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.

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.

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.

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).

Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:

- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation

- Dizziness or light-headedness

- Palpitations

- Chest pain or angina

- Shortness of breath

- Fatigue

- Headache

- Nausea

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.

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.

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body - because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to the layperson can look like normal spontaneous breathing, but it is in fact a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain. Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.

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.

Although there are many signs and symptoms associated with PVCs, PVCs may have no symptoms at all. An isolated PVC is hard to catch without the use of a Holter monitor. PVCs may be perceived as a skipped heart beat, a strong beat, or a feeling of suction in the chest. They may also cause chest pain, a faint feeling, fatigue, or hyperventilation after exercise. Several PVCs in a row becomes a form of ventricular tachycardia (VT), which is a potentially fatal abnormal heart rhythm. Overall it has been seen that the symptom felt most by patients experiencing a PVC is the mere perception of a skipped heartbeat. The more frequently these contractions occur, the more likely there are to be symptoms, despite the fact that these beats have little effect of the pumping action of the heart and therefore cause minimal if any symptoms.

Some other possible signs and symptoms of PVCs:

- Abnormal ECG

- Irregular heart beat

- Dyspnea

- Dizziness

- Feeling your heart beat (palpitations)

- Feeling of occasional, forceful beats

- Increased awareness of your heart beat

- Perception of a skipped heartbeat

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.

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.

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)

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.

A right bundle branch block (RBBB) is a heart block in the electrical conduction system.

During a right bundle branch block, the right ventricle is not directly activated by impulses travelling through the right bundle branch. The left ventricle however, is still normally activated by the left bundle branch. These impulses are then able to travel through the myocardium of the left ventricle to the right ventricle and depolarize the right ventricle this way. As conduction through the myocardium is slower than conduction through the Bundle of His-Purkinje fibres, the QRS complex is seen to be widened. The QRS complex often shows an extra deflection which reflects the rapid depolarisation of the left ventricle followed by the slower depolarisation of the right ventricle.

In most cases right bundle branch block has a pathological cause though it is also seen in healthy individuals in about 1.5-3%.

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.

The main symptom of AVNRT is the sudden development of rapid regular palpitations. Often, no provoking factor is identified, although some people affected by AVNRT report developing symptoms in stressful situations, and following consumption of alcohol or caffeine.

In some cases, the onset of the fast heart is associated with a brief drop in blood pressure. When this happens, the patient may experience dizziness or rarely lose consciousness (faint). If the heart rate is very fast, and the patient has underlying coronary artery disease (obstruction of the arteries of the heart by atherosclerosis), chest pain similar to angina may be experienced; this pain is band- or pressure-like around the chest and often radiates to the left arm and angle of the left jaw. AVNRT is rarely life-threatening.

SA blocks rarely give severe symptoms, because even if an individual had complete block at this level of the conduction system (which is uncommon), the secondary pacemaker of the heart would be at the AV node, which would fire at 40 to 60 beats a minute, which is enough to retain consciousness in the resting state. However SA block is capable of causing problematic symptoms even so, and may also hint at conduction issues elsewhere in the heart, and therefore SA blocks are - despite their lower level of lifethreatening risk - still "the most common indication for pacemaker implantation in the US".

Types of SA nodal blocks include:

- SA node Wenckebach (Mobitz I)

- SA node Mobitz II

- SA node exit block

In addition to the above blocks, the SA node can be suppressed by any other arrhythmia that reaches it. This includes retrograde conduction from the ventricles, ectopic atrial beats, atrial fibrillation, and atrial flutter.

The difference between SA node block and SA node suppression is that in SA node block an electrical impulse is generated by the SA node that doesn't make the atria contract. In SA node suppression, on the other hand, the SA node doesn't generate an electrical impulse because it is reset by the electrical impulse that enters the SA node.

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.

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node (AV node). In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia.

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

While atrial flutter can sometimes go unnoticed, its onset is often marked by characteristic sensations of the heart feeling like it is beating too fast or hard. Such sensations usually last until the episode resolves, or until the heart rate is controlled.

Atrial flutter is usually well tolerated initially (a high heart rate is for most people just a normal response to exercise), however, people with other underlying heart disease (such as coronary artery disease) or poor exercise tolerance may rapidly develop symptoms, such as shortness of breath, chest pain, lightheadedness or dizziness, nausea and, in some patients, nervousness and feelings of impending doom.

Prolonged atrial flutter with fast heart rates may lead to decompensation with loss of normal heart function (heart failure). This may manifest as exercise intolerance (exertional breathlessness), difficulty breathing at night, or swelling of the legs and/or abdomen.

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.

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

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)