3 cardiopulmonary resuscitation in small animal medicine- an

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Review

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 A n i m a l M e d i c i n e :An U p d a t e

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 too10 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.

In December 2005, the American Heart Association(AHA) published new guidelines for cardiopulmonary

cerebral resuscitation (CPCR) in humans for the 1st timein 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-basedguide for resuscitation practice, and collaborated to de-

velop the guidelines. The consensus statements werepublished in December 2005 in the journal Circulation.1

These guidelines are available without charge online atthe 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 researchand may be pertinent to the veterinary patient. The re-

vised recommendations particularly applicable to the petpopulation 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

use of bellows for apnea in 1530.2 Tossach documentedthe administration of mouth-to-mouth ventilation in1732.2 Various methods have been utilized to attempt to

save the life of the apparently deceased. Modern cardio-

pulmonary resuscitation had evolved by 1960 to includeendotracheal intubation, artificial ventilation, and cardi-

ac compressions. Since 1960, little improvement has beenmade in the success rate of CPCR in humans.2,3

Approximately 330,000 people in the United States dieevery 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.510 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 between4 and 9.6% for cats.11,12

Recognition of CPA

In veterinary medicine, there are several elementsof 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 theclient 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

clients desires. The decision to terminate CPCR shouldbe based on the patients disease process, the original

prognosis, and the clients 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

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:

[email protected].

Submitted April 2, 2007; Revised June 14, 2007; Accepted

October 2, 2007.Copyrightr 2008 by the American College of Veterinary Internal

Medicine

10.1111/j.1939-1676.2007.0033.x

J Vet Intern Med2008;22:925


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provided: patients with DNAR orders, external CPCR,

and those patients for whom everything possible shouldbe attempted, including open chest CPCR.

The most successful CPCR is the one avoided. In small

animal practice, there are many predisposing causes forCPA, including sepsis, cardiac failure, pulmonary disease,

neoplasia, coagulopathies, anesthesia, toxicities, multisys-

tem trauma, traumatic brain injury, and systemic in-flammatory response syndrome.1216 Anticipation of CPAand 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 inrespiratory depth, rate, or rhythm may occur, progress-

ing to gasping and finally agonal breaths at death.1720

Mucous membrane color and capillary refill time should

not be used to assess the patient for CPA because theymay 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 ventilatorybreaths, 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 chestcompressions 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 byplacement 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 includeplacement 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 beutilized to place the endotracheal tube and avoid vagal-

induced bradycardia from excessive manipulation of theepiglottis.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 hasbeen helpful to confirm endotracheal tube placement in

anesthetized animals.2527 A positive reading for exhaledCO2 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 propertube placement in these patients.25,28,29

Breathing

The veterinary patient is given 2 breaths 12 seconds in

duration, with positive pressure ventilation using 100%inspired oxygen, and then evaluated for spontaneousventilation.30 If the patient resumes spontaneous ventila-

tion, a full CPA situation may have been avoided. If thepatient has only respiratory arrest, acupuncture of the

Jen Chung (GV26) point should be considered. Thistechnique is performed by twirling a 25-G, 5/8-in. needleinserted 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 Reversalagents 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.

3234

If spontaneous ventilation does not return in the vet-

erinary patient, ventilations are begun at a rate of 1012breaths 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 chestwall.36 The ventilations delivered to the patient should be

neither too large nor too forcefully administered, orbarotrauma of the lungs may occur.14,37 An ambu bagor 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, 1215 bpm, may bebeneficial.22,37 Previous recommendations for veterinary

patients were to provide a ventilatory rate of 2024 bpm.22,30 Lower ventilation rates are an essential part

of the new guidelines.1 In humans, a ventilatory rate of

812bpm is recommended for adults and 1220 bpmfor pediatric patients and neonates.1,35,38 Delivery of anexcessive ventilatory rate should be avoided, because an

excessive rate has been shown to lower coronary perfusion

pressure and decrease the success rate of CPCRin human and in animal models.3840 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.38Although ventilatory rates are currently controversial,

a recent study published in the medical literature foundthat providing chest compressions alone in resuscitation

for out-of-hospital witnessed cardiac arrest resulted in ahigher 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 onlywhile awaiting assistance.41

