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Proceedings of the 34th World Small

Animal Veterinary Congress
WSAVA 2009
São Paulo, Brazil - 2009

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Reprinted in IVIS with the permission of the Congress Organizers

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WHAT’S NEW IN CPCR?

Dra. Adriana López Quintana, DVMT
alopezquintana@adinet.com.uy

Abstract
The keys to optimize success of CPCR are prompt intervention, adequate CPCR protocol, efficient
team work and frequent training. The etiology of the arrest should influence priorization of CPCR
technique. For cardiopulmonary arrest (CPA) the CAB protocol is advocated, Compressions first,
followed by Airway and Breathing, whereas, in the respiratory arrest ventilation is mandatory. The
new guidelines for CPCR emphasize the importance of providing continuous uninterrupted chest
compressions CCCPR, if necessary interruptions should be minimized to <10 seconds. The chest
wall should be allowed to completely recoil after being compressed at least 30% of the chest
diameter. Chest compressions must never be interrupted but if a second rescuer is available
orotracheal intubation is advocated. Each time positive ventilation is on board the intrathoracic
pressure increases thus reducing venous return to the heart, coronary perfusion and CPP. Current
recommendations include 1 sec. positive inspiration phase followed by complete relaxation at
respiratory rate < 10–12bpm. An impedance threshold device (ITD) limits air entry into the lungs
during chest recoil thus improving venous return, hemodynamic parameters, CPP, myocardial
perfusion and ROSC when used as an adjunct to CPCR in intubated cardiac arrest patients.
CCCPR for 60sec before defibrillation and for 2 minutes after a single shock before reassessment of
the rhythm by ECG is recommended for ventricular fibrillation. For asystole and pulseless electrical
activity resuscitation defibrillation is contraindicated, high-quality CCCPR is indicated. Vasopressin
has shown improved outcomes in human asystolic arrests and may show promise in veterinary
medicine. In order to prevent stone heart, the current recommended dose for epinephrine is lower
than ever 0,01-0.02mg/kg/iv/3-5min. Amiodarone is the medication of choice for treatment of
refractory ventricular fibrillation after defibrillation. Excessive IV fluids during CPCR reduce
coronary perfusion pressure, shock volumes are contraindicated. Allowing permissive hypothermia
post resuscitation has been found to be beneficial and may increase success rate.
In the event of cardiopulmonary arrest CPA, cardiopulmonary cerebral resuscitation CPCR provides
artificial ventilation and circulation until the return of spontaneous circulation ROSC. The reported
survival rate to hospital discharge SRDC for in hospital CPA is approximately 4.1% for dogs and
4.0-9.6% for cats, though discouraging similar outcomes have been described for humans. Recent
studies on experimental animals and human reviews for SHDC have shown that even when
performed by professionals, CPCR is generally inadequately performed. The main problems found
were lack of training, excessive ventilatory rates, low thoracic excursion, low frequency and
frequently interrupted chest compressions, as well as ineffective monitoring.

Recognition CPA
The major reasons for unsuccessful resuscitation are delayed recognition of CPA and delayed CPCR
initiation. Vigilant monitoring and anticipation of CPA in critical patients are essential. Frequent
monitoring of arterial blood pressure, CVP, core and peripheral temperature and critical diagnostic
tests and procedures (blood gases, lactate, K+, D-dimmer, PT, APTT, chest tap or tubing) may be
necessary. Changes in respiratory depth, rate or rhythm may occur and should prompt immediate
intervention. Clinical signs of CPA include loss of consciousness, absence of spontaneous
ventilation, absence of heart sounds on auscultation (BP<50mmHg) and absence of palpable
pulses (MAP<60mmHg).

Initiation of CPCR
Signed directives indicating client’s desires about resuscitation attempts must be obtained. All
hospitalized patients should be assigned to 1 of 3 groups, do not attempt resuscitation DNAR,
external CPCR and open chest CPCR and identified with a color code clearly posted on the patient
chart and on the cage door.

