Effects of dichloroacetate following canine asphyxial arrest

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.     

Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats

During cardiac arrest (CA), myocardial perfusion is solely dependent on cardiopulmonary resuscitation (CPR) although closed-chest compressions only provide about 10–20% of normal myocardial perfusion. The study was conducted in a whole animal CPR model to determine whether CPR-generated oxygen delivery preserves or worsens mitochondrial function. Male Sprague-Dawley rats (400–450 g) were randomly divided into four groups: (1) BL (instrumentation only, no cardiac arrest), (2) CA₁₅ (15 min cardiac arrest without CPR), (3) CA₂₅ (25 min cardiac arrest without CPR) and (4) CPR (15 min cardiac arrest, followed by 10 min CPR). The differences between groups were evaluated by measuring mitochondrial respiration, electron transport chain (ETC) complex activities and mitochondrial ultrastructure by transmission electron microscopy (TEM). The CA₂₅ group had the greatest impairment of mitochondrial respiration and ETC complex activities (I–III). In contrast, the CPR group was not different from the CA₁₅ group regarding all measures of mitochondrial function. Complex I was more susceptible to ischemic injury than the other complexes and was the major determinant of mitochondrial dysfunction. Observations of mitochondrial ultrastructure by TEM were compatible with the biochemical results. The findings suggest that, despite low blood flow and oxygen delivery, CPR is able to preserve heart mitochondrial function and viability during ongoing global ischemia. Preservation of complex I activity and mitochondrial function during cardiac arrest may be an important mechanism underlying the beneficial effects of CPR which have been shown in clinical studies.     

In-Hospital Cardiopulmonary Arrests in Patients With Left Ventricular Assist Devices

BackgroundBasic and advanced cardiac life support guidelines do not address resuscitation of patients with continuous-flow (CF) left ventricular assist devices (LVADs). As the population of LVAD patients increases, it becomes important to understand how to provide emergency care to such patients.Methods and ResultsWe retrospectively reviewed a consecutive series of patients with an implanted CF-LVAD who had an in-hospital cardiopulmonary arrest at our medical center from January 2011 to October 2013. We compared them with a matched cohort of patients without LVADs who had an in-hospital cardiopulmonary arrest during the same time period. Code documentation was used to determine arrest characteristics, perfusion assessment techniques, and time to cardiopulmonary resuscitation (CPR) initiation. There were 415 in-hospital arrests during the study period, and 4% (n = 16) occurred in patients with CF-LVADs. Response teams used various approaches to assess arterial perfusion, including palpation or Doppler of the arterial pulse and measurement of blood pressure by Doppler or arterial line. Nine of the 16 patients required CPR, but only 5 (56%) received CPR in <2 minutes. In the control group (n = 32) of patients without an LVAD, 22 received CPR, which was initiated within 2 minutes in all (100%) of the patients.ConclusionsCardiopulmonary arrests in LVAD patients accounted for 4% of all arrests in our center. We identified important time delays in CPR initiation, highlighting the need to develop resuscitation guidelines for this patient population.     

Advanced cardiac life support: Update on recent guidelines and a look at the future

The objectives of this article are to provide an update of the American Heart Association (AHA) 1992 National Conference guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care and to review the investigation and development of new methods of CPR which may be considered in future recommendations. Despite an organized approach to sudden cardiac arrest, survival in patients receiving CPR is in the range of 5–15%. The new AHA guidelines recommend standard manual CPR performed at a rate of 80–100 compressions/min and organized algorithms of advanced cardiac life support. These guidelines stress widespread community training and rapid response in the following sequence: (1) recognition of early warning signs, (2) activation of the emergency medical system (EMS), (3) basic CPR, (4) early defibrillation, (5) intubation, and (6) intravenous medication. Several new recommendations pertain specifically to in-hospital care and are, therefore, particularly relevant to physician management of cardiac arrest. The best predictor of survival in patients requiring circulatory support after cardiac arrest is attainable coronary and cerebral perfusion. Unfortunately, the minimal levels of end-organ perfusion required to sustain life are often difficult or impossible to achieve with standard manual cardiopulmonary resuscitation and several new techniques have therefore been introduced. The most promising of these techniques are (1) interposed abdominal compression, (2) pneumatic vest, and (3) active compression-decompression resuscitation. Each of these techniques offers unique advantages when compared with standard manual cardiopulmonary resuscitation. The 1992 National Conference recommendations provide a rational framework for the resuscitation of cardiac arrest victims. New methods of cardiopulmonary resuscitation are now available and investigation into these methods continues. In the future, these modalities may be incorporated in newer guidelines and be available on a widespread basis to supplement our current approach to cardiac arrest.     

