Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model

PurposePrevious studies implicate that the mitochondrial injury may play an important role in the development of post-resuscitation myocardial dysfunction, however few of them are available regarding the ultrastructural alterations of myocardial mitochondria, mitochondrial energy producing and utilization ability in the stage of arrest time (no-low) and resuscitation time (low-flow). This study aimed to observe the dynamic changes of myocardial mitochondrial function and metabolic disorders during cardiac arrest (CA) and following cardiopulmonary resuscitation (CPR).MethodsA total of 30 healthy male Sprague-Dawley rats were randomized into three groups: 1) VF/CPR: Ventricular fibrillation (VF) was electrically induced, and 5 min of CPR was performed after 10 min of untreated VF; 2) Untreated VF: VF was induced and untreated for 15 min; and 3) Sham: Rats were identically prepared without VF/CPR. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 min were calculated from ECG signals. The rats' hearts were quickly removed at the predetermined time of 15 min after beginning the procedure to gather measurements of myocardial mitochondrial function, high-energy phosphate stores, lactate, mitochondrial ultrastructure, and myocardial glycogen.ResultsThe mitochondrial respiratory control ratios significantly decreased after CA compared to sham group. CPR significantly increased respiratory control ratios compared with untreated VF animals. A significant decrease of myocardial glycogen was observed after CA, and a more rapid depletion of myocardial glycogen was observed in CPR animals. CPR significantly reduced the tissue lactate. The mitochondrial ultrastructure abnormalities in CPR animals were less severe than untreated VF animals. AMSA decayed during untreated VF; however, it was significantly greater in CPR group than the untreated VF group. In addition, AMSA was clearly positively correlated with ATP, but negatively correlated with myocardial glycogen.ConclusionImpairment of myocardial mitochondrial function and the incapability of utilizing glycogen were observed after CA. Furthermore, optimal CPR might, in part, preserved mitochondrial function and enhanced utilization of myocardial glycogen.     

Electrocardiographic prediction of the success of cardiac resuscitation.

OBJECTIVES: To identify a method for predicting the success or failure of a defibrillatory shock such as to avoid potentially detrimental interruptions of cardiopulmonary resuscitation (CPR). Such a method would also guide more optimal programming of automated external defibrillators. DESIGN: Prospective, observational animal study. SETTING: Medical research laboratory in a university-affiliated research and educational foundation. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation (VF) was electrically induced in 66 domestic pigs. After an interval of between 3 and 5 mins of untreated VF, precordial compression was begun. Electrocardiographic lead 2 was monitored and artifacts produced during precordial compression were removed by digital filtering. MEASUREMENTS AND MAIN RESULTS: In the derivation study, electrical defibrillation restored spontaneous circulation in 30 of the 66 animals. Successfully resuscitated animals had significantly greater coronary perfusion pressure, maximum VF amplitude, mean VF amplitude, and dominant VF frequency. No animals were resuscitated if the coronary perfusion pressure was <8 mm Hg, maximum amplitude was <0.48 mV, mean amplitude was <0.25 mV, or dominant frequency <9.9 Hz independently of the duration of untreated VF. When mean amplitude and dominant frequency were combined, the predictability was further improved. In an additional validation study of 14 animals, consecutive defibrillations were uniformly unsuccessful if the combination of mean amplitude and dominant frequency did not exceed the threshold values obtained in derivation study. CONCLUSION: Mean VF amplitude alone or in combination with dominant frequency of VF was expressed as a numerical score. It served as an objective noninvasive measurement on a par with that of coronary perfusion pressure for predicting the success of defibrillation. As such, it minimizes the detriment of repetitively interrupting mechanical interventions during CPR for electrical defibrillation when an electrical shock predictably fails to restore an effective rhythm.     

