Cardiac arrest and hemodynamic instability: urgent cardioversion
Patients who suffer a cardiac arrest from ventricular fibrillation, polymorphic ventricular tachycardia (VT), or rapid VT require CPR and prompt defibrillation.[46]Goldberger JJ, Cain ME, Hohnloser SH, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death: a scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. Circulation. 2008 Sep 30;118(14):1497-518.
http://circ.ahajournals.org/cgi/content/full/118/14/1497
http://www.ncbi.nlm.nih.gov/pubmed/18833586?tool=bestpractice.com
In this situation the chance of surviving the cardiac arrest decreases by 7% to 10% for every 1-minute delay in defibrillation.[47]Winkle RA, Mead RH, Ruder MA, et al. Effect of duration of ventricular fibrillation on defibrillation efficacy in humans. Circulation. 1990 May;81(5):1477-81.
http://circ.ahajournals.org/cgi/reprint/81/5/1477
http://www.ncbi.nlm.nih.gov/pubmed/2331763?tool=bestpractice.com
[48]De Maio VJ, Stiell IG, Wells GA, et al. Optimal defibrillation response intervals for maximum out-of-hospital cardiac arrest survival rates. Ann Emerg Med. 2003 Aug;42(2):242-50.
http://www.ncbi.nlm.nih.gov/pubmed/12883512?tool=bestpractice.com
[49]Rea TD, Eisenberg MS, Becker LJ, et al. Temporal trends in sudden cardiac arrest: a 25-year emergency medical services perspective. Circulation. 2003 Jun 10;107(22):2780-5.
https://www.doi.org/10.1161/01.CIR.0000070950.17208.2A
http://www.ncbi.nlm.nih.gov/pubmed/12756155?tool=bestpractice.com
Atrial fibrillation with ventricular preexcitation often requires immediate cardioversion because of the risk that the arrhythmia will degenerate into ventricular fibrillation. Long term anticoagulation should be considered based on thromboembolic risk.[5]Joglar JA, Chung MK, Armbruster AL, et al. 2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: a report of the American College of Cardiology/American Heart Association Joint Committee on clinical practice guidelines. Circulation. 2024 Jan 2;149(1):e1-156.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11095842
http://www.ncbi.nlm.nih.gov/pubmed/38033089?tool=bestpractice.com
In any situation where a tachycardia (regardless of the mechanism) is the cause of hemodynamic instability, angina, syncope, or decompensated heart failure, the priority should be toward rapid termination of the arrhythmia. In many cases (atrial fibrillation with rapid ventricular response, supraventricular tachycardia, VT) electrical cardioversion is the most efficient and reliable way to achieve sinus rhythm. It is useful to obtain a rhythm strip during and immediately after cardioversion in the event of reinitiation of the rhythm.[47]Winkle RA, Mead RH, Ruder MA, et al. Effect of duration of ventricular fibrillation on defibrillation efficacy in humans. Circulation. 1990 May;81(5):1477-81.
http://circ.ahajournals.org/cgi/reprint/81/5/1477
http://www.ncbi.nlm.nih.gov/pubmed/2331763?tool=bestpractice.com
[48]De Maio VJ, Stiell IG, Wells GA, et al. Optimal defibrillation response intervals for maximum out-of-hospital cardiac arrest survival rates. Ann Emerg Med. 2003 Aug;42(2):242-50.
http://www.ncbi.nlm.nih.gov/pubmed/12883512?tool=bestpractice.com
Regular wide-complex or regular narrow-complex tachycardia with hemodynamic stability: adenosine administration
In patients who are stable with a regular wide- or narrow-complex tachycardia, administration of adenosine is a therapeutic intervention and can provide useful diagnostic information.[14]Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020 Feb 1;41(5):655-720.
https://academic.oup.com/eurheartj/article/41/5/655/5556821
Adenosine should be administered in a closely monitored setting, with the patient supine, and with continuous ECG and hemodynamic monitoring.
Adenosine is metabolized rapidly by red blood cells and must therefore be given as a rapid bolus to be effective.
Adenosine transiently slows the sinus node or atrial tachycardia and transiently slows or blocks conduction in the atrioventricular (AV) node. Depending on the arrhythmia mechanism, adenosine may unmask the underlying rhythm (atrial flutter, atrial tachycardia) or may terminate arrhythmias that are dependent on the AV node (AV nodal reentrant tachycardia, AV reciprocating tachycardia).
Caution is required in the presence of atrial fibrillation and a possible accessory conduction pathway because adenosine can precipitate preferential rapid accessory tract conduction and degeneration to ventricular fibrillation.