There is no difference in pain and potential of ventricular fibrillation induction with lower energy levels. Previously, lower defibrillator outputs such as 50 J were employed to prevent pain, but the current recommendation is 200 J biphasic with either anteroposterior or midline and lateral defibrillation pad positioning. severe chest pain), synchronised direct current cardioversion is indicated to revert patients to sinus rhythm. In an acute setting, atrial flutter with hemodynamic compromise or rarely significant cardiac symptoms (i.e. It is important to understand that atrial flutter ablation has a high success rate unlike atrial fibrillation, and extreme methods of rate control such as pacemaker implantation and AV nodal ablation are rarely used as a management strategy. Rate control of atrial flutter can be very difficult to achieve pharmacologically. Various pharmacological agents which are used in non-invasive management are presented in Table 2. An emerging data however shows that less strict control such as heart rates less than an average 24-hour heart rate of less than 110 bpm is adequate. Typically, the aim is an average 24-hour heart rate over 24 hours of 80 bpm and a maximum of less than 130 bpm. The same parameters however could generally be applied as the goal is to avoid tachycardia-induced cardiomyopathy whilst preserving exercise capacity. There is debate in the literature about what exactly is adequate rate control this however pertains to atrial fibrillation as it has not been specifically studied in atrial flutter. Rate control is generally reserved for patients who are in permanent atrial flutter and have no or minimal symptoms and cannot achieve rhythm control due to co-morbidities or are not willing to undergo procedures or take medications. In this chapter, we will discuss the classification, pathophysiology, clinical presentation, electrocardiographic characteristics, electrophysiological testing and both the pharmacological and ablative management of atrial flutter. Re-entry however is still thought to play a role in atrial fibrillation, but its exact involvement is unknown. Currently these waves are considered chaotic and do not behave like the macro-reentry wavefront of atrial flutter. These mechanisms are distinct from that of atrial flutter which is macro-reentrant however, atrial tachycardia can also be re-entrant in mechanism similar to atrial flutter but on a microscopic level (re-entry around barriers of less than 2 cm).Ītrial fibrillation is due to fibrillatory waves in the atria with rates that are typically greater than 300 bpm in the atria. Its mechanism can be due to triggered activity or increased automaticity of atrial cells. As such, atrial flutter and atrial fibrillation often coexist.Ītrial tachycardia is typically characterised by atrial rates >100 bpm but less than 240 bpm with discrete activation sequences and non-sinus P waves including a baseline isoelectric period between these waves on ECG. If the tachycardia persists for a prolonged period, it frequently can degenerate into atrial fibrillation, particularly if the patient already has structural heart disease. It is generally paroxysmal in nature in a structurally healthy heart. The atrial rate in atrial flutter is approximately 240–360 beats per minute (bpm) with no distinct isoelectric period between the flutter ‘F’ waves. Atrial flutter has been traditionally defined as a macro-reentrant arrhythmia around a macroscopic (more than 2 cm in area) anatomical barrier that is confined within the atria. Although they are supraventricular in origin, apart from atrial tachycardia, they are not generally included in the nomenclature of supraventricular tachycardia. The more frequent clinically encountered atrial tachyarrhythmias include atrial tachycardia, atrial flutter and atrial fibrillation. Atrial arrhythmias are significant contributors for cardiac co-morbidity especially for stroke, heart failure and recurrent hospitalisations.
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