Cardiac arrhythmia I49.9

Author: Dr. med. S. Leah Schröder-Bergmann

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Last updated on: 29.10.2020

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Synonym(s)

HRS

History
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Although cardiac arrhythmias were recognised as such early on by measuring the pulse, it was only with the help of electrocardiography by Willem Einthoven (1860 - 1927) that they could be differentiated more precisely. Karl Frederik Wenckebach (1864 - 1949) is considered a pioneer of cardiac arrhythmias. In 1903, he was the first to publish a written treatise on cardiac arrhythmias "Arrhythmia as an expression of certain functional disorders of the heart" (Lewalter 2010).

At the end of the 19th century the connection between a ventricular arrhythmia and sudden cardiac death was already recognized (Kasper 2015). In 1914 Wenckebach published the book "Die unregelmäßige Herztätigkeit und ihre klinische Bedeutung" (The irregular heart activity and its clinical significance), which is still considered a classic of rhythmological literature today (Lewalter 2010).

Intracardiac ECGs have been used since the late 1960s. The therapeutically important application of high-frequency current for ablation of cardiac tissue has been available since the end of the 1980s (Kasper 2015).

Definition
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Cardiac arrhythmia (HRS) is a cardiac activity that deviates from the norm and can be caused by disturbances in the formation of stimuli and/or conduction of stimuli (Kasper 2015). HRS are not fundamentally pathological, they also occur in organically healthy people (Herold 2020).

Bradycardic HRS are always caused by disturbances in the formation of stimuli in the area of the sinus node or by disturbances in the transmission of stimuli:

  • between sinus node and right atrium (SA block)
  • between AV nodes and chambers (AV block)
  • Disturbance in the Tawara legs (Kasper 2015)

Tachycardia HRS result from

  • increased autonomy
  • Postdepolarization
  • Reentry (Kasper 2015)

Occurrence/Epidemiology
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The most common HRS is atrial fibrillation. About 2 million people in Germany currently suffer from this disorder (Frantz 2020).

Etiopathogenesis
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HRS can have myocardial, hemodynamic or extracardiac causes:

Pathophysiology
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A distinction is made in HRS between different pathophysiological mechanisms:

  • In sinus bradycardia or tachycardia, cellular mechanisms in the form of suppression or acceleration of phase 4 of excitation play a role.
  • In AV block, excitation is suppressed at the cellular level
  • In atrial fibrillation, repolarization results in a shortening of the action potential.
  • In autonomy (see definition), the ability to spontaneously depolarize forms the basis for autonomy.
  • In post-depolarisation (see definition), it is oscillations of the membrane voltage that occur at an action potential, either during (as early post-depolarisation) or after (as late depolarisation).
  • In reentry (see definition) two electrophysiologically different conduction paths are responsible for the pulse propagation around a non-excitable region. This results in the excitation circling around a non-excitable obstacle (Kasper 2015).

Clinical features
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Mild or only intermittent HRS may not be noticed by the patient.

The clinical symptoms are differentiated between subjective and objective complaints and arterial embolisms (Herold 2020).

  • 1. subjective complaints such as:
    • Palpitations
    • interruption of heartbeat
    • Tachycardia (Herold 2020)
  • 2. Objective symptoms due to reduction in cardiac output:
    • cerebral:
      • Dizziness
      • Swindle
      • Syncopes
      • epileptiform seizures
      • States of Confusion
      • Passagere visual or speech disorders
      • Cerebral infarction
    • cardiac:
  • 3. arterial embolisms:
    • Arterial embolisms occur especially in atrial fibrillation due to the detachment of cardiac thrombi (approx. 20 % of all strokes are caused by atrial fibrillation - Herold 2020)

Diagnostics
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The diagnostic procedure is very different for each individual. Two essential aspects for the further procedure are the medical history and the ECG (Kasper 2015).

Anamnesis: detailed anamnesis regarding the existing symptoms.

  • Drug history (especially regarding antiarrhythmic drugs, cardiac glycosides, tricyclic antidepressants)
  • are known to be heart valve vitae
  • C. M. Myocardial infarction
  • apoplexy
  • Z. n. Myocarditis
  • C.P.D.
  • there are indications of alcohol, medication or drug abuse

Inspection and auscultation: During inspection and auscultation, special attention should be paid to any signs of significant cardiopulmonary disease, such as:

  • evidence of oedema
  • persistent dysrhythmia
  • any existing heart murmurs
  • Signs of hypoxia
  • Currently undergoing lung resection (soon 2019)
  • arterial hypertension (Kasper 2015)

12- channel resting ECG: These are shown here for reference:

  • persistent dysrhythmia (e.g. atrial fibrillation)
  • Delta wave (e.g. in Wolff-Parkinson-White- Syndrome)
  • Epsilon wave (e.g. in arrhythmogenic right ventricular cardiomyopathy)
  • Extension or reduction of the QT time
  • Changes to the ST line (Kasper 2015)

Long-term ECG: The long-term ECG is important for the detection of intermittent HRS and for the quantification of HRS (Herold 2020).