Circulation

Standard manual CPCR was developed to pump

blood from the chest to the vital organs during chest

10 Plunkett and McMichael


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compression and enhance venous return into the chest

during relaxation of the chest wall. The goal is to maxi-mize cerebral and myocardial perfusion.4245 The differ-ence between mean arterial pressure and intracranial

pressure is cerebral perfusion pressure. Maintenance ofcerebral 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 andanimals have shown that successful return of spontaneous

circulation (ROSC) corresponds with maintenance ofsufficiently high myocardial perfusion pressures.46,48

Compression of the chest wall causes an increase inintrathoracic 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.42,4952 The decrease in in-tracranial pressure is the result of direct transfer of

pressure through the thoracic spine to the cerebrospinalfluid and increased venous drainage of the nonvalvular

veins of the paraspinal plexuses, resulting in increasedvenous return to the heart via the jugular veins.50,5355

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 numberand the duration of interruptions to o10 seconds, be-

cause interruptions allow a decrease in intrathoracic

pressure, intravascular pressure, and coronary perfusionpressure.1,5660 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 4050% of the

time and were associated with increased mortality.56,57,5961

Rapid auscultation of the chest for audible heartsounds is performed while simultaneously palpating for

the presence of a peripheral pulse. If heart sounds andpulses are absent, continuous external chest compres-

sions are begun. The thoracic pump theory, themechanism thought to be in effect in humans and medi-

um to large dogs, suggests that the application ofpressure to the chest wall in a rhythmic manner creates

blood flow by increasing intrathoracic pressure that istransmitted to arteries and veins, with a pressure gradientcausing forward blood flow, and also by compressing theheart directly.22,62 The cardiac pump theory is the meth-

od thought to be responsible for forward bloodmovement 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 thatare correctly performed in humans can generate systolic

arterial pressure peaks of 6080 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

chest compressions (the compressor) should be above

the patients chest.64,65 Placement of the compressorshands varies depending on the shape of the patientschest. For medium and large dogs (thoracic pump), the

compressors hands should be placed over the widest partof 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. Foranimals weighing 710 kg, the compressor should placehis or her hands directly over the apex of the heart, which

lies between the 4th and the 6th intercostal spaces at orslightly dorsal to the costochondral junction. Hands

should be placed slightly more dorsal in animals weigh-ing 410kg. For smaller dogs (o7 kg) and cats, the

fingers of 1 hand should be placed on 1 side of thechest and the thumb on the other side. Compressions

with the fingertips should be avoided.22,30,6668 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 80100 compressions per minute with a 1 : 1compression 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 patientsand 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 fromthe hospital.57,59,7173

Chest compressions should be continuous, with nopauses 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-hospitalcardiac 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 techniqueof interposed abdominal compression with chest com-

pressions may increase venous return to the heart, otherstudies have not shown any survival advantage.67,68

Evidence for or against the use of interposed abdominalcompression is lacking in the new CPCR guidelines.1

Compression Assist Devices

There are several compression assist devices availablefor CPCR in humans. The theory of the active compres-

sion-decompression device is that venous return to theheart can be increased during decompression by expand-

ing the chest cavity and decreasing intrathoracicpressure. 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

11Cardiopulmonary Resuscitation in Small Animals


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heart by increasing negative intrathoracic pressure dur-

ing the decompression phase of CPCR without affectingexhalation.42,7577 In animal models, the ITD can im-prove hemodynamic parameters, increase cerebral

perfusion by lowering intracranial pressure, improvemyocardial perfusion when intrathoracic pressure be-

comes increasingly negative, and improve ROSC when

used as an adjunct to CPCR in intubated cardiac arrestpatients.42,5052 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, intraoperativesudden cardiac arrest, and failure to achieve adequate

circulation within 25 minutes of external chest compres-sions, especially in dogs weighing 420kg.30,7880 The

surgical approach for internal cardiac massage has beendescribed 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 theremaining 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 carriedout 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 o4060 bpm in dogs and