Endocardial and transcutaneous cardiac pacing, calcium chloride, and epinephrine in postcountershock asystole and bradycardias

Clinically, asystole or a bradyarrhythmia may follow countershock of ventricular fibrillation (VF) in up to 40% of attempts. This study evaluated the effects of artificial cardiac pacing, calcium chloride (CaCl2), and epinephrine in postcountershock asystole/bradycardia. Micromanometer catheters were positioned in the aorta (Ao) and right atrium (RA) of ten dogs and VF induced by right ventricular (RV) stimulation. After 2 min of VF, a 400-J countershock was given. In six animals, asystole or a pulseless bradyarrhythmia followed one countershock. In four animals, up to three countershocks were needed to terminate VF and resulted in asystole or a pulseless bradyarrhythmia. Thirty seconds after termination of VF, cardiac pacing was begun in all animals using conventional RV endocardial pacing (RVEP) or a transcutaneous transthoracic pacing (TTP) technique. RVEP and TTP produced ventricular depolarizations, but electrical capture was never associated with Ao pressure fluctuations. After 2 min of pacing, CaCl2 was given and chest compressions and artificial ventilations (CPR) initiated. CaCl2 had no effect on CPR pressures. After 2 min of CPR, RVEP and TTP were again studied; capture without Ao pressure fluctuations was seen in all animals. Epinephrine was then given and CPR reinstituted. Epinephrine produced a significant increase in CPR Ao systolic pressure (58 +/- 13 to 84 +/- 24 mm Hg, p less than .001) and end-diastolic coronary perfusion pressure (Ao-RA) (9 +/- 4 to 34 +/- 8 mm Hg, p less than .001). Within 94 +/- 53 sec after epinephrine, spontaneous circulation was restored in eight animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

The duration of ventricular fibrillation required to produce pulseless electrical activity

The duration of untreated (no cardiopulmonary resuscitation) ventricular fibrillation (VF) needed to produce postdefibrillation pulseless electrical activity (PEA) was determined in 9 anesthetized swine ranging in weight from 20 to 30 kg. VF was induced electrically by a right ventricular catheter electrode, while arterial pressure and the electrocardiogram were recorded. VF was confirmed by the presence of VF waves in the electrocardiogram and a loss of pulsatile arterial pressure. VF was allowed to persist for 15-second increments (eg, 15, 30, 45, etc), after which defibrillation was achieved with transchest electrodes and the presence or absence of PEA was noted. If PEA was present, rhythmic chest compressions were applied to rescue the animal. Just after initiation of VF and just before defibrillation, VF wave frequency was measured. PEA was encountered in 100% of the trials after 180 seconds of VF. The threshold duration for PEA was 60 seconds. VF wave frequency decreased with the passage of time. At VF initiation, VF wave frequency (f0) ranged from 6 to 15 per second, with a mean of 10.1+/-2.1 per second. At 180 seconds (f180), the mean frequency was 4.0+/-0 per second. It was only possible to eliminate PEA and restore pumping in 1 animal when untreated VF lasted more than 180 seconds. There was no clear transition in the frequency of the VF waves with the passage of time that could predict the possibility of postdefibrillation PEA. Moreover, because of the different initial VF wave frequencies and the different rates of decrease with time, a measurement of VF wave frequency is unlikely to be informative on how long VF had been present. A consistent finding in this swine study of prolonged untreated VF was a rise in blood K+ which increased from a normal prefibrillation value of about 4 mEq/L to 8 to 12 mEq/L at 180 seconds. The longer the duration of VF, the higher the K+.     

Interactions between CPR and defibrillation waveforms: effect on resumption of a perfusing rhythm after defibrillation

