In its earliest forms, cardiopulmonary resuscitation (CPR) is most likely as old as human society itself.
In its earliest forms, cardiopulmonary resuscitation (CPR) is most likely as old as human society itself. Depictions of mouth-to-mouth ventilation appear in ancient Egyptian hieroglyphics, and descriptions appear in the bible. Modern CPR techniques emerged in the late 1950's and early 1960's. Since that time, there has been widespread acceptance of CPR as the cornerstone of basic cardiac life support. Despite more than 30 years of research, the methods used during CPR have changed very little. Survival rates in humans requiring CPR remain low (between 5% and 15% depending upon the study). In veterinary patients, rates for survival to hospital discharge have been reported to be between 5% and 10%. In recent years the term cardiopulmonary cerebral resuscitation (CPCR) has come into vogue. This change in terminology reflects a recognition, on the part of researchers, that maintenance of cerebral blood flow plays a central role in the success of resuscitation attempts.
Recently, the development of automated electrical defibrillators has provided an important step forward in CPR. The success of these devices is due to the fact that ventricular fibrillation and pulseless ventricular tachycardia are the most common arrest rhythms in people. In contrast, only about 20% of dogs had either of these two rhythms as their initial rhythm in one study. This means that a much smaller percentage of dogs and cats are likely to benefit from early defibrillation.
This discussion will assume a basic knowledge of both basic and advanced cardiac life support and will focus upon new advances and theories that may have an impact on the way CPCR is performed in small animals.
Defibrillation is considered the definitive therapy for ventricular fibrillation and pulseless ventricular tachycardia. The sooner defibrillation occurs, the higher the likelihood of successful resuscitation. When it is provided immediately after the onset of ventricular fibrillation the success rate of defibrillation is extremely high. Current recommendations in people are that chest compressions should be delayed in order to provide early defibrillation when indicated and the appropriate equipment is available. Some newer studies in people have questioned this approach. These studies showed that a short period of chest compressions (typically 2-3 minutes) followed by defibrillation may be more successful than immediate defibrillation. The theory behind this approach is that providing the myocardium with a short period of perfusion prior to defibrillation may improve outcome. In our institution, the installation of a continuous telemetry unit that records a history of EKG tracings for the prior 24 hours has shown that a significant number of patients have a period ventricular fibrillation before developing asystole. Intervention during this period of fibrillation would potentially improve patient outcome.
Interposed abdominal compression includes all the steps of ordinary CPR with the addition of external mid-abdominal compressions by a second or third individual, timed between chest compressions. The abdominal compressions are delivered in counterpoint to the rhythm of chest compressions, so that abdominal pressure is maintained whenever the chest is not being compressed. Pulses of central abdominal pressure are applied just cranial to the umbilicus. Hand position, depth, rhythm, and rate of abdominal compression are similar to those for chest compressions. This technique achieved some notoriety in the1990's after Sack et al. published a clinical study, involving several hundred patients, that suggested an approximate doubling or immediate resuscitation success and neurologically intact, long term survival. A recent meta-analysis of human clinical trials was favorable showing significant improvement in short-term survival.
Implementation of interposed abdominal compressions has occurred slowly in both humans and animals. This likely has occurred due to the practical difficulty associated with performing this technique. The way the technique is described, the individual performing chest compressions should say "one-and-two-and-three". The interposed abdominal compressions should be performed and the "and". In smaller patients, one individual may perform both the thoracic compressions and interposed abdominal compressions. Interposed abdominal compressions should not be performed in patients with hemoperitoneum due to the possibility of dislodging an established blood clot and causing further abdominal hemorrhage. We have found it difficult to coordinate the activity between the individual performing the thoracic compressions and the person performing the interposed abdominal compression. Potential improvement in patient outcome warrants strong consideration for the inclusion of interposed abdominal compressions in veterinary patients.
Epinephrine acts to increase coronary blood flow by increasing mean arterial blood pressure in patients undergoing CPCR. However, it is also associated with increased myocardial oxygen demand, ventricular arrhythmias, and myocardial dysfunction during the period after resuscitation. The theory behind using low dose epinephrine is that these myocardial side-effects can be minimized while still increasing mean arterial blood pressure. The current human guideline is to initially use low dose epinephrine (0.01 mg/kg). High-dose epinephrine (0.1 mg/kg) may be used if CPCR using low-dose epinephrine in unsuccessful. There are no studies of high versus low-dose epinephrine in clinical small animal patients.
The algorithm for performing CPCR in humans is undergoing major change. There is now a growing belief, particularly for out of hospital arrest, that chest compressions are more important to the ultimate outcome the airway management or ventilation. This stems from research in humans that found chest compressions were being performed only 38% of the time during CPCR. In other words, for more than half the time (62%) of the resuscitation effort no chest compressions were being performed. The most common reasons for interruption of chest compressions were repeatedly reassessing the patient, inserting a central line, and tracheal intubation. The consequences of chest compression interruptions are profound. Such interruptions compromise resuscitation hemodynamics by decreasing coronary perfusion pressure and resultant blood flow, and thereby lower survival. It takes up to 30 seconds of chest compressions to build maximal blood flow levels. After interrupting chest compressions for only 5 seconds, most forward blood flow has ceased.
Closed-chest cardiac compressions provide some ventilation to lungs and if only one person is present in the case of a cardiac arrest, attention should be concentrated on chest compressions until additional assistance arrives. Reassessment of the patient during CPCR should be limited. Interruptions to chest compressions should be limited even for endotracheal intubation or venous access. It should be noted that patients that die secondary to hypoxia (i.e. congestive heart failure) will have minimal to no ventilation during chest compression and these patients should receive positive pressure ventilation.
Epinephrine has been used during CPCR for more than 100 years. As discussed earlier, its use does not come without side effects including increased myocardial oxygen demand, and ventricular arrhythmias. Since it was found that endogenous vasopressin levels in successfully resuscitated patients were significantly higher than levels in patients who died, it was postulated that it might be beneficial to administer vasopressin during CPCR. Laboratory studies of CPCR revealed that vasopressin was associated with better blood flow to vital organs, delivery of cerebral oxygen, chances of resuscitation, and neurologic outcome than epinephrine. Vasopressin acts to increase mean arterial blood pressure by binding V1-receptors on vascular smooth muscle. It does not have the negative myocardial side effects seen with epinephrine.
A recent prospective study by Wenzel et al. found that vasopressin (0.8 units/kg IV) was least as good as epinephrine in humans with out of hospital cardiac arrest. Interestingly, the subgroup that benefited the most from vasopressin was patients with asystole. Since this is the most common arrest rhythm in small animals there very well may be a place for vasopressin in.
Once there is restoration of spontaneous circulation (ROSC) every effort should be made to identify and correct the underlying cause of the arrest. In the post-resuscitive phase most patients are at risk for another CPA and careful monitoring and early intervention are essential. It is estimated that 40-50% of animals that experience CPA will have ROSC. Despite this, a much smaller number (3-5%) will survive to hospital discharge.