Luisito S. Pablo, DVM, MS, DACVA
There are no specific guidelines on CPR primarily written for animals by a panel of veterinarians. Most of the information published on animal CPR are based on the authors' clinical experience and information published from animal experiments performed by non-veterinarians. There are no prospective randomized controlled trials in animals which will produce strong evidence that the steps we take during CPR are the most effective. Contrast this with human medicine where there have been 7 conferences on CPR and Emergency Cardiovascular Care since 1966. In 2000, the First International Guidelines Conference on CPR and ECC was held. This is considered a milestone because this is the first international conference on CPR and the recommendations were evidence-based.
There are eight levels of evidence the experts had to consider before arriving at a final class of recommendation. Interestingly, animal studies ranked low, only 6th, in the level of evidence. However, after analyzing the Guidelines, animal studies have played a great role in the inclusion of some of the recommendations.
We can learn from these guidelines and animal studies. It is important to choose the sections of the Guidelines that are applicable to our patients. The objective of this presentation is to present the current concepts of CPR (based on the 2000 Guidelines) and new research findings that are applicable to our practice with the goal of improving the outcome of our CPR in animals.
The current concepts presented here will be divided into the stages of CPR: 1) Basic cardiac life support, 2) Advanced cardiac life support and 3) Post-resuscitation care.
Basic cardiac life support (BCLS)
BCLS includes recognition of cardiac arrest and providing artificial breathing and circulation to the patient.
Animal and human studies have shown that chest compression rate > 80 per minute is needed to obtain optimal forward blood flow. Based on this, chest compression rates in dogs and cats of 90-120 per minute should be employed.
A high ventilatory rate (80-120 breaths per minute) during CPR occurs when simultaneous ventilation-compression CPR (SVC-CPR) is performed. Laboratory studies had conflicting results as to the efficacy of this technique compared with the standard CPR. On the other hand, clinical studies showed SVC-CPR to be worse than standard CPR based on hemodynamic parameters and survival. From these findings, it appears that lower ventilatory rates of 8-12 per minute in dogs and 12-15 per minute are reasonable choices during CPR as long as adequate tidal volume can be provided to the patient.
Alternative CPR Technique: Interposed Abdominal Compression (IAC-CPR)
IAC-CPR involves the compression of the abdomen during the relaxation phase of chest compression. The idea behind this technique is to generate external pressure on the aorta and vena cava. In turn, this will force the blood to the heart and brain and improve the perfusion of those organs. In dogs and cats, this technique can be done by one person by alternatively using one hand to compress the chest and the other hand to compress the abdomen. In humans, randomized clinical trials have shown improved outcome with IAC-CPR when compared with the standard CPR in in-hospital resuscitation. This is an alternative technique that shows promise in small animal CPR and should be tried.
Order of Priority
There are studies pointing to a change from the historic order of priority in basic life support. The typical sequence of basic life support dictates that the airway should be secured, ventilation supported and then chest compression started. It was shown that adequate oxygenation could be maintained for 5 to 10 minutes without ventilation provided that chest compressions were effective in producing forward blood flow. In addition, there was no difference in neurologic outcome in pigs that had chest compression with or without artificial breathing. Clinically, it is a good practice to initiate chest compression immediately once cardiac arrest has been recognized while another person intubates and provides artificial ventilation. A change in the order of priority to compression, followed by airway and breathing should be tried and may prove lifesaving.
Advanced Cardiac Life Support (ACLS)
Low-dose vs high-dose epinephrine
In the 2000 Guidelines, high doses of epinephrine may be used but are not recommended because of the potential for harm. Low-dose of epinephrine is used in the ACLS algorithm for ventricular fibrillation, ventricular asystole and pulseless electrical activity. In studies performed in pigs, 0.02 mg/kg was used as low (standard) dose for epinephrine while 0.2 mg/kg as high dose. This range represents clinically useful doses for the small animal practitioners. There are no clinical trials in veterinary medicine comparing the high and low doses of epinephrine. Clinical trials in humans and experimental studies in animals failed to show an improved survival and neurological outcome using high dose of epinephrine. Initially, the high-dose epinephrine given during resuscitation produced higher perfusion pressures. However, high-dose epinephrine resulted in post-resuscitation tachycardia, systemic hypertension and greater early mortality when compared with the low (standard) dose. Myocardial necrosis and worsened post-arrest cardiomyopathy were also reported following the use of the high-dose of epinephrine.
Based on the available references and clinical experience, the author recommends the use of the lower doses of epinephrine in dogs and cats which ranges from 0.02-0.05 mg/kg IV. This dose can be repeated every 3-5 minutes. The intracheal dose is twice the IV dose.
The inclusion of arginine vasopressin in ACLS is one of the highlights in the 2000 Guideline. Vasopressin is the naturally occurring antidiuretic hormone. Its main effect is peripheral vasoconstriction by stimulating the smooth muscle V1 receptors. It is recommended for ventricular fibrillation that is refractory to electrical defibrillation as an alternative to epinephrine. It has been shown to produce a greater vasoconstrictive effect during hypoxic and acidemic episodes compared with epinephrine. Its effects also last longer than epinephrine. In normal experimental animals, the half-life of vasopressin is 10-20 minutes. After the release of the 2000 Guidelines, more studies indicating the efficacy of vasopressin in CPR have been published. One study showed that pigs with ventricular fibrillation resuscitated using vasopressin had better pulmonary gas exchange than those that received epinephrine. Vasopressin was also evaluated experimentally in pigs with cardiac arrest following hypovolemic shock. It was shown that vasopressin produced a sustained vital organ perfusion and prolonged survival compared with high-dose epinephrine.
