Most people with Wenckebach (Type I Mobitz) do not show symptoms. However, those that do usually display one or more of the following:

- Light-headedness

- Dizziness

- Syncope (fainting)

Type 2 Second-degree AV block, also known as "Mobitz II," is almost always a disease of the distal conduction system (His-Purkinje System).

Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening. There is usually a fixed number of non-conducted P waves for every successfully conducted QRS complex, and this ratio is often specified in describing Mobitz II blocks. For example, Mobitz II block in which there are two P waves for every one QRS complex may be referred to as "2:1 Mobitz II block".

The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge. In this case, the person may experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death. The definitive treatment for this form of AV Block is an implanted pacemaker.

The impairment is usually below the AV node. Although the terms infranodal block or infrahisian block are often applied to this disorder, they refer to the "anatomic location" of the block, whereas Mobitz II refers to an "electrocardiographic pattern".

Trifascicular block is important to diagnose because it is difficult to tell based on the surface ECG whether the prolonged PR interval is due to disease in the AV node or due to diffuse distal conduction system disease.

- In the former case, if the block at the AV node level becomes complete, the escape rhythm will originate from the bundle of His, which typically will generate heart rates in the 40s, allowing the individual to survive and complain of symptoms of fatigue or near-syncope to their physician.

- In the latter case, however, because the conduction system disease is diffuse in nature, the escape rhythm may be fascicular or ventricular, which may be at rates that are life-threateningly low.

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.

Depending on the anatomical location of the defect which leads to a bundle branch block, the blocks are further classified into:

- Right bundle branch block

- Left bundle branch block

The left bundle branch block can be further sub classified into:

- Left anterior fascicular block. In this case only the anterior half of the left bundle branch (fascicle) is involved

- Left posterior fascicular block. Only the posterior part of the left bundle branch is involved

Other classifications of bundle branch blocks are;

- Bifascicular block. This is a combination of right bundle branch block (RBBB) and either left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB)

- Trifascicular block. This is a combination of right bundle branch block with either left anterior fascicular block or left posterior fascicular block together with a first degree AV block

- Tachycardia-dependent bundle branch block

Infra-Hisian block is that of the distal conduction system. Types of infra-Hisian block include:

- Type 2 second degree heart block (Mobitz II) –a type of AV block due to a block within or below the bundle of His

- Left anterior fascicular block

- Left posterior fascicular block

- Right bundle branch block

Of these types of infra-Hisian block, Mobitz II heart block is considered most important because of the possible progression to complete heart block.

A bundle branch block can be diagnosed when the duration of the QRS complex on the ECG exceeds 120 ms. A right bundle branch block typically causes prolongation of the last part of the QRS complex, and may shift the heart's electrical axis slightly to the right. The ECG will show a terminal R wave in lead V1 and a slurred S wave in lead I.

Left bundle branch block widens the entire QRS, and in most cases shifts the heart's electrical axis to the left. The ECG will show a QS or rS complex in lead V1 and a monophasic R wave in lead I. Another normal finding with bundle branch block is appropriate T wave discordance. In other words, the T wave will be deflected opposite the terminal deflection of the QRS complex.

Bundle branch block, especially left bundle branch block, can lead to cardiac dyssynchrony. The simultaneous occurrence of left and right bundle branch block leads to total AV block.

Third-degree atrioventricular block (AV block), also known as complete heart block, is a medical condition in which the impulse generated in the sinoatrial node (SA node) in the atrium of the heart does not propagate to the ventricles.

Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an "escape rhythm". Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG).

- The P waves with a regular P-to-P interval (in other words, a sinus rhythm) represent the first rhythm.

- The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is lack of any apparent relationship between P waves and QRS complexes.

Patients with third-degree AV block typically experience severe bradycardia (an abnormally-low measured heart rate), hypotension, and at times, hemodynamic instability.

Up to 80% of individuals with ARVD present have symptoms like syncope and dyspnea.The remainder frequently present with palpitations or other symptoms due to right ventricular outflow tract (RVOT) tachycardia (a type of monomorphic ventricular tachycardia).

Symptoms are usually exercise-related. In populations where hypertrophic cardiomyopathy is screened out prior to involvement in competitive athletics, it is a common cause of sudden cardiac death.

The first clinical signs of ARVD are usually during adolescence. However, signs of ARVD have been demonstrated in infants.

In a first degree sinoatrial block, there is a lag between the time that the SA node fires and actual depolarization of the atria. This rhythm is not recognizable on an ECG strip because a strip does not denote when the SA node fires. It can be detected only during an electrophysiology study when a small wire is placed against the SA node from within the heart and the electrical impulses can be recorded as they leave the p-cells in the centre of the node [ see pacemaker potential ], followed by observing a delay in the onset of the p wave on the ECG.

