Cardiopulmonary resuscitation: one size does not fit all.
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Asphyxia↗
Biomedical subjects
Wanchun Tang
Publications and source records attributed to Wanchun Tang.
A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation.
The objective of this research was to compare the effects of an alpha- and beta-adrenergic agonist, epinephrine, a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), and a non-adrenergic vasopressin on post-resuscitation myocardial function and duration of survival. Epinephrine continues to be the primary adrenergic agent for advanced cardiac life support. However, its major inotropic actions and especially its beta-adrenergic and, to a lesser extent, its alpha(1)-actions increase the severity of global ischemia during cardiac arrest and adversely affect post-resuscitation myocardial function and survival. We had previously observed significantly better outcomes with a selective alpha(2)-adrenergic agonist when compared with epinephrine. Non-adrenergic vasopressin also has promise of more favorable actions. The present study was, therefore, undertaken to compare a selective alpha(2)-adrenergic vasopressor drug with vasopressin, epinephrine, and saline placebo. Ventricular fibrillation (VF) was induced in 20 Sprague-Dawley rats. Mechanical ventilation and precordial compression were initiated after 8 min of untreated VF. About 2 min later, alpha-MNE in a dose of 100 microgram/kg, vasopressin in a dose of 0.4 U/kg, epinephrine in a dose of 30 microgram/kg, or saline control was administered. Defibrillation was attempted after 6 min of CPR. Left ventricular pressure, dP/dt(40), -dP/dt, and cardiac index were measured for an interval of 240 min after resuscitation. Except for saline controls, comparable increases in coronary perfusion pressure (CPP) were observed after each drug intervention. All animals were successfully resuscitated. Post-resuscitation myocardial function and survival were significantly better in animals treated with alpha-MNE. Both post-resuscitation myocardial function and survival were most improved after administration of the selective alpha(2)-adrenergic agonist, intermediate after vasopressin and least after epinephrine and saline placebo.
Analysis of Variance↗
Myocardial injury in children following resuscitation after cardiac arrest.
BACKGROUND: Myocardial dysfunction occurs immediately after successful cardiac resuscitation. Our purpose was to determine whether measurement of cardiac troponin I in children with acute out-of-hospital cardiac arrest predicts the severity of myocardial injury. METHODS AND RESULTS: This prospective, observational study was performed in the Pediatric Intensive Care Unit (PICU) on 24 patients following arrest, ranging in age from 8 months to 17 years. Troponin measurements were obtained on admission, and at 12, 24, and 48 h. Transthoracic echocardiograms were performed within 24 h after admission. Survival to hospital discharge was 29% (7/24). The mean age was 5.9+/-4.6 years for survivors and 4.2+/-5.3 years for non-survivors. The median (range) duration of cardiac arrest times for survivors was 6 min (3 to 63 min) versus 34 min (4 to 70 min) for nonsurvivors (P=0.02). Survivors received 1.3+/-2.2 doses of epinephrine (adrenaline) compared with 2.9+/-1.6 doses for non-survivors (P=0.02). Only one patient had ventricular fibrillation and defibrillation was unsuccessful. The ejection fraction for survivors averaged 73.2+/-11.2%, but for nonsurvivors only 55.4+/-19.8% (P=0.04). Ejection fraction correlated inversely with troponin at 12 h (r=-0.54, P=0.01) and at 24 h (r=-0.59, P=0.02). Circumferential fiber shortening for survivors was 37.5+/-7.8 and 25.5+/-10.7% for nonsurvivors (P=0.02). It also correlated inversely with troponin (r=-0.46, P=0.03 for survivors and r=-0.65, P=0.01, for nonsurvivors). CONCLUSION: After cardiac arrest and resuscitation in pediatric patients, the severity of myocardial dysfunction was reflected in troponin I levels.
Adolescent↗
Stroke volumes and end-tidal carbon dioxide generated by precordial compression during ventricular fibrillation.
