hands varies depending on the shape of the patient’s
chest. For medium and large dogs (thoracic pump), the
compressor’s hands should be placed over the widest part
of the chest and 1 hand should be placed on top of the
other hand with the hands parallel, applying even pres-
sure to the chest wall with the palm of the hand. For
animals weighing 7–10 kg, the compressor should place
his or her hands directly over the apex of the heart, which
lies between the 4th and the 6th intercostal spaces at or
slightly dorsal to the costochondral junction. Hands
should be placed slightly more dorsal in animals weigh-
ing 410 kg. For smaller dogs (o7 kg) and cats, the
fingers of 1 hand should be placed on 1 side of the
chest and the thumb on the other side. Compressions
with the fingertips should be avoided.22,30,66–68 The per-
son performing chest compressions should change every
2 minutes to maintain adequate force and rate.1,69,70
Chest compressions for veterinary patients should be
provided at 80–100 compressions per minute with a 1 : 1
compression to relaxation ratio (compression time
should equal relaxation time).13,22 The currently recom-
mended chest compression rate for humans is 100
compressions per minute for adult and pediatric patients
and 90 compressions per minute for neonatal patients.
The chest wall should be allowed to completely recoil af-
ter being compressed approximately 30% of the chest
wall diameter; otherwise, decreased coronary and cere-
bral perfusion and increased intrathoracic pressure
occur, leading to decreased survival to discharge from
the hospital.57,59,71–73
Chest compressions should be continuous, with no
pauses during administration of ventilatory breaths,
placement of IV catheters, endotracheal intubation,
ECG assessment, palpation of pulses, or administration
of medications.1,51,56,57,66 For witnessed out-of-hospital
cardiac arrest, a study in humans showed no improve-
ment in neurological outcome by adding mouth-
to-mouth ventilation to external chest compressions.41
Although some studies have shown that the technique
of interposed abdominal compression with chest com-
pressions may increase venous return to the heart, other
studies have not shown any survival advantage.67,68
Evidence for or against the use of interposed abdominal
compression is lacking in the new CPCR guidelines.1
Compression Assist Devices
There are several compression assist devices available
for CPCR in humans. The theory of the active compres-
sion-decompression device is that venous return to the
heart can be increased during decompression by expand-
ing the chest cavity and decreasing intrathoracic
pressure. The results of studies utilizing these devices
have been inconsistent.69,70,74 Such a device may be diffi-
cult to use in most veterinary patients because of the
hair coat.
An impedance threshold device (ITD) is a valve that
limits air entry into the lungs during chest recoil between
chest compressions to improve venous return to the
12 Plunkett and McMichael
heart by increasing negative intrathoracic pressure dur-
ing the decompression phase of CPCR without affecting
exhalation.42,75–77 In animal models, the ITD can im-
prove hemodynamic parameters, increase cerebral
perfusion by lowering intracranial pressure, improve
myocardial perfusion when intrathoracic pressure be-
comes increasingly negative, and improve ROSC when
used as an adjunct to CPCR in intubated cardiac arrest
patients.42,50–52 Although ITDs have been used in ani-
mals in research, their use is not yet reported in
veterinary practice.
Internal Cardiac Massage
The indications for internal cardiac massage include
penetrating chest wounds, thoracic trauma with rib frac-
tures, pleural space disease, diaphragmatic hernia,
pericardial effusion, hemoperitoneum, intraoperative
sudden cardiac arrest, and failure to achieve adequate
circulation within 2–5 minutes of external chest compres-
sions, especially in dogs weighing 420 kg.30,78–80 The
surgical approach for internal cardiac massage has been
described elsewhere.79,81 It has been suggested previously
to place a cross-clamp around the descending aorta, cau-
dal to the heart, to increase coronary and cerebral blood
flow.21,81,82 An alternative is to gently apply digital pres-
sure to the descending aorta, caudal to the heart, with
1 finger while cardiac compression is performed with the
remaining part of the hand.30,79 If a cross-clamp tourni-
quet or digital pressure is applied, it should be utilized for
o10 minutes and slowly withdrawn.81
Arrhythmias
Although rhythm analysis is important and ECG as-
sessment should occur early in CPA, it should be carried
out as briefly as possible to avoid impeding chest com-
pressions. There are only 4 rhythms that can cause a
pulseless cardiac arrest: asystole, ventricular tachycardia,
