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............................................................................................................................................................................. monitoring. The evaluation of a patient suspected of having POTS should eliminate other causes of sinus tachycardia such as hypovolaemia, anaemia, hyperthyroidism, pulmonary embolus, or pheochromocytoma.178 The clinical history should focus on defining the chronicity of the condition, possible causes of orthostatic tachycardia, modifying factors, impact on daily activities, and potential triggers.

11.1.1.4.2 Therapy. Non-pharmacological treatments should be attempted first in all patients. These include withdrawing medications that might worsen POTS, such as norepinephrine transport inhibitors, increasing blood volume with enhanced salt and fluid intake, reducing venous pooling with compression garments, and limiting deconditioning. Patients should engage in a regular, graduated, and supervised exercise programme featuring aerobic reconditioning with some resistance training for the thighs. Initially, exercise should be restricted to non-upright exercise, including the use of rowing machines and swimming, to minimize orthostatic stress on the heart.180182 If non-pharmacological approaches prove ineffective, pharmacological therapies may be targeted at specific aspects. Patients strongly suspected of having hypovolaemia should drink >_23 L of water per day, and dietary salt intake should be increased to 1012 g/day if tolerated. Midodrine significantly reduces orthostatic tachycardia but to a lesser degree than i.v. saline.170 Midodrine has a rapid onset with only brief effects and is usually administered three times daily. The drug should only be administered during daytime hours as it can cause supine hypertension. To reduce unpleasant sinus tachycardia and palpitations, low-dose propranolol [1020 mg per os (p.o.)] acutely lowers standing heart rate and improves symptoms in patients with POTS, while higher doses of propranolol are less well tolerated.172 Long-acting propranolol does not improve the quality of life of patients with POTS.167 Non-selective beta-blockers are preferable because they additionally block epinephrine-mediated beta-2-vasodilation, but other beta-blockers have not been adequately studied. Pyridostigmine, a cholinergic agonist that works by inhibiting acetylcholinesterase, can increase parasympathetic autonomic tone and has a lower risk of hypertension compared with other medications. Potential side effects include abdominal cramping, diarrhoea, and muscle cramps.173,174 Ivabradine slows sinus rates without affecting blood pressure, and in an open-label study 60% of patients with POTS had symptomatic improvement.175 Ivabradine should ideally be administered with concomitant beta-blockers for long-term therapy.151

11.1.2 Focal atrial tachycardia Focal AT is defined as an organized atrial rhythm >_100 b.p.m. initiated from a discrete origin and spreading over both atria in a centrifugal pattern. The ventricular rate varies, depending on AV nodal conduction. In asymptomatic young people (<50 years of age), the prevalence of focal AT has been reported to be as low as 0.34% with an increased prevalence of 0.46% in symptomatic arrhythmia patients.183 Most studies have reported no influence of sex. Symptoms may include palpitations, shortness of breath, chest pain, and rarely syncope or presyncope. The arrhythmia may be sustained or incessant. Dynamic forms with recurrent interruptions and reinitiations may be frequent.

In patients with PV-related AT, the focus is located at the ostium of the vein (or within 1 cm of the designated ostium)184 rather than further distally (24 cm).185

11.1.2.1 Diagnosis P wave identification from a 12 lead ECG recording during tachycardia is critical (Figure 7). Depending on the AV conduction and AT rate, the P waves may be hidden in the QRS or T waves. The P waves are monomorphic with stable CL, which helps to rule out organized AF. Adenosine injection can help by slowing the ventricular rate or, less frequently, by terminating focal AT. A discrete P wave with an intervening isoelectric interval suggests a focal AT. However, distinguishing focal from macro-re-entrant arrhythmias by surface ECG is not always possible. The presence of an isoelectric line does not rule out a macro-re-entrant mechanism, particularly in the presence of scar atrial tissue (from structural heart disease or previous extensive ablation/surgery procedures). In a normal heart and in the absence of previous ablation, the usual ECG localization rules apply,186 but their value in localizing the origin of the arrhythmia is also limited in this context. Focal AT may arise from any site in both atria, but particular sites of predilection in the normal heart rate are the crista terminalis, the tricuspid and mitral valve annulus, and within the thoracic veins joining the atria.46,186 A negative P wave in lead I and aVL suggests an LA origin. V1 is negative when the arrhythmia source or exit is in the lateral right atrium, while septal right atrial (RA) and LA origins show biphasic or positive P waves (Figure 7). Negative P waves in the inferior leads suggest a caudal origin, whereas positive P waves in those leads favour a superior location.

11.1.2.2 Acute therapy Hard data for an evidence-based choice of drugs for the acute therapy of focal AT are scarce. In general, acute therapy may be initiated with beta-blockers or calcium channel blockers, which may terminate focal ATs or slow the ventricular rate (Figure 8).92,94,187,188 Adenosine (i.v.) may terminate AT [delayed after-depolarizations (DAD)-triggered AT], but the tachycardia may also continue with AV block. Class IA, IC, and III drugs may also be effective, by prolonging refractoriness or suppressing automaticity.189191 Amiodarone may also be used for cardioversion or slowing of the ventricular rate,192 but the efficacy of rate control is unproven in critically ill patients with atrial arrhythmias.193 DC cardioversion is usually effective in acutely terminating the tachycardia, irrespective of the mechanism. However, in incessant forms of focal AT due to enhanced automaticity, the arrhythmia reinitiates, and repeating DC cardioversion is unlikely to be appropriate.

11.1.2.3 Catheter ablation Catheter ablation is the treatment of choice for recurrent focal AT, especially for incessant AT due to which TCM ensues (Figure 9).196 Distinguishing macro-re-entrant from focal ATs is critical for the ablation strategy. Focal ATs, as well as localized/ micro-re-entry ATs, display a centrifugal activation pattern that spreads throughout the atria. Mapping and ablation of focal ATs is based on determining the earliest activation site. In PV-related AT, focal ablation may be performed, but electrical isolation of both Downloaded from academic.oup.com/eurheartj/article/41/5/655/5556821 by guest on 07 October 2026