Question 6 from the first paper of 2005 asks the trainees to critically evaluate cardioversion in the ICU. Unlike defibrillation, cardioversion can be viewed as an elective thing. In many situations you may have a choice of whether to convert somebody's rhythm by electricity or by chemicals. The following discussion examines the electrical approach, mainly because that is what the college focused on in their model answer for Question 6. Of course, besides the option of chemical cardioversion, we also have mechanical cardioversion, which in modern practice is limited to the VT-stopping praecordial thump. When we choose to challenge our patient's heart with an electrical discharge, we have many different options of how we might want to deliver it. These options range from external electrodes and paddles to epicardial pacing wires.
As far as resources go, the time-poor candidate may safely limit themselves to the LITFL page on this subject. It is based on the model answer for Question 6 and covers all the important ground without any superfluous fluff. However, if one were for some reason after superfluous fluff, one may find it below.
Cardioversion is the use of a short ( 200msec) discharge of direct current which is synchronised with the QRS complexes, so as to convert an abnormal rhythm to sinus rhythm. It has not always been direct current (Claude Beck's 1947 model defibrillator used AC straight from the wall outlet, and generally only Soviet defibrillators were biphasic DC until the 1960s). Ultimately, direct current was found to be safer: a larger amount of energy could be delivered in a short period of time. The mechanism remains incompletely understood. Various groups have suggested various explanations. Direct current travels around the cells as well as through them; the effect is to change the transmembrane electrical potentials. One might expect all the cells to depolarise because all of the voltage-gated ion channels suddenly open, but the effect does not seem uniform: some cells depolarise and others hyperpolarise. In any case, this disrupts the normal propagation of action potentials. In this manner, DC current depolarises a sufficiently large amount of cardiac tissue, putting it into a refractory period and preventing the propagation of a reentrant current (which then dies away).
Mayr, Andreas, et al. "Effectiveness of direct-current cardioversion for treatment of supraventricular tachyarrhythmias, in particular atrial fibrillation, in surgical intensive care patients*." Critical care medicine 31.2 (2003): 401-405.
Trappe, Hans-Joachim, Bodo Brandts, and Peter Weismueller. "Arrhythmias in the intensive care patient." Current opinion in critical care 9.5 (2003): 345-355.
Sucu, Murat, Vedat Davutoglu, and Orhan Ozer. "Electrical cardioversion." Annals of Saudi medicine 29.3 (2009): 201.
Cakulev, Ivan, Igor R. Efimov, and Albert L. Waldo. "Cardioversion past, present, and future." Circulation 120.16 (2009): 1623-1632.
Plonsey, R., and R. C. Barr. "Effect of microscopic and macroscopic discontinuities on the response of cardiac tissue to defibrillating (stimulating) currents." Medical and Biological Engineering and Computing 24.2 (1986): 130-136.
Efimov, Igor R., et al. "Transmembrane voltage changes produced by real and virtual electrodes during monophasic defibrillation shock delivered by an implantable electrode." Journal of cardiovascular electrophysiology 8.9 (1997): 1031-1045.
Rosenqvist, Mårten. "Cardioversion without oral anticoagulation--is it risk-taking?." Europace: European pacing, arrhythmias, and cardiac electrophysiology: journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology 17.1 (2015): 3-4.
Hansen, Morten Lock, et al. "Thromboembolic risk in 16 274 atrial fibrillation patients undergoing direct current cardioversion with and without oral anticoagulant therapy." EP Europace 17.1 (2014): 18-23.