Second degree SA blocks are broken down into two subcategories just like AV blocks are:

The first is a second degree type I, or Wenckebach block. This rhythm is irregular, and the R-R interval gets progressively smaller, while the P-R interval remains constant, until a QRS segment is dropped. Note that this is quite different from the Wenckebach AV block, in which the PR interval gets progressively longer, before the dropped QRS segment. The pause of a second degree type I is less than twice the shortest R-R interval and is not a multiple of the P-R interval. The cause is a gradual lengthening of conduction time from the SA node to the atria. The p-cells in the centre of the node produce the rhythm at a regular rate, but their conduction across the node to where it meets atrial tissue is where the slowing occurs.

A second degree type II, or sinus exit block, is a regular rhythm that may be normal or slow. It is followed by a pause that is a multiple of the P-P interval usually (2-4) . Conduction across the SA node is normal until the time of the pause when it is blocked.

A third degree sinoatrial block looks very similar to a sinus arrest. However, a sinus arrest is caused by a failure to form impulses. A third degree block is caused by failure to conduct them. The rhythm is irregular and either normal or slow. It is followed by a long pause that is not a multiple of the P-R interval. The pause ends with a P wave, instead of a junctional escape beat the way a sinus arrest would.

There are three basic types of AV nodal block:

- First-degree AV block

- Second-degree AV block

- Type I second-degree AV block (Mobitz I), also known as Wenckebach block

- Type 2 second-degree AV block (Mobitz II) - due to a block in or below the bundle of His

- Third-degree AV block (complete heart block)

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.

First-degree atrioventricular block (AV block), or PR prolongation, is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds.

In first-degree AV block, the impulse conducting from atria to ventricles through the atrioventricular node (AV node) is delayed and travels slower than normal. It has a prevalence in the normal (young adult) population of 0.65-1.1% and the incidence is 0.13 per 1000 persons.

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.

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

No specific set of criteria has been developed for diagnosis of pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly documented in patients history, classified according to cause:

- Neurological - Dizziness, near syncope, and confusion.

- Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

- Hypotension - Seizure, mental status change, diaphoresis, and signs of orthostatic hypotension and shock.

- Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.

- Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds, and headache.

- Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should look for the following in the physical examination, as these are frequent findings at the time of admission:

- Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

- Pulse amplitude may vary, and blood pressure may fluctuate.

- Look for neck vein distension and cannon waves in the neck veins.

- Lungs may exhibit crackles.

- Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

- Liver may be pulsatile, and the RUQ may be tender to palpation. Ascites may be present in severe cases.

- The lower extremities may be edematous.

- Neurologic examination may reveal confusion, dizziness, or altered mental status.

While Ebstein's anomaly is defined as the congenital displacement of the tricuspid valve towards the apex of the right ventricle, it is often associated with other abnormalities.

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.

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.

Clinically, it is often asymptomatic by itself and considered benign in nature.

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)

Arrhythmogenic right ventricular dysplasia (ARVD) is an inherited heart disease.

ARVD is caused by genetic defects of the parts of heart muscle (also called "myocardium" or "cardiac muscle") known as desmosomes, areas on the surface of heart muscle cells which link the cells together. The desmosomes are composed of several proteins, and many of those proteins can have harmful mutations.

The disease is a type of nonischemic cardiomyopathy that involves primarily the right ventricle. It is characterized by hypokinetic areas involving the free wall of the right ventricle, with fibrofatty replacement of the right ventricular myocardium, with associated arrhythmias originating in the right ventricle.

ARVD can be found in association with diffuse palmoplantar keratoderma, and woolly hair, in an autosomal recessive condition called Naxos disease, because this genetic abnormality can also affect the integrity of the superficial layers of the skin most exposed to pressure stress.

ARVC/D is an important cause of ventricular arrhythmias in children and young adults. It is seen predominantly in males, and 30–50% of cases have a familial distribution.

Junctional rhythms (if a bradycardia) can cause decreased cardiac output. Therefore, the person may exhibit signs and symptoms similar to other bradycardia such as lightheadedness, dizziness, hypotension, and syncope. This rhythm can usually be tolerated if the rate is above 50 bpm.

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.

People with WPW are usually asymptomatic when not having a fast heart rate. However, individuals may experience palpitations, dizziness, shortness of breath, or infrequently syncope (fainting or near fainting) during episodes of supraventricular tachycardia. The telltale "delta wave" may sometimes be seen on an electrocardiogram (ECG/EKG).