Abstract:Extracorporeal membrane cardiopulmonary resuscitation (ECPR) during cardiopulmonary resuscitation (CPR) for selected cases and end-tidal carbon dioxide (ETCO2) could be used to guide initiation of ECPR. Ventricular fibrillation was induced in 12 pigs and CPR was performed until ETCO2 fell below 10 mmHg; then, ECPR was performed. Animals were divided into group short (GShort) and group long (GLong), according to time of CPR. Carotid blood flow was higher (p = 0.02) and mean arterial blood pressure lower in GLo… Show more
“…Notably, 12 hours into VA‐ECMO, lactate/pyruvate ratios and glycerol levels rise in CPR60 animals (Figure S1 ) but not significantly. This finding, also seen in another swine study of ECPR duration, 35 could indicate greater ischemic burden or progression of secondary injury processes 37 despite restoration of circulation. This would support development and use of postcardiac arrest neuromonitoring modalities that measure CBF, autoregulation, and oxygenation in real time, informing clinical management and prognostication.…”
Section: Discussionsupporting
confidence: 60%
“…All animals in both groups suffered severe neurological dysfunction and injury as measured by cerebral mitochondrial respirometry (Figure 4 ), neuropathologic analyses (Table S8 ), and cerebral microdialysis (Table S6 ), consistent with findings from other studies. 35 , 36 Interestingly, the proton gradient and inner membrane were not significantly different from sham animals as evidenced by state 4 o respiration without ATP production, which may suggest functional rather than structural mitochondrial injury. Notably, 12 hours into VA‐ECMO, lactate/pyruvate ratios and glycerol levels rise in CPR60 animals (Figure S1 ) but not significantly.…”
Background
The primary objective was to develop a porcine model of prolonged (30 or 60 minutes) pediatric cardiopulmonary resuscitation (CPR) followed by 22‐ to 24‐hour survival with extracorporeal life support, and secondarily to evaluate differences in neurologic injury.
Methods and Results
Ten‐kilogram, 4‐week‐old female piglets were used. First, model development established the technique (n=8). Then, a pilot study was conducted (n=15). After 80% survival was achieved in the final 5 pilot animals, a proof‐of‐concept randomized study was completed (n=11). Shams (n=6) underwent anesthesia only. Severe neurological injury was determined by a composite score of mitochondrial function, neuropathology, and cerebral metabolism: scale of 0–6 (severe: >3). Among 15 piglets in the pilot study, overall survival was 10 (67%); of the final 5, overall survival was 4 (80%). Eleven piglets were then randomized to 60 (CPR60, n=5) or 30 minutes of CPR (CPR30, n=5); 1 animal was excluded from prerandomization for intra‐abdominal hemorrhage (10/11, 91% survival). Three of 5 animals in the CPR60 group had severe neurological injury scores versus 1 of 5 in the CPR30 group (
P
=0.52). During ECMO, CPR60 animals had lower pH (CPR60: 7.4 [IQR 7.4–7.4] versus CPR30: 7.5 [IQR 7.4–7.5],
P
=0.022), higher lactate (CPR60: 6.8 [IQR 6.8–11] versus CPR30: 4.2 [IQR 4.1–4.3] mmol/L;
P
=0.012), and higher ICP (CPR60: 19.3 [IQR 11.7–29.3] versus CPR30: 7.9 [IQR 6.7–9.3] mm Hg;
P
=0.037). Both groups had greater mitochondrial injury than shams (CPR60:
P
<0.001; CPR30:
P
<0.001). CPR60 did not differ from CPR30 in mitochondrial respiration, neuropathology, or cerebral metabolism.
Conclusions
A pediatric porcine model of extracorporeal cardiopulmonary resuscitation after 60 and 30 minutes of CPR consistently resulted in 24‐hour survival with more severe lactic acidosis in the 60‐minute cohort.
“…Notably, 12 hours into VA‐ECMO, lactate/pyruvate ratios and glycerol levels rise in CPR60 animals (Figure S1 ) but not significantly. This finding, also seen in another swine study of ECPR duration, 35 could indicate greater ischemic burden or progression of secondary injury processes 37 despite restoration of circulation. This would support development and use of postcardiac arrest neuromonitoring modalities that measure CBF, autoregulation, and oxygenation in real time, informing clinical management and prognostication.…”
Section: Discussionsupporting
confidence: 60%
“…All animals in both groups suffered severe neurological dysfunction and injury as measured by cerebral mitochondrial respirometry (Figure 4 ), neuropathologic analyses (Table S8 ), and cerebral microdialysis (Table S6 ), consistent with findings from other studies. 35 , 36 Interestingly, the proton gradient and inner membrane were not significantly different from sham animals as evidenced by state 4 o respiration without ATP production, which may suggest functional rather than structural mitochondrial injury. Notably, 12 hours into VA‐ECMO, lactate/pyruvate ratios and glycerol levels rise in CPR60 animals (Figure S1 ) but not significantly.…”
Background
The primary objective was to develop a porcine model of prolonged (30 or 60 minutes) pediatric cardiopulmonary resuscitation (CPR) followed by 22‐ to 24‐hour survival with extracorporeal life support, and secondarily to evaluate differences in neurologic injury.
