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Wanchun Tang

Publications and source records attributed to Wanchun Tang.

At least 19 recordsLinked to original sources

Buccal capnometry to guide management of massive blood loss.

In both clinical and experimental settings, tissue P(CO2) measured in the oral mucosa is a practical and reliable measurement of the severity of hypoperfusion. We hypothesized that a threshold level of buccal tissue P(CO2) (P(CO2) BU)) would prognosticate the effects of volume repletion on survival. Twenty pentobarbital-anesthetized Sprague-Dawley male breeder rats, each weighing approximately 0.5 kg, were randomly assigned to one of four groups. Animals were bled over an interval of 30 min in amounts estimated to be 25, 30, 35, or 40% of total blood volume. One-half hour after the completion of bleeding, each animal received an infusion of Ringer lactate solution over the ensuing 30 min in amounts equivalent to two times the volume of blood loss. P(CO2) BU) was measured continuously with an optical P(CO2) sensor applied noninvasively to the mucosa of the left cheek. Arterial pressure and end-tidal CO2 were measured over the same interval. Neurological deficit and 72-h survival were recorded. Aortic pressures were restored to near baseline values for each of the four groups after fluid resuscitation. This contrasted with the improvement of P(CO2) BU), which differentiated between animals with short and long durations of postintervention survival. After electrolyte fluid resuscitation in rats subjected to rapid bleeding, noninvasive measurement of P(CO2) BU) was predictive of outcomes. Neither noninvasive end-tidal P(CO2) nor invasive aortic pressure measurements achieved such discrimination. Accordingly, P(CO2) BU) fulfills the criterion of a noninvasive and reliable measurement to guide fluid management of hemorrhagic shock.

Animals↗

Lay rescuer automated external defibrillator ("public access defibrillation") programs: lessons learned from an international multicenter trial: advisory statement from the American Heart Association Emergency Cardiovascular Committee; the Council on Cardiopulmonary, Perioperative, and Critical Care; and the Council on Clinical Cardiology.

Lay rescuer automated external defibrillator (AED) programs may increase the number of people experiencing sudden cardiac arrest who receive bystander cardiopulmonary resuscitation (CPR), can reduce time to defibrillation, and may improve survival from sudden cardiac arrest. These programs require an organized and practiced response, with rescuers trained and equipped to recognize emergencies, activate the emergency medical services system, provide CPR, and provide defibrillation. To determine the effect of public access defibrillation (PAD) programs on survival and other outcomes after SCA, the National Heart, Lung, and Blood Institute, the American Heart Association (AHA), and others funded a large prospective randomized trial. The results of this study were recently published in The New England Journal of Medicine and support current AHA recommendations for lay rescuer AED programs and emphasis on planning, training, and practice of CPR and use of AEDs. The purpose of this statement is to highlight important findings of the Public Access Defibrillation Trial and summarize implications of these findings for healthcare providers, healthcare policy advocates, and the AHA training network.

American Heart Association↗

Levosimendan improves postresuscitation myocardial dysfunction after beta-adrenergic blockade.

In earlier studies, we found that a nonselective beta-adrenergic blocking agent, propranolol, facilitated cardiac resuscitation, reduced postresuscitation myocardial ectopy, and improved postresuscitation survival. However, the potential adverse effects and specifically the negative inotropic actions of propranolol prompted our further investigation of the potential value of a non-beta-adrenergic inotropic drug, levosimendan, in conjunction with propranolol, for minimizing postresuscitation myocardial dysfunction after successful resuscitation from cardiac arrest. Ventricular fibrillation was induced and untreated for 7 minutes in 15 domestic pigs, which were divided into propranolol, propranolol plus levosimendan, and control groups. Propranolol was administered as a bolus dose of 0.1 mg/kg during cardiac arrest. Electrical defibrillation was attempted after 12 minutes of cardiac arrest including 5 minutes of precordial compression. Levosimendan was administered at 10 minutes after successful resuscitation in a dose of 20 microg/kg and followed by infusion of 0.4 microg/kg/min over the ensuing 220 minutes. Propranolol reduced energies or numbers of defibrillatory shocks and postresuscitation myocardial ectopy, and it improved postresuscitation myocardial dysfunction. When levosimendan was added, postresuscitation myocardial contractile function was improved even more.

