Arrhythmias - classification, causes and mechanisms of origin, circulatory consequences

Under construction / Forgotten

This article was marked by its author as Under construction, but the last edit is older than 30 days. If you want to edit this page, please try to contact its author first (you fill find him in the history). Watch the discussion as well. If the author will not continue in work, remove the template {{Under construction}} and edit the page. Last update: Wednesday, 21 Jan 2026 at 4.15 pm.

This article doesn't meet WikiLectures quality standards.

This article seems to not fulfill most of the items on our Editorial Process checklist. As such, it's going to be deleted soon. To the author of this article: if you still work on this article, make sure to replace this template with the Under construction template. However, be aware that if you don't make any changes to the article after that soon enough, the article will still be deleted. To find out what you need to do to improve this article, read Help:Editorial process. Feel free to ask for help on Forum:Support. To see how articles on WikiLectures should look like, check out articles in Category:Finished articles. For more information, contact the user who inserted this template, you can find them in the Page History (under the "Actions" button).

Arrhythmias (Dysrhythmias) – Disorders of Cardiac Rhythm

Clinical Presentation

From a symptomatic point of view, arrhythmias may present as:

• The patient perceives irregular heartbeats (palpitations), sometimes a sensation of acceleration, sometimes skipped beats; occasionally accompanied by weakness or presyncope.
• Recurrent loss of consciousness with absence of pulse, followed by spontaneous recovery.
• Sudden collapse with loss of consciousness, pulselessness, apnea, leading to death without immediate assistance.
• A young, otherwise healthy individual may occasionally perceive transient irregularity of heart rhythm.

Arrhythmias range from benign conditions to immediate life-threatening states.

---

Basic Diagnostic Evaluation

• ECG
• Long-term ECG monitoring (Holter monitoring)

Further diagnostic approach:

1. Identify and classify the type of arrhythmia
2. Search for the underlying cause
3. Treat both the arrhythmia and its cause

---

Main Causes of Cardiac Rhythm Disturbances

1. Autonomic Nervous System

• Sympathetic nervous system:
  • Increases heart rate and conduction velocity (sinus tachycardia)
  • Increases myocardial excitability → higher arrhythmia risk
• Parasympathetic nervous system:
  • Slows heart rate and conduction
  • Excessive vagal stimulation may cause syncope
• Drugs affecting the ANS:
  • Adrenaline – increases heart rate
  • Atropine – blocks acetylcholine
  • Beta-blockers – slow heart rate

---

2. Structural and Functional Myocardial Disorders

Any myocardial disease may cause arrhythmias:

• Ischemia, hypoxia, acidosis (ischemic heart disease), reperfusion injury
• Mechanical stress of myocytes: hypertrophy, marked dilation, cardiomyopathy
• Fibrosis, amyloidosis, post-infarction scar → electrical remodeling
• Inflammation (myocarditis)

---

3. Electrolyte Disorders

• Renal failure → hyperkalemia
• Increased mineralocorticoid activity → hypokalemia

---

4. Drugs and Toxic Influences

• Antiarrhythmic drugs
• Digitalis (prolongation of AV conduction)

---

5. Genetic Causes

• Mutations of ion channels

---

---

Mechanisms of Arrhythmia Development

Reentry

• Micro- or macro-reentry: circulating excitation
• Two pathways connected proximally and distally with different conduction properties (e.g., ischemia, fibrosis)
• Unidirectional conduction block in one pathway with retrograde conduction via an accessory pathway
  • Typical example: Wolff–Parkinson–White syndrome
• Frequently located in the AV node region
• Classic predisposition: accessory AV pathways in preexcitation syndromes

---

Increased Automaticity (Abnormal Automaticity)

• Disturbance of impulse generation
• Increased slope of phase 4 of the action potential
  • Influenced by autonomic tone, ions, ischemia
• Slowed in the SA node → bradycardia
• Accelerated in other regions → ectopic pacemakers, altered threshold potential

---

Triggered Activity

• Cyclic spontaneous depolarization of myocardium
• Membrane potential instability with repeated depolarization and repolarization without conduction system input
• Caused by abnormal repolarization
• Triggered by a preceding action potential