Methods and Results
Ten‐kilogram, 4‐week‐old female piglets were used. First, model development established the technique (n=8). Then, a pilot study was conducted (n=15). After 80% survival was achieved in the final 5 pilot animals, a proof‐of‐concept randomized study was completed (n=11). Shams (n=6) underwent anesthesia only. Severe neurological injury was determined by a composite score of mitochondrial function, neuropathology, and cerebral metabolism: scale of 0–6 (severe: >3). Among 15 piglets in the pilot study, overall survival was 10 (67%); of the final 5, overall survival was 4 (80%). Eleven piglets were then randomized to 60 (CPR60, n=5) or 30 minutes of CPR (CPR30, n=5); 1 animal was excluded from prerandomization for intra‐abdominal hemorrhage (10/11, 91% survival). Three of 5 animals in the CPR60 group had severe neurological injury scores versus 1 of 5 in the CPR30 group (
P
=0.52). During ECMO, CPR60 animals had lower pH (CPR60: 7.4 [IQR 7.4–7.4] versus CPR30: 7.5 [IQR 7.4–7.5],
P
=0.022), higher lactate (CPR60: 6.8 [IQR 6.8–11] versus CPR30: 4.2 [IQR 4.1–4.3] mmol/L;
P
=0.012), and higher ICP (CPR60: 19.3 [IQR 11.7–29.3] versus CPR30: 7.9 [IQR 6.7–9.3] mm Hg;
P
=0.037). Both groups had greater mitochondrial injury than shams (CPR60:
P
<0.001; CPR30:
P
<0.001). CPR60 did not differ from CPR30 in mitochondrial respiration, neuropathology, or cerebral metabolism.
Conclusions
A pediatric porcine model of extracorporeal cardiopulmonary resuscitation after 60 and 30 minutes of CPR consistently resulted in 24‐hour survival with more severe lactic acidosis in the 60‐minute cohort.
“…Olander et al exclusively investigated S100B as a neurological biomarker, however, there were no significant differences in S100B levels between different durations of ECPR. 37 Zhang et al demonstrated that the ECPR group had elevated levels of various cerebral inflammatory markers. 15 Wollborn et al’ s 2020 study showed an increased level of glial fibrillary acidic protein (GFAP), ionized calcium binding adapter molecule 1 (Iba1), and heme oxygenase-1 (HO-1).…”
“…Presently, extracorporeal cardiopulmonary resuscitation is commonly used, replacing traditional CPR to treat IHCA, and this method can effectively improve the survival rate [3,4]. In a study by Ölander et al [5], the effects of extracorporeal cardiopulmonary resuscitation under various end-tidal carbon dioxide levels were analyzed, and the results were veri ed using animal experiments. The post-resuscitation care for IHCA was analyzed in a study by Girotra et al [6], which included targeted temperature management, early coronary angiography, and comprehensive critical care.…”
Background: Both in-hospital and out-of-hospital cardiac arrest have several causes and complexities. Therefore, it is difficult to analyze and create targeted treatment plans for cardiac arrest. Moreover, even basic patient informationis insufficient or missing in many cases. To address these challenges, we developed an intelligent diagnosis and treatment system for cardiopulmonary resuscitation and restoration of spontaneous circulation to reasonably complete the diagnosis and treatment process and improve the success rate of treatment during in-hospital cardiac arrest.
Methods: Using 10 years of data from Utstein style in-hospital cardiac arrest registries in seven hospitals in China’s Hebei Province, we developed a two-stage intelligent diagnosis and treatment system based on the basic situation of different cases during cardiac arrest using deep reinforcement learning. This approach is aimed at maximizing the success rates of cardiopulmonary resuscitation and maintaining blood pressure at an optimal value during the restoration of spontaneous circulation. We employed Monte Carlo simulation to analyze the uncertainty.
Results: When comparing the actual diagnosis and treatment with those based on other models during cardiopulmonary resuscitation and restoration of spontaneous circulation in different conditions (sufficient and insufficient basic patient information), the average reward scores of the treatment plan provided by the intelligent diagnosis and treatment system developed in this study increased to 9.9–23 from 2.39.
Conclusions: The intelligent diagnosis and treatment system for in-hospital cardiac arrest based on deep reinforcement learning under the Utstein mode developed in this study can propose a reasonable diagnosis and treatment plan when in-hospital cardiac arrest occurs. Moreover, it can effectively induce cardiopulmonary resuscitation and restoration of spontaneous circulation processes in different patients even when basic patient informationis insufficient or missing.
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