Adrenergic beta-Antagonists↗

Levosimendan improves postresuscitation outcomes in a rat model of CPR.

In this study we sought to determine whether a calcium sensitizer, levosimendan, would have a more favorable effect on postresuscitation myocardial function and, consequently, postresuscitation survival than beta-adrenergic dobutamine. The extreme decrease in survival before hospital discharge of resuscitated victims is attributed, in part, to postresuscitation myocardial failure, and dobutamine has been recommended for the management of postresuscitation myocardial failure. We studied a total of 15 animals. Ventricular fibrillation was induced in Sprague-Dawley rats weighing 450 to 550 g. Cardiopulmonary resuscitation (CPR), including chest compressions and mechanical ventilation, was begun after 8 minutes of untreated cardiac arrest. Electrical defibrillation was attempted after 6 minutes of CPR. Each animal was resuscitated. Animals were randomized to undergo treatment with levosimendan, dobutamine, or saline-solution placebo. These agents were administered 10 minutes after the return of spontaneous circulation. Levosimendan was administered in a loading dose of 12 microg kg(-1) over a 10-minute period, followed by infusion of 0.3 microg kg(-1) min(-1) over the next 230 minutes. Dobutamine was continuously infused at a dosage of 3 microg kg(-1) min(-1). Saline-solution placebo was administered in the same volume and over the same amount of time as levosimendan. Levosimendan and dobutamine produced comparable increases in cardiac output and rate of left-ventricular pressure increase. However, administration of levosimendan resulted in lower heart rates and lesser increases in left ventricular diastolic pressure compared with both dobutamine and placebo. The duration of postresuscitation survival was significantly greater with levosimendan (16 +/- 2 hours), intermediate with dobutamine (11 +/- 2 hours) and least with saline-solution placebo (8 +/- 1 hour). Levosimendan and dobutamine both improved postresuscitation myocardial function. However, levosimendan produced more favorable postresuscitation myocardial function and increased the duration of postresuscitation survival.

Adrenergic beta-Agonists↗

Comparison between dobutamine and levosimendan for management of postresuscitation myocardial dysfunction.

OBJECTIVE: To investigate the effects of levosimendan, a nonadrenergic inotropic calcium sensitizer, in comparison with adrenergic dobutamine for the management of postresuscitation myocardial dysfunction following resuscitation from prolonged cardiac arrest. DESIGN: Randomized prospective animal study. SETTING: Animal research laboratory. SUBJECTS: Male Yorkshire-cross domestic pigs INTERVENTIONS: Ventricular fibrillation was induced in male domestic pigs weighing between 35 and 40 kg. Cardiopulmonary resuscitation, including precordial compression and mechanical ventilation, was started after 7 mins of untreated cardiac arrest. Electrical defibrillation was attempted after 5 mins of cardiopulmonary resuscitation. Each animal was successfully resuscitated without pharmacologic intervention. Resuscitated animals were randomized to treatment with levosimendan, dobutamine, or saline placebo. The inotropic agents or an equivalent volume of placebo diluents was administered 10 mins after restoration of spontaneous circulation. Levosimendan was administered in a loading dose of 20 microg.kg over 10 mins followed by a 220-min infusion of 0.4 microg.kg.min. Dobutamine was infused into the right atrium in an amount of 5 microg.kg.min. Treatment was continued for a total of 230 mins. MEASUREMENTS AND MAIN RESULTS: Levosimendan and dobutamine produced comparable increases in cardiac output. However, levosimendan produced significantly greater left ventricular ejection fraction and fractional area changes compared with dobutamine and saline placebo. CONCLUSIONS: Levosimendan has the potential of improving postresuscitation myocardial function. It is likely to serve as an alternative to dobutamine as an inotropic agent for management of postresuscitation myocardial dysfunction.

Analysis of Variance↗

How does interruption of cardiopulmonary resuscitation affect survival from cardiac arrest?