OBJECTIVE: The objective of this study was to measure stroke volumes produced by precordial compression during cardiopulmonary resuscitation and to quantitate relationships of stroke volume to measurements of end-tidal carbon dioxide. DESIGN: A prospective, observational animal study. SETTING: Medical research laboratory in a university-affiliated research and educational foundation. SUBJECTS: Domestic pigs. INTERVENTIONS: Eighteen anesthetized male, domestic pigs weighing between 40 and 45 kg were investigated. Ventricular fibrillation was electrically induced and continued for intervals ranging from 4 to 10 mins. Precordial compression was maintained at 80 per minute together with mechanical ventilation after endotracheal intubation. MEASUREMENTS AND MAIN RESULTS: Stroke volumes were measured with the aid of transesophageal echocardiographic imaging. End-tidal carbon dioxide was quantitated with conventional capnography. Baseline values of thermodilution cardiac output were highly correlated with echocardiographic measurements (r =.92). The stroke volume index produced by precordial compression averaged 0.45 mL/kg or approximately 37% of the average prearrest value of 1.22 mL/kg. The end-tidal carbon dioxide was highly predictive of stroke volume index (r =.88, p <.001) with a mean bias of 0.003 mL/kg. CONCLUSIONS: We confirmed that precordial compression produces approximately one third of prearrest stroke volumes during cardiopulmonary resuscitation and demonstrated that end-tidal carbon dioxide was quantitatively predictive of stroke volume index estimated by transesophageal echocardiographic imaging.
Animals↗
Vasopressor agents for cardiopulmonary resuscitation.
The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents produce systemic vasoconstriction. This increases aortic diastolic pressure, and consequently, coronary and cerebral perfusion pressures. The pharmacologic responses to the adrenergic agents are mediated by a group of receptors that are classified as alpha (alpha), including alpha1 and alpha2, and beta (beta), including beta1 and beta2. Epinephrine, which has each of these adrenergic actions, has been the preferred adrenergic agent for the management of cardiac arrest for almost 40 years. Its primary efficacy is due to its alpha-adrenergic vasopressor effects. This contrasts with its beta-adrenergic actions, which are inotropic, chronotropic, and vasodilator. Accordingly, beta-adrenergic actions prompt increases in myocardial oxygen consumption, ectopic ventricular arrhythmias, and transient hypoxemia due to pulmonary arteriovenous shunting. This may account for the failure to demonstrate that epinephrine improves ultimate outcomes in human victims of cardiac arrest. Major interest has more recently been focused on selective alpha-adrenergic agonists. Both alpha1-agonists and alpha2-agonists are peripheral vasopressors. However, rapid desensitization of alpha1-adrenergic receptors occurs during cardiopulmonary resuscitation. Moreover, alpha1-adrenergic receptors are present in the myocardium, and beta1-agonists, like beta-adrenergic agonists, increase myocardial oxygen consumption. If they cross the blood-brain barrier, alpha2-adrenoceptor agonists also have centrally acting vasodilator effects. In the absence of central nervous system access, alpha2-adrenergic agonists have selective peripheral vasoconstrictor effects. Under experimental conditions of cardiopulmonary resuscitation, selective alpha2-agonists, which do not gain entrance into the brain, produce only systemic vasoconstriction. Experimentally, these selective alpha2-agonists are as effective as epinephrine for initial cardiac resuscitation and have the additional advantage of minimizing myocardial oxygen consumption during the global myocardial ischemia of cardiac arrest. Accordingly, myocardial ischemic injury during cardiopulmonary resuscitation is minimized, and postresuscitation myocardial function is preserved with improved survival.
Adrenergic alpha-Agonists↗
Adverse outcomes of interrupted precordial compression during automated defibrillation.
BACKGROUND: Current versions of automated external defibrillators (AEDs) require frequent stopping of chest compression for rhythm analyses and capacity charging. The present study was undertaken to evaluate the effects of these interruptions during the operation of AEDs. METHODS AND RESULTS: Ventricular fibrillation was electrically induced in 20 male domestic swine weighing between 37.5 and 43 kg that were untreated for 7 minutes before CPR was started. Defibrillation was attempted with up to 3 sequential 150-J biphasic shocks, but each was preceded by 3-, 10-, 15-, or 20-second interruptions of chest compression. The interruptions corresponded to those that were mandated by commercially marketed AEDs for rhythm analyses and capacitor charge. The sequence of up to 3 electrical shocks and delays were repeated at 1-minute intervals until the animals were successfully resuscitated or for a total of 15 minutes. Spontaneous circulation was restored in each of 5 animals in which precordial compression was delayed for 3 seconds before the delivery of the first and subsequent shocks but in none of the animals in which the delay was >15 seconds before the delivery of the first and subsequent shocks. Longer intervals of CPR interventions were required, and there was correspondingly greater failure of resuscitation in close relationship to increasing delays. The durations of interruptions were inversely related to the durations of subthreshold levels of coronary perfusion pressure. Postresuscitation arterial pressure and left ventricular ejection fraction were more severely impaired with increasing delays. CONCLUSIONS: Interruptions of precordial compression for rhythm analyses that exceed 15 seconds before each shock compromise the outcome of CPR and increase the severity of postresuscitation myocardial dysfunction.
