Isolated first-degree heart block has no direct clinical consequences. There are no symptoms or signs associated with it. It was originally thought of as having a benign prognosis. In the Framingham Heart Study, however, the presence of a prolonged PR interval or first degree AV block doubled the risk of developing atrial fibrillation (irregular heart beat), tripled the risk of requiring an artificial pacemaker, and was associated with a small increase in mortality. This risk was proportional to the degree of PR prolongation.

A subset of individuals with the triad of first-degree heart block, right bundle branch block, and either left anterior fascicular block or left posterior fascicular block (known as trifascicular block) may be at an increased risk of progression to complete heart block.

Ouabain infusion decreases ventricular escape time and increases ventricular escape rhythm. However, a high dose of ouabain can lead to ventricular tachycardia.

Sinoatrial blocks are typically well-tolerated. They are not as serious as an AV block and most often do not require treatment. In some people, they can cause fainting, altered mental status, chest pain, hypoperfusion, and signs of shock. They can also lead to cessation of the SA node and more serious dysrhythmias. Emergency treatment, if deemed necessary, consists of administration of atropine sulfate or transcutaneous pacing.

It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block, sinus bradycardia, and other types of bradycardia (slow heart rate).

Sick sinus syndrome may also be associated with tachycardias (fast heart rate) such as atrial tachycardia (PAT) and atrial fibrillation. Tachycardias that occur with sick sinus syndrome are characterized by a long pause after the tachycardia. Sick sinus syndrome is also associated with azygos continuation of interrupted inferior vena cava.

The prognosis of patients with complete heart block is generally poor without therapy. Patients with 1st and 2nd degree heart block are usually asymptomatic.

Many conditions can cause third-degree heart block, but the most common cause is coronary ischemia. Progressive degeneration of the electrical conduction system of the heart can lead to third-degree heart block. This may be preceded by first-degree AV block, second-degree AV block, bundle branch block, or bifascicular block. In addition, acute myocardial infarction may present with third-degree AV block.

An "inferior wall myocardial infarction" may cause damage to the AV node, causing third-degree heart block. In this case, the damage is usually transitory. Studies have shown that third-degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks. The escape rhythm typically originates in the AV junction, producing a narrow complex escape rhythm.

An "anterior wall myocardial infarction" may damage the distal conduction system of the heart, causing third-degree heart block. This is typically extensive, permanent damage to the conduction system, necessitating a permanent pacemaker to be placed. The escape rhythm typically originates in the ventricles, producing a wide complex escape rhythm.

Third-degree heart block may also be congenital and has been linked to the presence of lupus in the mother. It is thought that maternal antibodies may cross the placenta and attack the heart tissue during gestation. The cause of congenital third-degree heart block in many patients is unknown. Studies suggest that the prevalence of congenital third-degree heart block is between 1 in 15,000 and 1 in 22,000 live births.

Hyperkalemia in those with previous cardiac disease and Lyme disease can also result in third-degree heart block.

The management includes identifying and correcting electrolyte imbalances and withholding any offending medications. This condition does not require admission unless there is an associated myocardial infarction. Even though it usually does not progress to higher forms of heart block, it may require outpatient follow-up and monitoring of the ECG, especially if there is a comorbid bundle branch block. If there is a need for treatment of an unrelated condition, care should be taken not to introduce any medication that may slow AV conduction. If this is not feasible, clinicians should be very cautious when introducing any drug that may slow conduction; and regular monitoring of the ECG is indicated.

Ventricular escape beats occur when the rate of electrical discharge reaching the ventricles (normally initiated by the heart's sinoatrial node (SA node), transmitted to the atrioventricular node (AV node), and then further transmitted to the ventricles) falls below the base rate determined by the rate of Phase 4 spontaneous depolarisation of ventricular pacemaker cells.

An escape beat usually occurs 2–3 seconds after an electrical impulse has failed to reach the ventricles

This phenomenon can be caused by the sinoatrial node (SA node) failing to initiate a beat, by a failure of the conductivity from the SA node to the atrioventricular node (AV node), or by atrioventricular block (especially third degree AV block). Normally, the pacemaker cells of the sinoatrial node discharge at the highest frequency and are thus dominant over other cells with pacemaker activity. The AV node normally has the second fastest discharge rate. When the sinus rate falls below the discharge rate of the AV node, this becomes the dominant pacemaker, and the result is called a junctional escape beat. If the rate from both the SA and AV node fall below the discharge rate of ventricular pacemaker cells, a ventricular escape beat ensues.

