Inducibility of human atrial fibrillation in an in silico model reflecting local acetylcholine distribution and concentration

Vagal nerve activity has been known to play a crucial role in the induction and maintenance of atrial fibrillation (AF). However, it is unclear how the distribution and concentration of local acetylcholine (ACh) promotes AF. In this study, we investigated the effect of the spatial distribution and concentration of ACh on fibrillation patterns in an in silico human atrial model. A human atrial action potential model with an ACh-dependent K+ current (I(KAch)) was used to examine the effect of vagal activation. A simulation of cardiac wave dynamics was performed in a realistic 3D model of the atrium. A model of the ganglionated plexus (GP) and nerve was developed based on the "octopus hypothesis". The pattern of cardiac wave dynamics was examined by applying vagal activation to the GP areas or randomly. AF inducibility in the octopus hypothesis-based GP and nerve model was tested. The effect of the ACh concentration level was also examined. In the single cell simulation, an increase in the ACh concentration shortened APD90 and increased the maximal slope of the restitution curve. In the 3D simulation, a random distribution of vagal activation promoted wavebreaks while ACh secretion limited to the GP areas did not induce a noticeable change in wave dynamics. The octopus hypothesis-based model of the GP and nerve exhibited AF inducibility at higher ACh concentrations. In conclusion, a 3D in silico model of the GP and parasympathetic nerve based on the octopus model exhibited higher AF inducibility with higher ACh concentrations.

Severe bradycardia and transient asystole during epidural anesthesia: A case report / 대한마취과학회지

The severe bradycardia and asystole are uncommon complications of epidural anesthesia but can be life threatening if not managed properly. A 73-year-old, ASA class 3, male patient was admitted for a total knee replacement under epidural anesthesia. Approximately 10 minutes after epidural anesthesia, the heart rate decreased significantly to 20 beats/min with asystole. The heart rate returned to 80 beats/min after administering atropine, ephedrine, and external cardiac compression. Severe bradycardia and asystole may be induced by vagal activation as a result of the low venous return and sympathetic blockade.