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.

The treatment for diffuse distal conduction system disease is insertion of a pacemaker. If the PR prolongation is due to AV nodal disease, a case may be made for observation, as it may never progress to complete heart block with life threateningly low heart rates.

Regardless of where in the conduction system the block is, if the block is believed to be the cause of syncope in an individual, a pacemaker is an appropriate treatment.

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.

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 underlying condition may be treated by medications to control hypertension or diabetes, if they are the primary underlying cause. If coronary arteries are blocked, an invasive coronary angioplasty may relieve the impending RBBB.

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.

An atrial septal defect is one possible cause of a right bundle branch block. In addition, a right bundle branch block may also result from Brugada syndrome, right ventricular hypertrophy, pulmonary embolism, ischaemic heart disease, rheumatic heart disease, myocarditis, cardiomyopathy or hypertension.

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.

The human heart is a four-chambered organ responsible for the distribution of blood throughout the body. While every physiological effort is made to ensure that such a vital organ can operate continuously without error, sometimes a pathological situation arises and the function of the heart is compromised. One such pathology arises when the electrical signal propagated throughout the heart (responsible for the heart's highly organized contractions) is hindered, resulting in a degradation of said conduction. This is referred to as a bundle branch block and is seen clinically as rate-dependent bundle branch block, right bundle branch block or left bundle branch block, in varying severity (first degree AV block, second degree AV block and third degree AV block)

A tachycardia-dependent bundle branch block (TDBBB) is a defect in the conduction system of the heart, and is distinct from typical bundle branch blocks due to its reliable, reproducible onset related to an increase in the rate of cardiac contraction. Tachycardia-dependent bundle branch block can prevent both ventricles from contracting efficiently and can limit the cardiac output of the heart.

The most common causes of first-degree heart block are an AV nodal disease, enhanced vagal tone (for example in athletes), myocarditis, acute myocardial infarction (especially acute inferior MI), electrolyte disturbances and medication. The drugs that most commonly cause first-degree heart block are those that increase the refractory time of the AV node, thereby slowing AV conduction. These include calcium channel blockers, beta-blockers, cardiac glycosides, and anything that increases cholinergic activity such as cholinesterase inhibitors. Digitalis is a sodium/potassium ATPase inhibitor and also prolongs AV conduction.

Trifascicular block is a problem with the electrical conduction of the heart. It is diagnosed on an electrocardiogram (ECG/EKG) and has three features:

- prolongation of the (first degree AV block)

- right bundle branch block

- either left anterior fascicular block or left posterior fascicular block.

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

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).

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.

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.

Atrioventricular block (AV block) is a type of heart block in which the conduction between the atria and ventricles of the heart is impaired. Under normal conditions, the sinoatrial node (SA node) in the atria sets the pace for the heart, and these impulses travel down to the ventricles. In an AV block, this message does not reach the ventricles or is impaired along the way. The ventricles of the heart have their own pacing mechanisms, which can maintain a lowered heart rate in the absence of SA stimulation.

The causes of pathological AV block are varied and include ischaemia, infarction, fibrosis or drugs, and the blocks may be complete or may only impair the signaling between the SA and AV nodes. Certain AV blocks can also be found as normal variants, such as in athletes or children, and are benign. Strong vagal stimulation may also produce AV block. The cholinergic receptor types affected are the muscarinic receptors.

There are three types:

- First-degree atrioventricular block - The heart’s electrical signals move between the upper and lower chambers of the heart.PR interval greater than 0.20sec.

- Second-degree atrioventricular block - The heart’s electrical signals between the upper and lower signals of the heart are slowed by a much greater rate than in first-degree atrioventricular block. Type 1 (a.k.a. Mobitz 1, Wenckebach): Progressive prolongation of PR interval with dropped beats (the PR interval gets longer and longer; finally one beat drops) . Type 2 (a.k.a. Mobitz 2, Hay): PR interval remains unchanged prior to the P wave which suddenly fails to conduct to the ventricles.

- Mobitz I is characterized by a reversible block of the AV node. When the AV node is severely blocked, it fails to conduct an impulse. Mobitz I is a progressive failure. Some patients are asymptomatic; those who have symptoms respond to treatment effectively. There is low risk of the AV block leading to heart attack. Mobitz II is characterized by a failure of the His-Purkinje cells resulting in the lack of a supra ventricular impulse. These cardiac His-Purkinje cells are responsible for the rapid propagation in the heart. Mobitz II is caused by a sudden and unexpected failure of the His-Purkinje cells. The risks and possible effects of Mobitz II are much more severe than Mobitz I in that it can lead to severe heart attack.

