Cardiac arrhythmiaI49.9

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).

Cardiac arrhythmias (HRS) are defined as cardiac activity that deviates from the norm and can be caused by stimulus generation disorders and/or conduction disorders (Kasper 2015). HRS are not fundamentally pathological; they also occur in organically healthy individuals (Herold 2020).

Bradycardic HRS always result from disturbances in stimulus formation in the area of the sinus node or from disturbances in stimulus conduction:

• between the sinus node and the right atrium (SA block)
• between AV node and ventricles(AV block)
• Disturbance in the tawara legs (Kasper 2015).

Tachycardic HRS are caused by

• increased autonomy
• Post depolarization
• Reentry (Kasper 2015)

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

HRS can have myocardial, hemodynamic, or extracardiac causes:

• myocardial causes such as:
  • coronary artery disease
  • Myocardial infarction
  • Myocarditis
  • cardiomyopathies (Herold 2020)
• hemodynamic causes such as:
  • Volume stress due to:
    • Vitiation with valvular insufficiency
    • shunt
  • Pressure loading due to:
    • arterial hypertension
    • pulmonary hypertension
    • valvular stenosis
    • stenosis of the outflow tract
    • hypertrophic obstructive cardiomyopathy (HOCM)
• extracardiac causes such as:
  • electrolyte disturbance (potassium, especially hypokalemia, calcium)
  • hyperthyroidism
  • hypoxia
  • Roemheld syndrome(functional cardiac symptoms associated with distended stomach or intestines (Gross 2011)
  • Medications (e.g. antiarrhythmics, cardiac glycosides, tricyclic antidepressants)
  • hyperreactive carotid sinus
  • psychovegetative factors
  • alcohol, drugs, caffeine, toxins (Herold 2020)
• postoperative arrhythmias after lung resection (Baldes 2019).

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).

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:
    • angina pectoris
    • Myocardial infarction
    • worsening of a pre-existing heart failure
    • generalized:
    • cardiogenic shock
    • sudden cardiac death
• 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)

The diagnostic procedure varies greatly from individual to individual. Two essential aspects for the further procedure are the medical history and the ECG (Kasper 2015).

Anamnesis: detailed anamnesis with regard to the existing symptoms.

• Drug history (especially regarding antiarrhythmics, cardiac glycosides, tricyclic antidepressants).
• are there any known valvular heart disease
• Z. n. myocardial infarction
• Z. n. apoplexy
• Z. n. myocarditis
• Z. n. cardiomyopathy
• There is evidence of alcohol, medication or drug abuse.

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

• evidence of edema
• persistent dysrhythmia
• possible presence of heart murmurs
• signs of hypoxia
• post lung resection (Baldes 2019)
• arterial hypertension (Kasper 2015)

12- channel- resting- ECG: These show here indications of:

• persistent arrhythmia (e.g. atrial fibrillation)
• Delta wave (e.g. in Wolff-Parkinson-White syndrome)
• Epsilon wave (e.g. arrhythmogenic right ventricular cardiomyopathy)
• Prolongation or shortening of the QT time
• Changes in the ST segment (Kasper 2015)

Long-term ECG: Long-term ECG is important for detecting intermittent HRS and quantifying HRS (Herold 2020).

Event recorder: If no events can be determined in the long-term ECG with typical symptoms, the use of an event recorder is recommended, since sporadically occurring HRS can also be recorded. Subjective symptoms can also be better identified.

Ergometry: With the help of ergometry:

• possible load-dependent HRS can be determined
• detect an insufficient increase in frequency (e.g. in sick sinus syndrome).

Pharmacological tests

• Ajmaline test: e.g. in case of a suspected Brugada syndrome (genetically caused functional disorder of the sodium channel with ST elevations in V1 to V3 and (in-) complete right bundle branch block; there is a risk of sudden cardiac death [Schuster 2005]).

Programmed pacing: In programmed pacing, the atria and ventricles can be paced separately.

• atrial pacing:
  • Detection of accessory pathways such as in Mahaim fibers, WPW syndrome, etc.
  • Determination of the refractory period of the atrium, AV node and possibly existing accessory pathways.
  • for diagnosis of supraventricular tachycardia
• ventricular pacing:
  • Detection of any accessory pathways
  • Determination of the refractory period of the ventricle, AV node and any accessory pathways present
  • Verification of the inducibility of hemodynamically intolerable ventricular tachycardias such as ventricular fibrillation (determination of the probability of sudden cardiac death)
  • Induction of ventricular re-entrant tachycardias
  • His bundle ECG with determination of AH time (conduction time from the atrium to the His bundle; corresponds to conduction delay in the AV node [Baenkler 2001]) and HV time (conduction time from the His bundle to the ventricle; corresponds to conduction in the His Purkinje system [Baenkler 2001])

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)

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

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)

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

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