Postcountershock pulseless rhythms: hemodynamic effects of glucagon in a canine model

Defibrillation after prolonged ventricular fibrillation (VF) is frequently followed by asystole or electromechanical dissociation (EMD) which are usually fatal. We studied the effects of glucagon, a known inotropic and chronotropic agent, during 19 episodes of postcountershock asystole/EMD in nine dogs. Systolic and diastolic aortic (Ao), left ventricular, pulmonary arterial, and right atrial (RA) pressures were recorded as was the instantaneous Ao-RA difference (coronary perfusion pressure) and coronary sinus blood flow (CSF) during closed-chest CPR. VF was induced electrically; 2 min later, a 400-J transthoracic shock was given. Countershock was always followed by asystole (n = 12) or EMD (n = 7). Conventional closed-chest CPR with a mechanical device was begun 30 to 60 sec after countershock and continued for 2 to 3 min. If a perfusing rhythm did not occur, glucagon (1 mg) was given iv and CPR continued for 2 to 3 min more. Glucagon had no significant effect on intravascular pressures, the coronary perfusion gradient, or CSF when compared to CPR alone. However, in 14 or 19 postcountershock episodes unresponsive to CPR alone, glucagon restored effective spontaneous circulation, i.e., successful cardiac resuscitation, due to its effects on the intrinsic pacemaker discharge rate. Glucagon has been previously shown to stimulate myocardial adenyl cyclase via nonadrenergic mechanisms. We conclude that when postcountershock asystole/EMD occurs, glucagon has a direct and favorable effect on cardiac resuscitation outcome due to its effects on pacemaker discharge rate which is not mediated by changes in myocardial blood flow or coronary perfusion pressure.     

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.     

Electrical therapy for post defibrillatory pulseless electrical activity

BACKGROUND: Defibrillation may convert ventricular fibrillation (VF) only to reveal profound mechanical dysfunction. Survival following this dysfunction, known as pulseless electrical activity (PEA) and electromechanical dissociation (EMD), is uncommon. We sought to evaluate an electrical therapy for primary post shock PEA following short duration VF. METHODS AND RESULTS: Forty-eight episodes of VF, lasting 110 +/- 25 s, were induced in 16 anesthetized dogs. Following defibrillation, 35 episodes met PEA criteria (ABP < or = 36 mmHg diastolic and pulse pressure < or = 14 mmHg in the first 20 s post shock). These post defibrillation PEA episodes were either Not Treated (NT) or Treated (T) with packets of 4-20 monophasic 0.2 ms 50-100 Hz pulses of 20-60 V applied across the tip and coil of an integrated bipolar transvenous defibrillation lead positioned in the right ventricle. The therapeutic endpoint was return of spontaneous circulation (ROSC; self-sustained ABP > or = 60 mmHg diastolic and/or > or = 100 mmHg systolic) for over 2 min. In the Not Treated group, only 4 of 19 (21%) episodes spontaneously recovered to ROSC in 123 +/- 49 s while in the Treated group, 11 of 16 (69%) of the PEA episodes achieved ROSC in 102 +/- 92 s. CONCLUSIONS: Electrical therapy increased the likelihood of ROSC in primary post defibrillation PEA three-fold (P < 0.01). Recovery occurred in the absence of thoracic compression, mechanical ventilation, or adjunctive drug therapy.     

Hemodynamic effects of ventricular defibrillation

Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage.Responses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO(2) increased but pO(2) and the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine.THESE RESPONSES WERE RELATED PRIMARILY TO CONVERSION OF VENTRICULAR FIBRILLATION RATHER THAN TO THE ELECTRICAL DISCHARGE OF COUNTERSHOCK BECAUSE COUNTERSHOCK WITHOUT VENTRICULAR FIBRILLATION CAUSED MORE TRANSIENT AND SMALLER RESPONSES THAN THOSE OBSERVED WITH DEFIBRILLATION: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.     