o120140 bpm in cats with a normal sinus rhythm on

ECG). Increased vagal tone, hypothermia, increasedintracranial pressure, and medications can cause sinus

bradycardia.83,84

Asystole and Pulseless Electrical ActivityIn humans, the survival rate from cardiac arrest with

asystole is very low.1 Asystole is the most commonarrest rhythm in dogs and cats.83,84 It can result from nu-

merous serious disease processes, trauma, and increasedvagal 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.8791 Resuscitation efforts should be directed at per-

forming high-quality CPCR with minimal interruptionsand 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 isan absence of myocardial contractility. Pulseless electri-cal activity was referred to previously as electrical

mechanical dissociation and has been combined withasystole under the new 2005 guidelines for humans.1 Un-

der the new guidelines, many rhythms are grouped in the

PEA category, including idioventricular rhythms andventricular 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 poorfor successful resuscitation.1

Ventricular Tachycardia

Ventricular tachycardia results from repetitive firing ofan 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 ofthe underlying cause should be addressed.83

Ventricular Fibrillation

Ventricular fibrillation is unorganized ventricular ex-citation resulting in poorly synchronized and inadequatemyocardial contractions that cause cardiac pump failure.

Sudden loss of cardiac output leads to global tissue is-

chemia, with the brain and myocardium being mostsusceptible. 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. Fineventricular fibrillation may be more difficult to convertto sinus rhythm than coarse ventricular fibrillation.85,86

Defibrillation

Defibrillation is defined as termination of ventricularfibrillation for at least 5 seconds after delivery of an elec-

tric shock that depolarizes myocardial cells andeliminates ventricular fibrillation. It is an electrophysio-

logic event that occurs 300500 ms after delivery of adefibrillatory shock.9395 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.9698

Chest compressions should be performed while the

defibrillator is being connected and charged. With



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a manual defibrillator, the defibrillator operator selects

the shock energy (in joules); however, it is the amplitudeof current flow (in amperes) that causes depolarizationof the myocardium and results in defibrillation.99 Alco-

hol, ultrasound gel, or other nonconductive gels shouldnot 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 paddlesor pad that will fit on the patients chest should be usedbecause small electrodes may cause myocardial necro-

sis.100102 The patient should be placed in dorsalrecumbency 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 contactwith the patient and anything connected to the patient,

and then 1 shock should be administered as quickly aspossible. The person administering the shock must avoid

contact with the patients 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 patients chest onthe down side, and a standard paddle can be used on the

upper side of the chest. The initial counter shock energyfor external defibrillation is 25 J/kg.103,104 Other dosage

recommendations for external defibrillation are to ad-minister 50 J for small dogs and cats, 100J for medium

dogs, and 200 J for large dogs or to administer 7 J/kg topatients o15 kg and 10 J/kg to patients 415 kg. For in-

ternal defibrillation, saline-soaked sponges should beplaced between the paddles and the heart. The energy of

the counter shock for internal defibrillation is 1/10 of thedosage used for external defibrillation (0.20.5 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 immediatelyafter defibrillation rarely is helpful and delays resump-

tion of postshock chest compressions.59,72,107109 Aftersuccessful defibrillation, a short period of a nonperfusing

rhythm, either asystole or pulseless electrical activity, iscommon before returning to normal sinusrhythm.96,110,111 Immediate chest compressions after at-

tempted defibrillation increase myocardial perfusion andare more likely to make conversion successful than theadministration of a 2nd shock.56,71,98,105,106,110115

In an unwitnessed, out-of-hospital arrest, the 2005CPCR guidelines recommend the administration ofexternal 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 beforereassessing the cardiac rhythm.116,117 In these situations,

a clinically relevant period of no perfusion may have oc-

curred. The responsiveness of ventricular fibrillation todefibrillation may be enhanced by previous chest com-

pressions and epinephrine administration.