BACKGROUND: Cardiopulmonary resuscitation (CPR) improves survival from cardiac arrest. The interactions between CPR and the new biphasic (BiP) defibrillation waveforms have not been defined. Our purpose was to compare the effect of CPR versus no CPR during BiP and damped sinusoidal (DS) shocks on the termination of ventricular fibrillation (VF) and the resumption of a perfusing rhythm. METHODS: We studied 20 pigs; VF was induced electrically and allowed to persist for 6 min. During VF episodes each pig received (in random order): (a) 6 min of full CPR (continuous ventilation and closed chest mechanical compression (Thumper, Michigan Instruments)) followed by DS defibrillation at 100 J; (b) no CPR, DS defibrillation; (c) 6 min of full CPR and BiP defibrillation at 100 J; and (d) no CPR, BiP defibrillation. RESULTS: BiP shocks with CPR terminated VF in 83% of attempts versus 45% without CPR (15/18 and 5/11 respectively, P<0.05). DS shocks with CPR were successful in terminating VF in 53% of attempts; DS shocks without CPR were successful in 44% (8/15 and 7/16, respectively, P=NS). No animal achieved a perfusing rhythm after shocks of either waveform if CPR did not precede the shocks during the 6-min VF period, whereas if CPR was administered during VF 46% (11/24) of the combined BiP/DS shocks restored a perfusing rhythm (P<0.01). CONCLUSION: In this experimental long duration VF model, CPR was essential for a perfusing rhythm after termination of VF by shocks with either waveform. CPR facilitated the termination of VF and resumption of a perfusing rhythm after biphasic waveform defibrillation but not after damped sinusoidal waveform defibrillation.     

Myocardial performance index following electrically induced or ischemically induced cardiac arrest

OBJECTIVES: We sought to investigate the echocardiographic myocardial performance index (MPI) to assess post-resuscitation myocardial function following electrically and ischemically induced ventricular fibrillation (VF). MATERIALS AND METHODS: VF was induced in fourteen anesthetized pigs weighing 38+/-4 kg. VF was induced electrically in seven animals and ischemically, following transient occlusion of the left anterior descending coronary artery (LAD), in the remaining seven animals. VF was untreated for 7 min after which CPR, including precordial compression and mechanical ventilation was begun. Defibrillation was attempted after 5 min of CPR. MPI, ejection fraction (EF) and fractional area change (FAC) were measured hourly during the following 4 h interval post-resuscitation. RESULTS: Five of seven animals were resuscitated in the electrically induced VF group, and four of seven animals in the ischemically induced VF group. No difference in EF and FAC were observed between the two groups. The MPI, however, was significantly greater at 60 min and 120 min post-resuscitation in animals after ischemically induced VF (p<0.05). CONCLUSION: In this model, left ventricular (LV) MPI was a more sensitive and useful quantitative parameter to assess the LV function than the EF and FAC measurements used routinely. MPI measurements indicated that post-resuscitation myocardial dysfunction may be more severe after ischemically induced VF compared to the electrically induced VF.     

新型大鼠心跳骤停和复苏的机械装置

目的研发由电磁阀系统总控制、压缩气体驱动的新型大鼠电刺激诱发心跳骤停和复苏的机械装置,并探讨其有效性和安全性。方法选用Sprague-Dawley雄性大鼠20只,应用自主开发研制的心跳骤停和复苏机械装置,持续交流电经右心室内膜致颤。在6min心室颤动后,开始给予6min的机械胸外按压和同步机械通气,随后双向波经胸体外除颤。结果15只大鼠复苏成功,自主循环恢复率为75%。电刺激后所有大鼠立刻出现心室颤动,3min的电刺激停止后动物持续表现为室颤而没有自发转复心律现象。心肺复苏期间恢复自主循环组其冠状动脉灌注压恒定在24mmHg左右,显著高于未能恢复自主循环组。结论本新型大鼠心跳骤停和心肺复苏装置的有效性和安全性高,可最大限度减少实验的误差,具有一定的推广应用前景。     