Pediatric defibrillation doses often fail to terminate prolonged out-of-hospital ventricular fibrillation in children

BACKGROUND: The recommended dose for pediatric defibrillation is 2 J/kg, based on animal studies of brief duration ventricular fibrillation (VF) and a single pediatric study of short duration in-hospital VF. In a piglet model of out-of-hospital (prolonged) cardiac arrest, this recommended dose was usually ineffective at terminating VF. We, therefore, hypothesized that pediatric dose defibrillation may be less effective for prolonged out-of-hospital pediatric VF. METHODS: We evaluated retrospectively all cardiac arrests in children less than 13 years old in Tucson from November 1998 to April 2003, with special attention to all children in ventricular fibrillation. We determined the rate of ventricular fibrillation termination after pediatric dose shocks in this cohort, and compared this rate with a published historical pediatric in-hospital defibrillation control group. A pediatric dose shock was defined as 2 J/kg (+/-10 J). All shocks in both groups were provided as monophasic damped sinusoidal waveforms. RESULTS: Thirteen of 151 (9%) children with out-of-hospital cardiac arrest had documented VF. Eleven children received a total of 14 pediatric dose shocks. The median minimum untreated dispatch-to-shock time in unwitnessed arrest or collapse-to-shock in witnessed arrest for those 11 children was 11 min (interquartile range 25-75%; 9-15.5 min). Seven of the 14 pediatric dose shocks terminated the VF (six to asystole, one to pulseless electrical activity). Nine children (68%) died in the emergency department and four (31%) in the pediatric intensive care unit; none survived to hospital discharge. Failure to terminate VF after a pediatric dose shock in this study group with prolonged out-of-hospital ventricular fibrillation was substantially more common than the previously reported in-hospital data (7/14 versus 5/57; OR 10.4; 95% CI 2.6-42; P=0.001). CONCLUSIONS: Termination of VF after a pediatric defibrillation dose is substantially worse for prolonged pediatric out-of-hospital VF cardiac arrest compared with in-hospital (short duration) ventricular fibrillation. The optimal pediatric defibrillation dose for prolonged VF is not known.     

The critical importance of minimal delay between chest compressions and subsequent defibrillation: a haemodynamic explanation

Outcome after prehospital defibrillation remains dire. The aim of the present study was to elucidate the pathophysiology of cardiac arrest and to suggest ways to improve outcome. Ventricular fibrillation (VF) was induced in air-ventilated pigs, after which ventilation was withdrawn. After 6.5 min of VF, ventilation with 100% oxygen was initiated. In six pigs (group I), defibrillation was the only treatment carried out. In another six pigs (group II), mechanical chest compression-decompression CPR (mCPR) was carried out for 3.5 min followed by a 40-s hands-off period before defibrillation. If unsuccessful, mCPR was resumed for a further 30 s before a second or a third, 40-s delayed, shock was given. In a final six pigs (group III) mCPR was applied for 3.5 min after which up to three shocks (if needed) were given during on-going mCPR. Return of spontaneous circulation (ROSC) occurred in none of the pigs in group I (0%), in 1 of six pigs in group II (17%) and in five of six pigs in group III (83%). During the first 3 min of VF arterial blood was transported to the venous circulation, with the consequence that the left ventricle emptied and the right ventricle became greatly distended. It took 2 min of mCPR to establish an adequate coronary perfusion pressure, which was lost when the mCPR was interrupted. During 30 s of mCPR coronary perfusion pressure was negative, but a carotid flow of about 25% of basal value was obtained. In this pig model, VF caused venous congestion, an empty left heart, and a greatly distended right heart within 3 min. Adequate heart massage before and during defibrillation greatly improved the likelihood of return of spontaneous circulation (ROSC).     

犬室颤心脏骤停模型的研究与改进

目的建立一种简单、有效、稳定的犬心脏骤停（CA）模型,为心肺脑复苏的实验研究奠定基础。方法选用健康成年犬30只,体质量（15±2）kg,雌雄不限,麻醉后经右颈外静脉置电极导管至右心室,以5mA电流诱发室颤的方法制作CA模型,根据CA时间不同随机分为CA3 min组、CA5 min组和CA8 min组,每组10只,随后进行电除颤及标准胸外心肺复苏术,比较各组的复苏成功率及存活情况。结果诱颤后所有犬心电图均显示室颤波,动脉血压下降并失去波动;各组自主循环恢复（ROSC）情况为CA 3min组：90％（9／10）、CA5min：80％（8／10）、CA8min：20％（2／10）;ROSC率CA3 min组和CA5 min组比较差异无统计学意义（P〉0.05）,CA8 min组与其他2组之间比较差异具有统计学意义（P〈0.05）;CA3rain组与CA5min、CA8 min组存活时间比较差异有统计学意义（P〈0.05）。结论犬经右心室导管诱发室颤制作的心脏骤停模型稳定且可靠,CA3 min后开始复苏具有较好的ROSC率和存活时间,能满足心肺脑复苏基础研究的需要。     

Diltiazem improves resuscitation from experimental ventricular fibrillation in dogs.

