Journal of Veterinary Emergency and Critical Care 22(2) 2012, pp 148–159

Clinical Practice Review doi: 10.1111/j.1476-4431.2012.00720.x

Updates in the American Heart Association

guidelines for cardiopulmonary resuscitation
and potential applications to veterinary
patients
Barbara L. Maton, DVM and Sean D. Smarick, VMD, DACVECC

Abstract

Objective – To review the updates in the American Heart Association (AHA) guidelines for cardiopulmonary
resuscitation (CPR) and identify potential applications to veterinary patients.
Etiology – Cardiopulmonary arrest is common in veterinary emergency and critical care, and consensus guide-
lines are lacking. Human resuscitation guidelines are continually evolving as new clinical and experimental
studies support updated recommendations. Synthesis of human, experimental animal model, and veterinary
literature support the potential for updates and advancement in veterinary CPR practices.
Therapy – This review serves to highlight updates in the AHA guidelines for CPR and evaluate their application
to small animal veterinary patients. Interventions identified will be evaluated for trans-species potential, raise
questions regarding best resuscitation recommendations, and offer opportunities for further research to continue
to advance veterinary CPR.
Prognosis – The prognosis for any patient undergoing cardiopulmonary arrest remains guarded.

(J Vet Emerg Crit Care 2012; 22(2): 148–159) doi: 10.1111/j.1476-4431.2012.00720.x

Keywords: consensus, cardiopulmonary resuscitation, emergency techniques, monitoring

ILCOR International Liason Committee on Resus-

Abbreviations citation (ILCOR)
ABC airway; breathing; compression IAHF InterAmerican Heart Foundation
AHA Americal Heart Association MAP mean arterial pressure
AED automated external defibrillators NDS neurological deficit scores
ANZCOR Australian and New Zealand Council on OPC overall performance categories
Resuscitation PETCO2 partial pressure of end-tidal CO2
CAB compression, airway, breathing PEA pulseless electrical activity
CPA cardiopulmonary arrest PaCO2 partial pressure of arterial CO2
CPP coronary perfusion pressure RCA Resuscitation Council of Asia
DAP diastolic arterial pressure RCSA Resuscitation Council of Southern Africa
ERC European Resuscitation Council ROSC return of spontaneous circulation
HSFC Heart and Stroke Foundations of Canada SCVO2 central venous oxygen saturation
ITD impedance threshold device SpO2 oxygen saturation
Sv̄O2 mixed venous oxygen saturation
SAP systolic arterial pressure

From AVETS, Monroeville, PA, 15146.

The authors declare no conflict of interests. Introduction

Address correspondence and reprint requests to
Dr. Barbara L. Maton, AVETS, 4224 Northern Pike, Monroeville, PA, 15146, The release of the 2010 American Heart Association
USA. (AHA) guidelines1 for cardiopulmonary resuscitation
Email: barb@maton.org
Submitted September 15, 2011; Accepted January 28, 2012.
(CPR) and emergency cardiovascular care coincided
with the 50th anniversary of the modern practice of

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human CPR. In 1992, the International Liaison Commit-
tee on Resuscitation (ILCOR) was formed to develop
consensus recommendations for human CPR. ILCOR is
a committee of 8 organizations including the AHA, Eu-
ropean Resuscitation Council (ERC), Heart and Stroke
Foundation of Canada (HSFC), Resuscitation Council of
Asia (RCA), Resuscitation Council of Southern Africa
(RCSA), the Australia and New Zealand Council on
Resuscitation (ANZCOR), and the InterAmerican Heart
Foundation (IAHF). This committee meets twice yearly
and serves to provide a mechanism for review of research
to help develop and disseminate consensus guidelines
for human CPR, as well as foster research in areas of
CPR where evidence may be lacking.1 ILCOR, in collab-
oration with AHA, has published updated CPR guide-
lines every 5 years since 2000.2–4 The 2010 AHA CPR
Guidelines are qualified by class of recommendation (I,
IIa, IIb, III based on risk-benefit ratio) and levels of evi-
dence (A, B, or C based on type of research, populations
analyzed, and the number of cases).1 This mechanism
for the development of human recommendations helps
to organize the effort to deliver recommendations that
are evidence-driven, peer-reviewed, and continuously
advancing.
In comparison, veterinary CPR recommendations
have been limited to review articles, retrospective
studies, and cross-sectional studies published in peer-
reviewed veterinary journals.5–21 These recommenda-
tions have often been extrapolated from the recommen-
dations for people, and despite being well referenced,
they do not have the benefit of consensus agreement as
is done when generating human guidelines. For veteri-
nary CPR, the next logical step is to emulate the pro-
cess of the development of CPR guidelines for people
and develop consensus guidelines for use in veterinary
patients.22
One of the challenges for the development of such
guidelines involves determining the appropriateness of
applying experimental models and human prospective
studies to clinical veterinary patients. Many experimen-
tal models of induced CPA (cardiopulmonary arrest)
utilize rodent or swine models, with questionable trans-
lation to canine and feline patients.23–26 Canine models
have been used to study resuscitation medicine since
the early 1900s.27, 28 When considering guidelines for use
in dogs, recommendations derived from these studies
may be stronger than those derived from human stud-
ies; however, subjects are often young healthy animals,
under anesthesia, with induced mechanisms of CPA dis-
similar to clinical patients. In considering these studies,
the model utilized, timing of interventions, type of inter-
ventions, and study endpoints must be critically evalu-
ated prior to drawing parallels with clinical veterinary
patients.

