Bradycardia: Causes of a Slow Pulse and Treatment

Bradycardia is a slow heart rate, usually less than 60 beats per minute in adults. It's important to immediately distinguish between two situations: "slow pulse without complaints" and "slow pulse with symptoms of poor circulation." [1]

In some people, bradycardia is physiological: during sleep, in trained athletes, and sometimes with high parasympathetic nervous system activity. In such cases, a slow rhythm may be normal, provided there are no fainting spells, severe weakness, shortness of breath, or chest pain. [2]

Bradycardia can be a symptom of disease if the heart's electrical system is malfunctioning, if there is a block in impulse conduction, if the myocardium is damaged, or if medications that "inhibit" the rhythm are used. In these cases, the danger is not so much related to the number of beats as to insufficient blood supply to the brain and organs. [3]

The modern approach is based on three questions: are there symptoms, is there a reversible cause, and are there indications for temporary or permanent pacing. This is the logic underlying international guidelines on bradycardia and conduction disorders. [4]

Code according to ICD-10 and ICD-11

In the International Classification of Diseases, 10th revision, bradycardia as a symptom or finding is coded as R00.1 Bradycardia, unspecified. Importantly, many causes of bradycardia have their own codes, for example, atrioventricular blocks, and then the primary cause is coded. [5]

The International Classification of Diseases, 11th revision, has separate codes for different types: for example, MC81.1 Bradycardia, unspecified and BC80.1 Sinus bradycardia. In clinical practice, this helps distinguish between "simple slow rhythm" and "sinus bradycardia." [6]

Table 1. ICD-10 and ICD-11 codes (guidelines for documentation) [7]

State	ICD-10	ICD-11
Bradycardia, unspecified	R00.1	MC81.1
Sinus bradycardia	usually R00.1 (as inclusion)	BC80.1

Epidemiology

Estimates of the prevalence of bradycardia in the general population vary widely due to different definitions and reporting methods, but a review of the global burden of bradycardia cites a range of 0.5%–2.0%. These figures refer to "bradycardia as a clinical problem" rather than to any episode of slow heart rate during sleep.[8]

When considering samples where rhythm is assessed using electrocardiograms, the proportion of "sinus bradycardia" may be higher. For example, in one 2025 study, sinus bradycardia was reported in 8.53% of 8,746 electrocardiograms, but such data cannot be automatically generalized to the entire population because the sample depends on the context of the examination. [9]

A more clinically important indicator is the incidence of "significant bradycardia," which leads to a diagnosis of bradycardia or requires treatment. Analysis of wearable device data suggests that the incidence of bradycardia may be as low as 0.89 cases per 1,000 person-years overall, and as high as 2.86 per 1,000 person-years in men aged 65-73. [10]

Sinus node dysfunction is a particular concern, being one of the main causes of symptomatic bradycardia in the elderly. Estimates of its incidence in reviews and clinical articles are approximately 0.8 cases per 1000 person-years, and an increase is expected due to the aging population. [11]

Table 2. Examples of epidemiological estimates (why the figures differ) [12]

Indicator	Grade	What exactly does it reflect?
Prevalence of bradycardia in the general population	0.5%-2.0%	"bradycardia as a clinical problem"
Sinus bradycardia according to electrocardiograms in the 2025 sample	8.53%	proportion of findings in the examined group
Frequency of bradycardia according to wearable devices	0.89 per 1000 person-years	new detections per year of observation
Frequency of sinus node dysfunction	0.8 per 1000 person-years	a disease that occurs more often in the elderly

Reasons

The causes of bradycardia are conveniently divided into physiological and pathological. Physiological bradycardia occurs during sleep and in trained individuals and does not require treatment unless there are symptoms or signs of conduction disturbances. [13]

Cardiac pathological causes include sinus node dysfunction and atrioventricular blocks. These two groups most often lead to the need for permanent cardiac pacing. [14]

A separate large group of causes are drug and toxic effects. Beta-blockers, some calcium channel blockers, digoxin, and other drugs can cause clinically significant slowing of the heart rate, especially when combined with age, conduction system diseases, and electrolyte disturbances. [15]

Finally, bradycardia can accompany systemic conditions: hypothyroidism, hypothermia, hyperkalemia, hypoxia, infectious and inflammatory processes. In such cases, treatment of the underlying cause becomes key. [16]

Table 3. Causes of bradycardia (short clinical chart) [17]