OBJECTIVE: To determine the effect of diltiazem on survival immediately after cardiac arrest and cardiopulmonary resuscitation (CPR) in dogs. DESIGN: Prospective, double-blind, randomized trial. SETTING: Laboratory at a large, university-affiliated medical center. SUBJECTS: Twenty-eight mongrel dogs, weighing 12 to 16 kg. INTERVENTIONS: After the administration of anesthesia, catheters were placed in the pulmonary artery, aortic arch, left ventricle, right ventricle, and great cardiac vein (12 dogs) for sample collection, pressure determinations, and induction of ventricular fibrillation. Dogs were randomized to receive either diltiazem, calcium chloride, or placebo (saline) either before or early during CPR. Dogs underwent 3 mins of unassisted fibrillatory arrest followed by 10 mins of standard CPR using a pneumatic device. After 13 mins of ventricular fibrillation, defibrillation was attempted repeatedly for less than or equal to 10 mins. Successful resuscitation was defined as an organized rhythm with an unassisted systolic BP of greater than 60 mm Hg for greater than or equal to 2 mins. MEASUREMENTS AND MAIN RESULTS: The resuscitation rate was significantly greater in diltiazem-treated animals (100%) than in those dogs receiving calcium (57%) or placebo (29%). Diltiazem-treated animals were resuscitated faster and required fewer defibrillation attempts than did dogs in the other groups. During CPR, coronary artery perfusion pressure and blood gases (arterial, venous, and myocardial) were similar among treatment groups. CONCLUSIONS: Diltiazem improves the resuscitation from experimentally induced ventricular fibrillation when administered before or early during CPR. This response may have important clinical implications in the treatment of patients undergoing cardiac arrest and CPR.     

Adjustable atrial and ventricular temporary electrode for low-energy termination of tachyarrhythmias early after cardiac surgery

Supraventricular and ventricular tachycardias are common and serious postoperative complications early after cardiac surgery. We introduce a completely removable temporary adjustable defibrillation electrode (TADE) for low energy cardioversion/defibrillation of postoperative atrial and ventricular tachyarrhythmias. The electrode consists of three loops of steel wires connected to one steel wire, which are movable within an isolation sheet for adjusting the active surface to the individual size of the heart chambers. Evaluation of the electrode was performed in 10 open-chest beagles with a mean weight of 25.5 kg. The electrodes were first positioned on the left and right atrium. Atrial fibrillation (AF) was induced via a bipolar temporary heart wire. Atrial defibrillation thresholds (DFTs) were measured according to a step-down shock protocol (5-0.4 J). Thereafter, the electrodes were adjusted and positioned on the right and left ventricle. Ventricular fibrillation (VF) was induced and DFTs were recorded the same way. Aortic flow and pressure and left ventricular pressure were continuously monitored throughout the experiment. For termination of AF, mean DFTs were 0.4 +/- 0 J (lowest possible shock level) with a mean shock impedance of 70 +/- 7.6 ohms. VF was terminated with a mean DFT of 3 +/- 1.1 J with a mean impedance 56.1 +/- 7.9 ohms. Complete transcutaneous removal of the electrodes was possible in all animals without any complications. In conclusion, successful low energy termination of AF and VF is possible with the tested temporary adjustable electrode. A clinical study is planned for further evaluation.     

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64 +/- 22 ms after unsuccessful defibrillation and 339 +/- 292 ms after successful defibrillation (P less than 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated. Thus, after both successful and unsuccessful defibrillation with epicardial shocks of greater than or equal to 1 J, an isoelectric window occurs during which no activation fronts are present; the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; unsuccessful shocks transiently synchronize activation before fibrillation regenerates; activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of greater than or equal to 1 J halt all activation fronts after which VF regenerates.     

