When PGE is administered to a newborn, it prevents the ductus arteriosus from closing, therefore providing an additional shunt through which to provide the systemic circulation with a higher level of oxygen.

Antibiotics may be administered preventatively. However, due to the physical strain caused by uncorrected d-TGA, as well as the potential for introduction of bacteria via arterial and central lines, infection is not uncommon in pre-operative patients.

Diuretics aid in flushing excess fluid from the body, thereby easing strain on the heart.

Analgesics normally are not used pre-operatively, but they may be used in certain cases. They are occasionally used partially for their sedative effects.

Cardiac glycosides are used to maintain proper heart rhythm while increasing the strength of each contraction.

Sedatives may be used palliatively to prevent a young child from thrashing about or pulling out any of their lines.

Palliative treatment is normally administered prior to corrective surgery in order to reduce the symptoms of d-TGA (and any other complications), giving the newborn or infant a better chance of surviving the surgery. Treatment may include any combination of:

Simple l-TGA has a very good prognosis, with many individuals being asymptomatic and not requiring surgical correction.

In a number of cases, the (technically challenging) "double switch operation" has been successfully performed to restore the normal blood flow through the ventricles.

For newborns with transposition, prostaglandins can be given to keep the ductus arteriosus open which allows mixing of the otherwise isolated pulmonary and systemic circuits. Thus oxygenated blood that recirculates back to the lungs can mix with blood that circulates throughout the body. The arterial switch operation is the definitive treatment for dextro- transposition. Rarely the arterial switch is not feasible due to particular coronary artery anatomy and an atrial switch operation is preferred.

After the surgery, some patients require intubation and mechanical ventilation for several days to allow adequate tracheal toilet, but most patients can have the tubes removed soon after the surgery. The obstructive airway symptoms may be worse in the first postoperative weeks. Only a few patients have immediate relief of stridor, but many obtain immediate relief of problems with swallowing (dysphagia). After extubation, it might be necessary to maintain positive airway pressure by appropriate flows of a humidified oxygen/air mixture.

The procedure is performed in general anesthesia. It is useful to place pulse oximeter probes on "both hands" and "one foot" so that test occlusion of one arch or its branches will allow confirmation of the anatomy. In addition blood pressure cuffs should also be placed on one leg and both arms to confirm the absence of a pressure gradient when the intended point of division of the lesser arch is temporarily occluded with forceps.

Treatment in emergency situations ultimately involves electrical pacing. Pharmacological management of suspected beta-blocker overdose might be treated with glucagon, calcium channel blocker overdose treated with calcium chloride and digitalis toxicity treated with the digoxin immune Fab.

Third-degree AV block can be treated by use of a dual-chamber artificial pacemaker. This type of device typically listens for a pulse from the SA node via lead in the right atrium and sends a pulse via a lead to the right ventricle at an appropriate delay, driving both the right and left ventricles. Pacemakers in this role are usually programmed to enforce a minimum heart rate and to record instances of atrial flutter and atrial fibrillation, two common secondary conditions that can accompany third-degree AV block. Since pacemaker correction of third-degree block requires full-time pacing of the ventricles, a potential side effect is pacemaker syndrome, and may necessitate use of a biventricular pacemaker, which has an additional 3rd lead placed in a vein in the left ventricle, providing a more coordinated pacing of both ventricles.

The 2005 Joint European Resuscitation and Resuscitation Council (UK) guidelines state that atropine is the first line treatment especially if there were any adverse signs, namely: 1) heart rate 3 seconds. Mobitz Type 2 AV block is another indication for pacing.

As with other forms of heart block, secondary prevention may also include medicines to control blood pressure and atrial fibrillation, as well as lifestyle and dietary changes to reduce risk factors associated with heart attack and stroke.

Acute management is as for SVT in general. The aim is to interrupt the circuit. In the shocked patient, DC cardioversion may be necessary. In the absence of shock, inhibition at the AV node is attempted. This is achieved first by a trial of specific physical maneuvers such as holding a breath in or bearing down. If these maneuvers fail, using intravenous adenosine; causes complete electrical blockade at the AV node and interrupts the reentrant electrical circuit. Long-term management includes beta blocker therapy and radiofrequency ablation of the accessory pathway.

