Focal atrial tachycardia I47.1

Synonyms

Chaotic atrial tachycardia; CAT;

Definition

Focal atrial tachycardia (FAT) is the occurrence of an atrial rhythm with a frequency of ≥ 100 beats per minute that originates in a circumscribed area of the atria and propagates centrifugally from there across both atria. Thereby, the frequency of the ventricles varies depending on the conduction in the AV- node (Brugada 2019).

Focal atrial tachycardias belong to the group of atrial tachycardias (Brugada 2019).

Focal atrial tachycardia is differentiated between:

- Unifocal FAT

- Multifocal FAT (Herold 2022), also referred to as MAT (Kasper 2015).

- Atrial reentry tachycardia (Haverkamp 2003).

No data are available on the prevalence of FAT (Liwanag 2022). Haverkamp (2003) describes the incidence of atrial tachycardia to be between 5-10%, and gender preference is roughly balanced. FAT accounts for approximately 10% of patients with paroxysmal supraventricular tachycardia who come for catheter ablation (Kasper 2015).

Multifocal atrial tachycardia (MAT) is relatively uncommon among atrial tachycardias. It occurs preferentially in neonates (Haas 2011).

FAT can basically be caused by all cardiac diseases affecting the atrium (Kasper 2015).

- Unifocal FAT is found in:

- healthy individuals

- in cases after cardiac surgery (Herold 2022).

- Multifocal FAT can occur due to:

- cardiac dysfunction e.g. in congenital heart defects, after cardiac surgery etc.

- severe heart failure

- theophylline intoxication

- cor pulmonale (Herold 2022)

- chronic lung diseases

- acute diseases (Kasper 2015)

Until proven otherwise, atrial tachycardia with AV block always indicates digitalis intoxication (Herold 2022).

FAT may occur in the setting of:

- chronic lung disease

- pulmonary hypertension

- ischemic heart disease

- hypoxia

- metabolic disorders

- digitalis intoxication (in multifocal FAT [Krehan 2017])

- increased sympathetic tone

- Ingestion of stimulants such as caffeine, cocaine, ephedrine, chocolate

- alcohol (Liwanag 2022)

- after ablation for atrial fibrillation (Müller- Edenborn 2021)

Unifocal FAT:

In most cases, these are due to:

- abnormal automaticity: This occurs due to spontaneous phase- 4 depolarization. During phase 4, the cardiomyocyte membrane is polarized and maintains the inward potassium channel in equilibrium. Due to an accelerated phase-4 increase, abnormal automaticity leads to cell depolarization (Liwanag 2022).

- triggered automaticity

- small reentry circuit (this is confined to the atrium or part of the atrial tissue and extends into the coronary sinus, a pulmonary vein, or the vena cava)

(Kasper 2015)

- Rarely by undetermined mechanism (Liwanag 2022).

Multifocal FAT:

- Automatic triggering of multiple atrial foci (Kasper 2015).

(Liwanag 2022)

FAT may be asymptomatic or primarily manifested by symptoms of the underlying disease. However, the following symptoms may also occur:

- Palpitations

- lightheadedness

- dyspnea

- pain or thoracic pressure

- irregular heartbeat

- sensations of rapid heart rate (Liwanag 2022)

Symptoms may be persistent or intermittent, triggered or exacerbated by stress, exercise, consumption of caffeinated products (Liwanag 2022).

ECG and determination of glycoside levels if the patient is digitized (Herold 2022). In cases of intermittent FAT, a long-term ECG should be performed (Kasper 2015).

ECG:

ECG may show:

- regular tachycardia at atrial level

- frequency between 100 - 250 BPM (Liwanag 2022)

- altered monomorphic P-wave configuration (Herold 2022).

- ventricular conduction may be variable:

- irregular or regular AV block with stable 1: 1

- stable 1: 1 conduction or

- stable 1: 2 (Mobitz type) or

- alternating 1: 2 (Wenckebach type)

- usually narrow QRS complexes, in case of cardiac dysfunction or high frequency these can also be deformed like a leg block

- often gradual onset or end of FAT, so called warming-up / cooling-down (Herold 2022)

Left atrium:

In case of tachycardia from the left atrium, a monophasic positive P- wave usually occurs in lead V 1 (Kasper 2015).

