Use of amplitude-integrated electroencephalography in decision-making for extracorporeal membrane oxygenation in comatose cardiac arrest patients whose eventual neurologic recovery is uncertain

Comatose cardiac arrest patients frequently experience cardiogenic shock or recurrent arrest. Extracorporeal membrane oxygenation (ECMO) can be used to salvage patients with cardiogenic shock or cardiac arrest refractory to conventional therapies. However, in comatose cardiac arrest patients whose neurologic recovery is uncertain, the use of ECMO is restricted because it requires considerable financial and human resources. Amplitude-integrated electroencephalography is an easily applicable, real-time electroencephalography monitoring tool that has been increasingly used to monitor brain activity in comatose cardiac arrest patients. We describe our experience of using amplitude-integrated electroencephalography in decision-making to place ECMO for comatose cardiac arrest patients whose eventual neurologic recovery appeared uncertain at the time of ECMO placement

Effect of pralidoxime on coronary perfusion pressure during cardiopulmonary resuscitation in a pig model

Objective Pralidoxime is widely used for the treatment of organophosphate poisoning. Multiple studies have reported its vasoconstrictive property, which may facilitate the restoration of spontaneous circulation (ROSC) after cardiac arrest by increasing the coronary perfusion pressure (CPP). 2,3-Butanedione monoxime, which belongs to the same oxime family, has been shown to facilitate ROSC by reducing left ventricular ischemic contracture. Because pralidoxime and 2,3-butanedione monoxime have several common mechanisms of action, both drugs may have similar effects on ischemic contracture. Thus, we investigated the effects of pralidoxime administration during cardiopulmonary resuscitation in a pig model with a focus on ischemic contracture and CPP. Methods After 14 minutes of untreated ventricular fibrillation, followed by 8 minutes of basic life support, 16 pigs randomly received either 80 mg/kg of pralidoxime (pralidoxime group) or an equivalent volume of saline (control group) during advanced cardiovascular life support (ACLS). Results Mixed-model analyses of left ventricular wall thickness and chamber area during ACLS revealed no significant group effects or group-time interactions, whereas a mixed-model analysis of the CPP during ACLS revealed a significant group effect (P=0.038) and group-time interaction (P<0.001). Post-hoc analyses revealed significant increases in CPP in the pralidoxime group, starting at 5 minutes after pralidoxime administration. No animal, except one in the pralidoxime group, achieved ROSC; thus, the rate of ROSC did not differ between the two groups. Conclusion In a pig model of cardiac arrest, pralidoxime administered during cardiopulmonary resuscitation did not reduce ischemic contracture; however, it significantly improved CPP

Autoimmune Hypoglycemia in a Patient with Characterization of Insulin Receptor Autoantibodies

BackgroundType B insulin resistance syndrome is a manifestation of autoantibodies to the insulin receptor that results in severe hyperglycemia and acanthosis nigricans. However, the mechanisms by which these autoantibodies induce hypoglycemia are largely unknown. In this paper, we report the case of patient with type B insulin resistance syndrome who presented with frequent severe fasting hypoglycemia and acanthosis nigricans.MethodsTo evaluate the mechanism of hypoglycemia, we measured the inhibition of insulin binding to erythrocytes and IM9 lymphocytes in a sample of the patient's dialyzed serum before and after immunosuppressive therapy.ResultsIn the patient's pre-treatment serum IgG, the binding of 125I-insulin to erythrocytes was markedly inhibited in a dose-dependent manner until the cold insulin level reached 10-9 mol/L. We also observed dose-dependent inhibition of insulin binding to IM9 lymphocytes, which reached approximately 82% inhibition and persisted even when diluted 1:20. After treatment with glucocorticoids, insulin-erythrocyte binding activity returned to between 70% and 80% of normal, while the inhibition of insulin-lymphocyte binding was reduced by 17%.ConclusionWe treated a patient with type B insulin resistance syndrome showing recurrent fasting hypoglycemia with steroids and azathioprine. We characterized the patient's insulin receptor antibodies by measuring the inhibition of insulin binding

Replication Data for: Relationship between hemodynamic parameters and severity of ischemia-induced left

This is a replication data for the study "Relationship between hemodynamic parameters and severity of ischemia-induced left ventricular wall thickening during cardiopulmonary resuscitation of consistent quality". Briefly, it contains hemodynamic and echocardiographic data obtained during cardiopulmonary resuscitation in pigs. After 14 minutes of untreated ventricular fibrillation, simulated basic life support, followed by advanced cardiovascular support, was provided. During cardiopulmonary resuscitation, hemodynamic data including arterial pressure and end-tidal carbon dioxide and echocardiographic data including left ventricular wall thickness and end-diastolic volume were monitored and obtained

Replication Data for: The effect of pralidoxime on coronary perfusion pressure during cardiopulmonary resuscitation in a pig model

This is a data of the study "The effect of pralidoxime on coronary perfusion pressure during cardiopulmonary resuscitation in a pig model". we investigated the effects of pralidoxime administration during cardiopulmonary resuscitation (CPR) in a pig model, with a focus on ischemic contracture and coronary perfusion pressure (CPP). After 14 minutes of untreated ventricular fibrillation, followed by 8 minutes of basic life support, 16 pigs randomly received either 80 mg/kg of pralidoxime (pralidoxime group) or an equivalent volume of saline (control group) during advanced cardiovascular life support (ACLS). Mixed-model analyses of left ventricular (LV) wall thickness and LV chamber area during ACLS revealed no significant group effects or group-time interactions, whereas a mixed-model analysis of the CPP during ACLS revealed significant group effect (P = 0.038) and group time interaction (P <0.001). Post-hoc analyses revealed significant increases in CPP in the pralidoxime group, starting at 5 minutes after pralidoxime administration. No animal, except one animal in the pralidoxime group, achieved ROSC; thus, the rate of ROSC did not differ between the two groups

Relationship between hemodynamic parameters and severity of ischemia-induced left ventricular wall thickening during cardiopulmonary resuscitation of consistent quality.

Ischemia-induced left ventricular (LV) wall thickening compromises the hemodynamic effectiveness of cardiopulmonary resuscitation (CPR). However, accurate assessment of the severity of ischemia-induced LV wall thickening during CPR is challenging. We investigated, in a swine model, whether hemodynamic parameters, including end-tidal carbon dioxide (ETCO2) level, are linearly associated with the severity of ischemia-induced LV wall thickening during CPR of consistent quality. We retrospectively analyzed 96 datasets for ETCO2 level, arterial pressure, LV wall thickness, and the percent of measured end-diastolic volume (%EDV) relative to EDV at the onset of ventricular fibrillation from eight pigs. Animals underwent advanced cardiovascular life support based on resuscitation guidelines. During CPR, LV wall thickness progressively increased while %EDV progressively decreased. Systolic and diastolic arterial pressure and ETCO2 level were significantly correlated with LV wall thickness and %EDV. Linear mixed effect models revealed that, after adjustment for significant covariates, systolic and diastolic arterial pressure were not associated with LV wall thickness or %EDV. ETCO2 level had a significant linear relationship with %EDV (P = 0.004). However, it could explain only 28.2% of the total variance of %EDV in our model. In conclusion, none of the hemodynamic parameters examined in this study appeared to provide sufficient information on the severity of ischemia-induced LV wall thickening