DefinitionThis section has been translated automatically.
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).
ClassificationThis section has been translated automatically.
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).
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Occurrence/EpidemiologyThis section has been translated automatically.
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).
EtiopathogenesisThis section has been translated automatically.
According to Stierle 2017, the most common cause of atrial flutter is
- organic heart diseases such as:
- heart valve defect
- Heart diseases such as:
- congenital vitia
- ...extracardiac conditions such as:
- Lung diseases
- under antiarrhythmic treatment of atrial fibrillation with:
Atrial flutter can also occur in otherwise healthy patients, mainly older patients (Herold 2020).
PathophysiologyThis section has been translated automatically.
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.
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.
Clinical featuresThis section has been translated automatically.
- angina pectoris
- Unrest (Wolff 2020)
- thoracic pressure
- (Pre-) Syncope
Remark: Sometimes patients are completely asymptomatic (Luik 2011)!
DiagnosticsThis section has been translated automatically.
12- channel ECG
The diagnosis is almost always possible with the help of the ECG (Mewis 2004). A regular chamber rhythm of 140 beats / min. with normal QRS complex is always suspicious of atrial flutter (Wolff 2020).
Typical for 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 at "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 can often not be detected in a 2:1 transition. In this case a carotid pressure test is recommended (this leads to a temporary AV blockage) (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 the P waves is not found here (Stierle 2017). In most cases an AV block II. degree with 2: 1 or 3: 1 transition occurs, which leads to a decrease of the chamber frequency. In this case the frequency of the chambers is about 140 beats / min. There is always the danger of a 1: 1 transition with threatening ventricular tachycardia (Herold 2020).
Transesophageal Echocardiography (TEE)
If the atrial flutter persists for longer than 48 h, thrombus exclusion by means of TEE is necessary. Excluded are patients with permanent anticoagulation (Kraemer 2018).
TherapyThis section has been translated automatically.
In atrial flutter, a distinction is made between acute therapy and antiarrhythmic therapy (Stierle 2017).
Primarily the ventricular frequency should be lowered with the following drugs:
- Beta blockers (e.g. metoprolol 5 mg - 10 mg i. v. under ECG control (Kraemer 2018)
- Calcium channel blockers: If there are 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 the potassium value (in case of hypokalemia first corresponding substitution with potassium) rapid digitalis saturation in case of very tachycardic atrial flutter. Recommended dosage: Digoxin 0.5 mg i. v. after 8 and 16 h each further 0.5 mg i. v., subsequent maintenance dose: 0.25 mg / d p. o. (Kraemer 2018)
- Anticoagulation: If there are no contraindications for anticoagulation, the following drugs can be used:
- High dose heparinization: e.g. enoxaparin 1 mg / kg KG s. c. 2 x /d (Remark: absolute contraindications: - malignant hypertension, florid ventriculo-duodenal ulcer, fresh cerebral haemorrhage, 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 was to eliminate the arrhythmia (Wolff 2020). This is possible with:
- Antiarrhythmics: The administration of an antiarrhythmic agent should be carried out under safe anticoagulation or by TEE- exclusion of thrombi (an exception are circulatory instable patients)(Wolff 2020). Dosage recommendation: Amiodarone 150 mg as a short infusion (Kraemer 2018) It is rarely possible to eliminate atrial flutter in the long term with medication (Wolff 2020).
- Atrial hyperstimulation (so-called "overdrive stimulation" [Herold 2020] or "overpacing" [Sattler 2007]): This is achieved by means of a venously inserted electrocatheter (Sattler 2007). With type I, over-stimulation is usually successful, but with type II it is only successful in 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 into atrial fibrillation. By applying higher energies, however, this can usually be converted into a sinus rhythm (van Aken 2001).
- catheter ablation
- In typical atrial flutter (type I): Catheter ablation is a curative procedure in 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 as it can be performed independently of the rhythm (Luik 2011). The success rate is > 95 % (Herold 2020)
- In atypical atrial flutter (type II): Since in atypical atrial flutter a surface ECG does not allow a clear localization of the reentry circle, this should be done in the form of a 3D mapping in experienced centers. The examination should be performed during the phase of arrhythmia or an arrhythmia should be indicated during the examination.
- During ablation it is important to avoid incomplete ablation lines at all costs, as they provide a breeding ground for new atypical reentry mechanisms. Ablation can be treated acutely in up to 80% of cases of left atrial flutter. However, the long-term prognosis is poor. Sufficient data are not available due to the rarity of the clinical picture (Mewis 2004) (Luik 2011).
Progression/forecastThis section has been translated automatically.
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).
LiteratureThis section has been translated automatically.
- van Aken H et al (2001) Intensive Care Medicine. Georg- Thieme- Publishing house 161 - 162
- Bob A and Bob K (2001) Internal Medicine. Special Edition MLP Dual Series Springer Verlag 1513
- Erdmann E (2009) Clinical Cardiology: Diseases of the heart, the circulation and the vessels near the heart. Springer publishing house 99 - 100
- Herold G et al (2020) Internal medicine. Herold Publisher 285 - 286
- Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 1484 - 1485
- Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publishing House 1811 - 1812
- Kraemer A (2018) Clinic guide night duty - feel safe and act confidently. Elsevier Urban und Fischer Publisher 150
- Luik A et al (2011) Typical and atypical atrial flutter. Cardio up 7 (29) 141 - 150
- Mewis C et al (2004) Cardiology compact: Everything for ward and specialist examination. Thieme Publishing House 555 - 561
- Paul T et al (2018) Guidelines Report Guideline: Tachycardic arrhythmias in childhood, adolescence and young adulthood (EMAH patients) AWMF Registry No. 023/022 Class: S2k
- Pinger S (2019) Repetitorium Kardiologie: For clinic, practice, specialist examination. German medical publisher. 705 – 724
- Sattler A M (2007) Casebook Cardiology and Angiology. Georg Thieme Publishing House
- Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer 406 - 408
- Wolff H P et al. (2020) Internal Therapy 2020 / 2021 Elsevier Urban und Fischer Verlag 395 - 396
Please ask your physician for a reliable diagnosis. This website is only meant as a reference.