34th World Small Animal Veterinary Congress 2009 - São Paulo, Brazil
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To reduce the elapsed time for intervention every essential supply should be on hand and ready to
go, including oxygen, an ambu bag, a crash cart and an ECG monitor. Even non-nursing staff
members should be trained on performing CPCR, time is precious and we never know who will be
the first-one to advert sudden CPA. They can be easily trained to perform chest compressions,
ventilate after intubation or draw up pre-calculated drugs.
Rapid auscultation for audible heart sounds is performed while simultaneously palpating for the
presence of peripheral pulse. If heart sounds and pulses are absent, continuous external chest
compressions are begun and the remainder of the CPCR team is alerted to begin the chain of
organized and trained responses. Now-a-days in the event of CPA the CAB protocol is advocated,
Compressions first, followed by Airway and Breathing. Chest compressions will provide circulation
as well as some gas exchange, thus simultaneous treating both circulatory and ventilatory failure.
Nevertheless, the etiology of the arrest should influence priorization of CPCR technique. In the
respiratory arrest ventilation is mandatory. In an asphysic animal model CPCR without ventilation
resulted in 100% mortality, whereas 100% survived in the group with ventilation.
Chest compressions are performed with the patient in right lateral recumbence with the rescuer
standing above the patient's chest, so that the whole upper body rather than just the arms are
involved in performing the compressions. Even pressure to the chest wall is applied with straight
arms and hands parallel one on top of the other. Compressions are performed over the widest part
of the thorax for patients >10kg, whereas for those between 7–10kg the hands should be placed
over the 4th-6th intercostal spaces at the costochondral junction. For smaller dogs and cats,
fingers of on hand are placed on one side of the chest and the thumb on the other. Compressions
rate should be 80-100/min, with a 1:1 compression to relaxation ratio.
The main priorities of CPCR are to maximize myocardial and cerebral perfusion pressure CPP. CPP
is determined by the difference between MAP and intracranial pressure ICP, whereas the difference
between aortic diastolic pressure and right atrial pressure determines myocardial perfusion. The
chest wall should completely recoil after being compressed at least 30% of the chest diameter. The
degree of chest compression directly affects cardiac output CO and arterial forward movement.
Meanwhile, the degree of chest wall recoil has a tremendous impact on the amount of venous
return, cardiac preload and on cerebrospinal fluid drainage thus favoring CPP. Compression
interruptions allow a decrease in intrathoracic differential pressure, MAP, CPP and coronary
perfusion, thus every effort should be made to provide continuous chest compression CCCPR and
to minimize the number and the duration of interruptions to <10sec. The person performing chest
compressions should change every 2 minutes to reduce rescuer’s fatigue and maintain adequate
force and rate. CCCPR have shown a significant difference on SHDC if compared to 15:2 CPR when
performed by one rescuer (10,4% vs. 14.6%). The same have proven truth in animal models.
Therefore, chest compressions must never be interrupted but if a second rescuer is available
orotracheal intubation is advocated. Sometimes manual or vacuum cleaning of secretions, blood
and debris is required. Proper placement should be confirmed by direct visualization and
appropriate chest wall excursions during ventilation. Some cases may require a cricothiroideal
puncture or a cricothirodectomy to place a tracheostomy tube. The patient is given 2 breaths 1–
2sec in duration, using 100%FiO2 and then evaluated for spontaneous ventilation. Reversal agents
for anesthetic drugs that may cause apnea are administered. Doxapram is contraindicated because
it decreases cerebral blood flow and increases cerebral oxygen demands. If spontaneous
ventilation does not return, ventilations are begun. Each time positive ventilation is on board the
intrathoracic pressure increases thus reducing venous return to the heart, coronary perfusion and
CPP. Current recommendations include 1 sec. positive inspiration phase at ≤20cmH2O airway
pressures followed by complete relaxation at respiratory rate of 10–12bpm. Pediatric ambu bags
are recommended because they have shown to reduce esophageal and gastric insufflation.
Several assist devices are available for CPCR in humans. The active compression-decompression
device can increase venous return to the heart by extra-expanding the chest cavity during
decompression. However, it may be difficult to use in most veterinary patients. An impedance
threshold device (ITD) is a valve that limits air entry into the lungs during chest recoil thus
improving venous return. In animal models, the ITD can improve hemodynamic parameters,
increase CPP by lowering ICP, improve myocardial perfusion and ROSC when used as an adjunct to
CPCR in intubated cardiac arrest patients.