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Updates in AHA guidelines for CPR and veterinary applications
In evaluating laboratory animal models of CPA, in-
cluding dogs, pig, sheep, and rats, it is important to
consider the model animal’s anatomy, potential recep-
tor variations, and normal vital signs. Despite most lab-
oratory animals having a laterally compressed thorax,
many experimental CPR models are performed deliver-
ing compressions in a ventrodorsal manner, contrary to
how canine and feline CPR is often performed in clinical
practice.5, 9, 29 In people, adenosine is recommended to
treat regular monomorphic tachyarrhythmias,30 and has
been studied in swine models of arrest.31 However, there
is some information to suggest a different adenosine re-
ceptor subtype in canine hearts (eg, dogs have predom-
inantly A2 receptor subtypes in the myocardium rather
than A1 ), which may limit the utility of adenosine for ar-
rhythmias in dogs.32 Canine models have been utilized
to study therapeutic hypothermia; however, the target
temperatures are more often determined relative to nor-
mal human body temperature, rather than taking into ac-
count normal canine temperature (ie, 1–2◦ C [1.8–3.6◦ F])
higher than people). Therapeutic hypothermia models
and temperature recommendations must therefore be in-
terpreted with caution.33, 34 Differences in anatomy, the
model species, and study design must be carefully eval-
uated in making correlations to small animal veterinary
patients.
The method of induction of CPA and timing of inter-
ventions are experimental considerations that may not
translate to veterinary patients. Many of the experimen-
tal animal models method of CPA induction do not mir-
ror clinical veterinary patients. For example, induced
ventricular fibrillation35–37 is often utilized as a model
of CPA. While this is the most common arrest rhythm
in people,38 this is not the most common arrest rhythm
for veterinary patients.7, 11 Models that utilize asphyxial
arrest23, 24 have some applicability to veterinary patients
that experience upper airway obstruction, however, this
population may be small in the clinical setting, and the
true incidence of airway obstruction in veterinary pa-
tients remains unknown.11, 14 Timing of interventions in
experimental models may be geared toward what is ex-
perienced in human CPA, with availability of prearrest
care and the paradigm of basic versus advanced life
support. For example, models may be designed with
an interval following induced CPA of no intervention
(ie, out-of-hospital CPA), followed by a period of ba-
sic life support (BLS, ie, bystander rescue), followed by
advanced life support (ALS, ie, paramedic support). Peo-
ple may receive more advanced therapy in the form of
fluid resuscitation, ventilation, drug administration, and
therapeutic hypothermia in transit to the hospital.29, 38 In
contrast, most veterinary patients with out-of-hospital
arrest receive minimal if any life support prior to ar-
rival at a veterinary facility. In people, the provision of
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B.L. Maton & S.D. Smarick
compressions and breathing (eg, mouth-to-mouth or
bag-mask ventilation) is considered BLS, and the place-
ment of an advanced airway and drug delivery consti-
tutes ALS. In contrast, veterinary CPR generally takes
place in a hospital setting and an advanced airway is
obtained at the recognition of the CPA with drugs avail-
able shortly thereafter. Some studies evaluate an inter-
vention prior to the induction of CPA,40, 41 which should
also be taken into account when attempting to apply the
intervention to veterinary patients. Despite deviations
of these models from CPA scenarios in clinical patients,
when canine and feline experimental animal models are
utilized, the animal model should be considered as the
species of interest.
Another important aspect to consider is the end-
point of experimental animal and human CPR stud-
ies. Endpoints utilized may include time to return of
spontaneous circulation (ROSC), short-term survival (ie,
12–96 hours), long-term survival (ie, 30-day survival),
or survival to hospital discharge. Beyond survival, at-
tempts to measure quality of life with neurologic deficit
scores (NDS), overall performance categories (OPC), and
whether human survivors function independently ver-
sus as permanent dependents are now often applied.
This focus on improved neurologic outcomes and ex-
tension of BLS to ALS with postarrest care was the ba-
sis of Peter Safar, MD, proposing and advocating the
term cardiopulmonary cerebral resuscitation (CPCR) since
the 1960s.28, 42 This term can still be found in the litera-
ture; however, the AHA 2010 Guidelines and current hu-
man literature predominantly use the term CPR which
includes the goal of an intact neurological patient.10, 43
As the recommendations in human medicine are re-
evaluated, further research in experimental animal mod-
els and clinical studies may offer benefit to our clinical
small animal patients. However, the results of such stud-
ies and the recommendations gleaned from them must
be critically evaluated prior to accepting them as the
standard of care.
Changes in the AHA Guidelines for CPR and poten-
tial application to veterinary patients
Assessment and Recognition of CPA
The first step in CPR is recognition of an arrested state in
the patient. Traditionally, this has been accomplished by
a “look, listen, and feel” approach, in which we recog-
nize an unresponsive patient that is not breathing, listen
for a heartbeat, and palpate for pulses.5, 44 The 2010 AHA
Guidelines advocate abandoning this approach and pur-
suing compressions in patients that are unresponsive,
apneic, or patients that are gasping.45 In people, the
presence of gasping (recognized in veterinary patients as
agonal5 or terminal breathing) often confuses the rescuer.
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Palpation for pulses can be challenging and unreliable,
even for trained healthcare providers.39, 46 Palpation for
pulses often leads to delays in initiation of CPR. In in-
stances where the healthcare provider performs a pulse
check, AHA recommends the assessment be kept under
10 seconds.39 In a study evaluating bystander CPR initi-
ated in 247 human patients that were not in CPA, the risk
of rib fracture was found to be 2%, with no documented
visceral organ injuries, whereas only 12% of patients ex-
perienced discomfort from the intervention.47 Therefore,
with a suggested low-risk of adverse effects from CPR
administered to patients not in arrest, and given the ben-
efit of early institution of CPR in arrested patients,11, 39, 48
it is recommended to defer palpation of pulses in the pa-
tient with signs of CPA, and when pursued, to limit the
time invested to less than 10 seconds. This recommenda-
tion may be considered in veterinary patients; however,
the complication rate of CPR in veterinary patients that
are not in a state of arrest is unknown.
Initiation: ABC versus CAB
In the AHA 2010 human recommendations, the tra-
ditional order of CPR initiation of airway, breathing,
compressions (ABC) has now formally been updated to
recommend initiation of CPR with compressions for out-
of-hospital sudden cardiac arrest, followed by airway
and breathing (CAB), and abandoning the administra-
tion of 2 rescue breaths for the immediate initiation
of chest compressions.39 Perfusion during cardiac ar-
rest is dependent on effective chest compressions; there-
fore it is advised to avoid any delays in the deliv-
ery of chest compressions.36, 39 In the early phases of
cardiac arrest, oxygen delivery is flow dependent.39, 49
Multiple studies in humans have found no change in
outcome for patients with out-of-hospital arrest treated
with compression-only CPR compared to traditional
CPR with compressions and ventilation.50–53 One study
identified improved neurologic outcome (30 days postar-
rest) for patients treated with compression-only CPR,
even when the cause of arrest was apnea.54 In a study
of human in-hospital arrests, shorter time to advanced
airway placement was not associated with improved
ROSC, although these patients received bag-valve-mask
ventilation during initial CPR.55 One limitation of these
studies is that in bystander-administered CPR in out-of-
hospital arrests, the efficacy of chest compressions can-
not be standardized for comparison. One of the goals
in investigating this alternative rescue method was to
improve bystander compliance in administering CPR,
given many lay people have hesitation in performing
“mouth-to-mouth” resuscitation.
There are several thoughts as to why out-of-hospital
arrest patients may have similar or improved outcomes