Animals↗
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.
Analysis of Variance↗
Myocardial dysfunction after electrical defibrillation.
We hypothesized that electrical shocks that defibrillate hearts successfully also produce myocardial injury, but only in settings in which the myocardium is underperfused. Myocardial function was measured in isolated, conventionally perfused or underperfused rat hearts during sinus rhythm and conventionally perfused or underperfused hearts during ventricular fibrillation (VF) after delivery of a sham, a 0.4 J, or a 0.7 J shock. In underperfused hearts, the dP/dt, negative dP/dt, left ventricular diastolic pressure and left ventricular pressure-volume relationships demonstrated significant impairment in myocardial function. Impairment increased with the higher energy shocks. This contrasted with normally perfused hearts, whether in sinus rhythm or during VF, in which shocks resulted in no significant impairment. Electrical shocks therefore produce myocardial injury but only when myocardial perfusion is reduced.
Animals↗
A selective alpha(2)-adrenergic agonist for cardiac resuscitation.
The effects of selective alpha(2)-adrenergic agonist alpha-methylnorepinephrine on the initial success of resuscitation and postresuscitation myocardial function were compared with nonselective alpha- and beta-adrenergic epinephrine in a swine model of cardiac arrest. Epinephrine, the primary pharmacological intervention in the treatment of cardiac arrest, improves immediate outcome. However, epinephrine increases the severity of myocardial dysfunction after cardiac resuscitation. Both inotropic and chronotropic actions provoke disproportionate increases in myocardial oxygen consumption by the ischemic heart, prompting this study, in which we hypothesized that a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), would moderate these adverse effects of epinephrine and minimize postresuscitation myocardial dysfunction. After 7 minutes of untreated ventricular fibrillation (VF) in 14 anesthetized male domestic pigs, precordial compression at a fixed rate of 80 compressions/min was begun, along with mechanical ventilation. Either alpha-MNE (100 microg/kg) or epinephrine (20 microg/kg) was administered as a bolus after 2 minutes of precordial compression. After an additional 4 minutes of precordial compression, defibrillation was attempted. Left ventricular systolic and diastolic function was quantitated with the use of transesophageal echo-Doppler imaging. Comparable increases in coronary perfusion pressure to 15 mm Hg were observed after the administration of both drugs. All animals were successfully resuscitated; epinephrine and alpha-MNE were equally quick in restoring spontaneous circulation after 7 minutes of untreated VF. Ejection fraction was reduced by 35% and 14% by epinephrine and alpha-MNE, respectively, after resuscitation. Epinephrine and alpha-MNE increased postresuscitation heart rate by 38% and 15%, respectively. Accordingly, significantly less postresuscitation impairment followed the administration of alpha-MNE. alpha-MNE, a selective alpha-adrenergic agonist, was as effective as epinephrine in restoring spontaneous circulation after 7 minutes of untreated VF in a porcine model for CPR and demonstrated lesser postresuscitation myocardial injury.
Adrenergic alpha-Agonists↗
Cardiopulmonary resuscitation for pulseless rhythms and asystole.
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Arrhythmias, Cardiac↗
Pharmacologic defibrillation.
Ventricular fibrillation (VF) is generally sustained. The mechanism is, at least in part, caused by progressive accumulation of intracellular sodium and calcium ions during untreated ventricular fibrillation, which subsequently increases defibrillation threshold. Cariporide, a potent and specific inhibitor of the sodium-hydrogen exchanger, has been shown to reduce intracellular sodium and calcium concentration in the setting of myocardial ischemia and reperfusion. We hypothesized that cariporide would facilitate defibrillation from prolonged ventricular fibrillation in a rodent model of cardiac arrest and resuscitation. Fifteen Sprague-Dawley rats were randomized to receive bolus injections of cariporide or placebo in a dose of 3 mg/kg into the right atrium either 5 mins before or at 8 mins after onset of ventricular fibrillation. Ventricular fibrillation was electrically induced and untreated for 8 mins. Precordial compression together with mechanical ventilation was then started and continued for an interval of 8 mins before attempted electrical defibrillation. All but one placebo-treated animal were successfully resuscitated. Spontaneous defibrillation with restoration of circulation was observed in both cariporide pretreatment and treatment groups but in none of the placebo-treated animals. The duration of postresuscitation survival was significantly increased in animals pretreated with cariporide. Therefore, sodium-hydrogen exchanger inhibitors may provide new options in settings of cardiopulmonary resuscitation to facilitate defibrillation.