PURPOSE OF REVIEW: Survival rates from cardiac arrest are unacceptably low. The present review aims to summarize recent contributions to cardiopulmonary resuscitation research in relation to hemodynamic consequences and especially survival resulting from interruption of chest compressions for defibrillation and rescue breathing. RECENT FINDINGS: Data from animal and human studies strongly support the negative consequences for overall survival when cardiopulmonary resuscitation is interrupted for rescue breathing and rhythm analysis. Furthermore, in settings of prolonged cardiac arrest, electrical defibrillation may not have the highest priority as initial intervention. SUMMARY: Interruption of cardiopulmonary resuscitation negatively affects survival from cardiac arrest. Fewer interruptions for interventions and interventions that take less time may improve survival.

Cardiopulmonary Resuscitation↗

Increases in both buccal and sublingual partial pressure of carbon dioxide reflect decreases of tissue blood flows in a porcine model during hemorrhagic shock.

BACKGROUND: Earlier studies had demonstrated that gastric partial pressure of carbon dioxide (PCO2) of the gastric wall is an early indication of perfusion failure. Because hypercarbia is a general phenomenon of perfusion failure, this study investigated whether sublingual and buccal mucosal tissue PCO2 also serve as a sensitive indicator of systemic blood flow during hemorrhagic shock. METHODS AND RESULTS: Hemorrhagic shock was induced in five male domestic pigs. Buccal and sublingual PCO2 increased from 60 to 129 mm Hg (p < 0.01) in parallel with average decreases in cardiac output to 44% (from 6.1 to 2.8 L/minute; p < 0.01), and mean arterial pressure to 47% (from 115 to 57 mm Hg; p < 0.01), over the 2-hour interval of shock. According to colored microspheres used for measurements, buccal mucosal flow decreased to 35% (from 6.3 to 2.2 mL/minute/100 g; p < 0.01) in close parallel with sublingual blood flow, which decreased to 34% (from 7.2 to 2.5 mL/minute/100 g; p < 0.01). Liver flow decreased to 56% (from 152 to 85 mL/minute/100 g;p < 0.01), and renal flow to 47% (from 272 to 128 mL/minute/100 g;p < 0.01) of baseline values. The procedure yielded to overall comparable volume exchanges in different animals. After reinfusion of shed blood, buccal PCO2, like sublingual PCO2, was restored to approximately baseline values (respectively, from 56 to 71 mm Hg and from 60 to 71 mm Hg; p = not significant), together with arterial pressure, cardiac output, and end-tidal CO2 (EtCO2) (respectively, from 115 to 115 mm Hg, from 6.1 to 6.3 L/minute, and from 35 to 39 mm Hg; p = not significant), but there was delayed reversal of lactic acidosis (from 0.7 to 2.5 mmol/L;p < 0.01). In five unbled control animals, no significant changes were observed over the same interval. CONCLUSION: The current study extends the rationale for noninvasive measurements to both buccal and sublingual mucosa for diagnosis and quantitation of hemorrhagic shock severity.

Animals↗

Carvedilol mitigates adverse effects of epinephrine during cardiopulmonary resuscitation.