ventricular fibrillation, and pulseless electrical activity
(PEA). Another arrhythmia of importance is sinus
bradycardia (a heart rate o40–60 bpm in dogs and
o120–140 bpm in cats with a normal sinus rhythm on
ECG). Increased vagal tone, hypothermia, increased
intracranial pressure, and medications can cause sinus
bradycardia.83,84
Asystole and Pulseless Electrical Activity
In humans, the survival rate from cardiac arrest with
asystole is very low.1 Asystole is the most common
arrest rhythm in dogs and cats.83,84 It can result from nu-
merous serious disease processes, trauma, and increased
vagal tone.1,83 Evaluation of all leads of an ECG is
important, because fine ventricular fibrillation can mim-
ic asystole.85,86 Administration of a defibrillation shock
to a patient in asystole may prove detrimental to sur-
vival.87–91 Resuscitation efforts should be directed at per-
forming high-quality CPCR with minimal interruptions
and to identify and treat reversible causes or complicat-
ing factors. No medications have been shown to be
effective in the treatment of asystole.1
Pulseless electrical activity is the condition in which,
despite a normal heart rate and rhythm on ECG, there is
an absence of myocardial contractility. Pulseless electri-
cal activity was referred to previously as electrical
mechanical dissociation and has been combined with
asystole under the new 2005 guidelines for humans.1 Un-
der the new guidelines, many rhythms are grouped in the
PEA category, including idioventricular rhythms and
ventricular escape rhythms.1 No medications have prov-
en effective in the treatment of PEA (ie defibrillation is
not beneficial), and resuscitation should focus on per-
forming high-quality CPCR and treatment of reversible
causes or complicating factors.1 The prognosis is poor
for successful resuscitation.1
Ventricular Tachycardia
Ventricular tachycardia results from repetitive firing of
an ectopic focus or foci in the ventricular myocardium or
Purkinje system and can precipitate ventricular fibrilla-
tion.83 Causes of ventricular tachycardia include
hypoxia, pain, ischemia, sepsis, electrolyte changes, trau-
ma, pancreatitis, gastric dilatation and volvulus, primary
cardiac disease, and other conditions.84,92 Treatment of
the underlying cause should be addressed.83
Ventricular Fibrillation
Ventricular fibrillation is unorganized ventricular ex-
citation resulting in poorly synchronized and inadequate
myocardial contractions that cause cardiac pump failure.
Sudden loss of cardiac output leads to global tissue is-
chemia, with the brain and myocardium being most
susceptible. Ventricular fibrillation may be either fine,
with lower amplitude and complete lack of organization,
or coarse, with higher amplitude and more orderly ap-
pearance.83,84 Orthogonal leads (lead I and aVF, lead II
and aVL) should be checked to verify fine ventricular
fibrillation, which can mimic asystole on the ECG. Fine
ventricular fibrillation may be more difficult to convert
to sinus rhythm than coarse ventricular fibrillation.85,86
Defibrillation
Defibrillation is defined as termination of ventricular
fibrillation for at least 5 seconds after delivery of an elec-
tric shock that depolarizes myocardial cells and
eliminates ventricular fibrillation. It is an electrophysio-
logic event that occurs 300–500 ms after delivery of a
defibrillatory shock.93–95 Ventricular fibrillation should
be identified as early as possible because it is more re-
sponsive to defibrillation if detected early. There are
2 types of defibrillators, monophasic and biphasic, refer-
ring to the type of current used. Newer defibrillators are
usually biphasic and are effective at terminating ventric-
ular fibrillation in humans at lower energy levels (120–
200 J) than are monophasic defibrillators (360 J). It is im-
portant to know the type of defibrillator available and
the energy level proven by the manufacturer to be effec-
tive at terminating ventricular fibrillation.96–98
Chest compressions should be performed while the
defibrillator is being connected and charged. With
 Cardiopulmonary Resuscitation in Small Animals
a manual defibrillator, the defibrillator operator selects
the shock energy (in joules); however, it is the amplitude
of current flow (in amperes) that causes depolarization
of the myocardium and results in defibrillation.99 Alco-
hol, ultrasound gel, or other nonconductive gels should
not be used on electrode paddles.1,36 Conductive paste
should be applied liberally to the paddles or self-adhesive
pads should be used. The largest electrode paddles
or pad that will fit on the patient’s chest should be used
because small electrodes may cause myocardial necro-
sis.100–102 The patient should be placed in dorsal
recumbency and the paddles should be placed with pres-
sure on opposite sides of the chest.
