Comparison of shock-first strategy and cardiopulmonary resuscitation-first strategy in a porcine model of prolonged cardiac arrest

Objective

The choice of a shock-first or a cardiopulmonary resuscitation (CPR)-first strategy in the treatment of prolonged cardiac arrest (CA) is still controversial. The purpose of this study was to compare the effects of these strategies on oxygen metabolism and resuscitation outcomes in a porcine model of 8 min CA.

Methods

Ventricular fibrillation (VF) was electrically induced. After 8 min of untreated VF, 24 male inbred Wu-Zhi-Shan miniature pigs were randomized to receive either defibrillation first (ID group) or chest compression first (IC group). In the ID group, a shock was delivered immediately. If the defibrillation attempt failed to attain restoration of spontaneous circulation (ROSC), manual chest compressions were rapidly initiated at a rate of 100 compressions min⁻¹, and the compression-to-ventilation ratio was 30:2. If VF persisted after five cycles of CPR, a second defibrillation attempt was made. In the IC group, chest compressions were delivered first, followed by a shock.

Results

Hemodynamic variables, the VF waveform and blood gas analysis outcomes were recorded. Oxygen metabolism parameters and the amplitude spectrum area (AMSA) of the VF waveform were computed. There were no significant differences in the rate of ROSC and 24 h survival between two groups. The ID group had lower lactic acid levels, higher cardiac output, better oxygen consumption and better oxygen extraction ratio at 4 and 6 h after ROSC than the IC group.

Conclusions

In a porcine model of prolonged CA, the choice of a shock-first or CPR-first strategy did not affect the rate of ROSC and 24 h survival, but the shock-first strategy might result in better hemodynamic status and better oxygen metabolism than the CPR-first strategy at the first 6 h after ROSC.     

Beta-blockade causes a reduction in the frequency spectrum of VF but improves resuscitation outcome: A potential limitation of quantitative waveform measures

Introduction

Methods to identify appropriate treatments for the various stages of ventricular fibrillation (VF) involve differentiating groups of subjects who will respond to defibrillation with return of spontaneous circulation (ROSC) and those who require other therapies (e.g., CPR, drugs) prior to defibrillation. The use of quantitative waveform measures (QWM) which measure the frequency and fractal dimension of the VF electrocardiogram have shown success in predicting response to defibrillatory shock in animal models. Patients in cardiac arrest are often taking medications affecting adrenergic activity such as the beta blocker metoprolol and the combined alpha and beta blocker, labetalol. How this exposure might alter the QWM and ROSC rates is not known.

Hyothesis

We sought to determine how pretreatment with adrenergic agents alters two QWM measures, the amplitude spectrum area (AMSA) and the detrended fluctuation analysis (DFA). We also examined how these medications alter the probability of ROSC after shock.

Methods

A swine model of ischemically induced VF cardiac arrest was used in which metoprolol and labetalol were administered prior to VF onset. 30 swine were randomly assigned to three groups of 10; control, metoprolol and labetalol. They were anesthetized, intubated and given the appropriate study drug. A balloon catheter was placed in the LAD coronary artery and inflated until VF occurred. ECG was recorded at 1000 Hz for 7 min of untreated VF. Closed chest compressions were then begun and after 1 min a 200 J shock was delivered. Resuscitation was continued with repeat defibrillation shocks as indicated for 15 min or until ROSC was achieved (defined: systolic BP > 60 for 10 min). The Fourier frequency spectra, AMSA and DFA measures from VF onset to 7 min were calculated using custom MATLAB routines. The QWM were compared over the electrical and circulatory phases of VF using generalized estimating equations. The rates of ROSC in the three groups were compared using relative risk measures.

Results

All 10 control animals fibrillated after coronary occlusion, 8 metoprolol and 7 labetalol animals fibrillated.The frequency spectrum in metoprolol treated animals demonstrated a reduction in mean frequencies from 1 to 3 min (electrical phase) and from 3 to 7 min (circulatory phase). Labetalol produced an even greater reduction in frequencies in these intervals. The decline in AMSA was similar in all three groups over the first 3 min. From 3 to 7 min the metoprolol group was significantly lower than the control group (p < 0.001) and the labetalol group was lower still (p < 0.001). The DFA demonstrated little difference between the control and metoprolol groups, but showed a linear increase over 7 min in the labetalol group (p < 0.001 vs compared to control and metoprolol groups).ROSC was noted in 2/10 in the control group, 7/8 in metoprolol group and 2/7 in the labetalol group. The frequentist analysis of ROSC showed a relative risk (RR) of ROSC of 4.4 when comparing control to metoprolol animals and 1.4 comparing control to labetalol animals.