Animals↗
Expanding automatic external defibrillators to include automated detection of cardiac, respiratory, and cardiorespiratory arrest.
The new Guidelines of the American Heart Association state that lay rescuers can no longer rely on the manual pulse check to confirm cardiac arrest in an unresponsive patient. We were therefore prompted to develop a method for automated determination of the presence or absence of cardiac contraction and breathing. The technique was designed to be incorporated into conventional automated external defibrillators and to work in conjunction with the information derived from rhythm analyses by the automated defibrillator. Using conventional electrocardiographic sensing and defibrillation electrodes, the transthoracic impedance was measured by passing a constant amplitude alternating current of 5 mA through the thorax at a frequency of 35 kHz. In five anesthetized male domestic swine, we observed pulses that were coincident with cardiac contraction documented by esophageal echocardiography. In addition, we observed larger signals of lower frequency that were time related to ventilation and documented by capnography. Both signals disappeared after inducing ventricular fibrillation. The impedance measurement identified respiratory arrest in anesthetized animals and primary cardiac arrest after ventricular fibrillation was induced. The cardiac arrest detector is therefore likely to augment the current information provided by automated defibrillators and to allow for more precise verbal prompting of lay rescuers.
Animals↗
Stroke volumes generated by precordial compression during cardiac resuscitation.
OBJECTIVES: To quantitate stroke volumes generated by precordial compression during cardiopulmonary resuscitation and to determine their relationship to coronary perfusion pressure and the success of resuscitation. DESIGN: Prospective, observational animal study. SETTING: Medical research laboratory in a university-affiliated research and educational foundation. SUBJECTS: Domestic pigs. INTERVENTIONS: Ventricular fibrillation was electrically induced in 25 anesthetized male domestic pigs. After an interval of 7 mins, electrical defibrillation was attempted. Failing to reverse ventricular fibrillation in each instance, precordial compression was begun coincident with mechanical ventilation. MEASUREMENTS AND MAIN RESULTS: Stroke volumes were computed from differences between diastolic and systolic areas of the left ventricle by utilizing transesophageal echocardiography. Both stroke volumes and coronary perfusion pressure were consistently greater in successfully resuscitated animals. Progressive decreases in stroke volumes during precordial compression were predictive of unsuccessful resuscitation. A linear correlation between stroke volume and coronary perfusion pressure (r =.70) was documented. CONCLUSION: These observations support the concept that stroke volumes generated by precordial compression are quantitatively related to the coronary perfusion pressure and to the success of cardiopulmonary resuscitation.
Analysis of Variance↗
Fixed-energy biphasic waveform defibrillation in a pediatric model of cardiac arrest and resuscitation.
OBJECTIVE: For adults, 150-J fixed-energy, impedance-compensating biphasic truncated exponential (ICBTE) shocks are now effectively used in automated defibrillators. However, the high energy levels delivered by adult automated defibrillators preclude their use for pediatric patients. Accordingly, we investigated a method by which adult automated defibrillators may be adapted to deliver a 50-J ICBTE shock for pediatric defibrillation. DESIGN: Prospective, randomized study. SETTING: A university-affiliated research institution. SUBJECT: Domestic piglets. INTERVENTIONS: We initially investigated four groups of anesthetized mechanically ventilated piglets weighing 3.8, 7.5, 15, and 25 kg. Ventricular fibrillation was induced with an AC current delivered to the right ventricular endocardium. After 7 mins of untreated ventricular fibrillation, a conventional manual defibrillator was used to deliver up to three 50-J ICBTE shocks. If ventricular fibrillation was not reversed, a 1-min interval of precordial compression preceded a second sequence of up to three shocks. The protocol was repeated until spontaneous circulation was restored, or for a total of 15 mins. In a second set of experiments, we evaluated a 150-J biphasic adult automated defibrillator that was operated in conjunction with energy-reducing electrodes such as to deliver 50-J shocks. The same resuscitation protocol was then exercised on piglets weighing 3.7, 13.5, and 24.2 kg. MEASUREMENTS AND MAIN RESULTS: All animals were successfully resuscitated. Postresuscitation hemodynamic and myocardial function quickly returned to baseline values in both experimental groups, and all animals survived. CONCLUSION: An adaptation of a 150-J biphasic adult automated defibrillator in which energy-reducing electrodes delivered 50-J shocks successfully resuscitated animals ranging from 3.7 to 25 kg without compromise of postresuscitation myocardial function or survival.