When the defibrillator is charged, the word ‘‘clear’’
should be shouted to warn personnel to cease contact
with the patient and anything connected to the patient,
and then 1 shock should be administered as quickly as
possible. The person administering the shock must avoid
contact with the patient’s limbs, the table, the ECG leads,
and everything connected to the patient. Doing so can be
difficult with the patient in dorsal recumbency. Alterna-
tively, the patient can remain in right lateral recumbency,
a flat paddle can be placed under the patient’s chest on
the down side, and a standard paddle can be used on the
upper side of the chest. The initial counter shock energy
for external defibrillation is 2–5 J/kg.103,104 Other dosage
recommendations for external defibrillation are to ad-
minister 50 J for small dogs and cats, 100 J for medium
dogs, and 200 J for large dogs or to administer 7 J/kg to
patients o15 kg and 10 J/kg to patients 415 kg. For in-
ternal defibrillation, saline-soaked sponges should be
placed between the paddles and the heart. The energy of
the counter shock for internal defibrillation is 1/10 of the
dosage used for external defibrillation (0.2–0.5 J/kg).104
Under the 2005 guidelines, to minimize the interrup-
tion in chest compressions, 1 shock should be
administered rather than the 3 successive shocks recom-
mended previously.56,71,105,106 Chest compressions
should immediately be resumed for 2 minutes before re-
assessing the cardiac rhythm and administration of an
additional shock.1 Assessment of an ECG immediately
after defibrillation rarely is helpful and delays resump-
tion of postshock chest compressions.59,72,107–109 After
successful defibrillation, a short period of a nonperfusing
rhythm, either asystole or pulseless electrical activity, is
common before returning to normal sinus
rhythm.96,110,111 Immediate chest compressions after at-
tempted defibrillation increase myocardial perfusion and
are more likely to make conversion successful than the
administration of a 2nd shock.56,71,98,105,106,110–115
In an unwitnessed, out-of-hospital arrest, the 2005
CPCR guidelines recommend the administration of
external chest compressions first for approximately 2
minutes, followed by 1 defibrillatory shock, regardless
of the type of defibrillator used, with immediate resump-
tion of chest compressions for 2 minutes before
reassessing the cardiac rhythm.116,117 In these situations,
a clinically relevant period of no perfusion may have oc-
curred. The responsiveness of ventricular fibrillation to
defibrillation may be enhanced by previous chest com-
pressions and epinephrine administration.71,106
13
When CPA occurs in a human hospital, immediate
defibrillation is recommended. If ventricular fibrillation
continues after 1 or 2 shocks plus compression, epineph-
rine should be administered every 3–5 minutes, or a
dose of vasopressin may be substituted for the 1st or the
2nd dose of epinephrine. If ventricular fibrillation con-
tinues after 2 or 3 shocks, compressions and admin-
istration of a vasopressor, followed by amiodarone, are
recommended.108,118–120
The likelihood of ROSC proportionately decreases
with delays in cardiac compressions from repeated
defibrillation, rhythm assessment, and other interrup-
tions.56,57,60,105,113,115 A precordial thump is no longer
recommended because research has shown that it can
lead to deterioration of cardiac rhythm, increased rate of
ventricular tachycardia, conversion of ventricular tachy-
cardia to ventricular fibrillation, complete heart block, or
asystole.121–123
Automated external defibrillators (AEDs) are comput-
erized devices that use voice and visual prompts to guide
safe defibrillation. They are useful for out-of-hospital
sudden cardiac arrest in public access areas such as air-
ports and sports venues.124–127 Microprocessors in the
AED analyze features of the surface ECG. The voice and
visual prompts along with diagrams guide the rescuer
and will not send a defibrillating shock unless the auto-
mated ECG rhythm analysis determines that
administration of a shock is indicated.57,61,124–127
Although manual defibrillators with dose adjustment
capabilities are recommended for children, AEDs
equipped with pediatric attenuator systems are available
for children 1–8 years of age.128–130 If an AED is to be
used on a small animal patient, studies in swine show that
it is advisable to use an AED equipped with a pediatric
dose attenuation system.103,131
Advanced Cardiac Life Support (ACLS)
Pharmacologic support of circulation and placement
of an advanced airway are some of the treatments con-
sidered to be a part of ACLS. These measures are
provided in addition to basic life support to increase the
likelihood of successful resuscitation and survival to dis-
charge from the hospital.
Routes of Administration for Medications and Fluid
Therapy
A central line is the preferred route for administration
of medication during CPCR. Unfortunately, one rarely is
in place before CPA, and a central line should not be
placed during CPCR because of the time-consuming na-
ture of placement.132,133 A peripheral IV catheter is the
next most preferred route, followed by intraosseous (IO)
administration and finally the intratracheal (IT)
route.36,134 Because of the rapid access to the IT route
and delays in placing peripheral catheters during CPA,
some prefer the IT route. Intracardiac injections should
be avoided, except possibly during open chest CPCR,
when the heart is directly observed. In addition to the
difficulty of injecting blindly into the left ventricle,
14 Plunkett and McMichael

intracardiac injections can result in numerous complica-
tions, including coronary vessel laceration, myocardial
ischemia, hemorrhage, arrhythmia, and pneumotho-