Discussion

Metoprolol results in a reduction in frequencies in the Fourier spectrum of VF as compared with controls. There is a further decrease in frequencies with labetalol. The AMSA reflects this reduction in frequencies with lower AMSA values from 3 to 7 min of VF. The DFA demonstrates consistent changes with labetalol treated animals over the 7 min, but the metoprolol treated animals do not differ from the controls. The marked improvement in ROSC seen with metoprolol (RR 4.4) is unexpected and is not seen in labetalol treated animals. Adrenergic blockade prior to VF induction affects quantitative measures of the VF waveform and may limit the ability of such measures to predict downtime or defibrillation outcome.     

Decoding twitter: Surveillance and trends for cardiac arrest and resuscitation communication

Aim of the study

Twitter has over 500 million subscribers but little is known about how it is used to communicate health information. We sought to characterize how Twitter users seek and share information related to cardiac arrest, a time-sensitive cardiovascular condition where initial treatment often relies on public knowledge and response.

Methods

Tweets published April–May 2011 with keywords cardiac arrest, CPR, AED, resuscitation, heart arrest, sudden death and defib were identified. Tweets were characterized by content, dissemination, and temporal trends. Tweet authors were further characterized by: self-identified background, tweet volume, and followers.

Results

Of 62,163 tweets (15,324, 25%) included resuscitation/cardiac arrest-specific information. These tweets referenced specific cardiac arrest events (1130, 7%), CPR performance or AED use (6896, 44%), resuscitation-related education, research, or news media (7449, 48%), or specific questions about cardiac arrest/resuscitation (270, 2%). Regarding dissemination (1980, 13%) of messages were retweeted. Resuscitation specific tweets primarily occurred on weekdays. Most users (10,282, 93%) contributed three or fewer tweets during the study time frame. Users with more than 15 resuscitation-specific tweets in the study time frame had a mean 1787 followers and most self-identified as having a healthcare affiliation.

Conclusion

Despite a large volume of tweets, Twitter can be filtered to identify public knowledge and information seeking and sharing about cardiac arrest. To better engage via social media, healthcare providers can distil tweets by user, content, temporal trends, and message dissemination. Further understanding of information shared by the public in this forum could suggest new approaches for improving resuscitation related education.     

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.     

长时程室颤先行心肺复苏对复苏效果的影响及机制研究

目的 比较7 min室颤先行心肺复苏2 min后除颤与直接除颤的复苏效果,并探讨其机制.方法 建立猪闭胸电诱发室颤模型,CPR First组优先心肺复苏2 min后连续三次除颤,Shock First组直接予连续三次除颤,观察冠脉灌注压、室颤波频率和振幅变化,计算除颤成功率和自主循环恢复率.结果 CPR First组先行心肺复苏2 min后可提高初次除颤前的冠脉灌注压、室颤波的频率和振幅, CPR First组比Shock First组有高的除颤成功率和自主循环恢复率(P＜0.05).结论 7 min室颤除颤前先行胸外按压和人工呼吸可明显提高复苏成功率,其机制与增加冠脉灌注,改善心脏能量储备,提高室颤波的频率和振幅有关.     

Myocardial infarction is a frequent cause of exercise-related resuscitated out-of-hospital cardiac arrest in a general non-athletic population

Background

Performing exercise is shown to prevent cardiovascular disease, but the risk of an out-of-hospital cardiac arrest (OHCA) is temporarily increased during strenuous activity. We examined the etiology and outcome after successfully resuscitated OHCA during exercise in a general non-athletic population.

Methods

Consecutive patients with OHCA were admitted with return of spontaneous circulation (ROSC) or on-going resuscitation at hospital arrival (2002–2011). Patient charts were reviewed for post-resuscitation data. Exercise was defined as moderate/vigorous physical activity.

