Min Of Untreated Cardiac Arrest Research Articles

Anesthetic regimen effects on a pediatric porcine model of asphyxial arrest

The effects of three anesthetic regimens on an established model of pediatric porcine hypoxic-hypercarbic arrest were examined. Twenty-four preadolescent miniature piglets were paralyzed, mechanically ventilated and anesthetized with one of three regimens: IM+IV pentobarbital ( n=8); IM+IV ketamine ( n=8); or IM ketamine+inhaled isoflurane ( n=8). Asphyxial cardiopulmonary arrest was induced and, after an 8 min cardiac arrest nonintervention interval, a standardized protocol of manual CPR with mechanical ventilation was performed. Outcome variables included incidence of ventricular fibrillation, time to cardiac arrest, endogenous plasma epinephrine levels and arteriovenous epinephrine gradients. IV Ketamine anesthesia produced the highest incidence of ventricular fibrillation ( P<0.01 vs. pentobarbital and isoflurane). Time to asphyxia induced cardiac arrest was greatest for the pentobarbital group ( P<0.05 vs. ketamine and isoflurane). During induction of asphyxial cardiac arrest (low cardiac flow), endogenous venous epinephrine accumulation was highest in the pentobarbital anesthetized group ( P<0.05). After 8 min of untreated cardiac arrest and 1 min of CPR (low flow), arterial epinephrine levels were highest in the ketamine group ( P<0.05). Endogenous epinephrine gradients were venous>arterial in all groups at the end of the 8 min cardiac arrest non-intervention interval (no flow). After 1 min of CPR, the gradients had either equalized or reversed to arterial>venous in all groups except for pentobarbital. As designed and expected, return of spontaneous circulation did not occur in any animal. We conclude that, in developing models of porcine asphyxial cardiopulmonary arrest and resuscitation to simulate pediatric human arrest, variations in anesthetic regimen produce significant differences in parameters that are important to consider: time to asphyxia induced cardiac arrest, fibrillation threshold, plasma epinephrine level and arteriovenous epinephrine gradient. Anesthetic effects need to be carefully considered and clearly explained to facilitate the interpretation of studies of interventions in cardiopulmonary arrest and resuscitation.

Myocardial dysfunction after resuscitation from cardiac arrest: An example of global myocardial stunning

Objectives. This study investigated the effect of prolonged cardiac arrest and subsequent cardiopulmonary resuscitation on left ventricular systolic and diastolic function.Background. Cardiac arrest from ventricular fibrillation results in cessation of forward blood flow, including myocardial blood flow. During cardiopulmonary resuscitation, myocardial blood flow remains suboptimal. Once the heart is defibrillated and successful resuscitation achieved, reversible myocardial dysfunction, or “stunning,” may occur. The magnitude and time course of myocardial stunning from cardiac arrest is unknown.Methods. Twenty-eight domestic swine (26 ± 1 kg) were studied with both invasive and noninvasive measurements of ventricular function before and after 10 or 15 min of untreated cardiac arrest. Contrast left ventriculograms, ventricular pressures, cardiac output, isovolumetric relaxation time (tau) and transthoracic Doppler-echocardiographic studies were obtained.Results. Twenty-three of 28 animals were successfully resuscitated and postresuscitation data obtained. Left ventricular ejection fraction showed a significant reduction 30 min after resuscitation (p < 0.05). Regional wall motion analysis revealed diffuse, global left ventricular systolic dysfunction. Left ventricular end-diastolic pressure increased significantly in the postresuscitation period (p < 0.05). Isovolumetric relaxation time (tau) was significantly increased over baseline by 2 h after resuscitation (p < 0.05). Similar findings were noted with the Doppler-echocardiographic analysis, including a reduction in fractional shortening (p <0.05), a reduction in mitral valve deceleration time (p < 0.05) and an increase in left ventricular isovolumetric relaxation time in 5 h after resuscitation (p < 0.05). By 24 h, these invasive and noninvasive variables of systolic and diastolic left ventricular function had begun to improve. At 48 h, all measures of left ventricular function had returned to baseline levels.Conclusions. Myocardial systolic and diastolic dysfunction is severe after 10 to 15 min of untreated cardiac arrest and successful resuscitation. Full recovery of this postresuscitation myocardial stunning is seen by 48 h in this experimental model of ventricular fibrillation cardiac arrest.

Intramyocardial hypercarbic acidosis during cardiac arrest and resuscitation.

To define changes in intramyocardial pH and PCO2 during cardiac arrest and resuscitation. Prospective and observational trial. Mammalian research laboratory utilizing a porcine model of cardiac arrest. Sixteen domestic pigs. Ventricular fibrillation was induced by an alternating current delivered to the epicardium. Precordial compression was begun after 3 mins of untreated cardiac arrest and was initially adjusted to produce a coronary perfusion pressure of 10 mm Hg. Electrical defibrillation was attempted after an additional 8 mins of precordial compression. A rapid-response, ion-selective field effect transistor sensor was adapted for measurement of intramyocardial PCO2. Intramyocardial PCO2 progressively increased from 54 to 346 torr (7.2 to 46.1 kPa) during the 11-min interval of cardiac arrest. Intramyocardial hydrogen ion concentrations were simultaneously measured with a glass electrode. The intramyocardial hydrogen ion value increased from 65 nmol/L (pH 7.20) to 441 nmol/L (pH 6.38) over the same interval. The increases in myocardial PCO2 were inversely correlated with coronary perfusion pressure and with the likelihood of successful resuscitation. Within 30 mins after successful cardiac resuscitation, myocardial PCO2 had almost completely returned to prearrest levels. Striking increases in myocardial PCO2 and hydrogen ion values accompany the global myocardial ischemia of cardiac arrest. The increases in myocardial PCO2, rather than decreases in pH, reflected more precisely the hemodynamic efficacy of the resuscitation effort, correlated inversely with coronary perfusion pressure, and predicted the likelihood of successful resuscitation.