An escape beat is a form of cardiac arrhythmia, in this case known as an ectopic beat. It can be considered a form of ectopic pacemaker activity that is unveiled by lack of other pacemakers to stimulate the ventricles. Ventricular pacemaker cells discharge at a slower rate than the SA or AV node. While the SA node typically initiates a rate of 70 beats per minute (BPM), the atrioventricular node (AV node) is usually only capable of generating a rhythm at 40-60 BPM or less. Ventricular contraction rate is thus reduced by 15-40 beats per minute.

If there are only one or two ectopic beats, they are considered escape beats. If this causes a semi-normal rhythm to arise it is considered an idioventricular rhythm.

The escape arrhythmia is a compensatory mechanism that indicates a serious underlying problem with the SA node or conduction system (commonly due to heart attack or medication side effect), and because of its low rate, it can cause a drop in blood pressure and syncope.

Sinoatrial arrest (also known as sinus arrest or sinus pause) is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. This condition is sometimes confused with sinoatrial block, a condition in which the pacing impulse is generated, but fails to conduct through the myocardium. Differential diagnosis of the two conditions is possible by examining the exact length of the interruption of cardiac activity.

If the next available pacemaker takes over, it is in the following order:

1. Atrial escape (rate 60–80): originates within atria, not sinus node (normal P morphology is lost).

2. Junctional escape (rate 40–60): originates near the AV node; a normal P wave is not seen, may occasionally see a retrograde P wave.

3. Ventricular escape (rate 20–40): originates in ventricular conduction system; no P wave, wide, abnormal QRS.

Treatment includes stop medications that suppress the sinus node (beta blocker, Calcium channel blocker, digitalis); may need pacing.

AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of abnormal fast heart rhythm. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medications, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.

AVNRT occurs when a reentrant circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as "part of" the AV node.

The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to muscular heart tissue of the heart's ventricles.

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart. There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff–Parkinson–White syndrome. Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.

They start from either the atria or atrioventricular node. They are generally due to one of two mechanisms: re-entry or increased automaticity. The other type of fast heart rhythm is ventricular arrhythmias—rapid rhythms that start within the ventricle. Diagnosis is typically by electrocardiogram (ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes such as hyperthyroidism or electrolyte abnormalities.

Specific treatments depend on the type of SVT. They can include medications, medical procedures, or surgery. Vagal maneuvers or a procedure known as catheter ablation may be effective in certain types. For atrial fibrillation calcium channel blockers or beta blockers may be used. Long term some people benefit from blood thinners such as aspirin or warfarin. Atrial fibrillation affects about 25 per 1000 people, paroxysmal supraventricular tachycardia 2.3 per 1000, Wolff-Parkinson-White syndrome 2 per 1000, and atrial flutter 0.8 per 1000.

Heart block is a disease or inherited condition that causes a fault within the heart's natural pacemaker due to some kind of obstruction (or "block") in the electrical conduction system of the heart. Despite the severe-sounding name, heart block may often cause no symptoms at all in some cases, or occasional missed heartbeats in other cases (which can cause lightheadedness, syncope (fainting), and palpitations), or may require an artificial pacemaker to be implanted, depending upon exactly where in the heart conduction is being impaired and how significantly it is affected.

In severe cases where the heart's ability to control and trigger heartbeats may be completely ineffective or unreliable, heart block can usually be treated by inserting an artificial pacemaker, a medical device that provides correct electrical impulses to trigger heart beats, compensating for the natural pacemaker's unreliability. Therefore, heart block frequently has no effects, or mild and occasional effects, and is not life-threatening in the vast majority of cases, and is usually treatable in more serious cases.

The human heart uses electrical signals to maintain and initiate the regular heart beat in a living person; incorrect conduction can lead to mild or serious symptoms depending upon the location of the blockage and how severely conduction is being blocked. Conduction is initiated by the sinoatrial node ("sinus node" or "SA node"), and then travels to the atrioventricular node ("AV node") which also contains a secondary "pacemaker" that acts as a backup for the SA nodes, then to the bundle of His and then via the bundle branches to the point of the apex of the fascicular branches (shown in the diagram on the right). Blockages are therefore classified based on where the blockage occurs - namely the SA node ("Sinoatrial block"), AV node ("AV block" or AVB), and at or below the bundle of His ("Intra-Hisian" or "Infra-Hisian block" respectively). Infra-Hisian blocks may occur at the left or right bundle branches ("bundle branch block") or the fascicles of the left bundle branch ("fascicular block" or "Hemiblock"). SA and AV node blocks are each divided into three degrees, with second degree blocks being divided into two types (written either "type I or II" or "type 1 or 2"). The term "Wenckebach block" is also used for second degree type 1 blocks of either the SA or AV node; in addition second degree blocks type 1 and 2 are also sometimes known as "Mobitz 1" and "Mobitz 2".

