Cardiac rhythm and conduction disorders: main types and diagnostics

Cardiac arrhythmias and conduction disorders are a general term for conditions in which electrical impulses in the heart originate inappropriately, travel along altered pathways, or are blocked. These include "too fast" rhythms of supraventricular and ventricular origin, "too slow" rhythms due to abnormalities in the nodes and bundles of the conduction system, and combined forms. Clinical significance varies: from incidental findings to life-threatening episodes that can lead to syncope, heart failure, and sudden death. Therefore, the approach to diagnosis and treatment is based not on a general arrhythmia but on the specific type and mechanism. [1]

The current strategy encompasses four parallel goals: reducing symptoms (palpitations, irregular heartbeats, shortness of breath), preventing complications (e.g., stroke in atrial fibrillation), reducing the risk of malignant arrhythmias, and improving quality of life and life expectancy. This is achieved through a combination of non-pharmacological measures, medications, catheter-based interventions, and, when indicated, implantable devices (pacemakers, cardiac resynchronization therapy systems, cardioverter-defibrillators). The choice is always individualized and depends on the type of arrhythmia, comorbidities, and patient preferences. [2]

In recent years, ablation technologies (targeted "switching off" arrhythmogenic foci) have advanced significantly. Along with traditional radiofrequency and cryoenergy, pulsed electric field ablation has emerged, which operates non-thermally and demonstrates a favorable safety profile in a number of situations. At the same time, "physiological stimulation" of the conduction system is developing—capture of the His bundle or the left bundle branch block—which helps maintain coordinated ventricular function and prevent cardiomyopathy caused by frequent right ventricular stimulation. [3]

It's important to understand that some rhythm disturbances are markers of other problems: high blood pressure, excess weight, sleep apnea, thyroid disease, previous myocarditis, or ischemia. Therefore, diagnosis always includes identifying and correcting the causes and risk factors—this reduces the frequency of attacks and allows for the use of fewer medications. [4]

Code according to ICD-10 and ICD-11

Coding helps to correctly record a diagnosis, plan treatment and keep statistics. In the International Classification of Diseases, Tenth Revision, rhythm and conduction disorders are divided into sections I44-I49: these include atrioventricular blocks, bundle branch block and fascicle block, pre-excitation syndromes, paroxysmal tachycardias, atrial fibrillation and flutter, and "other arrhythmias." A specific code is selected based on the clinical form and electrocardiographic features (e.g., I44.2 - complete atrioventricular block, I48 - atrial fibrillation and flutter, I47.1 - supraventricular tachycardia, I47.2 - ventricular tachycardia, I45.4 - nonspecific intraventricular block). [5]

The International Classification of Diseases, Eleventh Revision, uses more detailed categories: "Supraventricular arrhythmia," "Ventricular arrhythmia," "Conduction arrhythmia," and "Atrioventricular junction arrhythmia." This allows for more precise phenotype specification (e.g., supraventricular tachyarrhythmia, premature depolarizations, various types of block), which improves the accuracy of reporting and better aligns with modern treatment approaches. [6]

Table 1. Frequently used codes (approximate correspondences; the final choice depends on the ECG and the clinic)

Clinical category	ICD-10 (example)	ICD-11 (example)
Atrial fibrillation and flutter	I48 (with clarifications by type)	BC81 "Supraventricular tachyarrhythmia" and subcategories
Supraventricular tachycardia	I47.1	BC81 and the corresponding clarifying headings
Ventricular tachycardia	I47.2	BC70-BC7Z "Ventricular arrhythmias"
Atrioventricular blocks	I44.0-I44.3	BC63 "Conduction Disturbances"
Nonspecific intraventricular block	I45.4	BC63 "Conduction Disturbances"

Epidemiology

The prevalence of atrial fibrillation, the most common sustained tachyarrhythmia, is increasing as the population ages and detection rates improve. According to global estimates, more than 52 million people were living with atrial fibrillation and flutter in 2021, approximately one and a half to two times higher than in the 1990s. This increase is explained by demographics and improved diagnostics: age-standardized rates remain relatively stable. [7]