Results

A total of 1393 OHCA-patients were included with 91(7%) arrests occurring during exercise. Exercise-related OHCA-patients were younger (60 ± 13 vs. 65 ± 15, p < 0.001) and predominantly male (96% vs. 69%, p < 0.001). The arrest was more frequently witnessed (94% vs. 86%, p = 0.02), bystander CPR was more often performed (88% vs. 54%, p < 0.001), time to ROSC was shorter (12 min (IQR: 5–19) vs. 15 (9–22), p = 0.007) and the primary rhythm was more frequently shock-able (91% vs. 49%, p < 0.001) compared to non-exercise patients. Cardiac etiology was the predominant cause of OHCA in both exercise and non-exercise patients (97% vs. 80%, p < 0.001) and acute coronary syndrome was more frequent among exercise patients (59% vs. 38%, p < 0.001). One-year mortality was 25% vs. 65% (p < 0.001), and exercise was even after adjustment associated with a significantly lower mortality (HR = 0.40 (95%CI: 0.23–0.72), p = 0.002).

Conclusions

OHCA occurring during exercise was associated with a significantly lower mortality in successfully resuscitated patients even after adjusting for confounding factors. Acute coronary syndrome was more common among exercise-related cardiac arrest patients.     

亚低温治疗犬心脏骤停复苏后心功能研究

目的 明确亚低温对室颤复苏后犬心功能及心律失常的影响.方法 12头比格犬随机(随机数字法)分成两组(n=6):常温复苏组(37.0±0.2)℃和亚低温组(34.0±0.2)℃,通过快速电刺激诱导室颤,7 min后行心肺复苏,动态观察比较两组犬的心率、左心室收缩力指数、室性心律失常、除颤能量、肾上腺素用量及复苏后1周心超变化.结果 ①与室颤前比较,两组犬左心室收缩力指数在复苏后均有不同程度降低(P＜0.05),但亚低温组下降幅度小于常温组,且心率低于常温组(141±19)次/minvs.(163±31)次/min,P＜0.05.②与常温组比较,亚低温组犬室性心律失常发生的次数明显减少(P＜0.05),但是除颤次数、肾上腺素用量差异无统计学意义(P＞0.05).③复苏后1周,两组犬的心超结果显示,心脏结构及射血分数均恢复正常.结论 亚低温治疗可改善心脏骤停复苏后心肌收缩力,降低室性心律失常发生率.本研究结果提示,亚低温对复苏后心功能有一定的保护作用.     

A tourniquet assisted cardiopulmonary resuscitation augments myocardial perfusion in a porcine model of cardiac arrest

ObjectiveDuring cardiopulmonary resuscitation (CPR), myocardial blood flow generated by chest compression rarely exceeds 35% of its normal level. Cardiac output generated by chest compression decreases gradually with the prolongation of cardiac arrest and resuscitation. Early studies have demonstrated that myocardial blood flow during CPR is largely dependent on peripheral vascular resistance. In this study, we investigated the effects of chest compression in combination with physical control of peripheral vascular resistance assisted by tourniquets on myocardial blood flow during CPR.MethodsVentricular fibrillation was induced and untreated for 7 min in ten male domestic pigs weighing between 33 and 37 kg. The animals were then randomized to receive CPR alone or a tourniquet assisted CPR (T-CPR). In the CPR alone group, chest compression was performed by a miniaturized mechanical chest compressor. In the T-CPR group, coincident with the start of resuscitation, the thin elastic tourniquets were wrapped around the four limbs from the distal end to the proximal part. After 2 min of CPR, epinephrine (20 μg/kg) was administered via the femoral vein. After 5 min of CPR, defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 min before the next defibrillation. The protocol was continued until successful resuscitation or for a total of 15 min. Five minutes after resuscitation, the elastic tourniquets were removed. The resuscitated animals were observed for 2 h.ResultsT-CPR generated significantly greater coronary perfusion pressure, end-tidal carbon dioxide and carotid blood flow. There was no difference in both intrathoracic positive and negative pressures between the two groups. All animals were successfully resuscitated with a single shock in both groups. There were no significant changes in hemodynamics observed in the animals treated in the T-CPR group before-and-after the release of tourniquets at post-resuscitation 5 min.ConclusionsT-CPR improves myocardial and cerebral perfusion during CPR. It may provide a new and convenient method for augmenting myocardial and cerebral blood flow during CPR.     