INTRODUCTION: Earlier studies have implicated the adverse effects of beta- and alpha(1)-adrenergic receptors during cardiopulmonary resuscitation (CPR). Because carvedilol is both a nonselective beta- and alpha1-selective adrenergic receptor-blocking agent, we hypothesized that pretreatment with carvedilol would convert the actions of epinephrine to that of a selective alpha2-agonist. METHODS: Ventricular fibrillation (VF) was induced in Sprague-Dawley rats weighing approximately 500 g. Animals were randomized to 4 groups of 5 animals each: (1) placebo pretreatment and epinephrine treatment, (2) carvedilol pretreatment and placebo treatment, (3) carvedilol pretreatment and epinephrine treatment, and (4) placebo pretreatment and placebo treatment. Carvedilol (50 microg/kg) was injected as a bolus into the right atrium 15 minutes before VF was induced. VF was untreated for 8 minutes, after which CPR (chest compression and mechanical ventilation) was begun. Epinephrine (30 microg/kg) was injected into the right atrium 2 minutes after the start of CPR. Electrical defibrillation was attempted after 14 minutes of VF. RESULTS: All but 2 animals were successfully resuscitated. Approximately equivalent increases in coronary perfusion pressure from 23 +/- 1 mm Hg to 30 +/- 3 mm Hg were observed after the injection of epinephrine independently of carvedilol pretreatment. Carvedilol pretreatment followed by epinephrine treatment reduced early postresuscitation ventricular ectopy (116 +/- 147 vs 834 +/- 380, P < .01) and minimized increases in arterial blood lactate at 5 minutes after resuscitation (10.9 +/- 2.1 mmol/L vs 17.4 +/- 3.5 mmol/L, P < .01). The postresuscitation cardiac index measured 4 hours later was increased (307 +/- 43 mL x min(-1) x kg(-1) vs 210 +/- 6 mL x min(-1) x kg(-1), P < .05). Left ventricular diastolic pressures were decreased (6 +/- 1 vs 14 +/- 1 mm Hg, P < .05). Animals pretreated with carvedilol survived longer (71 +/- 1 vs 45 +/- 22 hours, P < .05) and with less postresuscitation neurologic deficit. CONCLUSION: After beta- and alpha1-adrenergic blockade with carvedilol before inducing cardiac arrest, epinephrine administered during CPR yielded better postresuscitation myocardial and neurologic functions and significantly increased postresuscitation survival.

Adrenergic Agonists↗

Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest.

INTRODUCTION: American Heart Association/American College of Cardiology guidelines recommend a compression-to-ventilation ratio (C/V ratio) of 15:2 during cardiopulmonary resuscitation (CPR) for out-of-the-hospital cardiac arrest. Recent data have shown that frequent ventilations are unnecessary and may be harmful during CPR, since each positive-pressure ventilation increases intrathoracic pressure and may increase intracranial pressure and decrease venous blood return to the right heart and thereby decrease both the cerebral and coronary perfusion pressures. HYPOTHESIS: We hypothesized that reducing the ventilation rate by increasing the C/V ratio from 15:2 to 15:1 will increase vital-organ perfusion pressures without compromising oxygenation and acid-base balance. METHODS: Direct-current ventricular fibrillation was induced in 8 pigs. After 4 min of untreated ventricular fibrillation without ventilation, all animals received 4 min of standard CPR with a C/V ratio of 15:2. Animals were then randomized to either (A) a C/V ratio of 15:1 and then 15:2, or (B) a C/V ratio of 15:2 and then 15:1, for 3 min each. During CPR, ventilations were delivered with an automatic transport ventilator, with 100% oxygen. Right atrial pressure, intratracheal pressure (a surrogate for intrathoracic pressure), aortic pressure, and intracranial pressure were measured. Coronary perfusion pressure was calculated as diastolic aortic pressure minus right atrial pressure. Cerebral perfusion pressure was calculated as mean aortic pressure minus mean intracranial pressure. Arterial blood gas values were obtained at the end of each intervention. A paired t test was used for statistical analysis, and a p value < 0.05 was considered significant. RESULTS: The mean +/- SEM values over 1 min with either 15:2 or 15:1 C/V ratios were as follows: intratracheal pressure 0.93 +/- 0.3 mm Hg versus 0.3 +/- 0.28 mm Hg, p = 0.006; coronary perfusion pressure 10.1 +/- 4.5 mm Hg versus 19.3 +/- 3.2 mm Hg, p = 0.007; intracranial pressure 25.4 +/- 2.7 mm Hg versus 25.7 +/- 2.7 mm Hg, p = NS; mean arterial pressure 33.1 +/- 3.7 mm Hg versus 40.2 +/- 3.6 mm Hg, p = 0.007; cerebral perfusion pressure 7.7 +/- 6.2 mm Hg versus 14.5 +/- 5.5 mm Hg, p = 0.008. Minute area intratracheal pressure was 55 +/- 17 mm Hg . s versus 22.3 +/- 10 mm Hg . s, p < 0.001. End-tidal CO(2) with 15:2 versus 15:1 was 24 +/- 3.6 mm Hg versus 29 +/- 2.5 mm Hg, respectively, p = 0.001. Arterial blood gas values were not significantly changed with 15:2 versus 15:1 C/V ratios: pH 7.28 +/- 0.03 versus 7.3 +/- 0.03; P(aCO(2)) 37.7 +/- 2.9 mm Hg versus 37.6 +/- 3.5 mm Hg; and P(aO(2)) 274 +/- 36 mm Hg versus 303 +/- 51 mm Hg. CONCLUSIONS: In a porcine model of ventricular fibrillation cardiac arrest, reducing the ventilation frequency during CPR by increasing the C/V ratio from 15:2 to 15:1 resulted in improved vital-organ perfusion pressures, higher end-tidal CO(2) levels, and no change in arterial oxygen content or acid-base balance.