Frequent atrial extrasystoles are more than just "harmless interruptions": high levels of them are associated with a two- to three-fold increase in the risk of developing atrial fibrillation, stroke, and even overall mortality. This doesn't mean that any single "glitch" is dangerous, but multiple episodes require monitoring and risk factor correction. [8]

Ventricular extrasystoles are also common. In people without structural heart disease, they are often benign, but with significant stress, they can be associated with deterioration of left ventricular function and an increased risk of other arrhythmias. In people with cardiomyopathy or coronary artery disease, ventricular arrhythmias are a significant predictor of sudden death. [9]

Prevalence estimates vary by method: a brief electrocardiogram (ECG) detects less than 24-hour monitoring or long-term recorders. Wearable devices and automated analysis algorithms contribute to detection rates, which is particularly noticeable in subclinical forms. [10]

Table 2. Epidemiological landmarks

Indicator	Current estimated data
The number of people with atrial fibrillation/flutter in the world	≈ 52-60 million (growth from 1990 to 2021)
Annual incidence of atrial fibrillation/flutter	≈ 4.5 million new cases (2021)
The relationship between atrial extrasystoles and the risk of fibrillation	2-3 times increased risk with high load
The role of monitoring	Long-term observation increases the detection of subclinical forms

Reasons

Causes are divided into "electrical" (automatism, trigger activity, reentry circuits) and "structural" (inflammation, ischemia, fibrosis, chamber dilation). Fibrosis and atrial distension create an environment for persistent tachyarrhythmias and facilitate their maintenance. This explains why blood pressure and weight control, and sleep apnea treatment, reduce the frequency of attacks. [11]

Predisposing factors include thyroid disease, electrolyte imbalances (low potassium and magnesium), stimulant use (large doses of caffeine, some cold and allergy medications), and alcohol. In some patients, the trigger is acute inflammation or myocarditis, including after viral infections. [12]

Ventricular arrhythmias are often associated with coronary artery disease and cardiomyopathy. Here, the danger is determined by the risk of sudden death and the presence of scar tissue, where reentry pathways occur. This mechanism requires a different approach—from beta-blockers and, when indicated, amedarone to catheter ablation and implantation of a cardioverter-defibrillator. [13]

Conduction disturbances (atrioventricular and intraventricular blocks) arise due to age-related changes, previous surgeries, inflammatory or infiltrative diseases, and drug effects. Sometimes they are reversible (for example, with drug-induced bradycardia), but often require constant stimulation. [14]

Risk factors

Non-modifiable risk factors include age and family history. The older a person is, the higher the likelihood of both tachyarrhythmias and heart blocks. A family history of atrial fibrillation or syncope due to conduction disturbances increases the individual risk. [15]

Modifiable factors include high blood pressure, excess body weight, diabetes, sleep apnea, alcohol abuse, high doses of caffeine and stimulants, chronic stress, and sleep deprivation. Correcting these factors is an integral part of treatment: without it, medications and procedural methods are less effective. [16]

For ventricular arrhythmias, the key factors remain a history of myocardial infarction, heart failure, and structural cardiomyopathy. The risk is also increased by certain drugs that prolong the electrical recovery of the heart and can provoke torsades de pointes. Therefore, it is important to evaluate potential interactions with any new therapy. [17]

Finally, a portion of rhythm disturbances are triggered by acute factors: dehydration, fever, significant electrolyte imbalances, and surgical stress. Timely correction of these factors often eliminates attacks without the need for long-term antiarrhythmic medications. [18]

Table 3. Risk factors and what to do about them

Factor	How does it affect	What helps?
Age, heredity	Increases the likelihood of arrhythmias and blockades	Regular check-ups and ECG screening as indicated
High blood pressure, overweight, diabetes	Remodeling of the atria and ventricles	Blood pressure and weight control, metabolic control
Sleep apnea	Destabilization of electrical activity	Diagnosis and treatment of sleep apnea
Alcohol, stimulants, lack of sleep	Increase ectopic activity	Sleep restriction and hygiene