Effect of epinephrine on defibrillation in ischemic ventricular fibrillation

Epinephrine is thought to improve the success of defibrillation with countershock therapy. However, a recent study failed to show any effect of epinephrine in dogs with normal coronary arteries undergoing electrically-induced ventricular fibrillation (VF). In the current study, the effects of epinephrine were examined in dogs with coronary occlusion undergoing both spontaneous and electrically-induced fibrillation. Forty pentobarbital-anesthetized dogs were prepared by placing snares around the circumflex and left anterior descending coronary arteries. Fibrillation and subsequent resuscitation were carried out with one coronary artery occluded. Dogs were randomly allocated so that half of the animals underwent spontaneous fibrillation and half were electrically fibrillated. In addition, half received epinephrine (1 mg) during resuscitation and half received normal saline solution (1 ml). After 3 minutes of cardiac arrest, cardiopulmonary resuscitation (CPR) was begun, and 30 seconds later epinephrine or saline were injected. One minute later defibrillation was attempted using successive stored energy doses of 1, 2, 4, 8, 16, and 32 J/kg. Delivered energy and transthoracic impedance were measured for each countershock. Successful defibrillation was defined as conversion to any rhythm other than VF or ventricular tachycardia that degenerated in VF within 10 seconds. No other drugs were given during resuscitation. Neither the type of fibrillation (electrically-induced versus spontaneous) or drug therapy (epinephrine versus placebo) had a significant effect on the incidence of defibrillation or the energy necessary for successful defibrillation. Epinephrine did significantly increase the incidence of resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sodium bicarbonate improves the chance of resuscitation after 10 minutes of cardiac arrest in dogs.

The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival.     

The Effect of Multiple Shocks on Canine Cardiac Defibrillation

FLAKER, G., ET AL.: The Effect of Multiple Shocks on Canine Cardiac Defibrillation. To determine if multiple shocks adversely affect the success of later shocks compared with early shocks, we analyzed the success rates of initial shocks (defibrillation attempts 1–5), first half shocks (defibrillation attempts 1–20) and second half shocks [defibrillation attempts 21–40) in a canine model. Epicardial patches were placed on the right and left ventricle in 28 dogs. Ventricular fibrillation was induced by a 60-Hz shock. After 30 seconds, defibrillation was attempted using 7, 12, 13, or 18 joules with either a uniphasic or biphasic rectangular waveform. The uniphasic waveform was 5 msec in duration; the biphasic waveform was 10 msec, with the lagging 5-msec pulse one-half the amplitude of the leading 5-msec pulse. For uniphasic shocks, the right ventricular patch was positive; for biphasic shocks, the right ventricular patch was positive during the leading 5 msec of the shock and negative during the lagging milliseconds. A total of 960 fibrillation episodes were evaluated; no dog was involved in more than 40 fibrillation episodes. The success rates of defibrillation attempts 1–5, defibrillation attempts 1–20, and defibrillation attempts 21–40 were similar at 12, 13, and 18 joules. This information supports the continued use of up to 40 fibrillation trials in canine cardiac defibrillation. However, at 7 joules defibrillation attempts 21–40 were more successful than defibrillation attempts 1–5, and 1–20. With our methodology, these data are consistent with the hypothesis that low energy shocks create a "sensitizing" effect on cardiac tissue, allowing more successful defibrillation with repeated shocks.     

Amiodarone and Bretylium in the Treatment of Hypothermic Ventricular Fibrillation in a Canine Model

Refractory ventricular fibrillation (VF) is a complication of severe hypothermia. Despite mixed experimental data, some authors view bretylium as the drug of choice in hypothermic VF. Bretylium was removed from Advanced Cardiac Life Support guidelines, and, to date, efficacy of amiodarone in hypothermia is unknown. OBJECTIVES: To compare defibrillation rates from hypothermic VF after drug therapy with amiodarone, bretylium, and placebo. METHODS: This was a randomized, blinded, and placebo-controlled laboratory experiment. Thirty anesthetized dogs were mechanically ventilated and instrumented to monitor coronary perfusion pressure (CPP), rectal core temperature, and electrocardiogram (ECG). Animals were cooled to 22 degrees C or the onset of spontaneous VF. Ventricular fibrillation was induced as needed with a transthoracic AC current. Cardiopulmonary resuscitation (CPR) was initiated and animals were randomized (n = 10 each group) to receive amiodarone 10 mg/kg (A), bretylium 5 mg/kg (B), or placebo (P) intravenously. CPR was continued while monitoring for chemical defibrillation. Rewarming was limited to removal from the cold environment. After 10 minutes, up to three escalating defibrillatory shocks were administered. Hemodynamic monitoring continued after resuscitation. Return of spontaneous circulation (ROSC) was defined as a sustainable ECG rhythm generating a corresponding arterial pressure tracing lasting a minimum of 15 minutes. Sample size permitted 80% power to detect a 60% difference in conversion rate between groups. RESULTS: CPR was adequate based on CPP > 15 mm Hg in all animals. Mean (+/-SD) CPP was 35.3 +/- 18.8 mm Hg with an overall lower trend in the amiodarone group (p = 0.06). Baseline variables were similar between groups. No instance of chemical defibrillation was noted. There was no significant difference in ROSC rates between groups. Resuscitation rates were: amiodarone = 1/10, bretylium = 4/10, and placebo = 3/10 (p = 0.45). CONCLUSIONS: In this model of severe hypothermic VF, neither amiodarone nor bretylium was significantly better than placebo in improving the resuscitation rate.     