when patients are only provided compressions. In a wit-
nessed cardiac arrest, during the first few minutes, oxy-
genated blood remains in the system despite cessation
of flow. In a canine model of induced ventricular fib-
rillation with compression-only resuscitation adminis-
tered within 1 minute of arrest, (with room air ventila-
tion prior to induction of ventricular fibrillation), dogs
maintained arterial oxygen saturation (SpO2 ) of 93.9 ±
3% for 4 minutes and the partial pressure of arterial CO2
pressure (PaCO2 ) did not rise above 35 mm Hg until af-
ter 8 minutes.56 Additionally, gasping or agonal breaths
are common, and may provide some ventilation.57, 58 In
a swine model of induced ventricular fibrillation, pre-
cordial compressions with gasping (and no mechanical
ventilation) produced minute volumes of 3 L, compared
to the mechanically ventilated group that had minute
volumes of 1 L. In this study, there was no significant
difference in PaCO2 for the first 2 minutes (maintained
under 40 mm Hg) between the groups, however, after 8
minutes, the positive pressure ventilation group had an
average PaCO2 of 28 mm Hg compared to 48 mm Hg in
the non-mechanically ventilated group.58 In the study by
Bobrow et al57 evaluating out-of-hospital arrest in peo-
ple, gasping was found to occur in 39% of arrests and
was associated with significantly higher survival to dis-
charge (39%) compared to those who did not gasp (9%).57
Passive recoil during chest compressions may also pro-
vide ventilation.56 Another argument is that during ar-
rested states, there are lower ventilatory needs to remove
CO2 given the reduced cardiac output (CO) and venous
return (only 10–15% of normal values) of the arrested
state.39, 56
In human bystander CPR, there is often a delay or
reluctance in initiation of CPR because of hesitation to
perform “mouth-to-mouth” ventilation due to a concern
for infectious diseases. For all of these reasons, AHA
no longer recommends 2 rescue breaths in initiation of
CPR, and chest compressions are advocated first, min-
imizing the delay of first compression. In lone-rescuer
untrained bystander CPR, “hands-only” CPR is recom-
mended until further help is available. In trained res-
cuer and healthcare provider CPR, compression: venti-
lation ratios of 30:2 are recommended, initiating with
compressions.39 Even in pediatric and infant arrests,
where ventricular fibrillation is less common and as-
phyxia is the predominant cause of arrest, AHA recom-
mends initiating with compressions; however bystander
integration of compressions with ventilations in a 30:2
ratio is recommended.59
There are several considerations in the application of
the CAB sequence recommendation for veterinary pa-
tients. These recommendations have been developed for
human patients with sudden-onset, witnessed out-of-
hospital cardiac arrest, which is most commonly associ-