Atrial septum:

If the tachycardia comes from the atrial septum, a shorter duration of P- waves is often found than in sinus rhythm (Kasper 2015).

Right atrium:

Tachycardia from the right atrium shows positive P- wave morphology in lead I (Kasper 2015) and biphasic P- wave morphology in lead V 1 with a sensitivity of 93% and a specificity of 88% and in lead aVL with a sensitivity of 88% and a specificity of 79% (Traykov 2015).

Superior districts of the atrium:

These are districts such as superior vena cava or superior pulmonary vein. The P-wave is positive in the inferior leads II, III and aVF (Kasper 2015).

Inferior districts of the atrium:

These involve, for example, the ostium of the coronary venous sinus. Negative P- waves are found in the inferior leads II, III and aVF (Kasper 2015).

Crista terminalis:

In this case, the P- wave resembles sinus tachycardia (Kasper 2015).

Unifocal FAT:

The ventricular complex is narrow (so-called narrow complex tachycardia) with a QRS- duration ≤ 120 ms (Brugada 2019). The frequency is between 100 - 250 beats / min. Typical monomorphic P- waves are recognizable before the QRS- complex, which differ from the P- waves of sinus rhythm (Krehan 2017).

Multifocal FAT:

At a minimum, 3 distinct P- configurations with alternating PP and PQ intervals are found in the ECG (Herold 2022), most recognizable in ll, lll, and V1. AV- conduction can be aberrant in a frequency-dependent manner, resulting in leg block-like deformed ventricular complexes (Haas 2011) with a QRS- duration of ≥ 120 ms (Kasper 2015). The frequency ranges from 100-160 beats/min (Krehan 2017). However, one finds, in contrast to atrial fibrillation clear isoelectric intervals between the P- waves (Kasper 2015).

This is a so-called irregular broad complex tachycardia (Brugada 2019).

- Electrolytes (especially potassium and calcium s.a. therapy)

- Glycoside levels in digitized patients (Herold 2022)

If a narrow, complex, regular tachycardia occurs, differential diagnosis should be made:

- sinus tachycardia (P-wave with superior axis)

- Atrial flutter (biphasic sawtooth-like F-wave)

- AV nodal reentry tachycardia (AVNRT): inverted P- wave before QRS complex or absent P- wave or P- wave disappears within S- wave.

- atrial tachycardia (focal)

- junctional tachycardia (P-wave is absent or inverted)

(Liwanag 2022)

When complex, irregular tachycardia occurs, differential diagnosis should be made from:

- Atrial fibrillation (Liwanag 2022)

- AV nodal dependent supraventricular tachycardia.

In this case, there is usually an AV block due to the dependence on the AV node (Kasper 2015).

- Tachycardia-induced cardiomyopathy.

This can develop even in younger and asymptomatic patients due to frequent FAT, regardless of frequency (Herold 2022).

- Triggering AV block (Liwanag 2022).

- Causal therapy:

Treatment of the underlying condition.

If the causal cause is digitalis intoxication, (most common cause of multifocal atrial tachycardia) it should be treated as follows (Herold 2022):

- Immediate discontinuation of digitalis

- Promote elimination of digitalis by:

- Antidote treatment with Fab antibody fragments such as DigiFab (Böhm 2000). Dosage:

- if the amount of digitalis is known: 80 mg antidigoxin- Fab bind 1 mg digoxin, so that the digoxin- level decreases by 1ng / ml and for digitoxin by 10 ng / ml (Flake 2021).

- If the amount of digitalis is unknown: bolus of 160 mg as a short infusion in 5% glucose over 20 min, then 20 mg / h over 12 h (Flake 2021)

- Symptomatic therapy of digitalis intoxication in the form of:

- temporary pacemaker

- Atropine for bradycardia (Herold 2022) Dosage: 1mg atropine i. v. (Böhm 2000).

- For ventricular extrasystoles, tachycardia and ventricular flutter use of:

- Magnesium 20 mval i. v. (2 mval = 1 mmol / l (Hartig 2004).

- Phenytoin 100 mg i. v.

- Lidocaine 100 mg i. v.