Pathogenesis

Tachyarrhythmias are based on three mechanisms. The first is increased automaticity, when cells themselves generate frequent impulses (for example, in atrial foci). The second is triggered activity, associated with "delayed" depolarization of cells after the main contraction. The third is re-entry, when the impulse "goes in circles" due to conduction inhomogeneities and refractoriness. Understanding the mechanism helps in choosing treatment: medications better suppress automaticity and triggers, and ablation more effectively "breaks" re-entry circles. [19]

Conduction disturbances are caused by damage to the conduction structures—the atrioventricular node, the bundle of His, its branches, and fascicles. With frequent right ventricular occlusion, "induced" cardiomyopathy can develop: the ventricles contract uncoordinatedly, and pumping function decreases over time. This triggers the development of physiological stimulation—the occlusion of the bundle of His or the left bundle branch, which restores synchrony. [20]

Atrial extrasystoles and other forms of ectopia alter the electrical environment of the atria: multiple "early" impulses promote remodeling and increase susceptibility to atrial fibrillation. Therefore, in some patients, combating triggers and managing risk factors reduces not only symptoms but also long-term risks. [21]

Ventricular arrhythmias in ischemic heart disease are more often maintained in scar tissue, where slow pathways and unilateral conduction blocks develop. Here, mechanistic treatment—targeted ablation and device therapy—takes center stage, and drug selection is subordinated to safety. [22]

Symptoms

Symptoms depend on the frequency and duration of episodes, as well as the condition of the myocardium. Typical complaints include palpitations, "thumps" or "drops" in the chest, shortness of breath during exertion, weakness, dizziness, and occasional fainting. Sometimes the only symptoms are anxiety and avoidance of activity. In some people, arrhythmias are asymptomatic and are detected during a random recording. [23]

With rapid supraventricular rhythms, sudden attacks of palpitations and shortness of breath are more common; prolonged high rates can lead to reversible "tachycarditis-induced" left ventricular dysfunction. With ventricular tachycardias, severe weakness, presyncope, and syncope are possible. This requires urgent evaluation. [24]

With bradycardia and heart blocks, the symptoms are different: fatigue, decreased exercise tolerance, brain fog, episodes of blurred vision, or brief loss of consciousness. Sometimes patients notice a rare, intermittent pulse. If the conduction system is severely damaged, implantation of a pacemaker is required. [25]

Some symptoms are triggered by factors such as alcohol, sleep deprivation, fever, and electrolyte imbalances. Identifying these factors and keeping a diary of episodes helps to more accurately tailor the treatment plan during the consultation. [26]

Table 4. Symptoms and possible forms

Symptom	What to think about	What to check
Sudden rapid heartbeat	Supraventricular tachycardia	Electrocardiogram, Holter
"Dips", tremors	Atrial or ventricular extrasystoles	Holter, electrolytes, thyroid
Dizziness, fainting	High blockades, ventricular tachycardia	Electrocardiogram, echocardiography, if indicated - hospitalization
Shortness of breath with rapid pulse	Tachycarditis-induced dysfunction	Echocardiography, discussion of debulking/ablation

Forms and stages

Based on their origin, a distinction is made between supraventricular (atrial and nodal) and ventricular arrhythmias. The former include atrial fibrillation and flutter, focal atrial tachycardia, and atrioventricular reciprocating tachycardia. The latter include ventricular tachycardia and ventricular fibrillation. Conduction disturbances are considered separately: atrioventricular and intraventricular blocks. [27]

Depending on the course of the disease, there are paroxysmal (attack-like), persistent (long-term), and permanent forms. For example, atrial fibrillation can be paroxysmal, persistent, or permanent; this determines the choice between rate control, rhythm control, and ablation. [28]

Severity ranges from asymptomatic to hemodynamically unstable conditions requiring emergency care. The importance of staging is that early intervention in symptomatic forms can prevent remodeling and deterioration of cardiac function. [29]