rax.16,135,136 Medication administered via a peripheral
catheter should be given as a bolus injection, followed by
0.9% NaCl IV and raising of the extremity for 10–20 sec-
onds.1,137,138 It usually takes 1–2 minutes for medication
administered via a peripheral vein to reach the central
circulation. The new guidelines recommend chest com-
pressions be administered for 2 minutes after drug
administration via a peripheral vein before checking the
ECG.132,133 The sites for IO administration include the
tibial crest, the femoral trochanteric fossa, and the prox-
imal humerus, and the technique has been described
elsewhere.139
The medications found to be well absorbed and
safe for administration via the IT route are atropine,
epinephrine, lidocaine, naloxone, and vasopressin (see
Table 1).140–145 IT administration of sodium bicarbonate
should be avoided because it inactivates the surfactant
and irritates tissues.16,140,146–151 Medications to be ad-
ministered via the IT route should be diluted in 5–10 mL
of sterile water, which is absorbed better than 0.9%
NaCl.146–149 If sterile water is not available, 0.9% NaCl
should be utilized.146,148 For IT administration, the dos-
age of most drugs should be increased 2–2.5 times their
IV dosage, except for epinephrine, which should be in-
creased by 3–10 times the IV dosage (0.03–0.1 mg/
kg).149,152–155 In studies of humans and animals, lower
dose epinephrine administered via the IT route caused
hypotension and decreased cerebral perfusion pressure
because of transient b-adrenergic effects.153,154,156–160
IV Fluid Therapy
The 2005 guidelines for humans state that IV fluids
should be administered if the patient is hypovolemic.1 IV
fluids should not be administered at shock dosages
(90 mL/kg for dogs and 45 mL/kg for cats) unless the pa-
tient was hypovolemic before CPA. In the euvolemic
CPA patient, the recommended dosage for crystalloid IV
fluids is a 20 mL/kg bolus for dogs and a 10 mL/kg bolus
for cats, as rapidly as possible. The administration of ex-
cessive volumes of IV fluids to euvolemic patients during
CPCR in animal studies decreased coronary perfusion
pressure because of an increase in right atrial pressure
relative to aortic pressure.12,161,162 If colloids are neces-
sary, the IV dosage of hetastarch or plasma is 20 mL/kg/
day for dogs and 5–10 mL/kg/day for cats. Hetastarch
may be administered as an IV bolus during CPCR at a
dosage of 5 mL/kg for dogs and 2–3 mL/kg for cats.163–
167
Hypertonic saline has been shown to improve survival
from ventricular fibrillation when compared with 0.9%
NaCl in animal studies.168,169 Although the concentra-
tions and dose recommendations are variable, the
authors recommend 3% hypertonic saline, at a dosage
of 4–6 mL/kg IV, slowly over 5 minutes.168,169 If hyper-

Table 1. Medications and shock energy doses used in CPCR.

Medication Canine Feline Details
Amiodarone 5.0 mg/kg IV, IO over 10 minutes Same Only 1 repeat dose, after 3–5 minutes, is
Repeat dose 2.5 mg/kg IV, IO over 10 recommended. Do not administer IT
minutes
Atropine 0.04 mg/kg IV, IO Same Can repeat every 3–5 minutes for a maxi-
0.08–0.1 mg/kg ITa mum of 3 doses
Calcium gluconate 10% 0.5–1.5 mL/kg IV slowly Same Do not administer IT
Epinephrine 0.01 mg/kg IV, IO Same Initial dose
0.03–0.1 mg/kg ITa Repeat doses should be administered every
Repeat dose 0.1 mg/kg 3–5 minutes
IV, IO, ITa
Lidocaine 2.0–4.0 mg/kg IV, IO 0.2 mg/kg IV, Use cautiously in cats
4.0–10 mg/kg ITa IO, IT
Magnesium sulfate 0.15–0.3 mEq/kg IV slowly over 10 Same Can repeat to a maximum of 0.75 mEq/kg
minutes Do not administer IT
Naloxone 0.02–0.04 mg/kg IV Same Opioid reversal agent
0.04–0.10 mg/kg ITa
Sodium bicarbonate 0.5 mEq/kg IV, IO Same Do not administer IT. Administer cau-
0.08  BW (kg)  base deficit 5 # of tiously after 10–15 minutes of CPA; can
mEq to administer repeat every 10 minutes
Vasopressin 0.2–0.8 U/kg IV, IO Same Repeat every 3–5 minutes or alternate with
0.4–1.2 U/kg ITa epinephrine
External defibrillation 2–5 J/kg 2–5 J/kg
shock energy (J) Or 50 J for small dogs, 100 J for medi- Or 50 J
um dogs, and 200 J for large dogs Or 7 J/kg if o15 kg
Or 7 J/kg if o15 kg and
10 J/kg if 415 kg
Internal defibrillation 0.2–0.5 J/kg Same
shock energy (J)
a
All medications administered IT should be diluted in 5–10 mL of sterile water.
IO, intraosseous; IT, intratracheal; CPCR, cardiopulmonary cerebral resuscitation.
 Cardiopulmonary Resuscitation in Small Animals
tonic saline is administered too rapidly, it can cause va-
gal-induced bradycardia and hypotension.168,169
Epinephrine
Epinephrine hydrochloride is a mixed adrenergic ago-
nist, acting on a- and b-receptors.170,171 It possesses both
b1-agonist (increased myocardial contractility, increased
heart rate, increased myocardial automaticity, and in-
creased myocardial oxygen consumption) and b2-agonist
(smooth muscle relaxation, peripheral vasodilatation,
systemic hypotension, and bronchial dilatation) ef-
fects.172,173 Epinephrine is administered during CPCR
mainly for its a2-adrenergic receptor-stimulating effects,
including peripheral arteriolar vasoconstriction, which
leads to increased coronary and cerebral perfusion pres-
sure.174,175 The a2-agonist effect of increased peripheral
arteriolar vasoconstriction overrides the b2-agonist–
induced hypotension and causes an increase in systemic
vascular resistance and increased arterial blood pressure,
which result in the shunting of blood to the brain, heart,
and lungs.174,176 The a1-agonist effects can be detrimen-
tal to the myocardium by increasing myocardial oxygen
demands and causing intramyocardial coronary arterio-
lar vasoconstriction and enhancing the reduction in
myocardial perfusion.174–184
The optimal dosage of epinephrine is not known.