Analysis of Variance↗
Cardiopulmonary resuscitation in the mouse.
We sought to develop a model of cardiac arrest and resuscitation on mice that would be comparable to that of large mammals and would allow for more fundamental investigations on cardiopulmonary arrest and cardiac resuscitation. A model of cardiopulmonary resuscitation previously developed by our group on rats was adapted to anesthetized, mechanically ventilated adult male Institute of Cancer Research mice that weighed 46 +/- 3 g. The trachea was intubated through the mouth, and end-tidal PCO(2) (PET(CO(2))) was measured with a microcapnometer. Catheters were advanced into the aorta and into the right atrium, and coronary perfusion pressure (CPP) was computed. A 1.5-mA alternating current was delivered to the right ventricular endocardium, which produced ventricular fibrillation or a pulseless rhythm. Precordial compression was begun 4 min later. Ten sequential studies were performed, during which five animals were successfully resuscitated and five failed resuscitation efforts. Successful resuscitation was contingent on the restoration of threshold levels of CPP and PET(CO(2)) during chest compression. As in rats, swine, and human patients, threshold levels of mean aortic pressure, CPP, and PET(CO(2)) were critical determinates of resuscitability in this murine model of threshold level of cardiac arrest and resuscitation.
Acid-Base Equilibrium↗
Cariporide for pharmacologic defibrillation after prolonged cardiac arrest.
BACKGROUND: We hypothesized that cariporide, a sodium-hydrogen exchange inhibitor, would be as cardioprotective during the global myocardial ischemia of prolonged cardiac arrest as it is in settings of coronary occlusion. METHODS AND RESULTS: Fifteen Sprague-Dawley rats were randomized to receive bolus injections of cariporide or placebo in a dose of 3 mgxkg(-1) into the right atrium either 5 minutes before, or at 8 minutes after, onset of ventricular fibrillation. Ventricular fibrillation was electrically induced and untreated for 8 minutes. Precordial compression, together with mechanical ventilation, was then started and continued for an interval of 8 minutes prior to attempted resuscitation. All but one placebo-treated animal were successfully resuscitated. Spontaneous defibrillation with restoration of circulation was observed in both cariporide-pretreatment and post-treatment groups but in none of the placebo-treated animals. Postresuscitation cardiac index, end-tidal CO(2), mean aortic pressure, left ventricular systolic pressure, left ventricular end-diastolic pressure, and left ventricular contractile and lusitropic functions (dP/dt(40), and -dP/dt) were significantly less impaired after cariporide, especially in the pretreated group, compared to electrically defibrillated controls. Postresuscitation ventricular premature beats were significantly reduced after cariporide. The duration of post-resuscitation survival was significantly increased in animals pretreated with cariporide. CONCLUSIONS: Cariporide, when administered prior to and during cardiac arrest, improved both the success of resuscitation and postresuscitation myocardial function.
Animals↗
Evolution of the stone heart after prolonged cardiac arrest.
OBJECTIVES: We hypothesized that progressive impairment in diastolic function during cardiopulmonary resuscitation (CPR) precedes evolution of the "stone heart" after failure of CPR. We therefore measured sequential changes in left ventricular (LV) volumes and free-wall thickness of the heart during CPR in an experimental model. DESIGN: Prospective, observational animal study. SETTING: Medical research laboratory in an university-affiliated research and educational institute. SUBJECTS: Domestic pigs. METHODS: Ventricular fibrillation (VF) was induced in 40 anesthetized male domestic pigs weighing between 38 kg and 43 kg. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Failing to reverse VF in each instance, precordial compression at a rate of 80/min was begun coincident with mechanical ventilation. Coronary perfusion pressures (CPPs) were computed from the differences in time-coincident diastolic aortic and right atrial pressures. Left ventricular (LV) systolic and diastolic ventricular volumes and thickness of the LV free wall were estimated with transesophageal echocardiography. The stroke volumes (SVs) were computed from the differences in decompression diastolic and compression systolic volumes. Free-wall thickness was measured on the hearts at autopsy. RESULTS: Significantly greater CPPs were generated with the 4 min of untreated cardiac arrest. Progressive reductions in LV diastolic and SV and increases in LV free-wall thickness were documented with increasing duration of untreated VF. A stone heart was confirmed at autopsy in each animal that failed resuscitative efforts. Correlations with indicator dilution method and physical measurements at autopsy corresponded closely with the echocardiographic measurements. CONCLUSION: Progressive impairment in diastolic function terminates in a stone heart after prolonged intervals of cardiac arrest.
Animals↗