Blocks are classified into degrees and levels of damage (node, His bundle, branches). High degrees of atrioventricular block and severe intraventricular conduction disturbances with symptoms are indications for pacemaker implantation or resynchronization therapy in patients with heart failure. [30]

Complications and consequences

Atrial fibrillation is associated with an increased risk of stroke and heart failure. Stroke risk assessment and timely administration of anticoagulants are essential, regardless of the chosen rhythm or rate control strategy. Insufficient rate control can lead to chamber dilation and decreased ejection fraction. [31]

Frequent atrial extrasystoles accelerate the "electrical aging" of the atria and increase the likelihood of transition to fibrillation. This is confirmed by observational studies and meta-analyses; therefore, with a high burden of extrasystoles, it is important to identify the causes and reduce their impact. [32]

Ventricular arrhythmias associated with structural heart disease are a major factor in sudden death. Proper risk stratification determines who requires beta-blockers, who requires ablation, and who requires implantable cardioverter-defibrillator (ICD) to terminate dangerous episodes. [33]

With chronic right ventricular imposition without synchronization, "induced" cardiomyopathy is possible. To avoid this, if long-term stimulation is necessary, physiological methods are considered—bundle of His or left branch block capture, and, in cases of heart failure, resynchronization therapy. [34]

When to see a doctor

Reasons for a routine visit include recurring episodes of heart palpitations, irregular heartbeats, and decreased exercise tolerance, especially if they are associated with triggers (alcohol, lack of sleep) and disrupt daily life. Even if you are young and consider yourself healthy, such symptoms warrant a basic assessment. [35]

Immediate medical attention is required for chest pain, severe shortness of breath, presyncope, fainting, or a very slow pulse accompanied by dizziness. These symptoms may indicate dangerous rhythm or conduction disturbances and require urgent diagnosis. [36]

If you have already been diagnosed with atrial fibrillation, it is important to discuss the need for anticoagulation and monitor your tolerability. Any bleeding, rash, progressive weakness, cough, or shortness of breath while taking amedarone are reasons for an unscheduled visit with your doctor. [37]

After implantation of devices (pacemaker, cardioverter-defibrillator), regular follow-up visits should be made and immediate medical attention should be sought if fever, redness in the pocket area, shock episodes, or new symptoms occur. [38]

Diagnostics

The first step is a resting electrocardiogram: it shows the heart rate, the width of ventricular complexes, the presence and shape of atrial activity, and the relationship between the atria and ventricles. If episodes are rare, 24-hour monitoring or long-term event recorders are prescribed, as well as wearable devices with confirmation by a clinician. [39]

Laboratory tests help identify reversible causes: electrolytes (potassium, magnesium), thyroid function, and inflammatory markers if myocarditis is suspected. A medication review is also conducted: certain medications and their combinations can provoke rhythm disturbances or prolong the cardiac electrical recovery. [40]

Echocardiography assesses the size and function of the chambers, the condition of the valves, and the presence of areas of hypokinesia. This influences the choice of tactics: with a reduced ejection fraction, one approach will be taken, while with a normal ejection fraction, another will be taken. For ventricular arrhythmias and before ablation, in-depth imaging and electrophysiological studies are used to precisely map "weak spots." [41]

Current guidelines emphasize the importance of risk stratification: some patients require observation and lifestyle modifications, some require medication, some require ablation, and some require device therapy. This helps avoid excessive drug therapy and promptly utilize proven methods. [42]

Table 5. Diagnostics: what, why and when

Method	What does it show?	When it is especially useful
Resting electrocardiogram	Rhythm type, conductivity, width of complexes	Any complaints of irregular heartbeats and palpitations
Holter and recorders	Arrhythmia burden and relationship with symptoms	Rare episodes, treatment evaluation
Laboratory tests	Electrolytes, hormones, inflammation	Search for reversible causes
Echocardiography	Structure and function of the heart	Choice of tactics for tachy- and bradyarrhythmias
Electrophysiological study	Mechanism and localization of foci	Ablation planning, complex cases