The dose of vasopressin used in swine studies was 0.4-0.8 u/kg. An intratracheal dose of 1.2 u/kg was shown to produce positive hemodynamic changes in dogs. Presently, we have been using vasopressin at a dose of 0.4-0.8 u/kg in dogs and cats. Our clinical experience is still limited and a positive clinical impression on vasopressin cannot be shared at this time.
Atropine is indicated in both ventricular asystole and slow pulseless electrical activity following epinephrine in the 2000 Guidelines. Atropine is an anticholinergic which works by reversing the cholinergic-mediated decreases in heart rate, blood pressure and systemic vascular resistance. The total vagolytic dose of atropine is recommended for asystolic cardiac arrest while lower atropine doses are indicated for pulseless electrical activity. The rationale behind this recommendation is that atropine will increase myocardial oxygen demand and can cause tachyarrhythmias especially if a total vagolytic dose is used. Atropine can be repeated every 3-5 minutes if lower dose is used.
Antiarrhythmic agents are used in the algorithm for ventricular fibrillation if there is no return to sinus rhythm after stacked electrical defibrillation, administration of epinephrine or vasopressin and another stacked electrical defibrillation.
Most veterinary practices do not have an electrical defibrillator. Converting ventricular fibrillation to sinus rhythm using drugs is very rare and difficult. This is a deficiency in veterinary practice that further reduces the success rate of CPR. In one study, ventricular fibrillation occurred in 19.8% of dogs and cats that suffered cardiac arrest. This figure is smaller than that observed in humans with an incidence of 33%. Still, it is unfortunate that about 19.8% of our small animal patients may not get the best resuscitation possible. Antiarrhythmic agents will be effective only when used in conjunction with electrical defibrillation.
In the ACLS algorithm for ventricular fibrillation, the following antiarrhythmic drugs were included: amiodarone, lidocaine, procainamide and magnesium sulfate. Bretylium was excluded in the Guideline primarily because of diminishing supply. It is also known to cause hypotension in the post-resuscitation period.
Amiodarone, a class III antiarrhythmic drug, increases the action potential duration. Presently, it is the antiarrhythmic drug of choice in the algorithm for ventricular fibrillation in humans. Clinical trials showed an improved survival in out-of-hospital victims with ventricular fibrillation given amiodarone. There are no clinical studies in dogs and cats evaluating the efficacy of amiodarone in the setting of ventricular fibrillation. The drug is very expensive and typical veterinary practices will not have amiodarone. It is unlikely that amiodarone will be the main antiarrhythmic agent in veterinary practice in the very near future, despite its efficacy in humans.
The dose of amiodarone in a canine experiment evaluating its efficacy in converting hypothermic ventricular fibrillation was 10.0 mg/kg IV. In this hypothermic model, amiodarone did not improve the resuscitation rate. In human cardiac arrest, initial dose (300 mg) is given as an slow IV push. If there is no response, another dose, which is one-half of the initial dose, is administered.
Lidocaine, in contrast to amiodarone, is readily available for veterinary practitioners. It is still included in the 2000 Guidelines as an antiarrhythmic for recurrent or persistent ventricular fibrillation. However, its use is classified as indeterminate. The available evidence supporting its efficacy is considered weak. More prospective clinical trials are needed to bring lidocaine to a higher level of recommendation. Regardless, lidocaine is an established drug and should be used if sinus rhythm is not attained following unsuccessful defibrillation and epinephrine administration. This is with the assumption that amiodarone is not available in a particular practice. In dogs, lidocaine is administered IV at 2.0-4.0 mg/kg while in cats, the recommended dose is 0.5 mg/kg. This can be repeated in 5-10 minutes. Lidocaine can also be administered intratracheally.
Procainamide is both a supraventricular and ventricular antiarrhythmic. It is specifically used only after a perfusing rhythm is attained but the patient returns to ventricular fibrillation. In dogs, procainamide is administered IV at 5-15 mg/kg. The rate of administration should be slower because rapid administration may cause hypotension.
Magnesium is included in the algorithm for ventricular fibrillation with two main indications: 1) cardiac arrest due to hypomagnesemia and 2) torsades de pointes. It is important to remember that magnesium sulfate depresses the CNS and respiratory system. It can also cause hypotension. The recommended dose for magnesium sulfate in cases of life-threatening ventricular arrhythmia is 100 mg/kg. Magnesium sulfate is diluted with 5% dextrose in water and given over 5-15 minutes.
Electrical defibrillation is recommended to be performed in a stacked fashion which means that shocking is done 3 times in a consecutive fashion without pulse check in between. The rhythm on the ECG monitor should be checked in between shocks and if it becomes sinus, defibrillation will be stopped.
In the new Guideline, defibrillators that deliver a biphasic waveform are acceptable.
The highlights in post-resuscitation care include the following recommendations:
1. Hyperventilation is not recommended unless there is a possibility of brain herniation. Hyperventilation will decrease blood flow to the brain and can result in an auto-PEEP (positive-end expiratory pressure). This auto-PEEP leads to increased cerebral venous and intracranial pressures.
2. It is important to correct hyperthermia during the post-resuscitation phase. If the patient is mildly hypothermic (>33 C [91.5F) but hemodynamically stable, active rewarming is not needed. This recommendation is based on the finding that mild hypothermia may be beneficial to neurological outcome. Despite this finding, the new Guideline does not recommend induction of hypothermia post-resuscitation.
There are other recommendations in the post-resuscitation phase. They are not included here because they are old concepts that still work.