Atrial flutter I48.9

Atrial flutter is a circular excitation fixed by anatomical and / or functional barriers, which can emanate from both atria and is transmitted to the chambers in a regular or irregular manner. The frequency-dependent definition of > 250 / min. described in some textbooks is now considered obsolete (Mewis 2004).

Atrial flutter belongs to the supraventricular tachycardias (Wolff 2020) and represents a special form of intraatrial reentry tachycardia (IART) (Paul 2018).

Type I atrial flutter (so-called isthmus dependent atrial flutter [Herold 2020] or typical atrial flutter):

• Type I occurs more frequently. Usually an anatomically defined macro- reentry is found in the right atrium, less frequently around scars in the right atrium.
• The flutter frequency is between 200 - 320 beats / min, mostly with 2: 1 transition to the ventricles.
• This type can degenerate in atrial fibrillation.

Type II atrial flutter (so-called non-isthmus-dependent atrial flutter [Herold 2020] or atypical atrial flutter [Kasper 2015]):

• This form is very rare. The frequency is between 250 - 350 beats / min. There is often an irregular transition (Stierle 2017).
• In type II the excitation can originate from both atria and is normally associated with scar areas (Kasper 2015).

Atrial flutter can occur at any age, even in the foetal period. However, the frequency increases with age. Atrial flutter occurs twice as frequently in men as in women (Luik 2011).

The incidence is 0.088 %.

Of those < 50 years of age 5/100,000 fall ill, of those > 80 years of age 587/100,000.

A so-called "lown atrial flutter" is rare. In 3 out of 4 patients there is also atrial fibrillation.

In 60 % of the affected patients a trigger is found, such as myocardial infarction, exacerbated COPD or heart or lung surgery (Pinger 2019).

According to Stierle 2017, the most common cause of atrial flutter is

• organic heart diseases such as:
  • heart valve defect
  • Heart diseases such as:
    • hypertensive
    • ischemic
    • inflammatory
  • congenital vitia
  • Cardiomyopathies
• ...extracardiac conditions such as:
  • Hyperthyroidism
  • Lung diseases
  • Drugs
  • under antiarrhythmic treatment of atrial fibrillation with:
  • Flecainide
    • propafenone
    • Sotalol
    • Dronedarone
    • Amiodarone

Atrial flutter can also occur in otherwise healthy patients, mainly older patients (Herold 2020).

A circular excitation, the so-called macro-reentry around the tricuspid valve annulus leads to right-atrial atrial flutter. The excitation passes through a narrowing between the tricuspid valve annulus and the inferior vena cava. This constriction is also called the sub-Eustachian or cavo-tricuspid isthmus.

(Kasper 2015)

The excitation usually takes place counterclockwise as so-called "counter- clock- wise" [Pinger 2019]) (Kasper 2015), but can also take place clockwise as "reverse typical atrial flutter" (Pinger 2019). The macro-reentry is maintained by the cavo-tricuspid isthmus and the crista terminalis (Herold 20209.

• palpitations
• angina pectoris
• Dyspnea
• Orthopnea
• agitation (Wolff 2020)
• Anxiety
• thoracic pressure sensation
• (pre-) syncope

Note: Sometimes patients are completely asymptomatic (Luik 2011)!

12- channel ECG

Diagnosis is almost always possible with the help of the ECG (Mewis 2004). A regular ventricular rhythm of 140 beats/min with a normal QRS complex is always suspicious for atrial flutter (Wolff 2020).

Typical in atrial flutter is the presence of a:

• Sawtooth-shaped deformation due to
  • negative P- waves in II, III and aVF at "counter- clock- wise" (see "Pathophysiology") with a frequency of 220 - 270 beats / min.
  • positive P- waves in II, III, aVF and V1 in "reverse typical atrial flutter" (see "Pathophysiology"), also with a frequency of 220 - 270 beats / min (Herold 2020 / Pinger 2019).

However, the typical sawtooth-shaped deformation may often not be apparent in a 2: 1 transition. In this case, a carotid pressure test is recommended (this leads to a temporary AV block) (Wolff 2020).

Type I (see classification):

• negative flutter waves in II, III, aVF are possible
• positive flutter wave in V1 possible

Type II (see classification):

• The typical morphology of P- waves is not found here (Stierle 2017). In most cases, an AV- block of II degree with 2: 1 or 3: 1 conduction occurs, which leads to a lowering of the ventricular frequency. The frequency of the ventricles in this case is about 140 beats / min.However, there is always a risk of 1: 1 conduction with threatening ventricular tachycardia (Herold 2020).