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Internal cardiac massage should be considered for penetrating chest wounds, chest wall trauma,
pleural space disease, pericardial effusion and lack of ROSC after 3-5min of external compressions.
During CPCR ETCO2 is more dependant on CO than on minute ventilatory volume and it has proven
to be the best tool to monitor the effectiveness of CPCR, providing almost immediate detection of
ROSC (ETCO2 increases to 18-24mmHg).
An ECG monitor should be attached to the patient in order to diagnose cardiac arrhythmias. For
asystole and pulseless electrical activity resuscitation, treatment of reversible causes (↑K+,
hypovolemia, tamponade) and high-quality CCCPR is indicated. Defibrillation shock to treat
asystole is contraindicated. Vasopressin, epinephrine and atropine alone or in alternation can be
used to try to recover an electrical cardiac rhythm. Unlike other drugs, vasopressin (0.8U/kg/iv/3–
5min) maintains its effectiveness in an acidotic, hypoxemic environment and has shown improved
outcomes in human asystolic arrests. The recommended dose for epinephrine is lower than ever,
0,01-0.02mg/kg/iv/3-5min or 0.03–0.1mg/kg/IT (diluted in 5-10ml of sterile water or 0.9% NaCl).
Atropine 0.04 mg/kg/IV/3–5min for a maximum of 3 doses may halt the progression of unstable
bradycardia to asystole or treat vagal-induced asystole.
Ventricular fibrillation can be the cause of CPA or the result of a minor success from the treatment
of asystole. CCCCPR for at least 60 seconds before defibrillation have shown to improve myocardial
perfusion, ATP storage and ROSC. Only one shock should be delivered, immediately followed by
CCCPR for at least 2 minutes prior to reassessing the ECG rhythm. The dose for a monophasic
defibrillator is 2-4joules/kg and 1-2joules/kg for a biphasic defibrillator. Amiodarone 5.0 mg/kg/iv-
io over 10 minutes is the drug of choice for refractory ventricular fibrillation, 2.5 mg/kg/IV may be
administered after 3–5min. Lidocaine may increase the defibrillation threshold and it is not
recommended for ventricular fibrillation. For ventricular arrhythmias after resuscitation, lidocaine
may be beneficial. The dosage of lidocaine in dogs is 2.0–4.0 mg/kg/IV-IO or 4-10mg/kg/IT.
Lidocaine should be used cautiously, if at all, in cats (0.2mg/kg/iv, IO or IT).
The best treatment for acidosis during CPA is to optimize perfusion and ventilation, NaHCO3 is not
recommended because it paradoxically reduces intracellular pH thus further impairing
mitochondrial work and myocardial response to CPCR.
The decision to terminate CPCR should be based on the original prognosis of the disease process
and the client's desires. In most cases, continued CPCR efforts are ended after 20 min. Respiratory
or CPA commonly recur after successful CPCR, close monitoring is essential. Common
complications that can be seen after CPCR include cerebral edema, hypoxemia, reperfusion injury,
abnormal hemostasis, acute renal failure, sepsis, multiple organ dysfunction syndrome. In
addition, treatment is needed to address the underlying disease process that resulted in the initial
CPA.
Supplemental oxygen at a FiO2 <50% to avoid oxygen toxicity and ventilatory support if necessary
should be provided. Permissive hypothermia (33–34°C) reduces metabolic O2 demands, neurologic
impairment and may increase the success rate from CPCR. Glucocorticoids are contraindicated,
they may worsen neurologic injury secondary to ischemia by causing hyperglycemia. Due to
increased right atrial pressure relative to aortic pressure excessive IV volumes during CPCR reduce
coronary perfusion pressure. Dobutamine 2.0–20.0μg/kg/min/CRI is the drug of choice to treat
normotensive decreased contractility. Dopamine 1.0–10.0μg/kg/min/CRI may work if dobutamine
does not, but may cause excessive vasoconstriction. In the hypotensive patient with normal
cardiac contractility, a CRI of a vasopressor is indicated but cautious administration is necessary
because excessive vasoconstriction may occur. The dosage for CRI of epinephrine is 0.1–
1.0 μg/kg/min, for vasopressin it is 0.01–0.04 U/min, whereas for norepinephrine it is 0.5–
1.0 μg/kg/min IV as a CRI, titrated to effect.
Nutritional support should be instituted as soon as possible depending on the patient's mentation
after resuscitation, original disease process, and underlying clinical status. A nasogastric tube and
microenteral fluid therapy can be started very soon after resuscutation, the placement of a
feeding tube should be considered later.

34th World Small Animal Veterinary Congress 2009 - São Paulo, Brazil