CPCR 2010: techniques and updates (Proceedings)

CPCR is the restoration of spontaneous circulation AND the preservation of neurologic function. CPCR techniques are constantly evolving through laboratory and clinical research. The most comprehensive review of currently accepted American Heart Association (AHA) Guidelines can be found in the 2005 AHA Guidelines for CPR and Emergency Cardiac Care.

CPCR should be instituted in any dog or cat that lacks a patent airway, spontaneous respiration, or spontaneous circulation. The decision to initiate CPCR ultimately lies with the appropriately informed owner of the pet. A "code" status is an important piece of information to require from owners whether the problem that their pet is presenting with is likely to result in a situation requiring CPCR or not. The code status will direct the team whether to resuscitate or not (DNR). In this system, the veterinarian would make appropriate decisions as to what techniques should be employed to optimize the likelyhood of successful resuscitation.

Facility Preparedness:

The first key to successful CPCR is preparedness. Preparedness originates with the appropriate equipment and education of team members. Mock CPCR drills on simulated animals are an excellent exercise to improve the functioning of the team. Supplies critical to initiating CPCR can be found in Table 1.

Table 1: Crash Box Contents. Shaded boxes indicate critical supplies.

Current Recommendations for Basic CPCR:

One of the keys to a successful "code" is for the team leader to rapidly assess the patient and delegate tasks to various members of the team. The leader must endotracheally intubate the patient (AIRWAY), as this step is THE MOST COMMON source of error in an arrest situation. One individual should be assigned to administering 10-24 breaths per minute (100% oxygen) (BREATHING) and maintaining endotracheal intubation by securing the endotracheal tube. A lower respiratory rate is most often utilized. This same individual should serve as a record keeper / timekeeper. One individual should institute chest compressions (CIRCULATION) at 100-120/minute. Chest compressions are most easily performed with the patient in right lateral recumbency with the hands placed atop one another over the base of the heart. The heart can be grasped and compressed between the hands in very small dogs and cats. In the situation in which a single rescuer is present, priority should be given to thoracic compressions over positive pressure ventilations. At this point in the "code", the team leader should assess whether compressions are generating a palpable pulse or improvement in mucous membrane color. If the compressions are not generating adequate pulses, the position of the hands should be altered slightly or other technical alterations made, and compressions resumed.

The decision to utilize open chest CPCR is based on the underlying pathology triggering the cardiac arrest, the size of the patient, and a lack of success of closed-chest CPCR. Absolute indicutions for immediate open-chest CPCR include pleural space (pneumothorax, pleural effusion, diaphragmatic hernia), pericardial space disease (pericardial effusion), and penetrating thoracic trauma that triggered the cardiac arrest. Open-chest CPCR should be considered in any animal in which closed chest CPCR is not successful.

Vascular Access and CPCR:

Vascular access has many purposes in the CPCR setting. Vascular access will allow for the administration of drug therapy in all patients and for IV fluids if the arrest occurred due to hypovolemia. The route of vascular access that can be acquired most rapidly is the best one for the situation. In a neonate, the intraosseous route is probably the most practical. In the event that vascular access cannot be rapidly established, drug therapy (epinephrine and atropine) can be administered at double the recommended dose down the endotracheal tube.

Drug therapy and Defibrillation in CPCR:

Electrocardiographic rhythm will dictate the necessity for drug therapy or defibrillation. Ventricular fibrillation necessitates immediate defibrillation. If a defibrillator is unavailable, a firm precordial "thump" may (although unlikely) restore a spontaneous rhythm.

Many arrest situations encountered in veterinary medicine are actually severe bradyarrhythmias ("vagal" arrests). Many of these bradyarrhythmias are associated with vomiting. Consequently, vomiting must be preemptively controlled in the critically-ill patient if possible. Bradyarrhythmias encountered in a CPCR setting should be treated with atropine. Atropine should be administered (0.04mg/Kg IV) once in any unwitnessed arrest and especially in those in which the arrest may have had a vagal origin.