Clinically speaking, the blocks tend to have more serious potential the closer they are to the 'end' of the electrical path (the muscles of the heart regulated by the heartbeat), and less serious effects the closer they are to the 'start' (at the SA node), because the potential disruption becomes greater as more of the 'path' is 'blocked' from its 'end' point. Therefore, most of the important heart blocks are AV nodal blocks and infra-Hisian blocks. SA blocks are usually of lesser clinical significance, since in the event of SA block, the AV node contains a secondary pacemaker which would still maintain a heart rate of around 40 - 60 beats per minute, sufficient for consciousness and much of daily life in the majority of individuals.

Some people with bundle branch blocks are born with this condition. Many other acquire it as a consequence of heart disease. People with bundle branch blocks may still be quite active, and may have nothing more remarkable than an abnormal appearance to their ECG. However, when bundle blocks are complex and diffuse in the bundle systems, or associated with additional and significant ventricular muscle damage, they may be a sign of serious underlying heart disease. In more severe cases, a pacemaker may be required to restore an optimal electrical supply to the heart muscle.

Sick sinus syndrome is a relatively uncommon syndrome in the young and middle age population. Sick sinus syndrome is more common in elderly adults, where the cause is often a non-specific, scar-like degeneration of the cardiac conduction system. Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

There are two non-distinct types of second-degree AV block, called "Type 1" and "Type 2". In both types, a P wave is blocked from initiating a QRS complex; but, in Type 1, there are increasing delays in each cycle before the omission, whereas, in Type 2, there is no such pattern.

Type 1 second-degree heart block is considered a more benign entity than type 2 second-degree heart block with type 1 not having structural changes found on histology.

Both types are named after Woldemar Mobitz. Type I is also named for Karel Frederik Wenckebach, and type II is also named for John Hay.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications that calls for the patients to be carefully monitored in the ICU. Complications include atrial fibrillation, thrombo-embolic events, and heart failure.

The initial impulse in a heart is usually formed in the Sinoatrial (SA) node and carried through the atria, down the internodal atrial pathways, and to the Atrioventricular (AV) node.

In normal conduction, the impulse would travel across the “bundle of His” (AV bundle), down the bundle branches, and into the Purkinje fibers. This would depolarize the ventricles and cause them to contract.

In an SA block, the electrical impulse is delayed or blocked on the way to the atria, thus delaying the atrial beat. This is different from an AV block, which occurs in the AV node and delays ventricular depolarization. SA blocks are categorized into three classes based on the length of the delay.

The true incidence of TIC is unclear. Some studies have noted the incidence of TIC in adults with irregular heart rhythms to range from 8% to 34%. Other studies of patients with atrial fibrillation and left ventricular dysfunction estimate that 25-50% of these study participants have some degree of TIC. TIC has been reported in all age groups.

A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node (e.g. digoxin toxicity), a pathological slowing of the SA discharge, or a complete AV block.

A number of physical acts can increase parasympathetic nervous supply to the heart, resulting in blocking of electrical conduction through the AV node. This can slow down or stop a number of arrhythmias that originate above or at the AV node (see main article: supraventricular tachycardias). Parasympathetic nervous supply to the heart is via the vagus nerve, and these maneuvers are collectively known as vagal maneuvers.

The cause is poorly understood. However several risk factors are associated with pacemaker syndrome.

Normally, the pacemaker of the heart that is responsible for triggering each heart beat (ventricular contraction) is the SA (Sino Atrial) node. However, if the ventricle does not receive triggering signals at a rate high enough from either the SA node or the AV (Atrioventricular) node, the ventricular myocardium itself becomes the pacemaker (escape rhythm). This is called Idioventricular Rhythm. Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes(> 0.12 sec). The rate is usually 20-40 bpm. If the rate is >40 bpm, it is called accelerated idioventricular rhythm. The rate of 20-40 is the "intrinsic automaticity" of the ventricular myocardium. It can be regarded as a physiological redundancy of the cardiac electrical system.

Second-degree atrioventricular block (AV block) is a disease of the electrical conduction system of the heart. It is a conduction block between the atria and ventricles. The presence of second-degree AV block is diagnosed when one or more (but not all) of the atrial impulses fail to conduct to the ventricles due to impaired conduction. It is classified as a block of the AV node and is categorized in between first-degree (slowed conduction) and third degree blocks (complete block).

A junctional escape beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. 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. It is a protective mechanism for the heart, to compensate for the SA node 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.

An episode of supraventricular tachycardia (SVT) due to AVNRT can be terminated by any action that transiently blocks the AV node. Various methods are possible.