Search

Aim of the study A reproducible long-term intensive care and outcome cardiac arrest model for exploring new cerebral preservation strategies is needed. We tried to determine effects and limitations of current therapies after different ‘no-flow’ times. Methods Thirty-five female Large White Breed pigs (26–37 kg) were included in the study. Three pigs served as sham animals without cardiac arrest (CA). Ventricular fibrillation (VF) CA was induced in 32 animals for 0, 7, 10 and 13 min (each group consisting of 8 animals), followed by 8 min of chest compressions, mechanical ventilation and vasopressors. Thereafter, up to 3 defibrillations were delivered. After restoration of spontaneous circulation (ROSC), the animals underwent intensive care for 20 h. Neurologic examination was performed at designated time points using a neurologic deficit (ND) and an overall performance category (OPC) score. Results Restoration of spontaneous circulation was achieved in 8 of 8 animals in the 0 min-group, 6 of 8 in the 7 min-group, 7 of 8 in the 10 min-group and 0 of 8 in the 13 min-group. All animals of the sham-group and 0 min-group were neurologically intact survivors; the 7 and 10 min-groups showed a median ND of 55%(26;94) and 73%(58;78), respectively. There were no significant differences between the 7 and 10 min-groups regarding OPC and NDS. Coronary perfusion pressure during CPR decreased concordantly with ‘no-flow’ times with a tendency towards significance. Conclusion This study established a reproducible cardiac arrest and resuscitation model in pigs which will be used to test novel resuscitation strategies to improve neurologic outcome after cardiac arrest.

Aim of the study Mild hypothermia after cardiac arrest should be induced as soon as possible. There is a need for improved feasibility and efficacy of surface cooling in ambulances. We investigated which and how much area of the body surface should be covered to guarantee a sufficient cooling rate. Methods Each of five adult, human-sized pigs (88–105kg) was randomly cooled in three phases with pads that covered different areas of the body surface corresponding to humans (100% or 30% [thorax and abdomen] or 7% [neck]). The goal was to quickly lower brain temperature (Tbr) from 38 to 33°C within a maximum of 120min. Linear regression analysis was used to test the association between cooling efficacy and surface area. Data are presented as mean±standard deviation. Results The 100% and 30% cooling pads decreased the pigs' Tbr from 38 to 33°C within 33±7min (8.2±1.6°C/h) and 92±24min (3.6±1.1°C/h). The 7% achieved a final Tbr of 35.8±0.7°C after 120min (1.1±0.4°C/h). The 30% and 7% cooling surface areas achieved 37±11% and 15±7% of the cooling rate compared to the 100% cooling pads. For every additional percent of surface area cooled, the cooling rate increased linearly by 0.07°C/h (95% CI 0.05–0.09, p =0.001). No skin lesions were observed. Conclusions The cooling pads were effective and safe for rapid induction of mild hypothermia in adult, human-sized pigs, depending on the percentage of body surface area covered. Covering only the neck, chest, and abdomen might achieve satisfactory cooling rates.

Aim of the study To evaluate all brain regions reported to be selectively vulnerable to global ischaemia in a pig cardiac arrest model with different durations of no-flow by establishing a semi-quantitative brain histopathologic scoring system and to compare histological damage with neurological deficits. Methods In a prospective randomised laboratory investigation, 35 female Large White pigs weighing 35–45 kg underwent ventricular fibrillation cardiac arrest for 0, 7, 10 or 13 min. In the brains of all animals that survived until the final endpoint (72 h post-arrest), 22 distinct regions were evaluated on paraffin-embedded sections in terms of type and extent of lesions. The results of the histological examination were compared to the results of a neurological outcome evaluation after 72 h. Results Significant differences were found in all cortex regions, the caudate nucleus and putamen, the hippocampal formation, the cerebellar cortex, and the thalamus between the ischaemic groups (7- and 10-min groups) and the control group (0-min group). No 13-min group animal survived. The main findings were neuronal necrosis and oedema. In animals from the 10-min group, many neurons were reabsorbed in the cerebral cortex, caudate nucleus and cerebellar granule cell layer. There was a highly significant correlation between histological damage and neurological deficits. Conclusions The pattern of neuronal lesions in this pig model bear good resemblance to the pattern known in humans and other animal models. The amount of histological lesions in selectively vulnerable brain regions correlates to neurological outcome.