Event recorder: If no events can be detected in the long-term ECG with typical symptoms, the use of an event recorder is recommended, since this can also be used to record sporadically occurring HRS. Also the subjective complaints can be better assigned.

Ergometry: With the help of ergometry:

Pharmacological tests

  • Ajmalin test: e.g. in V. a. Brugada syndrome (genetically caused dysfunction of the sodium channel with ST elevations in V1 to V3 and (in-) complete right thigh block; there is a risk of sudden cardiac death [Schuster 2005])

Programmed stimulation: With programmed stimulation, the atria and ventricles can be stimulated separately.

  • atrial stimulation:
    • Detection of accessory pathways such as Mahaim's fibres, WPW syndrome, etc.
    • Determination of the refractory time of the atrium, AV nodes and any accessory pathways
    • for the diagnosis of supraventricular tachycardia
  • ventricular stimulation:
    • Detection of any accessory pathways
    • Determination of the refractory time of the ventricle, AV node and possibly existing accessory pathways
    • Checking the inducibility of hemodynamically intolerable ventricular tachycardias such as ventricular fibrillation (determination of the probability of sudden cardiac death)
    • induction of ventricular reentry tachycardia
    • His-bundle ECG with determination of the AH time (transfer time from the atrium to the His-bundle; corresponds to the conduction delay in the AV node [Baenkler 2001]) and the HV time (transfer time from the His-bundle to the chamber; corresponds to the conduction in the His-Purkinje system [Baenkler 2001])

Imaging
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Echocardiography

Echocardiography may reveal indications of functional and structural disorders (Kasper 2015).

Cardio- MRT: With the MRT it is possible to localize:

  • scarred changes of the myocardium
  • Infiltrations of the heart muscle (Kasper 2015)

Laboratory
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  • Indications of an electrolyte disturbance
  • Thyroid hormones (Large 2011)

Therapy
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Since HRS also occur in otherwise healthy individuals, there is no general need for any therapeutic measures.

However, there is a need for treatment for:

  • Impairment of haemodynamics with decreasing cardiac output and pronounced symptoms
  • already existing or imminent tachycardiomyopathy
  • in case of increased risk of sudden cardiac death, which exists in:
    • Currently in resuscitation for ventricular fibrillation with rapid ventricular tachycardia
    • Presence of ventricular arrhythmias in severe underlying myocardial disease
    • ventricular arrhythmias with simultaneous restriction of the left ventricular pump function (Herold 20120)
    • ST- lifts in V1 to V3 and (in-) complete right leg block in Brugada- Syndrome (Schuster 2005)

The treatment of HRS can be causal or symptomatic (Herold 2020).

  • Causal treatment: treatment of the underlying condition
  • symptomatic treatment:
    • General measures: In acute cases of HRS, these consist of sedation of the patient, in case of tachycardia, sedation, vagus irritation by compression, Valsalva compression, ice tie, administration of O2, etc.
    • antiarrhythmic therapy:
      • Antiarrhythmics
      • Electrotherapy
      • Catheter ablation
      • antiarrhythmic cardiac surgery (Herold 2020)

Progression/forecast
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Prognosis and course depend on the respective underlying disease, the already existing damage and the therapeutic response rate.

Literature
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  1. Baenkler H W (2001) MLP Dual Series. Internal medicine: 299 syncopations, 611 tables Thieme Verlag 190
  2. Baldes N et al (2019) Postoperative arrhythmias. Central Bl Surgeon (144) 12 - 19
  3. Frantz S (2020) Cardiac arrhythmia. Dtsch Med Weekly (145) 509
  4. Groß D et al. (2011) History of medicine in the spotlight: Contributions of the "Rheinischer Kreis der Medizinhistoriker. Volume 2 Kassel university press. 116
  5. Herold G et al (2020) Internal medicine. Herold Publishing House 262 - 273
  6. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 273.e- 1 - 273e- 7
  7. Kasper D L et al (2015) Harrison's Internal Medicine. Georg Thieme Publisher 273.e- 1 - 273e- 8
  8. Lewalter B et al (2010) Cardiac arrhythmias: Diagnosis and therapy. Springer Medicine Publishing House 2 - 5
  9. Schuster H P et al (2005) ECG course for Isabel. Thieme Publishing House 100
  10. Stierle U et al (2014) Clinical Guide to Cardiology. Elsevier Urban and Fischer 373

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 29.10.2020