ObjectivePralidoxime 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.MethodsAfter 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).ResultsMixed-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.ConclusionIn a pig model of cardiac arrest, pralidoxime administered during cardiopulmonary resuscitation did not reduce ischemic contracture; however, it significantly improved CPP.
Unrecognized endobronchial intubation frequently occurs after emergency intubation. However, no study has evaluated the effect of one-lung ventilation on end-tidal carbon dioxide (ETCO2) during cardiopulmonary resuscitation (CPR). We compared the hemodynamic parameters, blood gases, and ETCO2 during one-lung ventilation with those during conventional two-lung ventilation in a pig model of CPR, to determine the effect of the former on ETCO2. A randomized crossover study was conducted in 12 pigs intubated with double-lumen endobronchial tube to achieve lung separation. During CPR, the animals underwent three 5-min ventilation trials based on a randomized crossover design: left-lung, right-lung, or two-lung ventilation. Arterial blood gases were measured at the end of each ventilation trial. Ventilation was provided using the same tidal volume throughout the ventilation trials. Comparison using generalized linear mixed model revealed no significant group effects with respect to aortic pressure, coronary perfusion pressure, and carotid blood flow; however, significant group effect in terms of ETCO2 was found (P < 0.001). In the post hoc analyses, ETCO2 was lower during the right-lung ventilation than during the two-lung (P = 0.006) or left-lung ventilation (P < 0.001). However, no difference in ETCO2 was detected between the left-lung and two-lung ventilations. The partial pressure of arterial carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2), and oxygen saturation (SaO2) differed among the three types of ventilation (P = 0.003, P = 0.001, and P = 0.001, respectively). The post hoc analyses revealed a higher PaCO2, lower PaO2, and lower SaO2 during right-lung ventilation than during two-lung or left-lung ventilation. However, the levels of these blood gases did not differ between the left-lung and two-lung ventilations. In a pig model of CPR, ETCO2 was significantly lower during right-lung ventilation than during two-lung ventilation. However, interestingly, ETCO2 during left-lung ventilation was comparable to that during two-lung ventilation.
The association between the initial lactate level and need for massive transfusion in severe trauma patients with and without traumatic brain injury Background: Exsanguination is a major cause of death in severe trauma patients. The purpose of this study was to analyze the prognostic impact of the initial lactate level for massive transfusion (MT) in severe trauma. We divided patients according to subgroups of traumatic brain injury (TBI) and non-TBI. Methods: This single-institution retrospective study was conducted on patients who were admitted to hospital for severe trauma between January 2016 and December 2017. TBI was defined by a head Abbreviated Injury Scale ≥ 3. Receiver operating characteristic analysis was used to analyze the prognostic impact of the lactate level. Multivariate analyses were performed to evaluate the relationship between the MT and lactate level. The primary outcome was MT. Results: Of the 553 patients, MT was performed in 62 patients (11.2%). The area under the curve (AUC) for the lactate level for predicting MT was 0.779 (95% confidence interval [CI], 0.742 to 0.813). The AUCs for lactate level in the TBI and non-TBI patients were 0.690 (95% CI, 0.627 to 0.747) and 0.842 (95% CI, 0.796 to 0.881), respectively. In multivariate analyses, the lactate level was independently associated with the MT (odds ratio [OR], 1.179; 95% CI, 1.070 to 1.299). The lactate level was independently associated with MT in non-TBI patients (OR, 1.469; 95% CI, 1.262 to 1.710), but not in TBI patients. Conclusions: The initial lactate level may be a possible prognostic factor for MT in severe trauma. In TBI patients, however, the initial lactate level was not suitable for predicting MT.
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