Influence of Ventricular Fibrillation Duration on Defibrillation Energy in Dogs Using Bidirectional Pulse Discharges

The automatic implantable defibrillator device typically discharges 5-30 seconds after detection of ventricular fibrillation. To investigate the importance of the duration of ventricular fibrillation on defibrillation, the effects of ventricular fibrillation durations of 5, 15, and 30 seconds on the energy requirements for successful internal defibrillation were compared in 15 closed chest dogs with internal electrodes. The electrode configuration utilized a transvenous right heart catheter with two electrodes and a precordial subcutaneous patch electrode, with a single bidirectional pulse discharged between the distal catheter electrode and the proximal catheter and patch electrodes. Curves of energy vs. percentage of successful defibrillation were constructed and logistic regression was used to derive 90% and 50% successful energy doses (ED90 and ED50). The mean ventricular fibrillation activation interval just prior to defibrillation was determined from discrete RV endocardial electrograms. Four dogs died during testing, all because of inability to defibrillate after 30 s of ventricular fibrillation. In the remaining 11 dogs, the ED90 increased from (mean +/- SD) 27 +/- 13J at 5 s to 41 +/- 14J at 30 s (p less than .01). The mean ventricular fibrillation activation interval decreased from 107 +/- 21 ms at 5 s to 95 +/- 18 ms at 30 s (p less than .01). In conclusion, the energy required for internal defibrillation in dogs using this electrode configuration increases with longer durations of ventricular fibrillation, and is associated with more rapid ventricular fibrillation activation intervals.     

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.     

自动体外除颤仪对猪心肺复苏的效果及对心功能的影响

目的 探讨自动体外除颤仪(AED)在抢救心搏骤停中的作用和应用方法,对比国产及进口AED的除颤和复苏效果.方法 14头北京长白猪,体质量(30±1)kg,于本院动物实验室,麻醉后左股静脉置入双腔临时起搏电极,连接医用程控刺激仪制作室颤模型.左股动脉置入动脉导管,连接PiCCO监护仪测量动脉血压及心输出量(CO)和肺血管外水指数(EVWI).心电监护证实室颤成功后,随机(随机数字法)将动物分为2组,每组7只,随机使用国产(M组)或进口(Z组)自动体外除颤仪(AED)除颤.胸骨两侧粘贴电极,按AED语音提示操作并除颤.以上过程反复进行4次,记录除颤次数及成功率.每次自主循环恢复(ROSC)后20 min进行心肌酶谱检测,同时监测CO及EVWI.实验数据计量资料采用重复测量方差分析,计数资料采用x2检验,以P＜0.05为差异有统计学意义.结果 14只动物共进行54次致颤,除Z组1只第二次致颤后未能成功复苏,其余均ROSC,复苏成功率为98.1%.M组放电37次,首次除颤成功率75.0%;Z组放电32次,首次除颤成功率80.8%.从AED开机到心电信号识别完毕平均需要(29±1)s.M组及Z组各2次在首次致颤后,AED未能成功识别室颤;Z组2次将ROSC后室性心动过速,误判为室颤,但按其提示除颤后未造成不良影响.实验过程中,所有动物心率、血压及CO未见明显波动,但EVWI和肌红蛋白(MYO)随时间变化进行性升高,其中第三、第四次除颤后与基础状态相比,有显著性差异.各项检测指标M组与Z组之间未发现显著性差异.结论 AED能够安全、有效地终止室颤;国产与进口AED在信号判别能力、除颤效果与对心肌损伤方面无显著差异;对于专业医护人员,推荐使用人工除颤器,以避免AED过度依赖自动化而产生的误判.     

Myocardial effects of ventricular fibrillation in the isolated rat heart.