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Updates in AHA guidelines for CPR and veterinary applications
ated with ventricular fibrillation and cessation of blood
flow. This has also been developed to simplify layperson
CPR and reduce the delay to first compression deliv-
ery. Conversely, PEA (pulseless electrical activity) and
asystole are more common arrest rhythms in veterinary
patients, and underlying respiratory pathology are com-
mon causes of arrest in veterinary patients.11, 18, 60 In a
swine model of ventricular fibrillation arrest in the pres-
ence of an obstructed airway, compression-only CPR was
inadequate to maintain arterial oxygen saturation, and
within 1.5–2 minutes of compression only CPR, there
was no arteriovenous difference in oxygen saturations.25
Although many critically ill veterinary patients have a
witnessed arrest, there are many veterinary patients that
present with out-of-hospital arrest that have been in an
arrested state for a prolonged period, at which point ven-
tilation is also integral to CPR. In veterinary medicine, at
the time of initiation of CPR, we often have more than 1
person available to assist in the resuscitation, and we less
frequently encounter the “lone-rescuer, layperson” effort
that commonly occurs in human out-of-hospital arrests.
In many of the lab animal models and human observa-
tional studies, the model involves cessation of compres-
sions to deliver ventilations to mimic the lone-rescuer
BLS administration.37, 52, 54 In contrast, for veterinary pa-
tients a resuscitation team pursuing compressions does
not necessarily do so at the exclusion of obtaining an
airway and starting positive pressure ventilation.
In the veterinary setting, while it is recognized that
veterinary patients commonly arrest from respiratory
causes (eg, pulmonary disease, pleural space disease,
airway obstruction), there is a population of patients
that arrest with normal respiratory function. In these pa-
tients, the CAB approach can be considered. Similar to
human patients, veterinary patients with agonal breath-
ing may be delayed in administration of CPR as they
still appear to have breathing, and an airway may not
be obtained due to jaw tone. From the moment agonal
breathing is recognized, chest compressions may be ad-
ministered until the airway may be instrumented. In the
instance of a cardiovascular arrest and a lone veterinary
rescuer, hands-only CPR may be considered.
Agonal breathing or gasping has gained attention in
the human literature as studies have shown this to be an
effective form of ventilation and self-resuscitation, and
associated with improved CPR outcomes.61, 62 Agonal
breathing is a preterminal form of respiration charac-
terized by an acute deep inspiration that results from
decreased oxygen delivery to the pneumotaxic and ap-
neustic breathing centers in the pons leading to stim-
ulation of respiratory pacemaker-like neurons in the
medulla.26, 63, 64 Laboratory studies in pigs and rats have
demonstrated that agonal breaths lead to significantly
increased CO and ventilation, and increases in CO of
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B.L. Maton & S.D. Smarick

up to 60% of baseline prefibrillation measurements are Breathing

obtained during agonal inspiration.65, 66 Experimental
In lone-rescuer trained bystander CPR, the recommen-
and observational studies have also shown that the pres-
dation is to begin with compressions in a 30:2 ratio
ence and frequency of gasping is correlated with im-
of compressions:ventilation. The AHA 2010 Guidelines
proved outcome in CPR.26, 62 Further prospective studies
continue to emphasize the importance of avoiding hy-
would be necessary to determine if there is an association
perventilation, with the recommendation of ventilation
with gasping and outcome in clinical veterinary patients
delivery of 8–10 breaths per minute (one breath every 6–8
with CPA. Based on available data, one may consider a
seconds).30 The recommendations for ventilation deliv-
rapid CAB approach in patients with agonal breathing.
ery are unchanged. The AHA 2010 guidelines still rec-
The ABC approach would still be recommended in
ommend the delivery of a breath over 1 second, with
patients with a respiratory cause of arrest or patients
a 1:1 I:E ratio and a tidal volume sufficient to result in
with hypoxemia as a contributing cause of arrest.67 These
a visible chest rise.29 The rescuer does not need to syn-
patients may have reversible pathology and CPR may
chronize breaths with compressions, and compressions
be more effective with efforts to reverse the underlying
should not be paused for ventilation.30, 70 The delivery of
cause of the arrest. Also, patients with prolonged CPA
100% oxygen during CPR until ROSC is obtained is still
prior to arrival to the hospital may benefit from the ABC
recommended.29
approach as they are less likely to have oxygenated blood
Impedance threshold devices (ITDs) have been found
in the circulatory system and more likely to have a sig-
to improve short-term outcomes in people (eg, survival
nificant component of respiratory acidosis which may
to hospital admit, short-term survival), but thus far have
affect vasopressor function.
not proven effect on long-term outcome measures (eg,
These updated recommendations in the initiation of
neurologic outcome, long-term survival).71 ITDs have
CPR in human patients may have some translation to
been evaluated in dogs with isoflurane-induced hy-
veterinary patients, and raise many questions regard-
potension, and were found to improve SAP (systolic
ing the application of a CAB approach in veterinary
arterial pressure) and cardiac index, however this study
CPR.
found no significant improvement in DAP (diastolic arte-
rial pressure) and MAP (mean arterial pressure).72 ITDs
Airway have also been evaluated in canine hemorrhagic shock
models, and found to increase SAP, MAP, and CO, with-
The AHA 2010 guidelines now recommend utilizing
out increasing DAP.73 Increased DAP is of importance
the partial pressure of end-tidal CO2 (PETCO2 ) to con-
as it is correlated to coronary perfusion pressure and
firm and monitor endotracheal tube positioning in early
ROSC.30 In both models, ITDs were found to decrease
CPA.30 Human endotracheal intubation is challenging,
pulmonary compliance.72, 73 The use of ITD in veteri-
particularly for inexperienced rescuers, and is associ-
nary patients with CPA requires further investigation.
ated with complications including trauma, tube dis-
Due to known potential adverse effects, they should not
placement, and obstruction.30 In contrast, the majority of
be used in patients with pulmonary disease, congestive
veterinary patients can be readily intubated using an en-
heart failure, small patients <10 kg, or patients with a
dotracheal tube, and the variation in veterinary patients’
compromised chest wall.72, 74
muzzle anatomy may make the application of many of
the human options such as the bag valve mask more
limited.
Circulation
The use of PETCO2 may still be helpful in veterinary
patients to help confirm an initial difficult intubation, The 2010 AHA Guidelines offer several updates in rec-
as well as assessing maintenance of proper endotracheal ommendations in the delivery of chest compressions,
tube positioning. In a canine model of induced ventricu- including increased frequency of compressions and in-
lar fibrillation, a median PETCO2 of 20 mm Hg was associ- creased depth of compressions. Previously, the 2005
ated with tracheal intubation, while a median PETCO2 of AHA Guidelines had recommended the delivery of
3 mm Hg was associated with esophageal intubation.68 about 100 compressions per minute, with a compression
Another study found consistent PETCO2 readings of 0 depth of 3.81–5 cm (1.5–2 inches), and at least 1/3 the
mm Hg from the esophagus and the stomach in sedated anterior-posterior chest dimension in children.3, 59 The
and anesthetized dogs.69 It is important to recognize 2010 AHA Guidelines recommend delivery of at least
that PETCO2 is not reliable in patients with prolonged ar- 100 compressions per minute and a compression depth
rest, massive pulmonary thromboembolism, severe pul- of at least 5 cm (2 inches).39 A duty cycle (ie, time spent in
monary edema, or colorimetric detector contamination compression to relaxation) of 50% is still recommended,
with secretions.30 as well as allowing full thoracic wall recoil.39 It is also