The need to resume chest compressions immediately after defibrillation attempts: An analysis of post-shock rhythms and duration of pulselessness following out-of-hospital cardiac arrest

AimCurrent consensus guidelines for cardiopulmonary resuscitation (CPR) recommend that chest compressions resume immediately after defibrillation attempts and that rhythm and pulse checks be deferred until completion of 5 compression:ventilation cycles or minimally for 2 min. However, data specifically confirming the post-shock duration of asystole or pulseless electrical activity before return of spontaneous circulation (ROSC) are lacking. Our aim was to describe the frequency of the various post-shock cardiac rhythms and the duration of post-shock pulselessness in out-of-hospital non-traumatic cardiac arrest.MethodUsing prospectively-collected data from the Resuscitation Outcomes Consortium (ROC) Epistry database, the investigators reviewed monitor-defibrillator recordings of 176 patients who received defibrillation attempts in the out-of-hospital setting for ventricular fibrillation (VF) or ventricular tachycardia (VT) with absent pulses,.ResultsAmong 376 different defibrillation attempts delivered in the 176 patients, there were 182 resulting episodes of post-shock asystole. The mean interval of asystole after defibrillation was 69 ± 136 s (median 20 s; IQR 36) and the mean interval for return of an organized rhythm was 64 ± 157 s (median 7 s; IQR 26). The mean time to ROSC was 280 ± 320 s (median 136 s; IQR 445).ConclusionAfter defibrillation attempts, the majority of patients remain pulseless for over 2 min and the duration of asystole before return of pulses is longer than 120 s beyond the shock gap in as many as 25%. These data support the recommendation to immediately resume chest compressions for 2 min following attempted defibrillation.     

Assessment of a three-phase model of out-of-hospital cardiac arrest in patients with ventricular fibrillation

AIM: Cardiac arrest with ventricular fibrillation (VF) has been divided into three phases in which phase-specific therapy may improve outcome. The aim of this study was to assess the relationship between call-to-shock time, bystander CPR (BCPR), and cardiac arrest outcomes. METHODS: In a retrospective analysis of prospectively-acquired data from witnessed VF out-of-hospital cardiac arrests (OHCA), patients were classified as phases 1, 2, or 3 based on call-to-shock time (<5, 5-8, and >8 min) and further stratified based on performance of BCPR. Groups were compared with regard to survival, neurological outcome, and restoration of spontaneous circulation (ROSC) with defibrillation only (no ALS interventions to achieve sustained ROSC). RESULTS: Survival, neurologically intact survival, and ROSC with defibrillation were different between phases 1 and 2 (p=0.014 and p=0.005, p<0.01) but not between phases 2 and 3. Patients were further classified as having received BCPR (N=111) or no BCPR (N=107). Neurologically intact survival with and without BCPR, respectively, was 61% versus 72% (phase 1), 44% versus 41% (phase 2), and 42% versus 29% (phase 3). ROSC with defibrillation only with and without BCPR, respectively, was 64% versus 56% (phase 1), 37.0% versus 29% (phase 2), and 33% versus 8% (phase 3). ROSC with defibrillation alone was statistically higher in univariate analysis in phase 3 with BCPR (p=0.033) but not in multivariate analysis (p=0.068). CONCLUSIONS: BCPR did not significantly improve survival in any phase of OHCA, though there was a trend toward increased neurologically intact survival and increased ROSC with defibrillation alone in phase 3.     

Causes for the declining proportion of ventricular fibrillation in out-of-hospital cardiac arrest