Predicting the success of defibrillation by electrocardiographic analysis

BACKGROUND: We investigated an electrocardiographic signal analysis technique for predicting whether an electrical shock would reverse ventricular fibrillation (VF) in an effort to minimize the damaging effects of repetitive shocks during CPR. METHODS AND RESULTS: An established model of CPR was utilized. VF was electrically induced in anesthetized 40 kg domestic pigs. Defibrillation was attempted after either 4 or 7 min of untreated VF. Failing to reverse VF, a 1 min interval of precordial compression and mechanical ventilation preceded each subsequent defibrillation attempt. The amplitude frequency spectrum of digitally filtered VF wavelets was computed with Fourier analysis during uninterrupted precordial compression from conventional right infraclavicular and left apical electrodes. Of a total of 34 electrical defibrillation attempts, 24 animals were restored to spontaneous circulation (ROSC). An amplitude spectrum analysis (AMSA) value of 21 mV Hz had a negative predictive value of 0.96 and a positive predictive value of 0.78. CONCLUSIONS: AMSA predicted when an electrical shock failed to restore spontaneous circulation during CPR with a high negative predictive value. This method potentially fulfills the need for minimizing ineffective defibrillation attempts and their attendant adverse effects on the myocardium.     

Postresuscitation electrolyte changes: role of arrhythmia and resuscitation efforts in their genesis

Hypokalemia frequently occurs after resuscitation from ventricular fibrillation (VF) in man. To test the casual roles of VF and resuscitation variables in this electrolyte change, we studied six groups of dogs: VF with CPR and electrical cardioversion (n = 9), control dogs with no intervention (n = 9), CPR without arrhythmia (n = 5), electrical cardioversion without arrhythmia (n = 5), CPR and cardioversion without arrhythmia (n = 5), and rapid right ventricular pacing (n = 5) (pacing rate 374 +/- 68 beat/min; BP 79/52 mm Hg during pacing). Blood for K, Ca, Mg, and glucose analysis was collected before each intervention (or at baseline in control animals) and sequentially for 3 hr. Mg had a maximum change of 0.3 mEq/L in the VF group 7 min after resuscitation, but did not change in the other groups (p less than .005). Glucose had a maximum change of 79 mg/dl in the VF group 7 min after resuscitation but did not change in the other groups (p less than .005). Ca had a maximum decrease of 0.4 mg/dl in the VF group 15 min after resuscitation but did not decrease in the other groups (p less than .005). K had a maximum decrease of 0.8 mEq/L in the VF group 60 min after resuscitation, whereas decreases were less in the other groups (p less than .005). Thus, VF caused a rapid rise in Mg and glucose followed by a fall in Ca and K. These changes were independent of resuscitation efforts as well as the moderate hypotension induced by rapid right ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Brain tissue oxygen pressure and cerebral metabolism in an animal model of cardiac arrest and cardiopulmonary resuscitation

OBJECTIVE: Direct measurement of brain tissue oxygenation (PbtO2) is established during spontaneous circulation, but values of PbtO2 during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO2 in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B. METHODS: In 12 pigs (12-16 weeks, 35-45 kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4 min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO2 1.0) with vasopressor therapy after 7, 12, and 17 min (vasopressin 0.4, 0.4, and 0.8 U/kg, respectively). Defibrillation was performed after 22 min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1h. RESULTS: After initiation of VF, PbtO2 decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO2 increased, and reached maximum values 8 min after start of CPR (25 +/- 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dl, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 microg/l after 13 min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC. CONCLUSIONS: Though PbtO2 returned to pre-arrest values during CPR, PbtO2 and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral low-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier.     

The frequency ratio: an improved method to estimate ventricular fibrillation duration based on Fourier analysis of the waveform

