Combination of cardiac pacing and epinephrine does not always improve outcome of cardiopulmonary resuscitation.

We hypothesized that the combination of cardiac pacing and epinephrine would yield a better efficacy for cardiopulmonary resuscitation (CPR) and the combination of 2 therapies at different opportunity would achieve the same results of CPR. Cardiac arrest was induced by clamping the tracheal tubes in 60 Sprague-Dawley rats. At 10 minutes of asphyxia, the animals were prospectively randomized into 5 groups (n = 12/group), and received saline (Sal-gro, 1 mL, intravenous [i.v.]), epinephrine (Epi-gro, 0.4 mg/kg, i.v.), pacing (Pac-gro, transesophageal cardiac pacing combined with saline 1 mL, i.v.), pacing + epinephrine group 1 (PE-gro1, transesophageal cardiac pacing combined with epinephrine 0.4 mg/kg, i.v.), or pacing + epinephrine group 2 (PE-gro2, transesophageal cardiac pacing combined with epinephrine 0.4 mg/kg, i.v., 4 minutes after the transesophageal cardiac pacing initiating and failing to resuscitate the animals), followed by initiation of CPR. Restoration of spontaneous circulation in Sal-gro was lower than in Epi-gro, Pac-gro, PE-gro1, and PE-gro2 (16.67% vs 66.67%, 66.67%, 100%, and 100%; P < .05 or P < .001, respectively). The proportions of withdrawing ventilator and 2-hour survival proportions in Pac-gro and PE-gro2 were higher than in Epi-gro and PE-gro1 (8/8, 10/12 vs 1/8, 2/12, respectively, P < .01, and 7/8, 8/12 vs 1/8, 2/12, respectively, P < .05 or P < .01). Mean survival time in Pac-gro and PE-gro2 were longer than in Epi-gro and PE-gro1 (P < .05 or P < .01). Therefore, the combination of 2 therapies does not always improve outcome of CPR. It is obvious that the combination of transesophageal cardiac pacing with delayed administration of epinephrine yields a better outcome compared to the combination of 2 therapies at the same time during CPR in a rat asphyxia cardiac arrest model.

A simpler cardiac arrest model in rats.

Two disadvantages of electrical induction of cardiac arrest used currently are that it is a technically complicated procedure and the consequent thermal injury, which prompts us to search for a simpler method with less adverse effect to induce ventricular fibrillation (VF) in rats. Different potential (18, 24, 30, and 36 V) of alternating current (AC) were administered to elicit VF in 15 rats via pacing electrode placed in esophagus. Four minutes after onset of VF, conventional cardiopulmonary resuscitation (CPR) was initiated. Restoration of spontaneous circulation was defined as the return of supraventricular rhythm with a mean aortic pressure of 20 mm Hg or greater for a minimum of 5 minute. Ventricular fibrillation was achieved by short interval of AC stimulation in all of the rats. After the termination of prolonged AC stimulation, electrocardiogram indicated VF occurred in 6 of 15 rats, asystole in 3 of 15 rats and pulseless electrical activity in 6 of 15 rats. Before CPR, however, electrocardiogram indicated that only 2 of 15 and 4 of 15 animals remained in VF and pulseless electrical activity, respectively, whereas 9 of 15 animals presented as asystole. After CPR, 11 of 15 animals were resuscitated. Necropsy showed that there was no gross evidence of thermal injury on the surface layer of the heart. Therefore, development of a rat cardiac arrest model by transesophageal AC stimulation is simpler and less adverse effect, which may have practical significance for facilitating experimental investigation on cardiac arrest and CPR.

A simpler cardiac arrest model in the mouse.