1. Early Afterdepolarizations (EAD)

• Occur before completion of repolarization (phase 3)
• Due to reopening of Na⁺ and Ca²⁺ channels
• Associated with long QT syndrome
• QT interval prolongation; clinically relevant QT dispersion
• QT corrected for heart rate: QTc = QT / √RR
• Acquired causes:
  • Electrolyte disturbances (hypokalemia, hypomagnesemia, hypocalcemia)
  • Drugs (antiarrhythmics, tricyclic antidepressants, antibiotics)
• Typical arrhythmia: torsades de pointes

---

2. Delayed Afterdepolarizations (DAD)

• Occur after repolarization
• Caused by excessive intracellular calcium leading to Na⁺ channel activation
• Occur in:
  • Tachycardia
  • Catecholamine stimulation
  • Digitalis toxicity
  • Ischemia
• Occur during the vulnerable period (transition between phases 3 and 4)
• On ECG: descending limb of the T wave
  • Extrasystole during this phase may trigger ventricular fibrillation (R-on-T phenomenon)

---

Conduction Disturbances

• Conduction velocity depends on the slope of phase 0 of the action potential
• Lower resting membrane potential reduces sodium channel activation and slows conduction

---

Congenital Channelopathies

• Romano–Ward syndrome – autosomal dominant
• Jervell–Lange–Nielsen syndrome – more severe, associated with deafness

---

Consequences of Arrhythmias

1. Benign, clinically insignificant
2. Marker of underlying disease (e.g. ischemia)
3. Electrical instability → progression of arrhythmias
4. Hemodynamic consequences
   • Excessively fast or slow heart rate impairs cardiac output
   • High heart rate → shortened diastole → decreased cardiac output
5. Impaired myocardial perfusion and metabolism
   • Very high heart rate shortens diastole → reduced coronary perfusion

---

Classification of Arrhythmias

1. According to Clinical Manifestation

• Bradycardia – regular, < 60 bpm
• Tachycardia – regular, > 100 bpm
• Bradyarrhythmia – irregular
• Tachyarrhythmia – irregular

---

2. According to Site of Origin

• Sinus
• Supraventricular – atrial and junctional
• Ventricular – AV node or ventricles

---

3. According to Pathogenetic Mechanism

• Disorders of impulse formation
• Disorders of impulse conduction
• Combined mechanisms

---

Arrhythmias in Childhood

• Common; usually benign in structurally normal hearts
• Normal rhythm in children:
  • Sinus rhythm
  • Sinus (respiratory) arrhythmia due to vagal tone changes during respiration

Physiological Dysrhythmias in Children

• Escape junctional rhythm due to vagotonia
  • During sleep in 19% of newborns and 45% of children
• Second-degree AV block
  • During sleep in 11% of healthy children
• Atrial extrasystoles – 14% of healthy infants
• Ventricular extrasystoles – 10–20% of children
  • Rare, uniform, isolated, disappear during exercise

---

Bradyarrhythmias in Childhood

• Sinus node dysfunction (vagotonia, hypothyroidism, drugs, postoperative states)
• Sinoatrial block
• Atrioventricular block (congenital, postoperative, postinflammatory)

---

Most Common Pediatric Arrhythmias

• Supraventricular arrhythmias

---

Therapeutic Interventions in Arrhythmias

Modulation of Autonomic Nervous System

• Vagal maneuvers (increase parasympathetic tone):
  • Carotid sinus massage
  • Valsalva maneuver
  • Ocular pressure
  • Diving reflex
• Drugs:
  • Sympatholytics (beta-blockers)
  • Sympathomimetics (adrenaline)
  • Parasympatholytics (atropine)

---

Pharmacological Treatment

• Antiarrhythmic drugs
• Beta-blockers
• Agents affecting ion channels

---

Electrical Therapy

• Defibrillation – termination of chaotic electrical activity, spontaneous restoration of sinus rhythm
• Implantable cardioverter-defibrillators (ICD)
• Cardioversion – treatment of atrial fibrillation or flutter
• Cardiac pacing

---

Other Treatment Options

• Catheter ablation
• Surgical treatment (e.g. elimination of accessory pathways)

Sources

Pathophysiology lectures 1.LK UK

Literature

• NEČAS, Emanuel, et al. Obecná patologická fyziologie. 1. edition. Karolinum, 2000. 380 pp. pp. 380. ISBN 80-246-0051-X.