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recommended to rotate the compressor every 2 minutes,
especially with higher compression rates as fatigue de-
creases efficacy of compressions, and may occur sooner
with increased compression frequency.75 In human CPR,
rescuer fatigue occurs within 1 minute however may not
be recognized until as late as 5 minutes.39, 76, 77
The concept of “push hard, push fast” was empha-
sized with the updated recommendation of at least
100 compressions per minute in the 2010 AHA recom-
mendations. Several human studies have shown im-
proved ROSC and survival with higher compressions
per minute.39, 78, 79 Compression rate is differentiated
from compressions per minute (which is affected by com-
pression rate and frequency and duration of pauses). In a
30-minute manual CPR model of dogs in ventricular fib-
rillation, compressions delivered at 120/minute led to
successful defibrillation in 12/13 dogs while compres-
sions delivered at 60/minute led to successful defibril-
lation in only 2/13 dogs.80 To the authors’ knowledge,
there are no recent prospective studies of compression
rate in dogs and cats, and further information is needed
in guiding the recommendations in dogs and cats. In peo-
ple, greater than 120 compressions/minute is considered
high frequency compressions, and there is insufficient
evidence to recommend this for human patients.71 One
must take into account the wide variations in individual
veterinary patients’ normal heart rates, and incorporate
this into the CPR strategy. While further research is nec-
essary to determine specific recommendations for com-
pression rates in veterinary patients, faster rates may be
considered.
Due to anatomical differences in chest wall configu-
ration, it is unknown if the recommendation of a com-
pression depth of 2 inches is appropriate or adequate for
dogs and cats. However, CO was found to be linearly
correlated with chest compression depth in dogs, and
for depths of 2.5 cm and greater, modest increases in
compression depth lead to relatively larger increases in
CO.29 This study found wide variations in CO related to
dog size when compression depth was used as a target,
and suggested that the use of esophageal pressure mea-
surements (with a target of 50 mm Hg) may be a more
reliable indicator of the compression depth required for
effective generation of CO. This study must be inter-
preted with caution as the compression model involved
sternal ventral-dorsal chest compression delivery.29 Cur-
rent veterinary recommendations are to compress 30%
of the chest wall diameter,5 and while there is not
enough information to recommend deeper compres-
sion, the authors emphasize attention to compression
depth in performing effective CPR. Ideal compression
depths in small animal veterinary patients still need to be
determined.