Differential diagnosis

The physician's task is to understand "where the roots are." Narrow ventricular complexes most often indicate a supraventricular origin, while wide ones indicate a ventricular origin or conduction with aberration. The shape and position of the atrial waves relative to the ventricular complexes are important: with rhythms originating from the atrioventricular junction, atrial waves may be retrograde and located after the complex, and with focal atrial tachycardias, they may have an atypical shape. [43]

Atrial fibrillation is distinguished by the absence of organized atrial waves and irregular intervals; atrial flutter is distinguished by "sawtooth" waves with typical conduction relationships. When in doubt, maneuvers affecting the atrioventricular node and recording in additional leads are helpful. [44]

Broad complexes require the exclusion of ventricular tachycardia, a dangerous condition, especially in structural heart disease. Here, the "dissociation" of the atria and ventricles, morphological criteria, and clinical context are taken into account. In the case of patient instability, diagnostic subtleties take a back seat—the most important thing is to quickly restore hemodynamics. [45]

Conduction disturbances are differentiated by the level of block and their impact on symptoms. For example, isolated right bundle branch block without symptoms often requires no intervention, whereas high degrees of atrioventricular block and severe ventricular asynchronousness require device therapy. [46]

Treatment

Non-pharmacological measures. The basic level is addressing risk factors: monitoring blood pressure and body weight, treating sleep apnea, limiting alcohol and stimulants, and practicing good sleep hygiene. For a significant proportion of people, this is sufficient to reduce the frequency and severity of episodes. When indicated, vagal maneuvers are taught to terminate certain types of supraventricular tachycardia. [47]

Medications. Beta-blockers or non-dihydropyridine calcium channel blockers are used to control the rate of rapid supraventricular rhythms. For rhythm control in selected patients without significant structural heart disease, drugs of the "fast sodium channel blocker" class (e.g., flecainide, propafenone) are used. For structural heart disease and ventricular arrhythmias, amedarone is used when indicated; sotalol is used with electrical recovery interval monitoring. Safety, electrolyte monitoring, and drug interaction assessment are important. [48]

Anticoagulants. In atrial fibrillation, the decision on anticoagulation is based on the stroke risk score; direct oral anticoagulants are preferable to classic vitamin K antagonists in most patients (except for mechanical valves and significant mitral stenosis). The choice of anticoagulant and dose depends on renal function, age, body weight, and concomitant medications. [49]

Catheter ablation. For symptomatic atrial fibrillation and a number of other supraventricular tachycardias, ablation is an effective method that is often superior to drug therapy for symptom control. Radiofrequency and cryoballoon technologies are available; the choice depends on the center's anatomy and experience. Newer pulsed electric field ablation technology demonstrates non-inferior efficacy compared with thermal methods and potentially lower risk of damage to adjacent structures; data are accumulating rapidly. For ventricular tachycardias, ablation of scar zones improves rhythm control and reduces the number of cardioverter-defibrillator discharges. [50]

Implantable devices. For symptomatic bradycardia and high-grade heart blocks, a pacemaker is used. "Physiological stimulation"—capture of the His bundle or left bundle branch block—is increasingly being discussed, which helps maintain or restore ventricular synchrony. In patients with heart failure and asynchronous contraction, resynchronization therapy is used. For the prevention of sudden death at high risk, a cardioverter-defibrillator is used. In certain clinical scenarios, leadless pacemakers are used. [51]

Table 6. Comparison of treatment methods

Target	Medicinal tactics	Procedural alternative
Relieve symptoms of supraventricular tachycardia	Frequency control, during selection - rhythm control	Catheter ablation
Preventing stroke in atrial fibrillation	Direct oral anticoagulants	Left atrial appendage occlusion in selected cases
Control of ventricular arrhythmias in structural disease	Beta-blocker, amedarone according to indications	Ablation, cardioverter-defibrillator
Symptomatic bradycardia/blocks	Medicines are limited	Pacemaker, physiological stimulation