In veterinary patients, epinephrine (1 : 1,000) should be
administered initially at 0.01 mg/kg IV, unless it is being
administered IT, in which case the dosage is 0.03–0.1
mg/kg.149,174,185,186 Epinephrine administration should
be repeated every 3–5 minutes if indicated. In veterinary
medicine, if repeated doses are not successful, vasopres-
sin can be administered instead or the epinephrine dosage
can be increased to 0.1 mg/kg IV.171,185–188 Many proto-
cols in human medicine now call for 1 dose of
epinephrine, followed by a dose of vasopressin IV before
repeating or increasing the dose of epinephrine.171,187,188
There have been no randomized clinical studies compar-
ing an epinephrine dosage of 0.01 mg/kg with placebo in
cardiac arrest.189 Placebo was shown to be superior to an
epinephrine dosage of 0.1 mg/kg in survival to discharge
in humans with CPCR.189–191 Although epinephrine
0.1 mg/kg IV appears to be superior for maximizing ce-
rebral blood flow and the aortic diastolic-right atrial
gradient, it is also associated with a higher refibrillation
rate and a lower survival rate.190–192
Vasopressin
Vasopressin is a nonadrenergic endogenous pressor
peptide that causes peripheral, coronary, and renal
vasoconstriction.193,194 At a dosage of 0.2–0.8 U/kg IV
or 0.4–1.2 U/kg IT, vasopressin stimulates specific V1A
receptors in the smooth muscle of the vasculature, leading
to nonadrenergic vasoconstriction.171,195–201 Vasopressin
may improve cerebral perfusion by causing dilatation of
cerebral vasculature. It causes less constriction in coro-
nary and renal blood vessels than in peripheral tissue,
resulting in preferential shunting of blood to the central
nervous system and heart.171,196,198,202
15
Because the outcome from pulseless cardiac arrest did
not differ in humans treated with vasopressin compared
with those treated with epinephrine, the 2005 guidelines
state that vasopressin can be used with or instead of epi-
nephrine in the treatment of ventricular fibrillation,
ventricular tachycardia, and PEA.1 In humans with
asystole, vasopressin was superior to epinephrine in sur-
vival to discharge from the hospital in some studies, and
it is recommended in the treatment of asystole.1,89,91,203
The utilization of vasopressin in CPCR of companion
animals is increasing because asystole is the most com-
mon arrest arrhythmia.90,204 Several studies in animals
with ventricular fibrillation showed that vasopressin
was superior to both epinephrine and placebo for
ROSC.87,89,193,205 The responses of the V1A receptors re-
main intact in an acidotic environment, as encountered in
cardiac arrest, allowing vasopressin to function, whereas
epinephrine and other catecholamines lose much of their
vasopressor effects in hypoxic and acidotic environ-
ments.171,195 According to a recent report in human
medicine, the initial dosage of vasopressin can be repeat-
ed every 3–5 minutes or vasopressin can be alternated
with epinephrine every 3–5 minutes.188
Atropine
Atropine sulfate is an anticholinergic parasympatho-
lytic that is effective at muscarinic receptors.206,207
During cardiac arrest, ventricular vagal tone is suspected
to be high, suppressing automaticity.207 Atropine revers-
es cholinergic-mediated responses and parasympathetic
stimulation and acts to increase heart rate, control hypo-
tension, and increase systemic vascular resistance.207 As
a vagolytic, it is most effective in the treatment of vagal-
induced asystole.207 It increases automaticity of the sin-
oatrial node and conduction of the atrioventricular
node.208,209 Although there are no prospective controlled
studies supporting the use of atropine in asystole or PEA
cardiac arrest, the 2005 guidelines recommend atropine
in these instances.1 The recommended dosage for atro-
pine during CPCR in dogs and cats is 0.04 mg/kg IV.104
If there is no effect, the dose can be repeated every 3–5
minutes for a maximum of 3 doses.210,211
Amiodarone
Amiodarone is a class III antiarrhythmic agent with
several effects, including prolongation of myocardial cell
action potential duration and refractory period by affect-
ing sodium, potassium, and calcium channels, and
noncompetitive a- and b-adrenergic inhibition.119,212 It
is the medication of choice for treatment of refractory
ventricular fibrillation after defibrillation, according to
the 2005 guidelines.1,118,120,213 Although numerous stud-
ies in humans and animals showed improvement in
response to defibrillation in patients treated with am-
iodarone compared with patients treated with lidocaine,
other studies dispute these findings.214 It should also be
noted that the rate of survival to hospital discharge
did not improve with the administration of amiodarone.1
Lidocaine and amiodarone are indicated for the treatment
16 Plunkett and McMichael
of atrial fibrillation, narrow-complex superventricular
tachycardia, ventricular tachycardia, wide-complex ta-
chycardia of uncertain origin, and refractory ventricular