71,106

When CPA occurs in a human hospital, immediate

defibrillation is recommended. If ventricular fibrillationcontinues after 1 or 2 shocks plus compression, epineph-rine should be administered every 35 minutes, or a

dose of vasopressin may be substituted for the 1st or the2nd dose of epinephrine. If ventricular fibrillation con-

tinues after 2 or 3 shocks, compressions and admin-

istration of a vasopressor, followed by amiodarone, arerecommended.108,118120

The likelihood of ROSC proportionately decreases

with delays in cardiac compressions from repeateddefibrillation, rhythm assessment, and other interrup-

tions.56,57,60,105,113,115 A precordial thump is no longerrecommended because research has shown that it can

lead to deterioration of cardiac rhythm, increased rate ofventricular tachycardia, conversion of ventricular tachy-

cardia to ventricular fibrillation, complete heart block, orasystole.121123

Automated external defibrillators (AEDs) are comput-erized devices that use voice and visual prompts to guide

safe defibrillation. They are useful for out-of-hospitalsudden cardiac arrest in public access areas such as air-

ports and sports venues.124127 Microprocessors in theAED analyze features of the surface ECG. The voice and

visual prompts along with diagrams guide the rescuerand will not send a defibrillating shock unless the auto-

mated ECG rhythm analysis determines thatadministration of a shock is indicated.57,61,124127

Although manual defibrillators with dose adjustmentcapabilities are recommended for children, AEDs

equipped with pediatric attenuator systems are availablefor children 18 years of age.128130 If an AED is to be

used on a small animal patient, studies in swine show thatit 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 thelikelihood of successful resuscitation and survival to dis-

charge from the hospital.

Routes of Administration for Medications and Fluid

TherapyA central line is the preferred route for administration

of medication during CPCR. Unfortunately, one rarely isin 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 routeand delays in placing peripheral catheters during CPA,

some prefer the IT route. Intracardiac injections shouldbe 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,



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intracardiac injections can result in numerous complica-

tions, including coronary vessel laceration, myocardialischemia, hemorrhage, arrhythmia, and pneumotho-rax.16,135,136 Medication administered via a peripheral

catheter should be given as a bolus injection, followed by0.9% NaCl IV and raising of the extremity for 1020 sec-

onds.1,137,138 It usually takes 12 minutes for medication

administered via a peripheral vein to reach the centralcirculation. The new guidelines recommend chest com-pressions be administered for 2 minutes after drug

administration via a peripheral vein before checking theECG.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).140145 IT administration of sodium bicarbonateshould be avoided because it inactivates the surfactant

and irritates tissues.

16,140,146151

Medications to be ad-ministered via the IT route should be diluted in 510 mL

of sterile water, which is absorbed better than 0.9%NaCl.146149 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 22.5 times their

IV dosage, except for epinephrine, which should be in-creased by 310 times the IV dosage (0.030.1 mg/

kg).149,152155 In studies of humans and animals, lower

dose epinephrine administered via the IT route caused

hypotension and decreased cerebral perfusion pressurebecause of transient b-adrenergic effects.153,154,156160

IV Fluid Therapy

The 2005 guidelines for humans state that IV fluidsshould 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 euvolemicCPA patient, the recommended dosage for crystalloid IV

fluids is a 20 mL/kg bolus for dogs and a 10 mL/kg bolusfor cats, as rapidly as possible. The administration of ex-

cessive volumes of IV fluids to euvolemic patients duringCPCR in animal studies decreased coronary perfusion

pressure because of an increase in right atrial pressurerelative 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 510 mL/kg/day for cats. Hetastarchmay be administered as an IV bolus during CPCR at adosage of 5 mL/kg for dogs and 23mL/kg for cats.163

167 Hypertonic saline has been shown to improve survivalfrom 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 dosageof 46 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 m g/kg IV, IO over 10 minutes