AimsThe reported proportion of ventricular fibrillation (VF) in out-of-hospital cardiac arrest (OHCA) has declined worldwide. VF decline may be caused by less VF at collapse and/or faster dissolution of VF into asystole. We aimed to determine the causes of VF decline by comparing VF proportions in relation to delay from emergency medical services (EMS) call to initial ECG (call-to-ECG delay), and VF dissolution rates between two study periods.MethodsData from the AmsteRdam REsuscitation STudies (ARREST), an ongoing OHCA registry in the Netherlands, were used. We studied cardiac OHCA in the study periods 1995–1997 (n = 917) and 2006–2012 (n = 5695). Cases with available ECG and information on call-to-ECG delay were included. We tested whether initial VF proportion and VF dissolution rates differed between both study periods using logistic regression.ResultsDespite a 15% VF decline between the periods, VF proportion around EMS call remained high in 2006–2012 (64%). The odds ratio (OR) for VF proportion in 2006–2012 vs. 1995–1997 was 0.52 (95%-CI 0.45–0.60, P < 0.001), with similar rates of VF dissolution in both periods (P = 0.83). VF decline was higher for unwitnessed collapse (OR 0.41, 95%-CI 0.28–0.58) and collapse at home (OR 0.50, 95%-CI 0.42–0.59), but not for categories of bystander CPR, age or sex.ConclusionVF proportion early after collapse remains high. VF decline is explained by the occurrence of less initial VF, rather than faster dissolving VF. An increase in unwitnessed OHCA and collapse at home contributes to the observed VF decline.     

Conceptual models of coronary perfusion pressure and their relationship to defibrillation success in a porcine model of prolonged out-of-hospital cardiac arrest

Introduction

The amount of myocardial perfusion required for successful defibrillation after cardiac arrest is unknown. Coronary perfusion pressure (CPP) is a surrogate for myocardial perfusion. One limited clinical study identifies a threshold of 15 mmHg required for return of spontaneous circulation (ROSC). Our exploration of threshold and dose models of CPP during the initial bout of CPR indicates higher levels than previously demonstrated are required. CPP required for shock success throughout on-going resuscitation is unknown and other conceptual models of CPP have not been explored.

Hypothesis

An array of conceptual models of CPP is associated with and predicts defibrillation success throughout resuscitation.

Methods

Data from 6 porcine cardiac arrest studies were pooled. Mean and area under the curve (AUC) CPP were derived for 30-s epochs. Five conceptual models of CPP were analyzed: threshold, delta, cumulative delta, dose, and cumulative dose. Comparative statistics were performed with one-way ANOVA and two-tailed t-test. Regression models assessed CPP trends and prediction of ROSC.

Results

For 316 defibrillation attempts in 124 animals, those resulting in ROSC (n = 75) had significantly higher threshold, delta, cumulative delta, dose, and cumulative dose CPP than those without. All conceptual models except delta CPP had significantly different values across successive defibrillation attempts and all five models were significant predictors of ROSC, along with experimental design.

Conclusions

Threshold, delta, cumulative delta, dose, and cumulative dose CPP predict individual defibrillation success throughout resuscitation.     

The effects of an automatic,low pressure and constant flow ventilation device versus manual ventilation during cardiovascular resuscitation in a porcine model of cardiac arrest

Background

Cardiac arrest is an important cause of mortality. Cardiopulmonary resuscitation (CPR) improves survival, however, delivery of effective CPR can be challenging and combining effective chest compressions with ventilation, while avoiding over-ventilation is difficult. We hypothesized that ventilation with a pneumatically powered, automatic ventilator (Oxylator^®) can provide adequate ventilation in a model of cardiac arrest and improve the consistency of ventilations during CPR.

Methods/results

Twelve pigs (∼40 kg, either sex) underwent 3 episodes each of cardiac arrest and resuscitation consisting of 30 s of untreated ventricular fibrillation, followed by 5 min of CPR, defibrillation, and ∼30 min of recovery. During CPR in each episode, pigs were ventilated in 1 of 3 ways in random balanced order: manual ventilation using AMBU bag (12 breaths/min), low pressure Oxylator^® (maximum airway pressure 15 cmH₂O with 20 L/min constant flow in automatic mode [Ox15/20]), or high pressure Oxylator^® (maximum airway pressure 20 cmH₂O with 30 L/min constant flow in automatic mode [Ox20/30]). During CPR, both Ox15/20 and Ox20/30 resulted in higher levels of positive end expiratory pressure than manual ventilation. Ox15/20 ventilation also resulted in higher arterial pCO₂ than manual ventilation. Ox20/30 ventilation yielded higher arterial pO₂ and a lower arterial–alveolar gradient than manual ventilation. All pigs were successfully defibrillated, and no measured haemodynamic variables were different between the groups.

Conclusion

Ventilation with an automatic ventilation device during CPR is feasible and provides adequate ventilation and comparable haemodynamics when compared to manual bag ventilation.     

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.     