BACKGROUND: CPR prior to defibrillation improves survival from prolonged ventricular fibrillation (VF) by over 10%, based on recent studies. Waveform analysis could identify those patients with VF of over 5 to 7-min duration who should receive CPR first. A method based on the changes in the Fourier-derived frequency spectrum over time could improve the ability to identify prolonged VF. METHODS AND RESULTS: The Fourier frequency spectra were calculated on 5-s epochs of VF from 45 swine for 12.5 min. The average power at each frequency shows a marked loss of frequencies above 8 Hz occurring at 5 min accompanied by an increase in the power in frequency spectra from 3 to 5 Hz. A measure termed the frequency ratio is defined as the ratio of the power in the high frequency band from 8 to 24 Hz compared to the power in the low frequency band from 3 to 5 Hz. The frequency ratio is shown to detect 90% of epochs with VF less than 5 min while allowing selection of 74% of those epochs over 5 min. When the frequency ratio is set to detect 90% of episodes of VF under 7 min, it is able to select 88% of those traces with VF over 7 min. The receiver operating curve (ROC) for the frequency ratio has an area under the curve of 0.91 at 5 min and 0.95 at 7 min of VF duration. CONCLUSIONS: The frequency ratio is an improved frequency-based measure of VF duration. Waveform analysis techniques could determine which patients should receive shock first and which should receive a period of CPR prior to shock, thereby increasing probability of survival.     

Left Ventricular Function after Monophasic and Biphasic Waveform Defibrillation: The Impact of Cardiopulmonary Resuscitation Time on Contractile Indices

Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.     

Transthoracic impedance does not decrease with rapidly repeated countershocks in a swine cardiac arrest model

STUDY PURPOSE: Successful defibrillation is dependent upon the delivery of adequate electrical current to the myocardium. One of the major determinant of current flow is transthoracic impedance. Prior work has suggested that impedance falls with repeated shocks during sinus rhythm. The purpose of this study was to evaluate changes in transthoracic impedance with repeated defibrillation shocks in an animal model of cardiac arrest due to ventricular fibrillation (VF). METHODS: VF was electrically induced in anesthetized swine. After 5 min of untreated VF, monophasic or biphasic waveform defibrillation was attempted using a standard sequence of 'stacked shocks' (200, 300, then 360 J, if necessary) administered via adhesive electrodes. If one of the first three shocks failed to convert VF, conventional CPR was initiated and defibrillation (360 J) attempted 1 min later. Strength-duration curves for delivered voltage and current were measured during each shock and transthoracic impedance calculated. Animals requiring a minimum of four shocks were selected for study inclusion. Impedance data from sequential shocks were analyzed using mixed linear models to account for the repeated-measures design and the variability of the initial impedance of individual animals. RESULTS: Thirteen animals (monophasic waveform, n=7, biphasic waveform, n=6) required at least four shocks to terminate VF (range 4-6). Transthoracic impedance did not change from the first shock in the 13 animals (46+/-8 Omega) to the fourth shock (46+/-9 Omega). In animals receiving more than four shocks, transthoracic impedance likewise did not change significantly from the first to the last shock, which terminated VF. The lack of a significant change in impedance was also observed when animals were analyzed according to defibrillation waveform. CONCLUSION: Transthoracic impedance does not change significantly with repeated shocks in a VF cardiac arrest model. This is likely due to the lack of reactive skin and soft tissue hyperemia and edema observed in non-arrest models.     

Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study

OBJECTIVES: To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF). DESIGN: Randomized, controlled trial. SETTING: University animal laboratory. SUBJECTS: Thirty swine (27 +/- 1 kg). INTERVENTIONS: After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks. MEASUREMENTS AND MAIN RESULTS: After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p <.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p <.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation.The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p <.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p <.0001) CONCLUSIONS: Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.     

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.     

Reducing CPR artefacts in ventricular fibrillation in vitro

CPR creates artefacts on the ECG, and a pause in CPR is therefore mandatory during rhythm analysis. This hands-off interval is harmful to the already marginally circulated tissues during CPR, and if the artefacts could be removed by filtering, the rhythm could be analyzed during ongoing CPR. Fixed coefficient filters used in animals cannot solve this problem in humans, due to overlapping frequency spectra for artefacts and VF signals.In the present study, we established a method for mixing CPR-artefacts (noise) from a pig with human VF (signal) at various signal-to-noise ratios (SNR) from -10 dB to +10 dB. We then developed a new methodology for removing CPR artefacts by applying a digital adaptive filter, and compared the results with this filter to that of a fixed coefficient filter. The results with the adaptive filter clearly outperformed the fixed coefficient filter for all SNR levels. At an original SNR of 0 dB, the restored SNRs were 9.0+/-0.7 dB versus 0.9+/-0.7 dB respectively (P<0.0001).     

