Bradycardia

Bradycardia (Greek βραδυκαρδία, bradykardía, "heart slowness"), in the context of adult medicine, is the resting heart rate of under 60 beats per minute, though it is seldom symptomatic until the rate drops below 50 beat/min. It may cause cardiac arrest in some patients, because those with bradycardia may not be pumping enough oxygen to their heart. It sometimes results in fainting, shortness of breath, and if severe enough, death.^[1]

Trained athletes or young healthy individuals may also have a slow resting heart rate (e.g. professional cyclist Miguel Indurain had a resting heart rate of 28 beats per minute).^[2] Resting bradycardia is often considered normal if the individual has no other symptoms such as fatigue, weakness, dizziness, lightheadedness, fainting, chest discomfort, palpitations or shortness of breath associated with it.

The term relative bradycardia is used in explaining a heart rate which although not actually below 60 beats per minute still is considered too slow for the individual's current medical condition.

Definition

Bradycardia in an adult is any heart rate less than 60 beats per minute, although symptoms usually manifest only for heart rates less than 50.^[3]

Classification

Atrial

Atrial bradycardias come in three different types. The first is respiratory sinus arrhythmia.. This is usually found in young and healthy adults. Heart rate increases during inhalation and decreases during exhalation. This is thought to be caused by changes in the vagal tone during respiration.^[4] If the decrease during exhalation drops the heart rate below 60bpm on each breath, this type of bradycardia is usually deemed benign and a sign of good autonomic tone.

Sinus bradycardia is a sinus rhythm of less than 60 bpm. It is a common condition found in both healthy individuals and those who are considered well conditioned athletes. Studies have found that 50 - 85 percent of conditioned athletes have benign sinus bradycardia, as compared to 23 percent of the general population studied.^[5] The reason for this is that their heart muscle has become conditioned to have a higher stroke volume and therefore requires fewer contractions to circulate the same volume of blood.^[4]

Sick sinus syndrome covers conditions that include severe sinus bradycardia, sinoatrial block, sinus arrest, and bradycardi-tachycardia syndrome (atrial fibillation, flutter, and paroxysmal supraventricular tachycardia).^[4]

Atrioventricular nodal

An atrioventricular nodal bradycardia or AV junction rhythm is usually caused by the absence of the electrical impulse from the sinus node. This usually appears on an EKG with a normal QRS complex accompanied with an inverted P wave either before, during, or after the QRS complex.^[4]

An AV junctional escape is a delayed heartbeat originating from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the SA node falls below the rate of the AV node.^[4] This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block.^[6] This is a protective mechanism for the heart, to compensate for a SA node that is no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so. This would present with a longer PR interval. A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node. Pathological causes include sinus bradycardia, sinus arrest, sinus exit block, or AV block.^[4]

Ventricular

A ventricular bradycardia, also known as ventricular escape rhythm or idioventricular rhythm, is a heart rate of less than 50 beats a minute. This is a safety mechanism that arises when there is lack of electrical impulse or stimuli from the atrium.^[4] Impulses originating from or below the His bundle, also known as ventricular, will produce a wide QRS complex with heart rates between 20 and 40 beats a minute. Those above the His bundle, also known as junctional, will typically range between 40 and 60 bpm with a narrow QRS complex.^[7][8] In a third degree heart block, approximately 61% take place at the bundle branch-Purkinje system, 21% at the AV node, and 15% at the His bundle.^[8] AV block maybe ruled out with an EKG indicating "a 1:1 relationship between P waves and QRS complexes."^[7] Ventricular bradycardias occurs with sinus bradycardia, sinus arrest, and AV block. Treatment often consist of the administration of atropine and cardiac pacing.^[4]

Infantile

For infants, bradycardia is defined as a heart rate of less than 100 beats per minute. (Normal is around 120-160 beats per minute.) Premature babies are more likely than full-term babies to have apnea and bradycardia spells; their cause is not clearly understood. Some researchers think the spells are related to centers inside the brain that regulate breathing and that may not be fully developed. Touching the baby gently or rocking the incubator slightly will almost always get the baby to start breathing again, which increases the heart rate. Medications (theophylline or caffeine) can be used to treat these spells in babies if necessary. NICU standard practice is to electronically monitor the heart and lungs for this reason.

Causes

This cardiac arrhythmia can be underlain by several causes, which are best divided into cardiac and non-cardiac causes. Non-cardiac causes are usually secondary, and can involve drug use or abuse; metabolic or endocrine issues, especially in the thyroid; an electrolyte imbalance; neurologic factors; autonomic reflexes; situational factors such as prolonged bed rest; and autoimmunity. Cardiac causes include acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary electrical disease. Ultimately, the causes act by three mechanisms: depressed automaticity of the heart, conduction block, or escape pacemakers and rhythms.

There are generally two types of problems that result in bradycardias: disorders of the sinoatrial node (SA node), and disorders of the atrioventricular node (AV node).

With sinus node dysfunction (sometimes called sick sinus syndrome), there may be disordered automaticity or impaired conduction of the impulse from the sinus node into the surrounding atrial tissue (an "exit block"). Only second degree sinostrial blocks can be detected by use of a 12-lead EKG.^[9] It is difficult and sometimes impossible to assign a mechanism to any particular bradycardia, but the underlying mechanism is not clinically relevant to treatment, which is the same in both cases of sick sinus syndrome: a permanent pacemaker.

Atrioventricular conduction disturbances (aka: AV block; 1^o AV block, 2^o type I AV block, 2^o type II AV block, 3^o AV block) may result from impaired conduction in the AV node, or anywhere below it, such as in the Bundle of His. The clinical relevance pertaining to AV blocks is greater than that of sinoatrial blocks.^[9]

Patients with bradycardia have likely acquired it, as opposed to having it congenitally. Bradycardia is more common in older patients.

Diagnosis

A diagnosis of bradycardia in adults is based on a heart rate less than 60. This is determined usually either via palpation or an ECG.

If symptoms occur, a determination of electrolytes may be helpful in determining the underlying cause.

Management

The treatment of bradycardia is dependent on whether or not the person is stable or unstable.^[3] If oxygen saturations are low supplemental oxygen should be provided.^[3]

Stable

Emergent treatment is not needed if the person is asymptomatic or minimally symptomatic.^[3]

Unstable

If a person is unstable the initial recommended treatment is intravenous atropine.^[3] Doses less than 0.5 mg should not be used as this may further decrease the rate.^[3] If this is not effective intravenous inotrope infusion (dopamine, epinephrine) or transcutaneous pacing should be used.^[3] Transvenous pacing may be required if the cause of the bradycardia is not rapidly reversible.^[3]

References