Group of reasons	Examples	What usually helps to distinguish
Physiological	sleep, endurance athletes	no symptoms, normal electrocardiography
Violation of automatism	sinus node dysfunction	pauses, weakness, fainting, age-related
Conduction disturbance	atrioventricular blocks	characteristic signs on an electrocardiogram
Medicinal and toxic	beta-blockers, digoxin	relationship with drug initiation or dose
Metabolic and systemic	hypothyroidism, hyperkalemia, hypoxia	changes in tests and clinical picture of the primary condition

Risk factors

Age is the most consistent risk factor for clinically significant bradycardia and sinus node dysfunction. Reviews emphasize that the disease is more common in older individuals and is associated with age-related wear and tear of the conduction system and associated cardiovascular diseases. [18]

Coronary artery disease, previous myocardial infarction, myocarditis, cardiomyopathy, and cardiac surgery increase the likelihood of conduction disturbances and the need for pacing. Clinically, this means that bradycardia associated with these conditions has a lower threshold for concern. [19]

Drug combinations, chronic kidney disease, diabetes, and hypertension increase the risk of drug-induced bradycardia and "mask" symptoms. Therefore, collecting a complete medication list is part of the risk assessment, not a formality. [20]

There are also "conditional" risk factors that can mimic the disease: high levels of athletic training and nocturnal episodes of bradycardia. These situations are usually harmless, but require distinguishing physiological from latent conduction pathology. [21]

Table 4. Risk factors and practical interpretation [22]

Factor	What increases	Practical conclusion
Age	risk of sinus node dysfunction and blockades	Symptom detection and monitoring are important
Cardiovascular diseases	risk of conductive disturbances	assessment for cardiac pacing is more often required
Drugs that affect rhythm	risk of iatrogenic bradycardia	a revision of therapy and interactions is needed
Electrolyte disturbances and hypoxia	risk of acute episodes	treat the cause and monitor tests
Training and sleep	"benign" bradycardia	treatment is usually not required if there are no symptoms

Pathogenesis

Bradycardia occurs either due to a decrease in the automaticity of the rhythm-setting cells or due to a disruption in impulse conduction through the conduction system. The former is most often associated with sinus node dysfunction, while the latter is associated with atrioventricular blocks of varying degrees. [23]

With sinus node dysfunction, the problem is often structural: fibrosis and degeneration of sinus tissue with age, the consequences of inflammation or ischemia. As a result, the heart sometimes fails to increase its rate under stress, and sometimes pauses occur, which causes symptoms. [24]

In impulse conduction blockades, the danger is determined not only by the frequency but also by the degree of blockade. High degrees of blockade can lead to an excessively slow "substitution" rhythm and a deterioration in the blood supply to the brain, which manifests itself in fainting and falls. [25]

A separate mechanism is drug-induced inhibition of automatism or conduction, especially when combined with several drugs and electrolyte imbalances. In such cases, correcting the underlying cause can quickly normalize the rhythm without device implantation. [26]

Symptoms

In many people, bradycardia is asymptomatic and is detected incidentally during pulse measurement or electrocardiography. In such situations, the context is typically assessed: sleep, exercise status, medications, age, and the presence of comorbidities. [27]

Symptoms appear when the heart fails to pump enough blood. The most typical symptoms include weakness, fatigue, dizziness, shortness of breath during exertion, and decreased tolerance for physical activity. [28]

Syncope or presyncope is one of the most significant symptoms because it can reflect pauses or episodes of high-grade block. In this situation, it is especially important to document the rhythm during the symptom using monitoring. [29]

Sometimes symptoms are masked: a person perceives drowsiness and weakness as "age" or "stress," but the cause turns out to be severe bradycardia due to medications or conduction disturbances. Therefore, symptoms are always assessed in conjunction with blood pressure, heart rate, and electrocardiography data. [30]

Table 5. Symptoms and red flags [31]

Manifestation	It often happens when	Why is it important?
No symptoms	physiological bradycardia	treatment is usually not required
Weakness, fatigue	sinus node dysfunction, medications	reduces the quality of life, requires finding the cause
Fainting	pauses, high-degree block	risk of injury and sudden deterioration
Chest pain, shortness of breath at rest	ischemia, heart failure	an emergency situation is possible
Confusion, cold sweat, drop in blood pressure	unstable hemodynamics	urgent help needed

Classification, forms and stages

Clinically, bradycardia is conveniently divided into sinus bradycardia, sinus node dysfunction, and impulse conduction block. This distinction is important because the prognosis and treatment differ fundamentally. [32]

Sinus bradycardia means that the rhythm remains sinus, but the rate is reduced. It can be physiological or pathological, and the key criteria are the presence of symptoms and the context. [33]