Use of naloxone during cardiac arrest and CPR: potential adjunct for postcountershock electrical-mechanical dissociation

Naloxone has been shown to increase arterial pressure in hemorrhagic and septic shock. To determine if naloxone has salutary effects during cardiac arrest with conventional closed-chest cardiopulmonary resuscitation (CPR), ten dogs were studied during 20 minutes of ventricular fibrillation (VF) and CPR and during a 30-minute postcountershock period. Central aortic (Ao) and right atrial (RA) systolic and end-diastolic (EDP) pressures, instantaneous Ao-RA pressure difference (coronary perfusion pressure), and electromagnetic Ao flow were measured. Ao and RA samples were analyzed during a control period and at five-minute intervals during CPR for PO2, PCO2, and pH. During VF, a piston-cylinder device was used to perform anteroposterior sternal depressions and positive pressure ventilations (100% O2) at standard rates and ratios. After 15 minutes of CPR, animals were randomized and given either naloxone (5 mg/kg) or epinephrine (1 mg). Defibrillation was attempted five minutes later using 1 J/kg and then, if necessary, 2, 4, 8, 12, and 16 J/kg until VF was terminated or the maximum energy dose was reached. If VF persisted or if countershock resulted in asystole or a nonperfusing rhythm (electrical-mechanical dissociation [EMD]), the alternate drug (naloxone or epinephrine) was then given. Measured systolic pressures, coronary perfusion pressures, aortic flow, and blood gases were not significantly different during the control period or at five, ten, and 15 minutes of VF and CPR between animal groups prior to drug administration. When compared to hemodynamic values measured at 15 minutes, naloxone had no significant effect on pressures or aortic flow measured five minutes after administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Inspiratory impedance during active compression-decompression cardiopulmonary resuscitation: a randomized evaluation in patients in cardiac arrest

BACKGROUND: Blood pressure is severely reduced in patients in cardiac arrest receiving standard cardiopulmonary resuscitation (CPR). Although active compression-decompression (ACD) CPR improves acute hemodynamic parameters, arterial pressures remain suboptimal with this technique. We performed ACD CPR in patients with a new inspiratory threshold valve (ITV) to determine whether lowering intrathoracic pressures during the "relaxation" phase of ACD CPR would enhance venous blood return and overall CPR efficiency. METHODS AND RESULTS: This prospective, randomized, blinded trial was performed in prehospital mobile intensive care units in Paris, France. Patients in nontraumatic cardiac arrest received ACD CPR plus the ITV or ACD CPR alone for 30 minutes during advanced cardiac life support. End tidal CO(2) (ETCO(2)), diastolic blood pressure (DAP) and coronary perfusion pressure, and time to return of spontaneous circulation (ROSC) were measured. Groups were similar with respect to age, gender, and initial rhythm. Mean maximal ETCO(2), coronary perfusion pressure, and DAP values, respectively (in mm Hg), were 13.1+/-0.9, 25.0+/-1.4, and 36.5+/-1.5 with ACD CPR alone versus 19.1+/-1.0, 43.3+/-1.6, and 56.4+/-1.7 with ACD plus valve (P<0.001 between groups). ROSC was observed in 2 of 10 patients with ACD CPR alone after 26.5+/-0.7 minutes versus 4 of 11 patients with ACD CPR plus ITV after 19.8+/-2.8 minutes (P<0.05 for time from intubation to ROSC). Conclusions-Use of an inspiratory resistance valve in patients in cardiac arrest receiving ACD CPR increases the efficiency of CPR, leading to diastolic arterial pressures of >50 mm Hg. The long-term benefits of this new CPR technology are under investigation.     

Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats

During cardiac arrest (CA), myocardial perfusion is solely dependent on cardiopulmonary resuscitation (CPR) although closed-chest compressions only provide about 10–20% of normal myocardial perfusion. The study was conducted in a whole animal CPR model to determine whether CPR-generated oxygen delivery preserves or worsens mitochondrial function. Male Sprague-Dawley rats (400–450 g) were randomly divided into four groups: (1) BL (instrumentation only, no cardiac arrest), (2) CA₁₅ (15 min cardiac arrest without CPR), (3) CA₂₅ (25 min cardiac arrest without CPR) and (4) CPR (15 min cardiac arrest, followed by 10 min CPR). The differences between groups were evaluated by measuring mitochondrial respiration, electron transport chain (ETC) complex activities and mitochondrial ultrastructure by transmission electron microscopy (TEM). The CA₂₅ group had the greatest impairment of mitochondrial respiration and ETC complex activities (I–III). In contrast, the CPR group was not different from the CA₁₅ group regarding all measures of mitochondrial function. Complex I was more susceptible to ischemic injury than the other complexes and was the major determinant of mitochondrial dysfunction. Observations of mitochondrial ultrastructure by TEM were compatible with the biochemical results. The findings suggest that, despite low blood flow and oxygen delivery, CPR is able to preserve heart mitochondrial function and viability during ongoing global ischemia. Preservation of complex I activity and mitochondrial function during cardiac arrest may be an important mechanism underlying the beneficial effects of CPR which have been shown in clinical studies.     

Cardiac arrest and resuscitation: brain iron delocalization during reperfusion

We hypothesize that brain injury from cardiac arrest occurs during reperfusion and is in part mediated by iron-dependent lipid peroxidation. We conducted a study to examine the time course of brain iron delocalization and lipid peroxidation in an animal model of cardiac arrest and resuscitation. Assays for brain tissue iron in low-molecular-weight species (LMWS iron) used the o-phenanthroline test on an ultrafiltered (molecular weight less than 30,000) tissue sample; malondialdehyde (MDA), a product of lipid peroxidation, in brain tissue was assayed by the thiobarbituric acid test (TBA). Samples of the parietal cortex from 11 nonischemic control dogs (Group 1) had LMWS iron levels of 9.6 +/- 4.9 nmol/100 mg tissue and MDA levels of 7.7 +/- 2.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 15 minutes of cardiac arrest (Group 2) had LMWS iron levels of 9.3 +/- 3.1 nmol/100 mg tissue and MDA levels of 6.1 +/- 1.0 nmol/100 mg tissue. Samples from the parietal cortex taken from five dogs after 45 minutes of cardiac arrest (Group 3) had LMWS iron levels of 6.7 +/- 3.3 nmol/100 mg tissue and MDA levels of 5.6 +/- 0.4 nmol/100 mg tissue. There was no significant difference among the three groups for either LMWS iron or MDA. Five dogs were subjected to 15 minutes of cardiac arrest and definitive resuscitation by internal cardiac massage and defibrillation (Group 4). Following resuscitation the chest was closed and the dogs were given intensive care for two hours.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bystander mouth-to-mouth ventilation and regurgitation during cardiopulmonary resuscitation

OBJECTIVES: To determine whether there is an association between bystander mouth-to-mouth ventilation and regurgitation in prehospital cardiac arrest patients. DESIGN: Prospectively conducted observational study. SETTING: Data were collected from patients treated by the emergency medical service (EMS) systems in three middle-sized or large Finnish urban communities, the Tampere District EMS and the physician-staffed Helicopter EMSs in the Helsinki and Turku areas in southern Finland. SUBJECTS: The study population consisted of 529 consecutive prehospital cardiac arrest patients with attempted resuscitation. Exclusion criteria were cardiac arrest due to trauma or drug overdose. MAIN OUTCOME MEASURES: Regurgitation in prehospital cardiac arrest patients documented by EMS personnel on the scene. RESULTS: Regurgitation occurred in a fourth of patients. Bystander cardiopulmonary resuscitation (CPR) with mouth-to-mouth ventilation was associated with a significantly increased risk of regurgitation compared with no CPR (P < 0.013) and CPR without ventilations (P < 0.01). CONCLUSIONS: The mode and role of bystander CPR in cardiac arrest needs to be further evaluated.     