Table 7. Safety of key antiarrhythmic drugs (what to monitor)

Preparation	Before the start	At the start	In dynamics
Flecainide/propafenone	Rule out structural disease (echo), electrocardiogram	Medical supervision	Electrocardiogram and symptoms
Sotalol	Electrocardiogram, potassium, magnesium, kidney function	Monitoring the electrical recovery interval	Outpatient electrocardiogram monitoring
Amedarone	Thyroid gland, liver, electrocardiogram	Load mode under control	Periodic monitoring of the thyroid gland, liver; assessment of the lungs if symptoms occur

Table 8. Ablation technologies: what are the differences?

Energy	Principle	Potential benefits	Comments
Radiofrequency	Thermal coagulation	Versatility, flexibility	Requires caution near risk structures
Cryoballoon	Freezing	Standardized applications	Features of approaches and anatomy
Pulsed electric field	Non-thermal electroporation	Selectivity to myocardium, short procedure time	Data accumulates quickly, selection by center and anatomy

Prevention

The foundation of prevention is risk factor management. Maintain a healthy weight, control blood pressure, avoid excess alcohol, and limit stimulants. Treat sleep apnea if diagnosed. These steps reduce the burden of arrhythmia and improve the results of any other therapy. [52]

Practice good sleep hygiene and breathing techniques to reduce stress. Moderate-intensity physical activity strengthens the cardiovascular system and has a beneficial effect on the heart's electrical stability. If you have symptoms, keeping a diary of your triggers can be helpful. [53]

Monitor electrolytes when taking diuretics and inform your doctor about all medications and supplements to avoid unwanted interactions and excessive prolongation of electrical recovery. [54]

If you are diagnosed with atrial fibrillation, discuss with your doctor not only rhythm or rate control, but also stroke prevention, which is carried out regardless of the antiarrhythmic strategy chosen. [55]

Forecast

The prognosis depends on the type of arrhythmia, its frequency, the presence of structural heart disease, and the quality of risk factor control. Many people with rare episodes and no structural pathology have a favorable prognosis. Proper lifestyle modification and adjustments to triggers often reduce the need for medications. [56]

In atrial fibrillation, the prognosis is largely determined by stroke prevention and the effectiveness of the chosen strategy—whether medications or ablation. Early referral for ablation in appropriate cases improves symptom control and reduces the risk of progression. [57]

For ventricular arrhythmias, the key factors are the risk of sudden death and the presence of myocardial scarring. Here, timely stratification and, when indicated, implantation of cardioverter-defibrillators and ablation determine outcomes. [58]

In patients with conduction disturbances, the prognosis improves with the introduction of physiological stimulation and cardiac resynchronization therapy in patients with heart failure. These technologies help maintain synchronous ventricular function and prevent induced cardiomyopathy. [59]

Questions and Answers (FAQ)

Should all arrhythmias be treated with medication?
No. If episodes are rare and don't affect quality of life, and examination reveals no dangerous causes, observation and risk factor management are sufficient. The decision is made on an individual basis. [60]

Which is better for atrial fibrillation: pills or ablation?
In many symptomatic patients, catheter ablation is superior to medications in controlling symptoms; in others, it can be considered as an early strategy. The final choice depends on anatomy, comorbidities, and center experience. [61]

Are frequent atrial extrasystoles without underlying structural heart disease dangerous?
Often, no, but a high load of atrial extrasystoles is associated with an increased risk of atrial fibrillation and stroke. It makes sense to discuss monitoring and correcting the underlying causes. [62]

When is a pacemaker needed?
For symptomatic bradycardia and high-grade atrioventricular block. Physiological stimulation of the conduction system is increasingly being used—it better maintains ventricular coordination. [63]

How does this fundamentally new pulsed ablation differ from older methods?
It is non-thermal and more selective in targeting the myocardium, potentially reducing the risk of damage to adjacent tissues. Randomized trials have demonstrated non-inferior efficacy compared to thermal methods. The choice of technology depends on the indications and the center's experience. [64]