Sinus node dysfunction encompasses a spectrum of manifestations: persistent bradycardia, pauses, sinus arrest, and alternating tachycardia-bradycardia syndrome. This group is characterized by the following rule: indications for stimulation are determined by symptoms, not a fixed rate. [34]

Atrioventricular blocks are classified by degree and level, and it is the higher degrees of block that most often require cardiac pacing. Here, the electrocardiographic picture and clinical instability are more important than "simply a slow pulse." [35]

Table 6. Practical classification of bradycardia [36]

Option	What does this mean?	Typical clinical decision
Sinus bradycardia	sinus rhythm, frequency below normal	observation or treatment of the cause
Sinus node dysfunction	pauses, inability to increase heart rate, symptoms	relationship of symptoms to rhythm, discussion of stimulation
Atrioventricular block	slowing or cessation of impulse conduction	assessment of the degree of blockade, often stimulation at a high degree
Drug-induced bradycardia	effect of therapy or intoxication	revision of the regimen, treatment of intoxication
Secondary bradycardia	hypoxia, electrolytes, endocrine causes	treatment of the primary condition

Complications and consequences

The main complication of symptomatic bradycardia is reduced blood flow to the brain, leading to falls, injuries, and a reduced quality of life. Particularly dangerous are sudden pauses and episodes of high-grade block, which can manifest as sudden syncope. [37]

In some patients, prolonged, severe bradycardia can worsen heart failure because the body is not receiving the required minute volume of blood during exercise. In such cases, treatment is aimed at restoring an adequate heart rate and eliminating the underlying cause. [38]

Drug-induced bradycardia is dangerous because it is sometimes accompanied by a drop in blood pressure and conduction disturbances, especially when combined with hyperkalemia. Therefore, this "side effect" may not be a trivial matter, but rather a serious emergency. [39]

A separate problem is the incorrect choice of tactics: for example, attempting to treat physiological bradycardia with devices or, conversely, ignoring symptoms in the case of high-grade block. Current guidelines emphasize the need to link the decision to symptoms and documented rhythm disturbances. [40]

When to see a doctor

Consulting a doctor is warranted for recurring episodes of dizziness, weakness, and shortness of breath during normal activity, accompanied by a slow pulse. This is especially important for people over 65 and for those taking medications that affect heart rate. [41]

Urgent evaluation is required if syncope, presyncope, sudden severe weakness with cold sweat, or a falling heart rate accompanied by a drop in blood pressure occurs. These signs are consistent with "unstable bradycardia," which may require emergency care. [42]

Immediate medical attention is necessary for chest pain, severe shortness of breath at rest, and increasing confusion. In this situation, bradycardia may be a manifestation of myocardial ischemia, severe electrolyte imbalances, or other dangerous causes. [43]

If bradycardia occurs after a change in medication dosage or the addition of a new drug, this is also a reason to promptly contact a doctor. Often, adjusting the therapy resolves the problem without further intervention. [44]

Diagnostics

The first step is to confirm bradycardia and assess symptoms. This typically begins with measuring heart rate and blood pressure, followed by an electrocardiogram (ECG) to determine whether the rhythm is sinus and whether there is conduction block. [45]

The second step is to search for reversible causes. Practical tests often include electrolytes, thyroid function tests, oxygen status assessment, and a review of all medications and supplements. If ischemia is suspected, an assessment is performed according to cardiology protocols. [46]

The third step is to "catch the rhythm during the symptom" if the complaints are episodic. This involves 24-hour ECG monitoring, external event recorders, and, in some cases, implantable monitoring devices if the episodes are rare but dangerous. [47]

The fourth step is to assess the cardiac structure and its consequences. Echocardiography is often required, especially if there is heart failure, a previous heart attack, or suspected cardiomyopathy, because structural disease influences the choice of pacing tactics. [48]

Table 7. Step-by-step diagnostics (clinical route) [49]

Step	What are they doing?	What does this give?
1	examination, pressure, ECG	confirmation of the type of bradycardia
2	tests: electrolytes, thyroid gland, hypoxia assessment	identification of reversible causes
3	24-hour monitoring and long-term recorders	connection of symptoms with rhythm
4	echocardiography	assessment of the structure and function of the heart
5	Consultation with an arrhythmologist if a high-degree block is suspected	decision on stimulation

Differential diagnosis

Physiological sinus bradycardia in trained individuals is distinguished by the absence of symptoms and normal heart rate adaptation to exercise. In questionable situations, exercise testing and monitoring, as well as assessment of the nocturnal rhythm profile, can be helpful. [50]