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Updates in AHA guidelines for CPR and veterinary applications
Another emphasis in the delivery of chest compres-
sions is allowing full thoracic wall recoil.39 Incomplete
thoracic recoil leads to increased intrathoracic pressure,
increased right atrial pressure, decreased coronary per-
fusion pressure, decreased cardiac index, and decreased
cerebral perfusion pressure.81, 82 It is common to lean
during CPR, especially when one becomes fatigued, and
this may not be recognized by the compressor. In a study
evaluating pediatric arrests, leaning was found to occur
in 89% of the compressions delivered.83 In people, real-
time automated feedback devices may be utilized to de-
crease the frequency of leaning, however have not been
found to completely eliminate leaning.83 Manikin stud-
ies suggest that allowing the heel of the hand to come
slightly off the chest helps to improve thoracic recoil.84
It is likely that this concept also applies to veterinary
patients.
Perfusion is dependent on effective chest compres-
sions during CPR, yet it is common for pauses to oc-
cur during CPR for instrumentation, defibrillation, ro-
tation of compressor, and assessment for ROSC. Chest
compression fraction, defined as “the proportion of time
spent delivering chest compressions” was determined to
be an independent predictor of survival in humans with
ventricular fibrillation, with higher compression frac-
tions significantly associated with increased survival.79
It is recommended to try to completely minimize any
pauses in chest compressions, and when necessary, to
keep the pause to under 10 seconds and synchronize the
pause with other adjustments that may require a pause
(ie, compressor rotation with defibrillation)39 A human
observational study of defibrillation success (in both in
and out-of-hospital arrests) found that longer preshock
pauses (time from last compression to shock delivery)
were independently and significantly associated with
defibrillation failure.85 Similarly, a swine model of in-
duced ventricular fibrillation demonstrated improved
success of defibrillation when preshock pauses were
minimized to 3 seconds, and found significantly re-
duced ROSC and increased myocardial dysfunction
when preshock pauses were 15 seconds or longer.86
These considerations likely have application to veteri-
nary patients however require further study in canine
and feline populations.
Drugs
Atropine is no longer recommended for routine use
for PEA or asystole in human CPR according to the
2010 AHA Guidelines.30 In people, atropine use in
PEA was associated with significantly decreased 30-
day survival.87 However, atropine is still recognized as
the treatment of choice for symptomatic bradycardia in
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B.L. Maton & S.D. Smarick
people.30 Similarly, in a canine model of PEA arrest in-
duced by asphyxia, atropine (0.04, 0.1, 0.2, and 0.4 mg/kg
IV) and epinephrine did not improve ROSC over dogs
that received epinephrine alone, and higher doses of at-
ropine were associated with decreased ROSC.88 Many
veterinary practitioners may not have ready access to an
ECG monitor43 , and given a relatively high incidence of
bradycardia associated with high vagal tone in veteri-
nary arrest patients (23% of dogs and 21% of cats in a
prospective study)11 , routine use of atropine in the ab-
sence of an ECG may still be considered. However, due
to the variety of potential arrest rhythms and differences
in their respective treatments, therapy should be guided
by the use of an ECG. The efficacy of atropine in arrest
rhythms other than severe sinus bradycardia in clinical
patients requires further investigation.
Stable paroxysmal supraventricular tachycardia and
now monomorphic wide complex supraventricular
tachycardia are initially managed with vagal maneuvers
and adenosine in people.30 However, adenosine is not
commonly used in dogs and cats, and there is some evi-
dence to suggest that dogs do not have the same cardiac
adenosine receptors as humans.32 The use of adenosine
in dogs requires further experimental and clinical explo-
ration.
Fibrillation Treatment
The 2010 AHA Guidelines now recommend the use of a
biphasic defibrillator, and a monophasic defibrillator can
be used if a biphasic defibrillator is not available.38 Clin-
ical trials in people have found biphasic defibrillators
to have higher success rates in defibrillation compared
to monophasic defibrillators.89, 90 The lower energy of
biphasic and other multiphasic defibrillators may induce
less postshock myocardial dysfunction.38 Biphasic defib-
rillators are used in almost all of the automated external
defibrillators (AEDs) and manual defibrillators now be-
ing manufactured.38
In a canine model of ventricular fibrillation, bipha-
sic defibrillation was associated with less injury to
the myocardium as assessed by the affect on my-
ocardial oxidative metabolism compared to monopha-
sic defibrillation.91 In a study of biphasic compared
to monophasic defibrillation in toy-breed dogs with
induced ventricular fibrillation, biphasic defibrillation
was found to require 30% less energy than monopha-
sic defibrillation, with less myocardial injury (as as-
sessed by cardiac biomarkers, ECG changes, and left
ventricular cardiac performance).92 Dogs that were
defibrillated with monophasic waveform defibrillators
developed increases in cardiac biomarker concentration
for 5 days (the increase in marker concentration was
154 
C Veterinary Emergency and Critical Care Society 2012, doi: 10.1111/j.1476-4431.2012.00720.x
also statistically higher than the biphasic group), pre-
mature ventricular contractions and ventricular arrhyth-
mias, and decreased left ventricular shortening fraction
compared to the biphasic group, in which biomarkers
returned to normal within 2 days, no malignant ECG
changes were noted, and shortening fraction was sig-
nificantly less affected. The authors concluded that a
biphasic defibrillator shock energy of 2–4 J/kg is ac-
ceptable for toy-breed dogs.92 Biphasic defibrillation has
been used in the clinical setting with success for defib-
rillation in a dog with refractory ventricular fibrillation
after a pacemaker implantation.93 The dog was admin-
istered CPR with 4 escalating monophasic shocks (up
to 9.9 J/kg) that were unsuccessful in conversion, 12
minutes after the onset of ventricular fibrillation, a sin-
gle biphasic shock (9.9 J/kg) was able to convert the
dog and the dog survived to discharge with no adverse
effects.93
Because biphasic defibrillators use one of several dif-
ferent waveforms, as well as fixed or escalating energy
levels, no standardized recommendation for shock en-
ergy dose is given, and it is advised to use the defib-
rillator manufacturer’s recommendations.38 Subsequent
shocks should be delivered at the same energy level
and higher energy levels may also be considered.38 The
recommendations available for veterinary patients is
to administer 2–5 J/kg up to 10 J/kg for monophasic
defibrillation,5 and as discussed previously, for biphasic
defibrillation, 2–4 J/kg may be considered but higher
dosages acceptable.92, 93 Biphasic defibrillation has been
used clinically in dogs however considerations remain
for standardization of shock doses.
It should be emphasized that electrical defibrillation
is the only proven effective treatment for ventricular
fibrillation.5, 7, 30 In people, amiodarone is considered for
ventricular fibrillation refractory to defibrillation, CPR,
and vasopressors; and this is unchanged from the 2005
AHA Guidelines.3, 30
Gauging Response
The 2010 AHA Guidelines now recommend the use of
PETCO2 for monitoring CPR efficacy. In people, it is rec-
ommended that a PETCO2 of <10 mm Hg should prompt
adjustment in techniques to try to further enhance CPR
delivery, while a normal PETCO2 of 35–40 mm Hg may
indicate ROSC.30 It is important to recognize that PETCO2
is not a reliable indicator of ROSC in asphyxial arrests.94
In a cross-sectional study of dogs and cats that under-
went CPA and had PETCO2 monitoring, 94% of dogs
with a PETCO2 of <15 mm Hg were NOT successfully
resuscitated, while 86% of dogs with a PETCO2 of ≥15
mm Hg were successfully resuscitated.11 In the same
study, 90% of cats with a PETCO2 ≥20 mm Hg were

