MATERIALS AND METHODS: Atrial arrhythmogenesis was investigated in Langendorff-perfused young (3-4 month) and aged (>12 month), wild type (WT) and peroxisome proliferator activated receptor-γ coactivator-1β deficient (Pgc-1β-/-) murine hearts modeling age-dependent chronic mitochondrial dysfunction during regular pacing and programmed electrical stimulation (PES).
RESULTS AND DISCUSSION: The Pgc-1β-/- genotype was associated with a pro-arrhythmic phenotype progressing with age. Young and aged Pgc-1β-/- hearts showed compromised maximum action potential (AP) depolarization rates, (dV/dt)max, prolonged AP latencies reflecting slowed action potential (AP) conduction, similar effective refractory periods and baseline action potential durations (APD90) but shortened APD90 in APs in response to extrasystolic stimuli at short stimulation intervals. Electrical properties of APs triggering arrhythmia were similar in WT and Pgc-1β-/- hearts. Pgc-1β-/- hearts showed accelerated age-dependent fibrotic change relative to WT, with young Pgc-1β-/- hearts displaying similar fibrotic change as aged WT, and aged Pgc-1β-/- hearts the greatest fibrotic change. Mitochondrial deficits thus result in an arrhythmic substrate, through slowed AP conduction and altered repolarisation characteristics, arising from alterations in electrophysiological properties and accelerated structural change.
METHODS: This was an observational manikin-based study. A total of 96 participants as well as two types of mechanical compression devices: Lucas-2 and AutoPulse, performed one minute of continuous chest compression on BT-CPEA programmed manikin while the ambulance travelled at different speeds, i.e., idle state, 30km/hr and 60km/hr. Seven outcome variables of chest compression were measured. Performance data of different groups of compressor were compared and analysed using repeated measures analysis of variance (ANOVA).
RESULTS: In manual chest compression, significant variation were noted among different speeds in term of average compression rate (p<0.001), average compression depth (p=0.007), fraction of adequate/insufficient compression depth and fraction of normal hands positioning with p=0.018, 0.022 and 0.034 respectively. Overall, AutoPulse and Lucas-2 were not affected by ambulance speed. Lucas- 2 showed more consistent average compression rate, higher fraction of adequate compression depth and reduced fraction of insufficient compression depth as compared to manual compression with p<0.001, 0.001 and 0.043 respectively.
CONCLUSION: In this study we found that ambulance speed significantly affected certain aspects of manual chest compression most notably compression depth, rate and hand positioning. AutoPulse and Lucas-2 can improve these aspects by providing more consistent compression rate, depth and fraction of adequate compression depth during transport.