Transesophageal echocardiography (TEE).

If atrial flutter persists for more than 48 h, thrombus exclusion by TEE is required. Patients on permanent anticoagulation are excluded (Kraemer 2018).

Atrial flutter is differentiated between acute therapy and antiarrhythmic therapy (Stierle 2017).

Acutetherapy:

Primarily, the ventricular rate should be lowered with the following medications:

• Beta blockers (e.g. metoprolol 5 mg - 10 mg i. v. under ECG control (Kraemer 2018).
• Calcium channel blockers: In case of contraindications to beta blockers, calcium channel blockers can be given, such as: Verapamil 5 mg - 10 mg i. v. under ECG- control (Kraemer 2018).
• Digitalis saturation: After control of potassium level (in case of hypokalemia first appropriate substitution with potassium) rapid digitalis saturation in case of very tachycardic atrial flutter. Dosage recommendation: digoxin 0.5 mg i. v. after 8 and 16 h each additional 0.5 mg i. v., subsequent maintenance dose: 0.25 mg / d p. o. (Kraemer 2018).
• Anticoagulation: If there are no contraindications to anticoagulation, the following drugs can be used:
  • High-dose heparinization: e.g. enoxaparin 1 mg / kg bw s. c. 2 x /d (Note: absolute contraindications: - malignant hypertension, florid ulcus ventriculi / duodeni, fresh cerebral hemorrhage, necrotizing pancreatitis, hemorrhagic diathesis, severe diabetes mellitus, liver cirrhosis with esophageal varices, Quick < 60 %, heparin-induced thrombocytopenia type II(Bob 2001)
  • low molecular weight heparin (NMH): e.g. enoxaparin (Clexane) 1 x 20 mg to 40 mg / d
  • NOAKs: e.g., rivaroxaban 2 x 150 mg / d (Kraemer 2018).

The next step should be to eliminate the arrhythmia (Wolff 2020). This is possible with:

• Antiarrhythmic drugs: The administration of an antiarrhythmic drug should be done under safe anticoagulation or by TEE- exclusion of thrombi (an exception are circulatory unstable patients)(Wolff 2020). Dosage recommendation: Amiodarone 150 mg as a short infusion (Kraemer 2018) However, it is rare to succeed in eliminating atrial flutter long-term with medication (Wolff 2020).
• Atrial overstimulation (so-called "overdrive stimulation" [Herold 2020] or "overpacing" [Sattler 2007]): This is performed by a venously inserted electrocatheter (Sattler 2007). In type I, overstimulation is usually successful, but in type II, it is successful in only about 10% (Stierle 2017).
• Electrocardioversion: This should be performed as primary treatment in patients with hemodynamic instability. Since the risk of thromboembolic events is very high, anticoagulation is recommended before cardioversion (see above [Kasper 2015]). The success rate of cardioversion is >90%. Sometimes atrial flutter converts to atrial fibrillation. However, by applying higher energies, this can usually be converted into sinus rhythm (van Aken 2001).
• Catheter ablation
  • In typical atrial flutter (type I): Catheter ablation is a curative procedure for typical atrial flutter. It can be used primarily or after failure of drug treatment (Erdmann 2009). Ablation involves electrical dissection of the cavo-tricuspid isthmus. The procedure can be planned electively because it can be performed regardless of rhythm (Luik 2011). The success rate is >95% (Herold 2020).
  • In atypical atrial flutter (type II): Since atypical atrial flutter cannot be clearly localized by a surface ECG, this should be done in the form of 3D mapping in experienced centers. The examination should be performed during the phase of an arrhythmia or an arrhythmia should be indicated during the examination.
  • During ablation, it is important to avoid incomplete ablation lines at all costs, as these contain a breeding ground for renewed atypical reentry mechanisms. Ablation can be treated acutely for left atrial flutter in up to 80%. However, the long-term prognosis is poor. Sufficient data are not available due to the rarity of the clinical picture (Mewis 2004) (Luik 2011).

After a successful ablation of the typical atrial flutter, regular monitoring is necessary, as it has been shown that 33% - 63% of patients developed atrial fibrillation and 6% developed an apoplexy (Pinger 2019).

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