叹息样呼吸与猪心肺复苏过程中血流动力学变化的研究

目的 研究CPR的病理生理过程,探讨叹息样呼吸对CPR过程中血流动力学的影响.方法 12头北京长白猪,体质量(30±1)kg,麻醉后气管插管,机械通气,连续记录实时呼吸参数.股动脉置管测量主动脉压(AOP),并抽取动脉血;肺动脉漂浮导管置测最右心房压(RAP)及心输出量(CO).以程控电刺激制作室颤(VF)模型.VF4 min后进行标准30:2 CPR 12 min,记录相关参数.结果 CPR过程中pH,PaCO2及乳酸逐渐升高,而PaO2逐渐降低,但PaO2在整个实验过程中均大于50mmHg.10只动物出现叹息样呼吸,但随时间推移逐渐减弱;未出现叹息样乎吸的2只动物均未复苏成功.标准心外按压在多数动物均可产生大干死腔量(VD)的被动通气,但其潮气量随时间推移逐渐减少.因此人工通气在总分钟通气量中所占比例逐渐增加.CO、冠脉灌注压(CPP)与叹息样呼吸分钟通气量(MVg)呈正相关(r分别等于0.736,0.721,P＜0.01);RAP与MVg呈负相关(r=-0.744,P＜0.01).结论 标准CPR能够维持机体12min的氧合;心外按压能够产生大于VD的被动通气;叹息样呼吸可以通过增加CO、CPP及降低RAP产生对自主循环的恢复产生有益的生理作用.

Abstract：

Objective Gasp was defined as a pathology respiration during cardiac arrest. This study was to investigate its effect on hemodynamics during CPR. Method Twelve domestic pigs, weighening (30 ± 1) kg,were anaesthetized. After tracheal intubation and mechanical ventilation, continuous respiratory variables were recorded. An artery catheter was inserted for reference blood samples and measuring aortic artery pressure (AOP).Right atrial pressure (RAP) and cardiac output (CO) were detected by Swan-Ganz catheter. Ventricular fibrillation (VF) was induced by programmed electrical stimulation instruments. After 4 minutes untreated VF, standard 30:2 CPR was done for 12 minutes and the parameters were recorded. Results pH, PaCO2 and lactic acid increased and PaO2 decreased progressively during CPR, whereas PaO2 was up to 50mmHg during the whole protocol. Gasps were observed in 10 animals, but weaken gradually; the left 2 animals with no gasp did not restore of spontaneous circulation (ROSC). Standard CPR could produce passive ventilation more than dead space (VD), but its tidal volume decreased gradually, which led to the percentage of rescue ventilation increased progressively. Positive correlations were found between CO, coronary perfusion pressure (CPP) and minute ventilation of gasps (MVg) (r was 0.736 and 0.721 respectively, both P ＜0.01); negative correlation were found between RAP and MVg (r= -0. 744, P ＜ 0.01). Conclusions Standard CPR could maintain 12 minutes oxygenation of body; compressions could produce enough passive ventilation more than VD; gasps were benefit to ROSC by increasing CO, CPP and decreasing RAP.     

T wave spectral variance for noninvasive identification of patients with idiopathic dilated cardiomyopathy prone to ventricular fibrillation even in the presence of bundle branch block or atrial fibrillation