老年人心肺复苏的特点及临床分析

目的了解6年来我院老年人心肺复苏（CPR）现状,分析其临床特点,研究防治对策。方法对本院2002年6月至2008年6月发生的335例心跳骤停（CA）的患者资料进行分析,按年龄分为老年组（年龄≥60岁）和非老年组（年龄〈60岁）,比较2组自主循环恢复（ROSC）成功率、脑复苏成功率; 分析2组CPR开始时间、人工气道开始建立时间、CPR持续时间、除颤次数、肾上腺素用量,组间进行比较。结果非老年组ROSC成功率为32.42%,脑复苏率为3.85%,老年组ROSC成功率为20.92%,脑复苏成功率为0.65%。2组之间CPR开始时间、人工气道开始建立时间方面无显著性差异（P〉0.05）,肾上腺素用量上有显著性差异（P〈0.05）。结论老年人CA患者CPR成功率相当低,重视老年人基础疾病的救治,完善急救医疗体系建设,是提高老年人CPR成功率的关键措施。     

Resuscitation of dogs from cold-water submersion using cardiopulmonary bypass

In cold-water drowning, attempts at restoration of spontaneous circulation (ROSC) by external cardiopulmonary resuscitation (CPR) often fail. We explored the longest period of asphyxial cardiac arrest from cold-water submersion (without inhalation of water) from which ROSC is possible using cardiopulmonary bypass (CPB). In 19 lightly anesthetized dogs the tracheal tube was clamped (simulating laryngospasm) and the dogs were immersed in ice water from 20, 40, 60, 90, or 120 minutes. Cardiac arrest occurred after six to 11 minutes of submersion. At start of resuscitation, rectal temperature ranged from 21 C (after 60 minutes) to 34 C (after 20 minutes of submersion), and cerebral temperature was between 7 C (after 120 minutes) and 27 C (after 20 minutes submersion). Resuscitation attempts were performed according to protocol in 16 dogs, using only CPB by venoarterial pumping with an oxygenator and a heat exchanger. Priming was with 400 to 800 mL Dextran 40 and Ringer's solution 1:1 plus heparin. CPB flows were 10 mL/kg/min, and they increased to achieve normotension and return of rectal temperature to 32 C. After one-half to three hours, of CPB, ROSC was successful in 75%. This percentage included one of three dogs after 90 minutes submersion, but not in the one dog after 120 minutes submersion. Spontaneous breathing and EEG activity returned in 56% at two to 24 hours, after 20 to 90 minutes of submersion. Failure of ROSC attempts apparently were due to clotting in large vessels during arrest and capillary leakage during reperfusion. CPB is effective for ROSC after prolonged hypothermic cardiac arrest, and it should be evaluated in animal outcome studies.     

Resuscitation time in ventricular fibrillation — a prognostic indicator

Length of resuscitation in prehospital ventricular fibrillation patients was studied to define its relationship to survival. Five hundred sixty-five patients presenting with the initial rhythm of ventricular fibrillation to the Milwaukee County Paramedic System between January 1978 and April 1982 were resuscitated successfully. Pediatric patients and patients with trauma, poisoning, and drowning were excluded. Of the 565 resuscitated patients, 262 (46%) were discharged alive and 303 (54%) died during hospitalization. For all 565 patients the resuscitation time and times from arrival of paramedics until the first sustained pulse were plotted against survival to define a curve. The curve demonstrated rapidly declining survival rates for resuscitation time up to 20 minutes; thereafter, survival declined more gradually with respect to resuscitation time. The mean resuscitation time for those eventually discharged alive was 12.6 minutes, which was statistically shorter (P less than .0001) than the mean resuscitation time of 23.9 minutes for those who eventually died. The overall survival curve of witnessed arrest patients was not statistically different from that of unwitnessed patients. The survival curve of those patients receiving bystander cardiopulmonary resuscitation (CPR) was similar to the curve of those who received no CPR. We conclude that resuscitation time is a heretofore undefined significant predictor of survival of resuscitated prehospital ventricular fibrillation patients.     