It is a common misconception that epinephrine "jump starts the heart". Epinephrine is used in the CPCR situation to improve blood pressure, increase blood flow to vital organs, and improve venous return to the heart through peripheral vasoconstriction (α-adrenergic effect). In the face of asystole or pulseless electrical activity (formerly termed electromechanical dissociation), epinephrine should be administered every 5 minutes. Both low dose and high dose epinephrine protocols are described in human medicine. It is recommended that low dose epinephrine initially be administered every 3-5 minutes during CPCR, switching to the high dose only if there is a lack of response to the lower doses. Epinephrine dosing may be rapidly calculated according to the following rule of thumb: 1 ml / 10Kg of the 1:10,000 formulation for low dose, or of the 1:1,000 formulation for high dose.

Updates of Techniques and Technologies:

Hypothermia: Hypothermia often develops spontaneously in patients undergoing CPCR. In addition, there is recent evidence in both animal and human trials that permissive hypothermia or active induction of mild to moderate hypothermia may have some protective benefit on neurologic outcome in patients that have undergone cardiac arrest.

Epinephrine vs. Vasopressin: Significant debate has arisen recently over the most appropriate vasopressor drug for administration during CPCR. Epinephrine and vasopressine both cause peripheral vasoconstriction, thus increasing mean arterial pressure and improving venous return. In humans, there appears to be no clear advantage in either survival or neurologic outcome when vasopressin is compared to epinephrine as the vasoconstrictor of choice for use in CPCR.

Inspiratory Impedence Threshold Valve Device (IITVD): During the decompression phase of the chest compression, intrathoracic pressure decreases slightly thus promoting venous return, however, air will also be drawn into the lungs during this phase of chest compression thus impairing some of this venous return. The IITVD prevents movement of gases into the lungs during the decompression phase of CPCR (making intrathoracic pressure more negative) thus improving venous return, stroke volume, cardiac output, and oxygen delivery to the tissues.

Biphasic Defibrillators: Most defibrillators used in veterinary medicine are monophasic defibrillators. Monophasic defibrillators (3-5J/Kg) deliver the shock in one direction. Biphasic defibrillators (2-4J/Kg) deliver half of the shock in one direction and the other half of the shock in the other direction. Biphasic defibrillators have been available for approximately 10 years, and most new defibrillators are biphasic in nature. Biphasic defibrillation has demonstrated better defibrillation abilities at a lower energy level than monophasic defibrillation with less cardiac injury.

Prognosis:

Despite often-heroic efforts, prognosis for dogs and cats that undergo cardiac arrest is extremely poor. A 1992 study from Kass et al. identified 198 dogs and cats that underwent cardiac arrest and CPCR. 56 dogs and cats (28.3%) had return of spontaneous circulation, and 6 (3%) lived more than one week following CPCR. Four of these 6 patients had cardiac arrest while undergoing anesthesia. Five (2.5%) were discharged from the hospital alive. Only 3 (1.5%) were still alive one month later. A more recent retrospective study by Hofmeister EH et al (JAVMA 2009) found a return of spontaneous circulation in 35% (56/161) of dogs and 44% (19/43) of cats. Survival to discharge from the hospital was 6%. The general poor prognosis in patients that undergo cardiac arrest should not preclude ongoing attempts to better the performance of our teams in CPCR situations nor the advancement of research designed to improve patient survival.

*Significant portions of these proceedings have been previously published for various veterinary continuing education meetings.

Further Reading:

1. Cole SG, Otto CM, et al. Cardiopulmonary cerebral resusucitation in small animals-a clinical practice review Part I. Journal of Veterinary Emergency and Critical Care 2002; 12: 261-267.

2. Cole SG, Otto CM, et al. Cardiopulmonary cerebral resusucitation in small animals-a clinical practice review Part II. Journal of Veterinary Emergency and Critical Care 2002; 13: 13-23.