Drug-induced bradycardia is characterized by a temporary relationship with the initiation of therapy, dose increases, or the combination of several drugs. Often, it is the discontinuation or replacement of one component that normalizes the rhythm. [51]

Sinus node dysfunction is important to distinguish from atrioventricular blocks because the indications for pacing and the choice of mode differ. The electrocardiogram pattern and documentation of pauses or blocks are crucial here. [52]

Finally, secondary causes such as hypothyroidism or hyperkalemia can produce marked bradycardia in the absence of primary conduction system disease. These conditions are confirmed by testing and require treatment of the underlying cause, sometimes urgently. [53]

Treatment

Treatment for bradycardia begins not with a pacemaker, but with determining whether there are symptoms and whether there is deterioration in blood circulation. If there are no complaints and the rhythm is explained by sleep or exercise, treatment is usually not required; observation and exclusion of underlying pathology in the presence of risk factors are sufficient. [54]

If symptoms are present, the first step is to eliminate reversible causes. In practice, this means reviewing medications, correcting electrolytes, treating hypoxia and endocrine disorders, and assessing myocardial ischemia if clinically indicated. This approach often allows for normalization of the rhythm without the use of devices. [55]

In the case of unstable bradycardia in an emergency, the algorithm is built around signs of poor perfusion: hypotension, altered consciousness, ischemic chest pain, and acute heart failure. Airway management, oxygen, monitoring, and rapid identification of the cause are recommended. [56]

The first-line drug for symptomatic bradycardia in adults in the advanced cardiopulmonary resuscitation algorithm is atropine: 1 milligram intravenously, repeated every 3-5 minutes for a total dose of 3 milligrams. This treatment is aimed at cases where there is a pronounced vagal component or certain types of conduction disturbances. [57]

If atropine is ineffective or the situation worsens, immediate rate-increasing measures are recommended: external electrical stimulation through the skin and/or infusions of drugs with a chronotropic effect. Algorithms specify ranges: dopamine 5-20 micrograms per kilogram per minute or epinephrine 2-10 micrograms per minute, titrated according to response. [58]

In drug intoxications, the approach is specific: for example, overdoses of beta-blockers or calcium channel blockers may require antidotes and intensive therapy, while temporary stimulation is used as a "bridge" until stabilization. In such cases, it is important to treat the cause, not just increase the frequency. [59]

In elective cardiology, the primary treatment for symptomatic sinus node dysfunction is permanent pacing when symptoms are documented to be associated with bradycardia or pauses. Bradycardia guidelines emphasize that there is no "magic" minimum rate at which pacing is indicated for everyone: the relationship to symptoms and the clinical context determine the decision. [60]

In high-degree atrioventricular blocks, the indications for pacing are usually more straightforward because of the risk of sudden pauses and an excessively slow replacement rhythm. Here, the decision is made based on the degree of block, the presence of symptoms, and concomitant structural heart disease. [61]

A separate modern section addresses the choice of pacing type and technology. Guidelines discuss physiological stimulation of the conduction system, including pacing of the His bundle and the left bundle branch, as ways to reduce the adverse effects of traditional right ventricular pacing in some patients. This refers to "new techniques" within modern electrophysiology. [62]

Another approach is leadless pacemakers, which may be considered in patients requiring single-chamber pacing and who are at high risk of device pocket infection or venous access problems. Such solutions are always individualized, taking into account the advantages and limitations of the technology. [63]

Table 8. Drugs that frequently cause or worsen bradycardia [64]

Group	Examples	Commentary for practice
Beta-blockers	metoprolol, bisoprolol	the risk is higher when combined with other "inhibitory" drugs
Non-dihydropyridine calcium channel blockers	verapamil, diltiazem	may cause conduction block
Cardiac glycosides	digoxin	risk of intoxication with decreased kidney function
Antiarrhythmic drugs	amiodarone, sotalol	pauses and blockades are possible
Potassium-increasing drugs	some treatment regimens	hyperkalemia increases conduction disturbances

Table 9. “New” stimulation technologies that are more frequently discussed in modern guidelines [65]

Technology	What is the idea?	Who is considered more often?
Bundle of His stimulation	more physiological conduction	if frequent stimulation is required and there is a risk of deterioration of left ventricular function
Left bundle branch block stimulation	an alternative with good capture parameters	when physiological stimulation is indicated
Leadless pacemaker	no pocket or in-water electrodes	high risk of infection, venous access problems

Prevention

Prevention of clinically significant bradycardia largely coincides with the prevention of heart disease: control of blood pressure, diabetes, smoking cessation, and correction of risk factors for coronary heart disease. This reduces the likelihood of structural causes of rhythm and conduction disturbances. [66]

