| BackgroundVentricular fibrillation (VF) is one of the most common arrhythmia causing sudden cardiac death. Previous studies have demonstrated that coronary perfusion pressure (CPP) is the best single predictor of successful defibrillation resulting in return of spontaneous circulation (ROSC). CPP was usually calculated as the aortic-to-right atrial pressure gradient during the relaxation phase of cardiopulmonary resuscitation (CPR). It is always used to evaluate the quality of CPR and the probability of successful CPR. There existed little information on the hemodynamics during VF before CPR. Whether there is hemodynamics during untreated VF before CPR and whether it can be used to predict the probability of ROSC? Whether VF waveform during untreated VF has some significance as a warning? All these questions are still needed to study.The most effective therapies for VF are defibrillation and CPR. However, with the duration of VF, the probability of successful defibrillation declined. Pharmacologic therapy to prevent or treat VF (as an adjunct to defibrillation) using currently available anti-arrhythmic agents has been limited by lack of efficacy and pro-arrhythmic effects. Thus, it is necessary to develop much safer and more effective drugs. Gap junction between cells is formed by different types of gap junction proteins (connexins), through which intercellular communication could be fulfilled. Therefore, disorder of the expression of connexins may lead to abnormal intercellular communication resulting in electrophysiological heterogeneity which may play an important role in arrhythmia. ZP123is a novel anti-arrhythmic peptide by regulating the gap junction proteins. It did not affect ionic channels and had no side effect of pro-arrhythmia. However, there are few studies on its effect on VF, especially prolonged VF. In the present study the effect of ZP123on prolonged VF was evaluated by analyzing hemodynamic variables and VF waveform during untreated VF before CPR.Objectives(1) To evaluate whether CPP and VF waveform during untreated VF could be used to predict the probability of ROSC;(2) To analyze whether VF waveform could be used to substitute for CPP to predict the probability of ROSC as noninvasive indicators;(3) To investigate the effect of ZP123on prolonged VF in swine.MethodsVF was electrically induced in40pigs. Twenty animals were not given special interventions before VF. The other twenty animals randomly received either ZP123or saline control infusion before VF. Untreated VF lasted for8min. If a shock was unsuccessful, a ’rescue shock’ of higher joule was applied from an initial70J to100J (the second time) then150J (the third time), and the subsequent energy was150J. All animals were given2min of chest compression before every defibrillation. Adrenaline and atropine were given when necessary during the process of rescue. The rescue was stopped until the animals attained ROSC or the whole rescue time lasted for30min. Hemodynamics (aortic systolic pressure:AOSP, diastolic aortic pressure:AODP, right atrial pressure:RAP, coronary perfusion pressure:CPP), VF mean frequency (VFmf) and VF mean amplitude (VFma) during untreated VF were analyzed by a multipurpose polygraph. After the experiment, the non-intervention20animals were divided into two groups, ROSC or no-ROSC group. Hemodynamics, VFmf, and VFma were compared between the two groups. Meanwhile, VFmf, VFma, hemodynamics, the rate of the first three successful defibrillation and ROSC were compared between the drug and control groups. ResultsThere were7animals in ROSC group and13in no-ROSC group. Hemodynamic variables were better and both VFmfand VFma were higher in the ROSC animals than those in the no-ROSC animals (AOSP:38.75±20.41mmHg vs.24.52±11.69mmHg; AODP:31.34±16.81mmHg vs.18.48±8.47mmHg; RAP:22.44±4.20mmHg vs.18.17±4.69mmHg; CPP:8.24±16.12mmHg vs.0.82±4.55mmHg; VFmf:11.33±2.02Hz vs.9.96±1.59Hz; VFma:0.31±0.15mV vs.0.18±0.07mV, all P＜0.01). CPP, VFmf and VFma during untreated VF could be used to predict the probability of ROSC (area of ROC curve:0.86,0.76, and0.82, respectively). Both VFmf and VFma had a positive correlation with CPP (r=0.67; r=0.71, P=0.005; P=0.002, respectively). Compared with control group, VFmf was higher but VFma was lower during the8min of VF in the drug group (11.8±2.1Hz vs.10.4±2.0Hz;0.24±0.10mV vs.0.31±0.16mV, P=0.0001; P=0.01, respectively). Hemodynamic variables in the two groups were comparable (AOSP:28.58±12.09mmHg vs.29.42±7.31mmHg; AODP:22.55±6.39mmHg vs.23.05±3.63mmHg; RAP:21.68±3.44mmHg vs.21.21±2.82mmHg; CPP:2.28±4.44mmHg vs.2.22±1.20mmHg, all P＜0.05). The defibrillation threshold was lower and the rate of successful defibrillation was higher in the drug group than those in the control group (92.2±26.4J vs.133.3±28.9J;90%vs.30%, P=0.045; P=0.02, respectively). The rate of ROSC was no difference between the two groups (40%vs.30%,P=1.00).Conclusions(1) Both CPP and VF waveform during untreated VF before CPR have a higher predictive value for ROSC;(2) VF waveform could be used to substitute for CPP to predict the probability of ROSC as noninvasive indicators;(3) In prolonged VF, ZP123could decrease the defibrillation threshold and improve the rate of successful defibrillation. However, it could not improve the rate of ROSC which may be related with its side-effect of decreasing VFma. |
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