fibrillation that is unresponsive to compressions, defi-
brillation, and vasopressor administration.118,120,212–214
The dosage of amiodarone is 5.0 mg/kg IV or IO over
10 minutes. One repeated dose of amiodarone, at a dos-
age of 2.5 mg/kg IV, may be administered after 3–5
minutes.119,215
Lidocaine
Lidocaine is a class Ib antiarrhythmic agent that stabi-
lizes cell membranes by sodium channel blockade and
also acts as a local anesthetic. In clinical trials, in com-
parison with amiodarone, lidocaine resulted in decreased
ROSC and increased incidence of asystole after defibril-
lation.118,216 Because it has no proven efficacy in cardiac
arrest, the 2005 guidelines state that lidocaine should
be considered an alternative treatment to amiodarone.1
Lidocaine is not recommended for treatment of ventric-
ular fibrillation if defibrillation is planned, because it may
make electrical defibrillation more difficult by increasing
the defibrillation threshold and decreasing myocardial
automaticity.217,218 For ventricular arrhythmias after re-
suscitation, lidocaine may be beneficial and should be
considered if amiodarone is not available.118,213,214 The
dosage of lidocaine in dogs is 2.0–4.0 mg/kg IV or
IO.12,25 For IT administration in dogs, the lidocaine dos-
age is increased 2–2.5 times and it is diluted in sterile
water.12,25,143,144 Lidocaine should be used cautiously, if
at all, in cats at a dosage of 0.2 mg/kg IV, IO, or IT.219,220
Sodium Bicarbonate
Sodium bicarbonate was recommended previously for
the treatment of severe acidosis during CPCR. Evidence
for its efficacy is lacking and the new guidelines recom-
mend it only in the treatment of tricyclic antidepressant
overdose, severe pre-existing metabolic acidosis, and
severe hyperkalemia.221–227 For these conditions, sodi-
um bicarbonate may be administered at a dosage of 0.5
mEq/kg IV.221–227 The best treatment for the respiratory
acidosis and nonrespiratory (metabolic) acidosis that
occur during CPA is to maximize ventilation and perfu-
sion.1,153,228,229 Sodium bicarbonate may inactivate
catecholamines that are administered simultaneously
and can cause hypernatremia, hyperosmolality, extracel-
lular alkalosis, decreased systemic vascular resistance,
left shift of the oxyhemoglobin curve, and decreased re-
lease of oxygen from hemoglobin.23
Calcium
Calcium was thought to be useful for increasing cardi-
ac contractility during CPCR, but there is no proven
benefit for the administration of calcium during
CPCR.230–232 Calcium is currently recommended for
the treatment of calcium channel blocker toxicity, hyper-
kalemia, and documented ionized hypocalcemia, rather
than routine use during CPCR.231 When indicated,
the dosage of 10% calcium gluconate is 0.5–1.5
mL/kg slowly IV.233 In critically ill patients, serum total
calcium concentration is an inadequate reflection
of serum ionized calcium concentration, which is affect-
ed by interactions of serum pH, individual serum
protein-binding capacity and affinity, and serum protein
concentration.232,234–236
Magnesium Sulfate
Magnesium sulfate is an essential enzyme cofactor
with numerous roles in cellular metabolism. A deficiency
of magnesium may result in altered depolarization,
repolarization, and pacemaker activity because of abnor-
malities of potassium and sodium homeostasis from
decreased sodium, potassium-adenosinetriphosphatase
(Na1, K1-ATPase) activity. Magnesium also affects
vascular tone.237–240 The administration of magnesium
sulfate may be beneficial in the treatment of refractory
ventricular arrhythmias, including ventricular fibrillation
and torsades de pointes (a life-threatening, polymor-
phic form of ventricular tachycardia).1,241–243 Decreased
intracellular concentrations of magnesium increase myo-
cardial excitability, potentially resulting in ventricular
arrhythmias.241–244 The dosage of magnesium sulfate
during cardiac arrest is 0.15–0.3 mEq/kg administered
slowly IV over 10 minutes, repeated to a maximum dos-
age of magnesium sulfate of 0.75 mEq/kg/day.215
Glucose
Glucose administration is not recommended during
CPCR unless the patient has documented hypoglycemia.
Neurologic outcome after resuscitation is worse in pa-
tients with hyperglycemia.228,245–248
Bretylium Tosylate
Bretylium tosylate is a type III antiarrhythmic agent
with both direct myocardial and adrenergic effects. It is no
longer recommended because of its hypotensive effects,
antiadrenergic effects, and lack of proven efficacy.36,249,250
Reversal Agents
If CPA is associated with sedation or anesthesia, ad-
ministration of a reversal agent if one is available and
appropriate is recommended. Reversal agents include a2-
adrenergic antagonists (yohimbine or atipamezole, 0.1–
0.2 mg/kg IV slowly), benzodiazepam antagonists (flu-
mazenil, 0.02 mg/kg IV), and opioid antagonists
(naloxone, 0.02–0.04 mg/kg IV).251 The administration
of inhalation anesthetics should be stopped and the
breathing circuit should be evaluated before CPCR is
initiated.