急性心肌梗死心肺复苏后紧急介入治疗的作用

目的探讨紧急介入治疗能否改善急性心肌梗死心肺复苏后患者的预后。方法回顾性分析院前及急诊室发生心脏骤停的急性心肌梗死患者32例,分为在心肺复苏后同时进行紧急介入治疗组(n= 12)和保守治疗组(n=20)．比较两组的住院期间病死率、严重心律失常、心力衰竭、心原性休克和严重出血的发生率。结果介入组住院期间死亡2例(17%),保守组死亡14例(70%),p＜0．01;心肺复苏后发生心力衰竭者两组分别为3例(25%)和16例(80%),P＜0．01;两组的严重心律失常、心原性休克和严重出血发生率差异无统计学意义(P＞0．05);Logistic回归分析表明,急诊介入治疗能显著降低病死率,而心肺复苏时间＞20min,将增加病死率。结论早期紧急介入治疗能显著改善急性心肌梗死心肺复苏患者的预后。     

Public perceptions and experiences of myocardial infarction, cardiac arrest and CPR in London

INTRODUCTION: The lay public have limited knowledge of the symptoms of myocardial infarction ("heart attack"), and inaccurate perceptions of cardiac arrest survival rates. Levels of CPR training and willingness to intervene in cardiac emergencies are also low. AIMS: To explore public perceptions of myocardial infarction and cardiac arrest; investigate perceptions of cardiac arrest survival rates; assess levels of training and attitudes towards CPR, and explore the types of interventions considered useful for increasing rates of bystander CPR among Greater London residents. METHODS: A quantitative interview survey was conducted with 1011 Greater London residents. Eight focus groups were also conducted to explore a range of issues in greater depth and validate trends that emerged in the initial survey. RESULTS: Chest pain was the most commonly recognised symptom of "heart attack". Around half of the respondents were aware that a myocardial infarction differs from a cardiac arrest, although their ability to explain this difference was limited. The majority overestimated that at least a quarter of cardiac arrest patients in London survive to hospital discharge. Few participants had received CPR training, and most were hesitant about performing the procedure on a stranger. CONCLUSIONS: Awareness and knowledge of CPR, and reactions to cardiac emergencies, reflect relatively low levels of CPR training in London. Publicising cardiac arrest survival figures may be instrumental in prompting members of the public to train in CPR and motivating those who have been trained to intervene in a cardiac emergency.     

Potassium induced cardiac standstill during conventional cardiopulmonary resuscitation in a pig model of prolonged ventricular fibrillation cardiac arrest: A feasibility study

Aim of the study

Potassium-based cardioplegia has been the gold standard for cardioprotection during cardiac surgery. We sought to evaluate the feasibility and the effects of potassium-induced cardiac standstill during conventional cardiopulmonary resuscitation (CPR) in a pig model of prolonged ventricular fibrillation (VF).

Methods

VF was induced in 20 pigs, and circulatory arrest was maintained for 14 min. Animals were then resuscitated by standard CPR. Coincident with the start of CPR, 20 ml of saline (control group) or 0.9 mequiv. kg⁻¹ of potassium chloride diluted to 20 ml (potassium group) was administered into right atrium.

Results

Administration of potassium resulted in asystole lasting for 1.0 min (0.2) in the potassium group animals. VF reappeared in all but one animal, in which wide QRS complex bradycardia followed. Restoration of spontaneous circulation (ROSC) was attained in two animals (20%) in the control group and in seven animals (70%) in the potassium group (p = 0.070). Resuscitated animals in the potassium group required fewer countershocks (3, 4 vs. 2 (1–2)), smaller doses of adrenaline (1.84, 1.84 vs. 0.94 (0.90–1.00) mg), and shorter duration of CPR (8, 10 vs. 4.0 (4.0–4.0) min) than did the control group. Potassium concentrations normalised rapidly after ROSC in both groups, and the potassium concentrations at 5 min (5.5, 6.6 vs. 6.8 (6.5–7.8) mequiv. l⁻¹) and 4 h (4.9, 5.4 vs. 5.9 (5.1–6.4) mequiv. l⁻¹) after ROSC were similar in the both groups.

Conclusion

In a pig model of untreated VF cardiac arrest for 14 min, resuscitation with potassium-induced cardiac standstill during conventional CPR was found to be feasible.