Animals↗

The effects of biphasic waveform design on post-resuscitation myocardial function.

OBJECTIVES: This study examined the effects of biphasic truncated exponential waveform design on survival and post-resuscitation myocardial function after prolonged ventricular fibrillation (VF). BACKGROUND: Biphasic waveforms are more effective than monophasic waveforms for successful defibrillation, but optimization of energy and current levels to minimize post-resuscitation myocardial dysfunction has been largely unexplored. We examined a low-capacitance waveform typical of low-energy application (low-energy biphasic truncated exponential [BTEL]; 100 microF, < or =200 J) and a high-capacitance waveform typical of high-energy application (high-energy biphasic truncated exponential [BTEH]; 200 microF, > or =200 J). METHODS: Four groups of anesthetized 40- to 45-kg pigs were investigated. After 7 min of electrically induced VF, a 15-min resuscitation attempt was made using sequences of up to three defibrillation shocks followed by 1 min of cardiopulmonary resuscitation. Animals were randomized to BTEL at 150 J or 200 J or to BTEH at 200 J or 360 J. RESULTS: Resuscitation was unsuccessful in three of the five animals treated with BTEH at 200 J. All other attempts were successful. Significant therapy effects were observed for survival (p = 0.035), left ventricular ejection fraction (p < 0.001), stroke volume (p < 0.001), fractional area change (p < 0.001), cardiac output (p = 0.044), and mean aortic pressure (p < 0.001). Hemodynamic outcomes were negatively associated with energy and average current but positively associated with peak current. Peak current was the only significant predictor of survival (p < 0.001). CONCLUSIONS: Maximum survival and minimum myocardial dysfunction were observed with the low-capacitance 150-J waveform, which delivered higher peak current while minimizing energy and average current.

Animals↗

Delta-opioid receptor agonist reduces severity of postresuscitation myocardial dysfunction.

Postresuscitation myocardial dysfunction is recognized as a leading cause of early death after initially successful cardiopulmonary resuscitation (CPR). In the present study, we hypothesized that a delta-opioid receptor agonist would decrease the severity of postresuscitation myocardial dysfunction and improve survival. Fifteen Sprague-Dawley rats, fasted overnight with access to water, were anesthetized by an injection of 45 mg/kg ip pentobarbital sodium. Additional doses of 10 mg/kg were administered at hourly intervals but not within 30 min before induced ventricular fibrillation (VF). Either the delta-opioid receptor agonist pentazocine (300 microg/kg), pentazocine pretreated with the opioid receptor-blocking agent naloxone (1 mg/kg), or saline placebo was injected into the right atrium after 5 min of untreated VF and 3 min before initiation of CPR. After an additional 8 min of CPR administration, defibrillation was attempted. All animals were successfully resuscitated. Left ventricular rate of pressure increase at 40 mmHg and cardiac index values were significantly improved in pentazocine-treated animals, which also had significantly longer survival times (60 +/- 11 vs. 16 +/- 7 h; P < 0.01). Except for ease of defibrillation, the beneficial effects of pentazocine were completely abolished by pretreatment with naloxone. The concept of pharmacological hibernation employing a delta-opioid receptor agonist is a novel and promising intervention for minimizing global ischemic injury during CPR and postresuscitation myocardial dysfunction.