Transposition of the great vessels (TGV) is a group of congenital heart defects involving an abnormal spatial arrangement of any of the great vessels: superior and/or inferior venae cavae, pulmonary artery, pulmonary veins, and aorta. Congenital heart diseases involving only the primary arteries (pulmonary artery and aorta) belong to a sub-group called transposition of the great arteries.

l-TGA can sometimes be diagnosed in utero with an ultrasound after 18 weeks gestation. However, many cases of simple l-TGA are "accidentally" diagnosed in adulthood, during diagnosis or treatment of other conditions.

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

The goal of treatment is to prevent the development or continuation of neurologic deficits. Treatments include observation, anticoagulation, stent implantation and carotid artery ligation.

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.

An acyanotic heart defect, also known as non-cyanotic heart defect, is a class of congenital heart defects. In these, blood is shunted (flows) from the left side of the heart to the right side of the heart due to a structural defect (hole) in the interventricular septum. People often retain normal levels of oxyhemoglobin saturation in systemic circulation.

This term is outdated, because a person with an acyanotic heart defect may show cyanosis (turn blue due to insufficient oxygen in the blood).

According to a study in cyanotic congenital heart disease (CCHD) in Sohag University, Upper Egypt. 50 neonates were diagnosed as suffering from cyanotic congenital heart disease (CCHD), they concluded that cyanotic congenital heart disease (CCHD) frequency was significant (9.5%) with D-TGA being the commonest type. Majority of neonates with Cyanotic congenital heart disease (CCHD) showed survival with suitable management.

Cor triatriatum (or triatrial heart) is a congenital heart defect where the left atrium (cor triatriatum sinistrum) or right atrium (cor triatriatum dextrum) is subdivided by a thin membrane, resulting in three atrial chambers (hence the name).

Cor triatriatum represents 0.1% of all congenital cardiac malformations and may be associated with other cardiac defects in as many as 50% of cases. The membrane may be complete or may contain one or more fenestrations of varying size.

Cor triatrium sinistrum is more common. In this defect there is typically a proximal chamber that receives the pulmonic veins and a distal (true) chamber located more anteriorly where it empties into the mitral valve. The membrane that separates the atrium into two parts varies significantly in size and shape. It may appear similar to a diaphragm or be funnel-shaped, bandlike, entirely intact (imperforate) or contain one or more openings (fenestrations) ranging from small, restrictive-type to large and widely open.

In the pediatric population, this anomaly may be associated with major congenital cardiac lesions such as tetralogy of Fallot, double outlet right ventricle, coarctation of the aorta, partial anomalous pulmonary venous connection, persistent left superior vena cava with unroofed coronary sinus, ventricular septal defect, atrioventricular septal (endocardial cushion) defect, and common atrioventricular canal. Rarely, asplenia or polysplenia has been reported in these patients.

In the adult, cor triatriatum is frequently an isolated finding.

Cor triatriatum dextrum is extremely rare and results from the complete persistence of the right sinus valve of the embryonic heart. The membrane divides the right atrium into a proximal (upper) and a distal (lower) chamber. The upper chamber receives the venous blood from both vena cavae and the lower chamber is in contact with the tricuspid valve and the right atrial appendage.

The natural history of this defect depends on the size of the communicating orifice between the upper and lower atrial chambers. If the communicating orifice is small, the patient is critically ill and may succumb at a young age (usually during infancy) to congestive heart failure and pulmonary edema. If the connection is larger, patients may present in childhood or young adulthood with a clinical picture similar to that of mitral stenosis. Cor triatriatum may also be an incidental finding when it is nonobstructive.

The disorder can be treated surgically by removing the membrane dividing the atrium.

Treatment for alcoholic cardiomyopathy involves lifestyle changes, including complete abstinence from alcohol use, a low sodium diet, and fluid restriction, as well as medications. Medications may include ACE inhibitors, beta blockers, and diuretics which are commonly used in other forms of cardiomyopathy to reduce the strain on the heart. Persons with congestive heart failure may be considered for surgical insertion of an ICD or a pacemaker which can improve heart function. In cases where the heart failure is irreversible and worsening, heart transplant may be considered.

Treatment will possibly prevent the heart from further deterioration, and the cardiomyopathy is largely reversible if complete abstinence from alcohol is maintained.