successfully resuscitated. Therefore, PETCO2 is suggested
to be of benefit in monitoring the efficacy of CPR in
veterinary patients and should be considered. Coro-
nary perfusion pressure (CPP) monitoring has previ-
ously been recommended to guide CPR, and a value of
≥15 mm Hg is believed to correlate with ROSC.3 CPP is
equivalent to aortic diastolic pressure minus right atrial
diastolic pressure, and may be determined using arterial
and central venous catheters. The 2010 updated AHA
guidelines discuss the use of arterial diastolic pressure
as a surrogate for CPP determination, and while there
is no specific target known for arterial diastolic pres-
sure, a pressure <20 mm Hg should prompt efforts to
improve CPR.30 Also, continuous monitoring of arterial
pulse pressure can detect ROSC if the pulse wave and
rhythm check are in agreement. This monitoring may be
of benefit in veterinary ICU and anesthesia patients that
already have arterial catheters in place prior to a CPA
event, although similar to people, the arterial diastolic
pressure target remains to be determined.
The use of central venous oxygen saturation (ScvO2 )
is now recommended to help monitor the efficacy of
CPR, and the 2010 AHA Guidelines recommend im-
proving CPR if ScvO2 is <30% (reference intervals in
people range from 60–80%).30 In a canine model of open-
chest CPR, Sv̄O2 was found to not be a reliable indica-
tor of Sv̄O2 (mixed venous oxygen saturation), therefore
not an acceptable surrogate measurement.95 ScvO2 mea-
surement requires a central venous catheter, and either
a central venous oximetric tipped catheter or cooxime-
ter. This may be of value in critically ill patients that
arrest with a central venous catheter in place, and fur-
ther study would be necessary to develop specific target
recommendations.
Postarrest Care
The 2010 AHA Guidelines recommend maintaining nor-
motension, and while the ideal target blood pressure
is unknown, suggest maintaining a mean arterial pres-
sure ≥ 65 mm Hg and systolic pressures ≥ 90 mm
Hg.96 The ideal target postresuscitation blood pressure
for veterinary patients is unknown. The AHA Guide-
lines also recommend early titration of oxygen delivery
to the minimum supplementation necessary to maintain
arterial saturation of ≥ 94% to avoid oxygen toxicity.96
A study of dogs with induced CPA and 9 minutes of
resuscitation with hyperoxic (Fi O2 = 1.0), hyperoxic
(Fi O2 = 1.0) and antioxidant, and normoxic (Fi O2 =
0.21) treatment revealed the hyperoxic dogs to have
significantly more neurologic impairment at 12 and 24
hours postresuscitation compared to normoxic dogs; this
was attenuated by antioxidant treatment.40 This sug-
gests a link between hyperoxic treatment and neuro-

C Veterinary Emergency and Critical Care Society 2012, doi: 10.1111/j.1476-4431.2012.00720.x
Updates in AHA guidelines for CPR and veterinary applications
logic oxidant damage.40 Further research in veterinary
patients is necessary to develop formal recommenda-
tions for Fi O2 during CPR. Moderate glycemic control
(8–10 mmol/L [144–180 mg/dL]) with the avoidance of
hypoglycemia is recommended in the management of
human postarrest patients.96 The recommendation for
blood glucose target in the postarrest veterinary patient
is unknown; however, as with any critical patient, ideally
hypoglycemia and profound hyperglycemia should be
avoided.
The 2010 AHA Guidelines formally recommend ther-
apeutic hypothermia (32–34◦ C, [89.6–93.2◦ F]) be insti-
tuted for 12–24 hours for any patient that is comatose
after an out-of-hospital ventricular fibrillation arrest,
and recommend it be considered for any other rhythm
including PEA and asystole.96 Also, active rewarm-
ing should be avoided if mild hypothermia develops
(>32◦ C, [89.6◦ F]) for 48 hours after ROSC.96 In a study
of dogs with induced ventricular fibrillation after 20
minutes of CPR followed by another 20 minutes of
CPR with targeted cooling, moderate (tympanic tem-
perature 27◦ C [80.6◦ F]) or mild (tympanic temperature
34◦ C, [93.2◦ F]) therapeutic hypothermia improved out-
come assessed by survival, neurologic function, brain
histology, and myocardial damage scores compared to
dogs with normothermia.33 In this study, therapeutic hy-
pothermia was achieved using venovenous extracorpo-
real shunt cooling, and found to be beneficial when ini-
tiated during the CPR.33 In another study of dogs with
induced ventricular fibrillation for 9 minutes followed
by cold carotid arterial flush (4◦ C, [39.2◦ F]) that resulted
in reduction of tympanic temperatures to 34◦ C (93.2◦ F)
while systemic temperatures (rectal and esophageal tem-
peratures) were maintained >35◦ C (95◦ F), dogs treated
with cold carotid arterial flush had significantly im-
proved neurologic deficit scores compared to dogs that
were maintained normothermic.97 While the recommen-
dations for target temperatures in veterinary patients
require further evaluation, laboratory studies support
benefit to the use of therapeutic hypothermia in veteri-
nary arrest patients.
Prognosis
A recent cross-over study evaluating CPR in dogs and
cats (a total of 161 dogs and 43 cats) revealed that ROSC
was obtained in roughly 35% of dogs and 44% of cats,
and of all arrests, 6% of dogs and 7% of cats survived
to hospital discharge.11 When anesthetic arrests are con-
sidered, survival to discharge improved to 47% com-
pared to 2% that did not have an anesthesia-associated
arrest. None of the patients that had out-of-hospital ar-
rest survived to discharge, and patients with multiple
155
B.L. Maton & S.D. Smarick

Table 1: Updates in the AHA Guidelines for CPR and potential applications to veterinary patients