OBJECTIVE: Ventricular fibrillation (VF) is known to increase myocardial oxygen requirements and to alter coronary vascular physiology. However, the significance of these effects during cardiac arrest and resuscitation is not well understood. A model was developed in the isolated rat heart to investigate the myocardial effects of VF during a simulated episode of cardiac arrest and resuscitation. We hypothesized that VF would intensify the severity of myocardial ischemia and consequently accentuate postischemic myocardial dysfunction. DESIGN: Prospective and randomized. SETTING: Research laboratory. SUBJECTS: Twenty Sprague-Dawley rats. INTERVENTIONS: Hearts were harvested and perfused at a constant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. In five hearts, VF was induced by a 0.05-mA current delivered to the right ventricular endocardium. The perfusate flow was then stopped for a 10-min interval and resumed at 20% of baseline flow for another 10 mins. After 20 mins of VF, the perfusate flow was returned to baseline and a sinus rhythm reestablished by epicardial electrical shocks. The studies were randomized and included three additional groups to control for the effects of ischemia without VF (n = 5), the effects of VF without ischemia (n = 5), and the stability of the preparation (n = 5). MEASUREMENTS AND MAIN RESULTS: Isovolumic indices of left ventricular function were obtained using a latex balloon advanced through the mitral valve and distended to an end-diastolic pressure of 10 mm Hg. The coronary effluent was collected from the right ventricular cavity. VF during myocardial ischemia was associated with a higher coronary effluent PCO2, increased coronary vascular resistance, and development of ischemic contracture as indicated by increases in left ventricular pressure from 9+/-3 to 33+/-6 mm Hg (p < .05). After defibrillation, contractility and relaxation rapidly returned to baseline values, whereas the isovolumic end-diastolic pressure remained elevated for 20 mins. These changes were much less prominent when ischemia was not accompanied by VF. CONCLUSIONS: These findings indicate that VF may adversely affect myocardial ischemia by hastening the development of ischemic contracture, increasing coronary vascular resistance, and favoring the development of diastolic pump failure early after resuscitation from cardiac arrest.     

Emergency Defibrillation Using a Temporary Pacing Electrode Catheter

Direct application of electrical current to the heart utilizing special equipment such as implantable defibrillators or specially designed catheters has been useful in patients with recurrent ventricular tachyarrhythmias. We describe a patient who developed intractable ventricular fibrillation (VF) during the course of electrophysiologic testing. VF continued for 50 minutes, during which time multiple transthoracic shocks of 360 joules failed to convert the arrhythmia. Intracardiac shocks were then delivered via a transvenous 6 French standard quadripolar pacing catheter positioned in the right ventricular apex by direct application of the defibrillator paddle to the catheter, with the patient lying on the posterior paddle. Energy of up to 300 joules failed to defibrillate the patient, but use of 360 joules delivered in this fashion defibrillated the patient twice. Despite the protracted time of cardiac arrest, the patient recovered without sequelae. We report this case to demonstrate that VF refractory to transthoracic defibrillation may be converted by intracardiac shocks using a temporary pacing catheter without special equipment.     

Effects of pretreatment with propranolol on potassium, calcium, and magnesium shifts after ventricular fibrillation in dogs

Hypokalemia and other electrolyte changes have been observed after resuscitation from ventricular fibrillation. We studied the effect of propranolol on postresuscitation electrolytes in a canine model of ventricular fibrillation and cardiac resuscitation by randomizing 40 anesthetized dogs to four groups: ventricular fibrillation--no drug (VF), ventricular fibrillation--propranolol pretreatment (VF-prop), control-no drug (NoVF), control--propranolol (NoVF-prop). We measured serum electrolytes at baseline and periodically for 3 hours. In VF dogs, serum potassium decreased from 3.9 +/- 0.4 to 3.2 +/- 0.2 mEq/L 60 minutes after resuscitation (p less than 0.001). The decrease in potassium was prevented (p less than 0.001) by propranolol. Serum calcium decreased from 10.6 +/- 0.8 to 10.2 +/- 0.8 mg/dl in VF dogs 15 minutes after resuscitation (p less than 0.05); this decrease was not blocked by propranolol (p = NS). Serum magnesium increased from 1.5 +/- 0.2 to 1.8 +/- 0.1 mEq/L in VF dogs 7 minutes after resuscitation (p less than 0.001); this rise was partially blocked by propranolol (p less than 0.01). Serum glucose increased from 105 +/- 6 to 183 +/- 27 mg/dl in VF dogs 7 minutes after resuscitation (p less than 0.001); this increase was diminished by propranolol (p less than 0.001). Thus propranolol prevents the decrease in serum potassium after ventricular fibrillation in this canine model, providing evidence that postresuscitation hypokalemia is caused by the beta-adrenergic effects of catecholamines secreted in response to cardiac arrest. Propranolol blocks the rise in magnesium and glucose but does not block the decrease in calcium after resuscitation.