Ionized hypocalcemia during prolonged cardiac arrest and closed-chest CPR in a canine model

STUDY BACKGROUND: Free or ionized calcium (Ca+2) is known to play a critical role in normal cardiovascular function, and Ca+2 administration in the setting of ionized hypocalcemia has been shown to improve indexes of cardiac function. The value of Ca+2 administration in the setting of cardiac arrest and resuscitation is unproven and controversial, in large part because ionized Ca+2 levels during cardiac arrest and resuscitation have not been adequately studied and exogenous calcium therapy may worsen ischemic cellular injury. STUDY PURPOSE: To measure free calcium during prolonged cardiac arrest and CPR in a canine model. METHODS AND MEASUREMENTS: Central arterial and venous catheters were positioned in nine dogs, and ventricular fibrillation (VF) was induced electrically. After seven and one-half minutes of VF, countershocks were administered, and CPR was initiated and performed in accordance with current recommendations for 20 minutes. At five-minute intervals during resuscitation efforts, arterial pH, ionized Ca+2, and lactate as well as aortic pressure were measured. RESULTS: During resuscitation, average systolic arterial pressure was 50 mm Hg. Within five minutes of instituting CPR, ionized Ca+2 significantly decreased from control values (5.1 +/- 0.1 at control to 4.0 +/- 0.1 mg/dL); after 20 minutes of attempted resuscitation, it averaged 3.2 +/- 0.2 mg/dL (P less than .05 vs control). There was no change in total Ca+2 during the arrest period (9.2 +/- 0.5 at control to 8.6 +/- 0.8 mg/dL at 27.5 minutes). Arterial lactate significantly increased throughout the arrest and resuscitation period (1.9 +/- 0.2 at control to 7.5 +/- 0.4 mM/L at 27.5 minutes). A significant correlation was demonstrated between ionized Ca+2 and lactate concentrations (r = -.72, P less than .001) but not between ionized calcium and pH (r = -.22, P greater than .20). CONCLUSION: Ionized hypocalcemia occurs during prolonged cardiac arrest and resuscitation, and ionized hypocalcemia during prolonged arrest and resuscitation may be due to binding by lactate, as has been demonstrated in vitro.     

Limitations of open-chest cardiac massage after prolonged, untreated cardiac arrest in dogs

STUDY OBJECTIVES: Open-chest cardiac massage is an effective method of resuscitation if instituted within 15 minutes of normothermic cardiac arrest that has failed to respond to ongoing closed-chest CPR efforts. The usefulness of invasive forms of CPR after various periods of untreated cardiac arrest is less certain. This study was performed to determine the effectiveness of open-chest resuscitation after prolonged periods of untreated cardiac arrest. SETTING AND DESIGN: Prospective, controlled laboratory investigation using an animal model of cardiac arrest. Open-chest cardiac massage initially was compared to standard closed-chest compression CPR. The efficacy of open-chest CPR then was evaluated after ten and 40 minutes of untreated ventricular fibrillation. TYPE OF PARTICIPANTS: Twenty mongrel dogs (24 +/- 1 kg). MEASUREMENTS AND MAIN RESULTS: After 20 minutes of untreated ventricular fibrillation, open-chest resuscitation was significantly better than closed-chest efforts for the production of coronary perfusion pressure (58 +/- 14 vs 2 +/- 1 mm Hg; P less than .05) and initial resuscitation success (five of five vs one of five; P less than .03). Open-chest cardiac massage was equally effective for initial resuscitation if begun after ten or 20 minutes of untreated ventricular fibrillation (five of five vs five of five), but if untreated ventricular fibrillation continued for 40 minutes prior to instituting open-chest massage, no resuscitation benefit was found (none of five; P less than .005). There were marked differences in 24-hour survival depending on the length of time untreated cardiac arrest continued prior to instituting open-chest resuscitation efforts. After 20 minutes of ventricular fibrillation, initial resuscitation was successful with open-chest massage, but long-term survival was poor. CONCLUSION: Open-chest cardiac massage did not produce long-term survival if untreated cardiac arrest persisted for 20 or more minutes prior to invasive resuscitation efforts.     