Animals↗

Spontaneous gasping generates cardiac output during cardiac arrest.

OBJECTIVES: To measure stroke volumes coincident with spontaneous gasping during untreated ventricular fibrillation and to evaluate the effects of gasping. DESIGN: Prospective study in laboratory animals. SETTING: University-affiliated research institute. SUBJECTS: Male Yorkshire-X domestic pigs. INTERVENTIONS: Pigs were anesthetized (ketamine, 20 mg/kg intramuscularly and sodium pentobarbital, 30 mg/kg intravenously), intubated, and mechanically ventilated. Ventricular fibrillation was electrically induced and untreated for 7 mins. The right femoral artery and vein were cannulated. A 5.5/7.5-MHz biplanar transesophageal echocardiography transducer was advanced into the esophagus. MEASUREMENTS AND MAIN RESULTS: Stroke volumes were measured as the product of the transaortic blood flow velocity and transesophageal echocardiographic measurements of valve area. In addition, left ventricular volumes were echocardiographically estimated at peak inspiration and at peak expiration of each gasp by transesophageal methods. The stroke volume produced by gasping averaged 23 +/- 6 mL, which represented approximately 60% of a precardiac arrest stroke volume (38 +/- 8 mL, p <.001). Increases in end-tidal carbon dioxide tension coincident with each gasp were consistent with comparable increases in pulmonary blood flow and therefore stroke volumes. Both were associated with increases in aortic pressure from 20 +/- 3 to 33 +/- 8 mm Hg (p <.001) and coronary perfusion pressure from 4 +/- 3 to 13 +/- 7 mm Hg (p <.001). CONCLUSIONS: Our studies confirm that preterminal gasping during ventricular fibrillation increases both ventilation and forward blood flow.

Animals↗

A lazaroid mitigates postresuscitation myocardial dysfunction.

OBJECTIVE: Lazaroids, a series of 21-aminosteroids, reduce free radical mediated injury after ischemia and reperfusion. We hypothesized that the lazaroid U-74389G would minimize postresuscitation myocardial dysfunction and thereby improve neurologically meaningful survival in a rodent model after resuscitation from 8 mins of ventricular fibrillation. DESIGN: Randomized, controlled laboratory study. SETTING: University-affiliated research institute. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Ventricular fibrillation was electrically induced in ten anesthetized Sprague-Dawley rats. The lazaroid agent U-74389G in a dose of 1 mg.kg-1 or its vehicle serving as a placebo was injected into the right atrium after 7 mins of untreated ventricular fibrillation. One minute after injection of the compound, precordial compression was begun together with mechanical ventilation and continued for 6 mins before attempted electrical defibrillation. MEASUREMENTS AND MAIN RESULTS: All animals were successfully resuscitated. Postresuscitation cardiac index, left ventricular end-diastolic pressure, the rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg, and the maximum rate of left ventricular pressure decline were significantly less impaired in lazaroid-treated animals. This contrasted with control animals, which had significantly greater myocardial impairment, greater neurologic deficit, and lesser duration of survival. CONCLUSIONS: The lazaroid compound U-74389G, administered during cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved survival.

Animals↗

Beta1-adrenergic blockade during cardiopulmonary resuscitation improves survival.

OBJECTIVE: The short-acting beta1-selective adrenergic blocking agent, esmolol, was administrated during cardiopulmonary resuscitation with the hypothesis that initial resuscitation and postresuscitation survival would be improved. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: Ventricular fibrillation was induced in 18 male Sprague-Dawley rats, which were then left untreated for 6 mins before attempted resuscitation with precordial compression, mechanical ventilation, and electrical defibrillation. Animals were randomized to receive 300 microg/kg esmolol in a volume of 200 microL or an equivalent volume of saline placebo during cardiopulmonary resuscitation. Electrical defibrillation was attempted after 12 mins of ventricular fibrillation. MEASUREMENTS AND MAIN RESULTS: Esmolol-treated animals required a significantly smaller number of electrical shocks before resuscitation. Each of the esmolol-treated but only five of nine placebo-treated animals were successfully resuscitated. Postresuscitation contractile and left ventricular diastolic functions of resuscitated animals were significantly better after esmolol administration and duration of survival was significantly increased. CONCLUSIONS: A short-acting beta1-selective adrenergic blocking agent, when administered during cardiopulmonary resuscitation, significantly improved initial cardiac resuscitation, minimized postresuscitation myocardial dysfunction, and increased the duration of postresuscitation survival.

