Takashi Kamohara

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.

Alpha-methylnorepinephrine, a selective alpha2-adrenergic agonist for cardiac resuscitation☆

OBJECTIVES The purpose of this study was to investigate the effects of a selective alpha2-adrenergic agonist, alpha-methylnorepinephrine (alphaMNE) as an alternative vasopressor agent during cardiopulmonary resuscitation (CPR). BACKGROUND For more than 40 years, epinephrine has been the vasopressor agent of choice for CPR. Its beta- and alpha1-adrenergic effects increase myocardial oxygen consumption, magnify global myocardial ischemia and increase the severity of postresuscitation myocardial dysfunction. METHODS Ventricular fibrillation (VF) was induced in 20 Sprague-Dawley rats. After 8 min of untreated VF, mechanical ventilation and precordial compression began. AlphaMNE, epinephrine or saline placebo was injected into the right atrium 2 min after the start of precordial compression. As an additional control, one group of animals was pretreated with alpha2-receptor blocker, yohimbine, before injection of alphaMNE. Defibrillation was attempted 4 min later. Left ventricular pressure, dP/dt40, negative dP/dt and cardiac index were measured for an interval of 240 min after resuscitation. RESULTS Except for saline placebo and yohimbine-treated animals, comparable increases in coronary perfusion pressure were observed after each drug intervention. All animals were successfully resuscitated. Left ventricular diastolic pressure, cardiac index, dP/dt40 and negative dP/dt were more optimal after alphaMNE; this was associated with significantly better postresuscitation survival. Pretreatment with vohimbine abolished the beneficial effects of alphaMNE. CONCLUSIONS The selective alpha2-adrenergic agonist, alphaMNE, was as effective as epinephrine for initial cardiac resuscitation but provided strikingly better postresuscitation myocardial function and survival.

Echo-doppler observations during cardiac arrest and cardiopulmonary resuscitation

We describe a series of investigations that used transesophageal echo-Doppler observations during cardiac arrest and cardiopulmonary resuscitation. Regular contractions of the left atrium persisted during the initial 7 mins of untreated ventricular fibrillation. Ventricular chamber deformation and mitral valve closing and opening followed precordial compression and relaxation. Stroke volumes computed from differences between diastolic and systolic areas of the left ventricle were predictive of the success of the resuscitation. Progressive decreases in left ventricular compliance were associated with decreases in left ventricular diastolic and stroke volumes and progressed to a stone heart.

A lazaroid mitigates postresuscitation myocardial dysfunction.

ObjectiveLazaroids, 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. DesignRandomized, controlled laboratory study. SettingUniversity-affiliated research institute. SubjectsSprague-Dawley rats. InterventionsVentricular 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 ResultsAll 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. ConclusionsThe lazaroid compound U-74389G, administered during cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved survival.