Repeat dose 2.5mg/kg IV, IO over 10

minutes

Same Only 1 repeat dose, after 35 minutes, is

recommended. Do not administer IT

Atropine 0.04 mg/kg IV, IO

0.080.1 mg/kg ITaSame Can repeat every 35 minutes for a maxi-

mum of 3 doses

Calcium gluconate 10% 0.51.5 mL/kg IV slowly Same Do not administer IT

Epinephrine 0.01 mg/kg IV, IO

0.030.1 mg/kg ITa

Repeat dose 0.1 mg/kg

IV, IO, ITa

Same Initial dose

Repeat doses should be administered every

35 minutes

Lidocaine 2.04.0 mg/kg IV, IO

4.010 mg/kg ITa0.2 mg/kg IV,

IO, IT

Use cautiously in cats

Magnesium sulfate 0.150.3mEq/kg IV slowly over 10

minutes

Same Can repeat to a maximum of 0.75 mEq/kg

Do not administer IT

Naloxone 0.020.04 mg/kg IV

0.040.10mg/kg IT

a

Same Opioid reversal agent

Sodium bicarbonate 0.5 mEq/kg IV, IO

0.08 BW (kg) base deficit5 # of

mEq to administer

Same Do not administer IT. Administer cau-

tiously after 1015 minutes of CPA; can

repeat every 10 minutes

Vasopressin 0.20.8 U/kg IV, IO

0.41.2 U/kg ITaSame Repeat every 35 m inutes o r alternate w ith

epinephrine

External defibrillation

shock energy (J)

25J/kg

Or 50 J for small dogs, 100J for medi-

um dogs, and 200 J for large dogs

Or 7 J/kg ifo15kg and

10 J/kg if415kg

25 J/kg

Or 50 J

Or 7 J/kg ifo15kg

Internal defibrillation

shock energy (J)

0.20.5 J/kg Same

aAll medications administered IT should be diluted in 510 mL of sterile water.

IO, intraosseous; IT, intratracheal; CPCR, cardiopulmonary cerebral resuscitation.



7/18

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, increasedheart 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 CPCRmainly 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 peripheralarteriolar vasoconstriction overrides the b2-agonist

induced hypotension and causes an increase in systemicvascular 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 oxygendemands and causing intramyocardial coronary arterio-lar vasoconstriction and enhancing the reduction in

myocardial perfusion.174184

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 beingadministered IT, in which case the dosage is 0.030.1mg/kg.149,174,185,186 Epinephrine administration should

be repeated every 35 minutes if indicated. In veterinary

medicine, if repeated doses are not successful, vasopres-sin can be administered instead or the epinephrine dosagecan be increased to 0.1 mg/kg IV.171,185188 Many proto-

cols in human medicine now call for 1 dose ofepinephrine, 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 incardiac 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.189191 Although epinephrine0.1 mg/kg IV appears to be superior for maximizing ce-

rebral blood flow and the aortic diastolic-right atrialgradient, it is also associated with a higher refibrillationrate and a lower survival rate.190192

Vasopressin

Vasopressin is a nonadrenergic endogenous pressor

peptide that causes peripheral, coronary, and renalvasoconstriction.193,194 At a dosage of 0.20.8 U/kg IV

or 0.41.2 U/kg IT, vasopressin stimulates specific V1Areceptors in the smooth muscle of the vasculature, leading

to nonadrenergic vasoconstriction.171,195201 Vasopressinmay 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

Because the outcome from pulseless cardiac arrest did

not differ in humans treated with vasopressin comparedwith those treated with epinephrine, the 2005 guidelinesstate 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, andit 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 vasopressinwas 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, whereasepinephrine 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 35 minutes or vasopressin can be alternated

with epinephrine every 35 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 suspectedto 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 Asa 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 atrioventricularnode.208,209 Although there are no prospective controlled

studies supporting the use of atropine in asystole or PEA

cardiac arrest, the 2005 guidelines recommend atropinein 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 35

minutes for a maximum of 3 doses.210,211

Amiodarone

Amiodarone is a class III antiarrhythmic agent with

several effects, including prolongation of myocardial cellaction potential duration and refractory period by affect-

ing sodium, potassium, and calcium channels, andnoncompetitive a- and b-adrenergic inhibition.119,212 It

is the medication of choice for treatment of refractoryventricular 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 benoted 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



8/18

of atrial fibrillation, narrow-complex superventricular

tachycardia, ventricular tachycardia, wide-complex ta-chycardia of uncertain origin, and refractory ventricularfibrillation that is unresponsive to compressions, defi-

brillation, and vasopressor administration.118,120,212214

The dosage of amiodarone is 5.0mg/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 35minutes.119,215