Intervention AHA 2005 AHA 2010 Veterinary patients

Initiation Rescue breath, then pulse check for
up to 10 seconds prior to
compressions
Initiation ABC∗ versus CAB† ABC∗
Airway PETCO2 ‡ is considered adjunct to
confirm airway placement
Circulation 100 compressions per minute, depth
of 3.81–5 cm (1.5–2 inches)
Drugs Consider atropine as routine in
PEA§ /asystole
Fibrillation Biphasic or monophasic defibrillator
Gauging PETCO2 ‡ is a safe indicator of cardiac
output (CO)
Gauging Target CPP¶ ≥ 15 mmHg calculated
from central venous and arterial
pressures
Gauging Arterial blood gas to estimate
hypoxemia but not a reliable
indicator of acidosis
Post-arrest care Target blood pressure not discussed
Post-arrest care Target arterial oxygen saturation not
discussed, recommend maintain
normocarbia
Post-arrest care Monitor blood glucose frequently,
treat hyperglycemia with insulin
and avoid hypoglycemia
Post-arrest care Consider therapeutic hypothermia for
out-of-hospital arrest (32–34◦ C,
[89.6–93.2◦ F])
∗
Airway, breathing, compressions.
†
Compressions, airway, breathing.
‡
Partial pressure of end tidal carbon dioxide.
§ Pulseless electrical activity.
¶ Coronary perfusion pressure.
∗∗
Return of spontaneous circulation.
††
Central venous oxygen saturation.
Begin compressions in any patient
unresponsive, apneic, or gasping
CAB†
PETCO2 ‡ should be used to confirm
and monitor airway placement
At least 100 compressions per minute
Depth of at least 5 cm (2 inches)
Do not consider atropine routine in
PEA§ /asystole
Recommend biphasic defibrillator
PETCO2 ‡ is recommended to gauge
response with a target of >10
mm Hg
Target arterial diastolic pressure >20
mm Hg as a surrogate for CPP¶
use pulse waveform with rhythm
check for ROSC confirmation
Target ScvO2 †† > 30% to gauge
response and adjust efforts
Target blood pressure MAP ≥ 65 mm
Hg and Systolic ≥ 90 mm Hg
Wean oxygen supplementation to the
minimum necessary to maintain
arterial saturation ≥ 94%
Moderate glycemic control: blood
glucose target 144–180 mg/dL,
[8–10 mmol/L] with the avoidance
of hypoglycemia
Recommend therapeutic
hypothermia (32–34◦ C,
[89.6–93.2◦ F]) for 12–24 hours
for any patient comatose after
out-of-hospital ventricular
fibrillation arrest
Does the risk of delayed
compressions in veterinary
patients outweigh the benefit of
pulse palpation?
Are there instances in which
veterinary patients would benefit
from a CAB† approach?
Can PETCO2 ‡ be used to help confirm
intubation in arrested veterinary
patients?
Would faster and deeper
compressions benefit arrested
veterinary patients?
Is atropine beneficial for routine use
in arrested veterinary patients?
Should biphasic defibrillation be
recommended over monophasic
defibrillation in veterinary
patients?
Should PETCO2 be used to gauge the
response of resuscitative efforts
in arrested veterinary patients? If
so, what is the target PETCO2 ‡ ?
Is arterial diastolic pressure
correlated to ROSC∗∗ in arrested
veterinary patients, and what
should be the target pressure?
What is the best gauge of oxygen
delivery in arrested veterinary
patients, and is there a target
ScvO2 †† ?
What is the target blood pressure in
the postarrest veterinary patient?
What is the safest arterial oxygen
supplementation parameter in the
postarrest veterinary patient?
What should be the target glycemic
regulation in postarrest veterinary
patients?
Should therapeutic hypothermia be
implemented in postarrest
veterinary patients?

disease conditions were less likely to be successfully re- survival.11 Dopamine continuous rate infusion and vaso-
suscitated. In cats, having more people involved with pressin administration improved the likelihood of ROSC
the resuscitation effort was correlated to survival, while in dogs.11 In a study evaluating veterinary survivors of
shock as a cause of arrest was correlated with decreased CPA (18 patients), most common initial arrest rhythms

156 
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included asystole (72%), ventricular fibrillation (17%),
and pulseless electrical activity (PEA, 11%).14 Of all
patients in this study, 55% had an anesthetic-related
arrest.
As discussed, there are veterinary reviews and recom-
mendations available on CPR initiation, delivery, and
postarrest care.5–7, 10, 15 However, despite what may be
available as a standard of care, when veterinary prac-
titioners were surveyed, it was discovered that many
of these recommendations are not being practiced.43 It
is possible that the information is not well dissemi-
nated, formal consensus recommendations are not avail-
able, or resources (including equipment, drugs, and
personnel) may be limited. With these challenges in
mind, veterinarians set forth to draw parallels and
help develop recommendations for CPR for veterinary
patients.
Overall, previous veterinary CPR recommendations
have been derived from human studies and guidelines,
as well as experimental animal studies. It is unknown
how well this information translates to clinical veterinary
patients, and there is a great need for further research in
veterinary CPR. Table 1 outlines the changes from the
AHA 2005 to the 2010 human guidelines and lists some
questions to be considered in the development of vet-
erinary guidelines. With the continuous advancements
in human medicine, and the finding of improved results
following standardized practice and recommendations,
there is an urging need to develop parallel standards
for veterinary patients. Given this need, a new initiative
is near completion and aims to review the available in-
formation and produce the first consensus of veterinary
CPR recommendations, as well as guide further research
efforts. This initiative is called the Reassessment Cam-
paign on Veterinary Resuscitation (RECOVER),22 and the
publication of the RECOVER findings is forthcoming.
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