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 following stimulants, conditions and triggers may increase your risk of the more frequent occurrence of premature ventricular contractions:

- Caffeine, tobacco and alcohol

- Exercise

- High blood pressure (hypertension)

- Anxiety

- Underlying heart disease, including congenital heart disease, coronary artery disease, heart attack, heart failure and a weakened heart muscle (cardiomyopathy)

- African American ethnicity- increased the risk of PVCs by 30% in comparison with the risk in white individuals

- Male sex

- Lower serum magnesium or potassium levels

- Faster sinus rates

- A bundle-branch block on 12-lead ECG

- Hypomagnesemia

- Hypokalemia

Premature ventricular contractions can occur in a healthy person of any age, but are more prevalent in the elderly and in men. They frequently occur spontaneously with no known cause. Heart rate turbulence (HRT) is a phenomenon representing the return to equilibrium of the heart rate after a PVC. HRT parameters correlate significantly with mortality after myocardial infarction (heart attack). Some possible causes of PVCs include:

- Adrenaline excess;

- High blood calcium;

- Cardiomyopathy, hypertrophic or dilated;

- Certain medicines such as digoxin, which increases heart contraction or tricyclic antidepressants

- Chemical (electrolyte) problems in the blood;

- Contact with Carina (trachea/bronchi) when performing medical suctioning stimulates vagus nerve

- Drugs such as:

- Alcohol;

- Caffeine;

- Cocaine

- Theobromine;

- Myocardial infarction;

- Hypercapnia (CO poisoning);

- Hypokalemia—low blood levels of potassium

- Hypomagnesaemia—low blood levels of magnesium

- Hypoxia;

- Ischemia;

- Lack of sleep/exhaustion;

- Magnesium and potassium deficiency;

- Mitral valve prolapse;

- Myocardial contusion;

- Myocarditis;

- Sarcoidosis;

- Smoking

- Stress;

- Thyroid problems;

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.

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

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.

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.

In otherwise healthy patients, occasional premature atrial contractions are a common and normal finding and do not indicate any particular health risk. Rarely, in patients with other underlying structural heart problems, PACs can trigger a more serious arrhythmia such as atrial flutter or atrial fibrillation. In otherwise healthy people, PACs usually disappear with adolescence.

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.

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.

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.

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.

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.

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

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.

Hypertension, or abnormally high blood pressure, often signifies an elevated level of both psychological and physiological stress. Often, hypertension goes hand in hand with various atrial fibrillations including premature atrial contractions (PACs). Additional factors that may contribute to spontaneous premature atrial contractions could be:

- Increased age

- Abnormal body height

- History of cardiovascular disease (CV)

- Abnormal ANP levels

- Elevated cholesterol

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.

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.

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).

In the human heart the sinoatrial node is located at the top of the right atrium. The sinoatrial node is the first area of the heart to depolarize and to generate the action potential that leads to depolarization of the rest of the myocardium. Sinoatrial depolarization and subsequent propagation of the electrical impulse suppress the action of the lower natural pacemakers of the heart, which have slower intrinsic rates.

The accelerated idioventricular rhythm occurs when depolarization rate of a normally suppressed focus increases to above that of the "higher order" focuses (the sinoatrial node and the atrioventricular node). This most commonly occurs in the setting of a sinus bradycardia.

Accelerated idioventricular rhythm is the most common reperfusion arrhythmia in humans. However, ventricular tachycardia and ventricular fibrillation remain the most important causes of sudden death following spontaneous restoration of antegrade flow. Prior to the modern practice of percutaneous coronary intervention for acute coronary syndrome, pharmacologic thrombolysis was more common and accelerated idioventricular rhythms were used as a sign of successful reperfusion. It is considered a benign arrhythmia that does not require intervention, though atrioventricular dyssynchrony can cause hemodynamic instability, which can be treated through overdrive pacing or atropine.

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.

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.