Lidocaine

Lidocaine is a class Ib antiarrhythmic agent that stabi-

lizes cell membranes by sodium channel blockade andalso acts as a local anesthetic. In clinical trials, in com-

parison with amiodarone, lidocaine resulted in decreasedROSC and increased incidence of asystole after defibril-

lation.118,216 Because it has no proven efficacy in cardiacarrest, 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 maymake electrical defibrillation more difficult by increasing

the defibrillation threshold and decreasing myocardialautomaticity.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 2.04.0 mg/kg IV orIO.12,25 For IT administration in dogs, the lidocaine dos-

age is increased 22.5 times and it is diluted in sterilewater.12,25,143,144 Lidocaine should be used cautiously, if

atall, in cats at a dosage of 0.2 mg/kg IV, IO, or IT.219,220

Sodium Bicarbonate

Sodium bicarbonate was recommended previously forthe 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 antidepressantoverdose, severe pre-existing metabolic acidosis, andsevere hyperkalemia.221227 For these conditions, sodi-

um bicarbonate may be administered at a dosage of 0.5mEq/kg IV.221227 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 inactivatecatecholamines 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 duringCPCR.230232 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 0.51.5

mL/kg slowly IV.233 In critically ill patients, serum total

calcium concentration is an inadequate reflectionof serum ionized calcium concentration, which is affect-ed by interactions of serum pH, individual serum

protein-binding capacity and affinity, and serum proteinconcentration.232,234236

Magnesium Sulfate

Magnesium sulfate is an essential enzyme cofactorwith 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 fromdecreased sodium, potassium-adenosinetriphosphatase(Na1, K1-ATPase) activity. Magnesium also affects

vascular tone.237240 The administration of magnesium

sulfate may be beneficial in the treatment of refractoryventricular arrhythmias, including ventricular fibrillation

and torsades de pointes (a life-threatening, polymor-phic form of ventricular tachycardia).1,241243 Decreasedintracellular concentrations of magnesium increase myo-

cardial excitability, potentially resulting in ventricular

arrhythmias.241244 The dosage of magnesium sulfateduring cardiac arrest is 0.150.3 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 duringCPCR unless the patient has documented hypoglycemia.Neurologic outcome after resuscitation is worse in pa-

tients with hyperglycemia.228,245248

Bretylium Tosylate

Bretylium tosylate is a type III antiarrhythmic agent

with both direct myocardial and adrenergic effects. It is nolonger 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, 0.02mg/kg IV), and opioid antagonists(naloxone, 0.020.04 mg/kg IV).251 The administrationof inhalation anesthetics should be stopped and the

breathing circuit should be evaluated before CPCR isinitiated.

Monitoring the Effectiveness of CPCR

To assess the effectiveness of CPCR efforts, the pa-

tients ETCO2 level should be monitored as an indicationof 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,



9/18

patients who could not be resuscitated had significantly

lower ETCO2 levels than those who were successfullyresuscitated.245,252255 The presence of a palpable carotidor femoral pulse may not be a reliable indicator of suc-

cessful CPCR, because venous pulses may be felt in theabsence 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 beperformed by placement of a Doppler ultrasound trans-ducer on the lubricated cornea.258,259 Assessment of

oxygenation at the tissue level during CPCR can beachieved by monitoring central venous blood gases

from a pulmonary artery catheter sample.25 Evaluationof central venous blood gases provides a more

accurate assessment of tissue acid-base status duringCPCR because it takes into consideration the effects

of low peripheral blood flow and the resulting tissuehypoxia, 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 oftissue acidosis or tissue hypoxemia.260263 Pulse oximetry

is not helpful because peripheral pulsatile blood flow isinadequate.1,245

Care of the Patient After Successful Resuscitation

Respiratory or CPA commonly recur after successfulCPCR 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.264266

The following parameters should be monitored: pulserate, 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 patientcomfort.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 oxygenkennel.36 Initially, the patient should be ventilated with

100% oxygen, but the oxygen concentration should bedecreased too60% as quickly as possible to avoid oxy-

gen toxicity.108,267271 If continued ventilation isrequired, arterial blood gases and direct arterial blood

pressure or indirect systolic blood pressure should bemonitored continuously.