Comparison of central venous and arterial pH and PCO2 during open-chest CPR in the canine model

Arterial blood gases are difficult to obtain during cardiopulmonary resuscitation (CPR) in human beings, and the possibility of venous sampling is raised frequently. The reliability of central venous gases as a substitute for arterial blood gases in assessing acid base status, however, has not been investigated adequately under conditions of CPR. Therefore, femoral arterial and central venous catheters were placed in 24 mongrel dogs, and ventricular fibrillation was electrically induced. After varying predetermined downtimes from five to 60 minutes, open-chest CPR was begun, and arterial and central venous blood gases were simultaneously drawn every five minutes during a 30-minute period. Arterial pH (pHa) was consistently higher than central venous pH (pHcv) by an average of .048 units. A significant correlation existed between the pHa and pHcv at all times during CPR, with an overall r = .9771 (P less than .0001). The difference between central venous PCO2 (PcvCO2) and arterial PCO2 (PaCO2) was 5.17 mm Hg prior to cardiac arrest, but it increased 300% to a mean of 15.51 mm Hg during CPR. Correction of pHcv using conventional methods to account for this respiratory component decreased the correlation between pHa and pHcv to r = .6905. The ability of pHcv to substitute for pHa was assessed, and showed a sensitivity of 100% when pHa of 7.2 was used as a criterion for treatment. In this model, pHcv is a sensitive indicator of pHa and it may be used to guide bicarbonate therapy. The increased PcvCO2 during CPR probably results from the marked tissue lactic acid production and subsequent shift of the bicarbonate buffer into free carbon dioxide.     

兔模型心脏骤停标准的探讨

目的：比较心肺复苏动物模型的2种心脏骤停判断标准,以确立适合于心脏骤停后综合征研究的心脏骤停判断标准。方法：大耳白兔30只,随机分为心电图标准组（A组）、动脉压标准组（B组）。采用夹闭气管建立心脏骤停模型,分别使用2种不同的心脏骤停判断标准,心脏骤停5min时立即复苏,观察复苏成功率和兔存活时间,监测心脏骤停前、复苏后24、48、72、96、120h6个时间点兔血神经元特异性烯醇化酶（NSE）、谷丙转氨酶（ALT）、血肌酐及肌钙蛋白I水平,分析复苏后多器官功能障碍综合征（MODS）发生情况。结果：心肺复苏即刻成功率A组为33%,B组为86%,2组比较有显著差异（P〈0.05）。兔存活时间A组为（1.38±1.04）h,B组存活时间为（58.0±41.5）h,2组比较有显著差异（P〈0.01）。B组兔复苏后24、48、72h时间点血NSE、ALT、肌酐及肌钙蛋白I水平明显升高,与心脏骤停前比较有显著差异（P〈0.01）。复苏后24～72h,兔出现多器官功能障碍综合征（MODS）表现。结论：以平均动脉压为标准判断心脏骤停优于心电图标准,适用于标准化心脏骤停后综合征的兔模型的建立。     

Recent Advances in Cardiopulmonary Resuscitation

Recent Advances in CPR. Mechanical and pharmacologic measures intended to increase blood now to vital organs are the mainstay of therapy for patients in cardiac arrest. Several new cardiopilmonary resuscitation (CPR) techniques as well as novel devices and pharmacologic agents have been developed and tested since the first report of manual closed chested CPR over three decades ago. These recent mechanical and pharmacologic advances in the treatment of cardiac arrest are described. Some of these new techniques, devices, and drug therapies are presently undergoing clinical evaluation in patients in cardiac arrest. While many of these new methods and techniques have shown promise in small clinical trials in humans, none have yet lo be found to be conclusively superior to manual closed chested CPR and treatment with standard pharmacologic agents.     

Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.     

Strategy analysis of cardiopulmonary resuscitation training in the community

Bystander cardiopulmonary resuscitation (CPR) is a crucial therapy for sudden cardiac arrest. This appreciation produced immense efforts by professional organizations to train laypeople for CPR skills. However, the rate of CPR training is low and varies widely across communities. Several strategies are used in order to improve the rate of CPR training and are performed in some advanced countries. The Chinese CPR training in communities could gain enlightenment from them.