The second level of prevention is the safe administration of rhythm-modifying medications. Regular pulse monitoring and electrocardiography, especially with increasing doses and drug combinations, helps prevent drug-induced bradycardia. [67]

The third level is prevention of complications through early detection. For people with episodic syncope and suspected rare pauses, a monitoring strategy is important because early diagnosis prevents injury and recurrent syncopal episodes. [68]

Finally, for some patients, correction of concomitant conditions, such as sleep apnea, is important. Guidelines emphasize that treatment of sleep apnea can reduce nocturnal bradycardia and the need for pacing, unless otherwise indicated. [69]

Forecast

The prognosis for bradycardia depends on the cause and the presence of symptoms. Physiological sinus bradycardia in a healthy person usually has a favorable prognosis and does not require treatment. [70]

In sinus node dysfunction, life prognosis is often determined by comorbid cardiovascular diseases, and symptoms and risk of falls are usually well controlled with continuous cardiac pacing. The effect of pacing is particularly noticeable in the reduction of syncope and improvement in exercise tolerance. [71]

In high-grade atrioventricular blocks, timely pacing significantly reduces the risk of syncope and sudden pauses. In this group, early diagnosis is important because symptoms may be subtle, but the risk remains high. [72]

If the cause of bradycardia is reversible, such as drug- or metabolic-related, the prognosis is usually good with correct treatment. Therefore, accurate diagnosis of the cause is actually part of the prognosis, not a separate "formality." [73]

FAQ

Is bradycardia normal?
Yes, during sleep and in trained individuals, the heart rate can be less than 60 beats per minute without clinical problems if there are no symptoms. [74]

What rate is considered dangerous?
Danger is determined not by a single number, but by symptoms of poor perfusion and the type of abnormality on the electrocardiogram. In sinus node dysfunction, guidelines emphasize that there is no fixed "minimum" rate for deciding on pacing. [75]

What should you do if bradycardia develops while taking medications?
You should contact your doctor to review your medication, as discontinuing or adjusting the dose often resolves the issue. Severe weakness, fainting, or a drop in blood pressure require immediate medical attention. [76]

Does everyone with bradycardia need a pacemaker?
No, pacing is indicated for certain conduction disturbances and/or a proven connection between symptoms and bradycardia or pauses, as well as for high-grade heart blocks. The decision depends on the electrocardiogram and clinical examination. [77]

How are dangerous episodes confirmed if they are rare?
Long-term monitoring is used: 24-hour recorders, event recorders, and sometimes implantable monitors to record the rhythm during the symptom. [78]

Key points from guidelines and expert opinions

Professor Fred M. Kusumoto, MD, a cardiologist and electrophysiologist at Mayo Clinic, and co-authors of the American College of Cardiology, American Heart Association, and Heart Rhythm Society guidelines formulate the principle for sinus node dysfunction as follows: “There is no established minimum threshold for rate or pause duration at which continuous pacing is indicated for all.” Translation into Russian. [79]

A review of the key points of the same guideline emphasizes the position on nocturnal bradycardia: “for sleep-related bradycardia, continuous pacing is not performed unless otherwise indicated; treatment of sleep apnea often resolves the problem.” Translation into Russian. [80]

Professor Michał Glikson, cardiologist and electrophysiologist, Shaare Zedek Medical Center, and co-authors of the European Society of Cardiology guidelines indicate that the most common indications for a permanent pacemaker are “sinus node dysfunction and high-grade atrioventricular block.” Translation into Russian. [81]

The American Heart Association's algorithm for managing symptomatic bradycardia emphasizes that in the case of instability, protocol should be followed, with atropine used as a first-line agent, followed by external stimulation and infusion chronotropic support if ineffective. Translation of the algorithm into Russian. [82]

Table 10. Summary of theses from the guidelines [83]

Thesis	Source
The decision to permanently stimulate sinus node dysfunction requires a relationship between symptoms and bradycardia; there is no fixed rate threshold.	American College of Cardiology, American Heart Association, and Heart Rhythm Society 2018 Guidelines
In nocturnal bradycardia associated with sleep apnea, primary treatment is sleep apnea correction; stimulation is usually not needed without other indications.	A review of key points from the American College of Cardiology guidelines
The main indications for a permanent pacemaker are sinus node dysfunction and high-grade atrioventricular block.	European Society of Cardiology Guidelines 2021
In case of unstable bradycardia, an emergency care algorithm with atropine and possible external stimulation is used.	American Heart Association 2025 Algorithm