Monitoring the Effectiveness of CPCR
To assess the effectiveness of CPCR efforts, the pa-
tient’s ETCO2 level should be monitored as an indication
of perfusion.25,29,252 If ventilation during CPCR is rela-
tively constant, changes in cardiac output are reflected
by changes in ETCO2 levels.25 In studies of humans,
 Cardiopulmonary Resuscitation in Small Animals
patients who could not be resuscitated had significantly
lower ETCO2 levels than those who were successfully
resuscitated.245,252–255 The presence of a palpable carotid
or femoral pulse may not be a reliable indicator of suc-
cessful CPCR, because venous pulses may be felt in the
absence of adequate arterial blood flow during CPCR
because of backflow of blood from the caudal vena
cava.256,257 Assessment of cerebral blood flow can be
performed by placement of a Doppler ultrasound trans-
ducer on the lubricated cornea.258,259 Assessment of
oxygenation at the tissue level during CPCR can be
achieved by monitoring central venous blood gases
from a pulmonary artery catheter sample.25 Evaluation
of central venous blood gases provides a more
accurate assessment of tissue acid-base status during
CPCR because it takes into consideration the effects
of low peripheral blood flow and the resulting tissue
hypoxia, hypercarbia, and acidosis that occur during
CPA.1,25,260 Studies have shown that evaluation of arteri-
al blood gases during CPCR does not adequately
reflect the effectiveness of ventilation or the severity of
tissue acidosis or tissue hypoxemia.260–263 Pulse oximetry
is not helpful because peripheral pulsatile blood flow is
inadequate.1,245
Care of the Patient After Successful Resuscitation
Respiratory or CPA commonly recur after successful
CPCR in veterinary patients.12 A ‘‘sepsis-like syndrome’’
characterized by coagulopathy, immunologic dysfunc-
tion, and multiple organ failure has been documented
after successful resuscitation in people because of the
presence of global ischemia and reperfusion injury.264–266
The following parameters should be monitored: pulse
rate, rhythm and character, mental status, ECG, pulse
oximetry, body temperature, lung sounds, mucous mem-
brane color, capillary refill time, urine output,
electrolytes, blood gases, PCV and total solids, blood
glucose concentration, serum lactate concentration, cen-
tral venous pressure, neurologic function, and patient
comfort.228,245,246
Supplemental oxygen should be provided via ventila-
tory support if inadequacies in spontaneous ventilation
are present, or via a nasal catheter, a hood, or an oxygen
kennel.36 Initially, the patient should be ventilated with
100% oxygen, but the oxygen concentration should be
decreased to o60% as quickly as possible to avoid oxy-
gen toxicity.108,267–271 If continued ventilation is
required, arterial blood gases and direct arterial blood
pressure or indirect systolic blood pressure should be
monitored continuously.
If the animal has mild hypothermia or becomes
hypothermic during CPCR, permissive hypothermia
should be allowed.272,273 Permissive hypothermia is the
term used when hypothermia is allowed to continue
without taking steps to rewarm the patient to a normal
body temperature. This term differs from induced hypo-
thermia, in which the human patient is manipulated via
medical treatment and external devices to a body tem-
perature of 32–34 1C and maintained at this low body
temperature for 12–24 hours.272–274 Although induced
17
hypothermia may be useful in human patients, it requires
advanced monitoring and medical devices not typically
available in veterinary practice. Complications of hypo-
thermia include arrhythmias and coagulopathy.1,272–275
The target temperature for dogs and cats is 33–
34 1C.276,277 Permissive hypothermia diminishes the oxy-
gen demands of tissues, reduces neurologic impairment
after CPA, and may increase the success rate from
CPCR.272–280
IV fluid therapy should be administered cautiously.
Crystalloids should not be administered at shock fluid
dosages unless the patient was hypovolemic before CPA.
To improve peripheral perfusion and cardiac output, it
may be beneficial to administer an IV bolus of a colloid
such as hetastarch (5–10 mL/kg IV for dogs and 2–3
mL/kg IV slowly over 15 minutes for cats.)166,281 If the
colloid bolus does not improve cardiac output, blood
pressure, and peripheral perfusion, it may be beneficial to
administer a positive inotrope or vasopressor.
After an adequate IV fluid bolus, if the patient is
normotensive, with decreased perfusion and decreased
cardiac contractility as evaluated by echocardiography,
administration of a positive inotrope (eg dobutamine or
dopamine) may be indicated. Peripheral perfusion can be
evaluated by assessing serum lactate concentration, urine
output, capillary refill time, and rectal and peripheral
temperatures. Dobutamine is usually the drug of choice
to improve cardiac output without causing excessive va-
soconstriction. The dosage of dobutamine for infusion is
2.0–20.0 mg/kg/min IV as a constant rate infusion (CRI)
titrated to effect.282,283
The administration of dopamine may be beneficial
if dobutamine does not produce the desired response.
