Cardioversion in the ICU

Created on Fri, 11/06/2015 - 21:51
Last updated on Thu, 05/31/2018 - 17:08


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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.

Rationale for the use of direct current to convert cardiac rhythm

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).

Advantages of DC cardioversion over chemical cardioversion

  • Electrical cardioversion is immediately effective (when it is effective)
  • It may be life-saving in a haemodynamically unstable arrhythmia
  • Automated devices ensure synchronisation so that  R-on-T phenomena should not occur
  • There are relatively few long-term side effects associated with it (i.e. unlike long-term amiodarone it won't give you pulmonary fibrosis) 

Disadvantages of electrical cardioversion in comparison to antiarrhythmic drugs

  • It is not a long-term strategy: if the underlying pathology has not been fixed, reversion to sinus rhythm will not be sustained.
  • There is the risk of arterial thromboembolism, although this is probably much the same risk as with pharmacological cardioversion, or with spontaneous reversion to sinus rhythm for that matter. "There are no data supporting that pharmacological cardioversion is associated with a lower risk for TE", wrote Mårten Rosenqvist in an editorial responding to the publication of a massive study of thromboembolic risk in AF (Hansen et al, 2014)
  • It requires a sedated patient.
  • It will result in a raised troponin, which may obscure the presence of genuine myocardial infarction.
  • It requires the accurate diagnosis of rhythm

Accepted applications of electrical cardioversion

  • Atrial flutter (good chance of success)
  • Supraventricular tachycardia (good chance of success)
  • VT
  • Atrial fibrillation (poor chance of success, especially if the AF has been going on for a very long time).

Potential complications of electrical cardioversion

  • Ventricular fibrillation may develop due to lack of synchronization.
  • Sudden restoration of sinus rhythm can dislodge intracardiac thrombi.
  • Transient left bundle branch block may develop. In fact any sort of conduction block may develop, including complete heart block.
  • Transient left ventricular systolic dysfunction may develop. In fact you could cause myocardial damage.
  • There may be skin burns due to incorrect use of the equipment.
  • If the patient has a pacemaker, you may damage it with the direct current. 
  • If the patient has digoxin toxicity, one may induce VF in such a patient.



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.