If the animal has mild hypothermia or becomeshypothermic during CPCR, permissive hypothermia

should be allowed.272,273 Permissive hypothermia is theterm used when hypothermia is allowed to continue

without taking steps to rewarm the patient to a normalbody temperature. This term differs from induced hypo-

thermia, in which the human patient is manipulated viamedical treatment and external devices to a body tem-

perature of 3234 1C and maintained at this low body

temperature for 1224 hours.272274

Although induced

hypothermia may be useful in human patients, it requires

advanced monitoring and medical devices not typicallyavailable in veterinary practice. Complications of hypo-thermia include arrhythmias and coagulopathy.1,272275

The target temperature for dogs and cats is 3334 1C.

276,277 Permissive hypothermia diminishes the oxy-

gen demands of tissues, reduces neurologic impairment

after CPA, and may increase the success rate fromCPCR.272280

IV fluid therapy should be administered cautiously.

Crystalloids should not be administered at shock fluiddosages unless the patient was hypovolemic before CPA.

To improve peripheral perfusion and cardiac output, itmay be beneficial to administer an IV bolus of a colloid

such as hetastarch (510 mL/kg IV for dogs and 23mL/kg IV slowly over 15 minutes for cats.)166,281 If the

colloid bolus does not improve cardiac output, bloodpressure, 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 decreasedcardiac contractility as evaluated by echocardiography,

administration of a positive inotrope (eg dobutamine ordopamine) may be indicated. Peripheral perfusion can be

evaluated by assessing serum lactate concentration, urineoutput, capillary refill time, and rectal and peripheral

temperatures. Dobutamine is usually the drug of choiceto improve cardiac output without causing excessive va-

soconstriction. The dosage of dobutamine for infusion is2.020.0mg/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 vasoconstrictionwithout an additional increase in cardiac output. The

dosage of dopamine to produce a positive inotropiceffect is 1.010.0mg/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 dobutamineor dopamine added to a total volume of 100 mL 0.9%

NaCl. When this preparation is delivered at 1.0 mL/h IV,1.0mg/kg/min is administered. The CRI solution should

be protected from light.284

After an adequate IV fluid bolus, if the patient ishypotensive, with normal cardiac contractility as evalu-

ated by echocardiography, the administration of avasopressor (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 0.11.0mg/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,0.1mg/kg/min is administered. The CRI solution should

be protected from light.

284

The dosage of vasopressin for



10/18

infusion is 0.010.04 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 remainshypotensive despite adequate volume replacement and

treatment with other, less potent, inotropes such as

dopamine.1,288,289

Cardiac contractility, cardiac oxygendemand, heart rate, and stroke volume increase after theadministration 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 wateror 5% dextrose in normal saline before administration.

The dosage of norepinephrine is 0.51.0 mg/kg/min IV asa CRI, titrated to effect.1,284

Neurologic dysfunction occurs commonly afterCPCR. Often, the clinical abnormalities resolve over

2448 hours. The patient should be allowed a minimumof 48 hours before a prognosis is made regarding neuro-

logic abnormalities.73,84,292,293 To avoid increasing thebrains 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 causedby 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 toischemia by causing hyperglycemia.248,294 Nutritional

support should be instituted as soon as possible depend-ing on the patients 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 supportshould 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, absentpupillary response, absent withdrawal response to pain,

and absent motor response.73,292

Common complications that can be seen after

CPCR include cerebral edema, hypoxemia, reperfusioninjury, 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 initialCPA.264,265,278,280,295297

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 CPCRhave been conducted on dogs, providing useful informa-

tion for veterinarians. The new AHA guidelines forhumans 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 includethe administration of chest compressions continuallythroughout 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 lidocainefor the treatment of refractory ventricular tachycardia orfibrillation after defibrillation, and allowance of mild per-

missive hypothermia in the postarrest period.

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