Dopamine has a greater impact on systemic arterial
blood pressure but may cause excessive vasoconstriction
without an additional increase in cardiac output. The
dosage of dopamine to produce a positive inotropic
effect is 1.0–10.0 mg/kg/min IV as a CRI titrated to
effect.282,283 The following formula may be used to cal-
culate a dobutamine or dopamine CRI: 6  body weight
in kilograms 5 the number of milligrams of dobutamine
or dopamine added to a total volume of 100 mL 0.9%
NaCl. When this preparation is delivered at 1.0 mL/h IV,
1.0 mg/kg/min is administered. The CRI solution should
be protected from light.284
After an adequate IV fluid bolus, if the patient is
hypotensive, with normal cardiac contractility as evalu-
ated by echocardiography, the administration of a
vasopressor (eg epinephrine, vasopressin, or norepineph-
rine) IV as a CRI titrated to effect may be beneficial to
increase systemic arterial blood pressure and cardiac out-
put, but cautious administration is necessary because
excessive vasoconstriction may occur.282,285 The dosage
of epinephrine (1 : 1,000) for infusion is 0.1–1.0 mg/kg/
min IV as a CRI titrated to effect.283 The following for-
mula may be useful to calculate an epinephrine CRI: 0.6
 body weight in kilograms 5 the number of milligrams
of epinephrine added to a total volume of 100 mL 0.9%
NaCl. When this preparation is delivered at 1.0 mL/h IV,
0.1 mg/kg/min is administered. The CRI solution should
be protected from light.284 The dosage of vasopressin for
18 Plunkett and McMichael
infusion is 0.01–0.04 U/min IV as a CRI titrated to
effect.286,287
Norepinephrine is a potent vasoconstrictor and ino-
tropic agent with mixed a- and b-adrenergic receptor
action that may be indicated in the patient who remains
hypotensive despite adequate volume replacement and
treatment with other, less potent, inotropes such as
dopamine.1,288,289 Cardiac contractility, cardiac oxygen
demand, heart rate, and stroke volume increase after the
administration of norepinephrine.1,284 Renal, splanch-
nic, and pulmonary vasoconstriction also occurs.1,290,291
Norepinephrine is available in 2 forms. Norepinephrine,
1 mg, is equivalent to 2 mg of norepinephrine bitartate.
Norepinephrine, 4 mg, or 8 mg of norepinephrine bitar-
tate, should be diluted in 250 mL of 5% dextrose in water
or 5% dextrose in normal saline before administration.
The dosage of norepinephrine is 0.5–1.0 mg/kg/min IV as
a CRI, titrated to effect.1,284
Neurologic dysfunction occurs commonly after
CPCR. Often, the clinical abnormalities resolve over
24–48 hours. The patient should be allowed a minimum
of 48 hours before a prognosis is made regarding neuro-
logic abnormalities.73,84,292,293 To avoid increasing the
brain’s oxygen requirements, hyperthermia should be
avoided and antiepileptic treatment should be adminis-
tered to a patient with seizures. Situations that cause
increased intracranial pressure such as sneezing caused
by nasal oxygen cannulas and neck wraps for jugular
catheters or esophagostomy tubes should be avoided.
Glucocorticoid administration is contraindicated in these
patients and may worsen neurologic injury secondary to
ischemia by causing hyperglycemia.248,294 Nutritional
support should be instituted as soon as possible depend-
ing on the patient’s mentation after resuscitation,
original disease process, and underlying clinical status.
If oral enteral nutritional support is not possible, place-
ment of a feeding tube or parenteral nutritional support
should be considered.
Studies in humans identified 4 clinical signs that corre-
late with poor neurologic outcome when observed
24 hours after resuscitation: absent corneal reflex, absent
pupillary response, absent withdrawal response to pain,
and absent motor response.73,292
Common complications that can be seen after
CPCR include cerebral edema, hypoxemia, reperfusion
injury, abnormal hemostasis, acute renal failure, sepsis,
multiple organ dysfunction syndrome, and recurrent
CPA. In addition, treatment is needed to address the un-
derlying disease process that resulted in the initial
CPA.264,265,278,280,295–297
Conclusion
The goal of resuscitation is survival to hospital dis-
charge, and hopefully continued quality of life after
discharge. Many of the experimental studies of CPCR
have been conducted on dogs, providing useful informa-
tion for veterinarians. The new AHA guidelines for
humans have many applications to small animal veteri-
nary medicine. These new guidelines should be instituted
in the protocol for CPCR of dogs and cats where practi-
cal and applicable. The new recommendations for
humans that are applicable to veterinary patients include
the administration of chest compressions continually
throughout CPCR, keeping interruptions as brief and
few as possible, avoiding excessive ventilatory rates,
application of 1 defibrillation shock, followed immediate-
ly by chest compressions rather than 3 successive shocks,
the utilization of amiodarone in preference to lidocaine
for the treatment of refractory ventricular tachycardia or
fibrillation after defibrillation, and allowance of mild per-
missive hypothermia in the postarrest period.
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