Cyanotic heart defect is a group-type of congenital heart defect (CHD) that occurs due to deoxygenated blood bypassing the lungs and entering the systemic circulation or a mixture of oxygenated and unoxygenated blood entering the systemic circulation. It is caused by structural defects of the heart (i.e.: right-to-left, bidirectional shunting, malposition of the great arteries), or any condition which increases pulmonary vascular resistance. The result being the development of collateral circulation.

Left to right shunting heart defects include:

- Ventricular septal defect (VSD) (30% of all congenital heart defects)

- Atrial septal defect (ASD)

- Atrioventricular septal defect (AVSD)

- Patent ductus arteriosus (PDA)

- Previously, Patent ductus arteriosus (PDA) was listed as acyanotic but in actuality it can be cyanotic due to pulmonary hypertension resulting from the high pressure aorta pumping blood into the pulmonary trunk, which then results in damage to the lungs which can then result in pulmonary hypertension as well as shunting of blood back to the right ventricle. This consequently results in less oxygenation of blood due to alveolar damage as well as oxygenated blood shunting back to the right side of the heart, not allowing the oxygenated blood to pass through the pulmonary vein and back to the left atrium.

- (Edit - this is called Eisenmenger's syndrome and can occur with Atrial septal defect and ventricular septal defect as well (actually more common in ASD and VSD) therefore PDA can still be listed as acyanotic as, acutely, it is)

Others:

- levo-Transposition of the great arteries (l-TGA)

Acyanotic heart defects without shunting include:

- Pulmonary stenosis (a narrowing of the pulmonary valve)

- Aortic stenosis

- Coarctation of the aorta

Early treatment includes removing fluids from the stomach via a nasogastric tube, and providing fluids intravenously. The definitive treatment for duodenal atresia is surgery (duodenoduodenostomy), which may be performed openly or laparoscopically. The surgery is not urgent. The initial repair has a 5 percent morbidity and mortality rate.

Differentiation of DIOS from constipation is generally performed by unit specializing in the treatment of cystic fibrosis. Adequate hydration and an aggressive regimen of laxatives are essential for treatment and prevention of DIOS. Osmotic laxatives such as polyethylene glycol are preferred. Individuals prone to DIOS tend to be at risk for repeated episodes and often require maintenance therapy with pancreatic enzyme replacement, hydration and laxatives (if the symptoms are also mild).

Oral contrast instillation into the colon/ileum under radiological control has been found to reduce the need for surgical intervention.

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.

Atrioventricular reentrant tachycardia, atrioventricular reciprocating tachycardia or AVRT, is a type of abnormal fast heart rhythm and is classified as a type of supraventricular tachycardia (SVT). AVRT is most commonly associated with Wolff-Parkinson-White syndrome, in which an accessory pathway allows electrical signals from the heart's ventricles to enter the atria and cause earlier than normal contraction, which leads to repeated stimulation of the atrioventricular node.

Wellens' syndrome is an electrocardiographic manifestation of critical proximal left anterior descending (LAD) coronary artery stenosis in patients with unstable angina. It is characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads. A less common variant is biphasic T wave inversions in the same leads.

First described by Hein J. J. Wellens and colleagues in 1982 in a subgroup of patients with unstable angina, it does not seem to be rare, appearing in 18% of patients in his original study. A subsequent prospective study identified this syndrome in 14% of patients at presentation and 60% of patients within the first 24 hours.

The presence of Wellens' syndrome carries significant diagnostic and prognostic value. All patients in the De Zwann's study with characteristic findings had more than 50% stenosis of the left anterior descending artery (mean = 85% stenosis) with complete or near-complete occlusion in 59%. In the original Wellens' study group, 75% of those with the typical syndrome manifestations had an anterior myocardial infarction. Sensitivity and specificity for significant (more or equal to 70%) stenosis of the LAD artery was found to be 69% and 89%, respectively, with a positive predictive value of 86%.

Wellens' sign has also been seen as a rare presentation of Takotsubo cardiomyopathy or stress cardiomyopathy.

A systematic review of the evidence found that exercise may or may not reduce the size of the gap in pregnant or postpartum women. The authors looked at 8 studies totaling 336 women and concluded, “Due to the low number and quality of included articles, there is insufficient evidence to recommend that exercise may help to prevent or reduce DRAM” also stating that "non-specific exercise may or may not help to prevent or reduce DRAM during the ante- and postnatal periods."