Adrenergic beta-Antagonists↗

Nonselective beta-blocking agent improves the outcome of cardiopulmonary resuscitation in a rat model.

OBJECTIVE: Postresuscitation myocardial dysfunction has been recognized as a leading cause of early death after initial successful resuscitation. Recent experimental and clinical studies have indicated that the beta-adrenergic effect of epinephrine significantly increases the severity of postresuscitation myocardial dysfunction. The fact that beta-adrenergic stimulation increases myocardial oxygen consumption during ventricular fibrillation is an important implication with respect to both the exogenous in terms of pharmacologic interventions during cardiopulmonary resuscitation and the endogenous as the result of intense sympathetic activation of cardiovascular collapse. Earlier experimental evidence has indicated that oxygenation improved by beta-blockade and beta1-blocking agent did offset the adverse effect of epinephrine. This prompted us to investigate the effect of beta-blockade on both exogenous and endogenous beta stimulation in an established rat model. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTIONS: In this series of studies, propranolol was administrated before ventricular fibrillation as a pretreatment combined with epinephrine treatment during precordial compression and then alone in a prolonged cardiac arrest setting. MEASUREMENTS AND MAIN RESULTS: Improved postresuscitation myocardial dysfunction (cardiac index, dP/dt40, -dP/dt) was observed with propranolol, a nonselective beta-adrenergic blocker, in pretreated animals such that the beneficial effects were associated with better postresuscitation survival. CONCLUSION: Nonselective beta-blockade improved the outcome of cardiopulmonary resuscitation in a rat model and deserves further evaluation in settings of cardiopulmonary resuscitation.

Adrenergic beta-Antagonists↗

Amplitude spectrum area: measuring the probability of successful defibrillation as applied to human data.

OBJECTIVE: The objective of our study was to examine the effectiveness of an electrocardiographic predictor, amplitude spectral area (AMSA), for the optimal timing of defibrillation shocks in human victims of cardiac arrest. Based on the spectral characteristics of ventricular fibrillation potentials, we examined the probability of successful conversion to an organized viable rhythm, including the return of spontaneous circulation. The incentive was to predict the likelihood of successful defibrillation and thereby improve outcomes by minimizing interruptions in chest compression and minimizing electrically induced myocardial injury due to repetitive high-current shocks. DESIGN: Observational study on human electrocardiographic recordings during cardiopulmonary resuscitation. SETTING: Medical research laboratory of a university-affiliated research and educational institute. PATIENTS: Victims of out-of-hospital cardiac arrest. INTERVENTIONS: Iteration of electrocardiographic records, representing lead 2 equivalent recordings on 108 defibrillation attempts with an automated external defibrillator, of 46 victims of cardiac arrest due to ventricular fibrillation. MEASUREMENTS AND MAIN RESULTS: Three seconds of ventricular fibrillation, recorded immediately preceding delivery of a shock, were analyzed utilizing the AMSA algorithm. AMSA represents a numerical value based on the sum of the magnitude of the weighted frequency spectrum between 3 and 48 Hz. The greater the AMSA value, the greater was the probability of reversal of ventricular fibrillation. At an AMSA value of >13.0 mV-Hz, successful defibrillation yielded a sensitivity of .91 and a specificity of .94. CONCLUSION: AMSA predicts the success of electrical defibrillation with high specificity. AMSA therefore serves to minimize interruptions of precordial compression and the myocardial damage caused by delivery of repetitive and ineffective electrical shocks.

Databases, Factual↗