- defibrillation

- Cardioversion (Böhm 2000)

- Potassium:

Hyperkalemia increases the risk of AV block (Lemmer 2007). Therefore, in case of hyperkalemia, antidote treatment with Fab antibody fragments (see above) should be given immediately (Mori 2012). If no antidote is available, the shift of potassium into the intracellular space can be treated with glucose, insulin, and bicarbonate (Gertsch 2007).

However, potassium is always contraindicated in pre-existing conduction disorders (Lemmer 2007). In case of hypokalemia, potassium should be substituted, except in case of pre-existing conduction disorders (Mori 2012).

- Calcium:

Ca2+ enhances the effect of digitalis and thus promotes toxicity. From there, calcium supplements are contraindicated in digitalis intoxication. Existing hypercalcemia should be corrected promptly (Karow 2021).

- Symptomatic therapy of FAT:

- Drug therapy with e.g.

- beta blockers (Herold 2022)

- Calcium channel blockers

- Adenosine (Kasper 2015)

- antiarrhythmic drugs

- Ivabradine (Brugada 2019).

Beta blockers and antiarrhythmics

Beta-blockers, such as metoprolol or esmolol, and calcium channel blockers, such as verapamil or diltiazem (IIa C [Brugada 2019]), may slow ventricular rate by enhancing AV block, which in turn may improve tolerance to arrhythmias (Kasper 2015).

They should also be used when adenosine administration fails (IIa B [Brugada 2019]).

Nucleoside

The nucleoside adenosine can be used i. v. as a bolus of 6-18 mg for regular narrow complex tachycardia (I B) and for multifocal atrial tachycardia (IIa C [Brugada 2019]).

Administration of adenosine abates some forms of FAT, but there may also be transient enhancement of AV block (in the case of reentry cause, for example) without termination of tachycardia (Kasper 2015).

Antiarrhythmics

Ibutilide i. v. (llb) or amiodarone / flecainide / propafenone (IIb C) may be considered as acute therapy for FAT. However, ibutilide is not available in Germany (Brugada 2019).

Ivabradine

Ivabradine can be considered together with a beta-blocker (see above) as long-term therapy in FAT (llb [Brugada 2019]).

- Cardioversion:

In hemodynamically unstable patients, the guideline (I B) recommends synchronized direct current cardioversion as the first therapeutic measure. If therapy is not successful, antiarrhythmic drugs such as ibutilide, amiodarone / flecainide / propafenone (ll b C) should be used (Brugada 2019).

In hemodynamically stable patients, it is recommended to use synchronized direct current cardioversion only after failure of the above drugs (l B [Brugada 2019]).

- Ablation:

This should be applied when there is a risk of tachycardia-induced cardiomyopathy or when drug therapy is permanently required (Herold 2022), as well as in recurrent FAT (Brugada 2019).

Primarily, adenosine (IIa B) is recommended therapeutically in patients with FAT. If this therapy is unsuccessful, beta blockers (lla C) or calcium channel blockers (lla C) should be used. If this also fails, antiarrhythmic drugs such as ibutilide, flecainide, or propafenone (llb C) should be used. If therapeutic success fails despite drug measures, synchronized direct current cardioversion (l B) is recommended (Brugada 2019).

Long-term therapy

Long-term therapy options include:

- 1. catheter ablation (l B) if FAT is persistent or has already caused cardiomyopathy (Brugada 2019).

- 2. if ablation is not desired by the patient, drug therapy can be used in structurally heart healthy patients in the form of:

- Beta-blockers (see above) or.

- non-dihydropyridine calcium antagonists such as verapamil or diltiazem or

- Flecainide or propafenone (lla C).

In patients without evidence of heart failure with reduced left ventricular ejection fraction (HFrEF), verapamil or diltiazem are recommended (Brudaga 2019).

- 3. if the above options fail, ivabradine should be used in conjunction with a beta-blocker or amiodarone (llb C) if there is no response (Brugada 2019).

The prognosis of FAT is ultimately dependent on the precipitating condition, but overall is considered a benign tachycardia (Liwanag 2022).

- Ablation:

Ablation is shown to be successful in over 80% of cases (Herold 2022). The complication rate is 1.4%. However, recurrence occurs in approximately 20% thereafter (Brugada 2019).

- Tachycardia-induced cardiomyopathy:

This is usually reversible after successful therapy (Herold 2022).

Patients with congenital heart disease should be anticoagulated if FAT occurs (l C [Brugada 2019]).

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