OBJECTIVE: Delivering alternating currency (AC) to right ventricular endocardium to induce ventricular fibrillation (VF) in mice is complicated. We tried to validate whether transoesophageal AC stimulation could induce VF and how long AC stimulation had to be sustained to prevent the spontaneous cardioversion of VF in mice. METHODS: A pacing electrode was inserted orally into the oesophagus and AC was delivered to esophagus through the pacing electrode to stimulate the heart and induce VF in 15 mice. The incidence of VF and time of AC stimulation were recorded 4min after onset of VF cardiopulmonary resuscitation (CPR) was started. RESULTS: VF was induced by short AC stimulation in all 15 mice. With the prolongation of AC stimulation, the incidences of spontaneous cardioversion of VF decreased whereas the incidence of pulseless electrical activity (PEA) increased accordingly. Following the termination of prolonged AC stimulation, VF occurred only in 1 of 15 mice, but PEA in 14 of 15 mice. Before CPR 1 of 15 and 12 of 15 animals remained in VF and in PEA, respectively, while 2 of 15 animals developed into asystole. After CPR, 11 of 15 animals were successfully resuscitated. CONCLUSION: VF can be induced by a short period of transoesophageal AC stimulation in mice. However, prolonged AC stimulation is prone to induce PEA other than VF. Nonetheless, the development of a mouse CA model in this manner is simpler and easier, which may have practical significance for facilitating experimental investigation on CA and CPR.

Epinephrine, but not vasopressin, improves survival rates in an adult rabbit model of asphyxia cardiac arrest.

Although vasopressin has been reported to be more effective than epinephrine for cardiopulmonary resuscitation in ventricular fibrillation animal models, its efficacy in asphyxia model remains controversy. The purpose of this study was to investigate the effectiveness of vasopressin vs epinephrine on restoration of spontaneous circulation (ROSC) in a rabbit model of asphyxia cardiac arrest. Cardiac arrest was induced by clamping endotracheal tube. After 5 minutes of basic life-support cardiopulmonary resuscitation, animals who had no ROSC were randomly assigned to receive either epinephrine alone (epinephrine group; 200 microg/kg) or vasopressin alone (vasopressin group; 0.8 U/kg). The coronary perfusion pressure (CPP) was calculated as the difference between the minimal diastolic aortic and simultaneously recorded right atrial pressure. Restoration of spontaneous circulation was defined as an unassisted pulse with a systolic arterial pressure of 60 mm Hg or higher for 5 minutes or longer. We induced arrest in 62 rabbits, 15 of whom had ROSC before drug administration and were excluded from analysis. The remaining 47 rabbits were randomized to epinephrine group (n = 24) and vasopressin group (n = 23). Before and after drug administration, CPP in epinephrine group increased significantly (from -4 +/- 4 to 36 +/- 9 mm Hg at peak value, P = .000), whereas CPP in vasopressin group increased only slightly (from 9 +/- 5 to 18 +/- 6 mm Hg at peak value, P = .20). After drug administration, 13 of 24 epinephrine rabbit had ROSC, and only 2 of 23 vasopressin rabbit had ROSC (P < .01). Consequently, we conclude that epinephrine, but not vasopressin, increases survival rates in this adult rabbit asphyxia model.

Ventricular fibrillation induced by transoesophageal cardiac pacing: a new model of cardiac arrest in rats.

OBJECTIVE: To investigate whether transoesophageal cardiac pacing can induce ventricular fibrillation (VF) and how long the cardiac pacing has to be sustained to prevent the reversion of the VF induced. METHODS: A pacing electrode was inserted orally into the oesophagus and high-frequency ventricular pacing was performed so as to elicit VF in 25 Sprague-Dawley rats. Incidences of VF and time of cardiac pacing were observed and recorded. Four minutes after onset of VF cardiopulmonary resuscitation (CPR) was initiated. RESULTS: A short interval of high-frequency ventricular pacing caused an immediate drop of blood pressure, loss of pulse and increase of right atrial pressure in the same time frame. When the cardiac pacing was terminated, VF was elicited at least once or more than once in all of the 25 rats. However, the VF elicited by the burst stimulation could be defibrillated spontaneously. With the prolongation (120-180 s) of cardiac pacing, the incidence of defibrillation of VF decreased from 100 to 0%. VF persisted in 19 of 25 animals, developed into asystole in 5 of 25 animals and converted into pulseless electrical activity in 1 of 25 animals prior to CPR. Following CPR 22 of 25 animals were resuscitated. CONCLUSIONS: Transoesophageal cardiac pacing can induce VF in rats. However, the cardiac pacing is required for at least 120-180 s to ensure that VF does not spontaneously convert. We can use the technique to establish a new and simpler rat cardiac arrest (CA) model, which may facilitate experimental investigation on CPR.