Conventional methods using Holter ECG recordings for noninvasive risk stratification are limited in patients with idiopathic dilated cardiomyopathy (IDC) prone to ventricular fibrillation (VF) having atrial fibrillation (AF) or bundle branch block (BBB). We therefore investigated, whether spectral assessment of beat-to-beat alternations of repolarization is associated with VF in these patients. Twenty-four-hour Holter ECG recordings in 462 patients with IDC were used. The VF group comprised of 64 consecutive patients who survived cardiac arrest, the no VF group consisted of 398 consecutive patients without a history of malignant ventricular arrhythmia. One hundred patients with ischemic cardiomyopathy (ICM) served as a control group. In each patient, 1,024 consecutive T waves were aligned using cross correlation methods. Two-dimensional Fourier transform (2D FFT) used the data matrix of 1,024 consecutive 200-ms segments centered to the T wave peak. Power spectra of the 2D FFT revealed the frequency content of the T wave in the first dimension and the periodicity of this frequency content in the second dimension. The ratio between periodic frequency contents and the sum of nonperiodic and periodic frequency contents between 0.5 and 50 Hz is equal to the T wave spectral variance (TWSV) index. Thus, TWSV index = 0 would mean that all 1,024 T waves are identical and TWSV index = 1 would mean that the 1,024 T waves are totally variable. The TWSV index was significantly higher in the VF group (0.93 +/- 0.14) than in the no VF group (0.53 +/- 0.13, P < 0.01). The best cutoff between the VF and the no VF group was achieved by using a TWSV index of 0.75 (sensitivity = 89%, specificity = 78%). No significant differences were observed between patients with and without AF or with and without BBB, and between patients with IDC and ICM. Even in the presence of BBB or AF spectral assessment of T wave alternations by TWSV index using 2D FFT in Holter ECG recordings, allows the identification of patients with IDC at risk for VF.     

A new device producing manual sternal compression with thoracic constraint for cardiopulmonary resuscitation

OBJECTIVE: Blood flow during conventional cardiopulmonary resuscitation (CPR) is usually less than adequate to sustain vital organ perfusion. A new chest compression device (LifeBelt) which compresses both the sternum and the lateral thoraces (compression and thoracic constraint) has been developed. The device is light weight, portable, manually powered and mechanically advantaged to minimize user fatigue. The purpose of this study was to evaluate the mechanism of blood flow with the device, determine the optimal compression force and compare the device to standard manual CPR in a swine arrest model. METHODS: Following anesthesia and instrumentation, intravascular contrast injections were performed in four animals and the performance characteristics of the device were evaluated in eight animals. In a comparative outcome study, 42 anesthetized and instrumented swine were randomized to receive LifeBelt or manual CPR. Ventricular fibrillation (VF) was induced electrically and was untreated for 7.5 min. After 7.5 min, countershocks were administered and chest compressions initiated. Pulseless electrical activity (PEA) was observed after one to three shocks in all animals. CPR was continued until restoration of spontaneous circulation (ROSC) or for 10 min after the first shock. If ROSC had not occurred within 5 min of beginning CPR, 0.01 mg/kg of epinephrine (adrenaline) was administered. During CPR, peak systolic aortic pressure (Ao), diastolic coronary perfusion pressure (CPP-diastolic aortic minus diastolic right pressure) and end-tidal CO(2) were measured. RESULTS: Angiographic studies demonstrated cardiac compression as the mechanism of blood flow. Optimal performance, determined by coronary perfusion pressure, was observed at a sternal force of 100-130 lb (45-59 kg). In the comparative trial, significant differences in the measured CPP were observed between LifeBelt and manual CPR both at 1 min (15+/-8 mmHg versus 10+/-6 mmHg, p<0.05) and 5 min (17+/-4 mmHg versus 13+/-7 mmHg, p<0.02) of chest compression. A greater (p<0.05) ETCO(2), a marker of cardiac output and systemic perfusion, was observed with LifeBelt CPR (20+/-7 mmHg) than with manual CPR (15+/-5 mmHg) at 1 min. Peak Ao pressures were not different between methods. With the device, 86% of animals were resuscitated compared to 76% in the manual group. CONCLUSIONS: Blood flow with the LifeBelt device is primarily the result of cardiac compression. At a sternal force of 100-130 lb (45-59 kg), the device produces greater CPP than well-performed manual CPR during resuscitation from prolonged VF.