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.

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.

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)

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.

Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.

VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.

- Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.

The restrictive VSDs (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmenger's syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

Symptoms include difficulty breathing (dyspnea) and bluish discoloration on skin and lips (cyanosis). A newborn baby will show signs of heart failure such as edema, fatigue, wheezing, sweating and irregular heartbeat.

A defect in the ostium primum is occasionally classified as an atrial septal defect, but it is more commonly classified as an atrioventricular septal defect

On ECG superior axis deviation is generally found in primum ASD, but an RSR pattern (M pattern) in V1 is characteristic. Fixed splitting of the second heart sound occurs because of equal filling of the left and right atria during all phases of the respiratory cycle.

Patients with Atrial Septal Defects may have Atrial Fibrillation, Atrial Tachycardia, or Atrial Flutter, but these arrythmias are not usually seen until patients grow older. Features also seen on the EKG include Right Atrial Enlargement, PR prolongation and advanced AV block. When you suspect a patient has an ASD based on the findings of an incomplete Right Bundle Branch Block with a rSr' or rSR' the next thing you should do is examine the frontal plane QRS. The frontal plane QRS is the most helpful clue to help you differentiate Secundum ASD from Primum ASD. In Primum defects left axis deviation is seen in most patients with an axis of > -30 degrees and very few patients have right axis deviation. In contrast Secundum defects have an axis between 0 degrees and 180 degrees with most cases to the right of 100 degrees.

In the ECG above, you can see an example of the rSR' pattern in V1 with a R' greater than S with T wave inversion which is commonly seen in volume overload Right Ventricular Hypertrophy.

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%.

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.

If there is a defect in the septum, it is possible for blood to travel from the left side of the heart to the right side of the heart, or the other way around. Since the right side of the heart contains venous blood with a low oxygen content, and the left side of the heart contains arterial blood with a high oxygen content, it is beneficial to prevent any communication between the two sides of the heart and prevent the blood from the two sides of the heart from mixing with each other.

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.

Pre-excitation syndrome is an abnormal heart rhythm in which the ventricles of the heart become depolarized too early, which leads to their partial premature contraction.

Left bundle branch block (LBBB) is a cardiac conduction abnormality seen on the electrocardiogram (ECG). In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.

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

In the case of 2:1 block (2 P waves for every QRS complex) it is impossible to differentiate type I from type II Mobitz block based solely on the P:QRS ratio or on a pattern of lengthening PR intervals. In this case, a lengthened PR interval with a normal QRS width is most likely indicative of a type I-like pathology, and a normal PR interval with a widened QRS is most likely indicative of a type II-like pathology.

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)

Normally, the atria and the ventricles are electrically isolated, and electrical contact between them exists only at the "atrioventricular node". In all pre-excitation syndromes, at least one more conductive pathway is present. Physiologically, the normal electrical depolarization wave is delayed at the atrioventricular node to allow the atria to contract before the ventricles. However, there is no such delay in the abnormal pathway, so the electrical stimulus passes to the ventricle by this tract faster than via normal atrioventricular/bundle of His system, and the ventricles are depolarized (excited) before (pre-) normal conduction system. This creates the ventricular pacemaker type of ectopic pacemaker.

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.

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.

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.

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)

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.

In cardiology, Ventricular dyssynchrony is a difference in the timing, or lack of synchrony, of contractions in different ventricles in the heart. Large differences in timing of contractions can reduce cardiac efficiency and is correlated with heart failure.