- Third-degree atrioventricular block - No association between P waves and QRS complexes. The heart’s electrical signals are slowed to a complete halt. This means that none of the signals reach either the upper or lower chambers causing a complete blockage of the ventricles and can result in cardiac arrest. Third-degree atrioventricular block is the most severe of the types of heart ventricle blockages. Persons suffering from symptoms of third-degree heart block need emergency treatment including but not limited to a pacemaker.

In order to differentiate between the different degrees of the atrioventricular block (AV block), the First-Degree AV block occurs when an electrocardiogram (ECG) reads a PR interval that is more than 200 msec. This degree is typically asymptomatic and is only found through an ECG reading. Second-Degree AV block, although typically asymptomatic, has early signs that can be detected or are noticeable such as irregular heartbeat or a syncope. A Third-Degree AV block, has noticeable symptoms that present itself as more urgent such as: dizziness, fatigue, chest pain, pre syncope, or syncope.

Laboratory diagnosis for AV blocks include electrolyte, drug level and cardiac enzyme level tests. A clinical evaluation also looks at infection, myxedema, or connective tissue disease studies. In order to properly diagnose a patient with AV block, an electrocardiographic recording must be completed (ECG). Based on the P waves and QRS complexes that can be evaluated from these readings, that relationship will be the standardized test if an AV block is present or not. In order to identify this block based on the readings the following must occur: multiple ECG recordings, 24-hour Holter monitoring, and implant loop recordings. Other examinations for the detection of an AV block include electrophysiologic testing, echocardiography, and exercise.

Management includes a form of pharmacologic therapy that administers anticholinergic agents and is dependent upon the severity of a blockage. In severe cases or emergencies, atropine administration or isoproterenol infusion would allow for temporary relief if bradycardia is the cause for the blockage, but if His-Purkinje system is the result of the AV block then pharmacologic therapy is not recommended.

A bundle branch block is a defect of the bundle branches or fascicles in the electrical conduction system of the heart.

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

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.

Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the heart, which works in parallel with the SA node. Parasystolic pacemakers are protected from depolarization by the SA node by some kind of "entrance block". This block can be complete or incomplete.

Parasystolic pacemakers can exist in both the atrium or the ventricle. Atrial parasystolia are characterized by narrow QRS complexes

Two forms of ventricular parasystole have been described in the literature, fixed parasystole and modulated parasystole. Fixed ventricular parasystole occurs when an ectopic pacemaker is protected by entrance block, and thus its activity is completely independent from the sinus pacemaker activity. Hence, the ectopic pacemaker is expected to fire at a fixed rate.

Therefore, on ECG, the coupling intervals of the manifest ectopic beats will wander through the basic cycle of the sinus rhythm. Accordingly, the traditional electrocardiographic criteria used to recognize the fixed form of parasystole are:

- the presence of variable coupling intervals of the manifest ectopic beats;

- inter-ectopic intervals that are simple multiples of a common denominator;

- fusion beats.

According to the modulated parasystole hypothesis, rigid constancy of a pacemaker might be expected if the entrance block were complete, but if there is an escape route available for the emergence of ectopic activity, then clearly there must be an effective ionic communication, not complete insulation, between the two tissues. If there is an electrical

communication between the two, then the depolarization of the surrounding ventricle may influence the ectopic pacemaker. That influence will be electrotonic; depolarization of the surrounding field will induce a partial depolarization

of the pacemaker cells. Therefore, appropriate diagnosis of modulated parasystole relies upon the construction of a “phase response curve” as theoretical evidence of modulation of the ectopic pacemaker cycle length by the electrotonic activity generated by the sinus discharges across the area of protection. In this case, the timing of the arrival of the electronic stimulus will serve to delay or advance the subsequent pacemaker activation. In this case, the coupling intervals between the manifest ectopic and sinus discharges will be either fixed or variable, depending on the cycle length relations between the two pacemakers.

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.

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.

Third degree AV block can be treated with Cilostazol which acts to increase Ventricular escape rate

Among the causes of LBBB are:

- Aortic stenosis

- Dilated cardiomyopathy

- Acute myocardial infarction

- Extensive coronary artery disease

- Primary disease of the cardiac electrical conduction system

- Long standing hypertension leading to aortic root dilatation and subsequent aortic regurgitation

- Lyme disease

- Side effect of some cardiac surgeries (e.g., aortic root reconstruction)