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An atrioventricular block (or AV block) is a type of heart block involving impairment of the conduction between the atria and ventricles of the heart. It usually involves the atrioventricular node, but it can involve other structures.The atrioventricular node (abbreviated AV node) is an area of specialized tissue between the atria and the ventricles of the heart, specifically in the posteroinferior region of the interatrial septum near the opening of the coronary sinus, which conducts the normal electrical impulse from the atria to the ventricles.
The atrioventricular node delays impulses for a while (aprox. 0.12s) before allowing impulses through to the His-Purkinje conduction system, which spreads impulses to the ventricular walls. The reason it is important to delay the cardiac impulse is to ensure that the atria have ejected their blood into the ventricles before the ventricles contract.
First degree AV block or PR prolongation is a disease of the electrical conduction system of the heart in which the PR interval is lengthened. In first degree heart block, the disease is almost always at the level of the atrioventricular node (AV node). It has a prevalence in the normal (young adult) population of 0.65-1.1% and the incidence is 0.13 per 1000 persons.
First degree AV block may be due to conduction delay in the AV node, in the His-Purkinje system (made up by the bundle of His and the Purkinje fibers), or a combination of the two. The majority of cases are due to a dysfunction of the AV node; however, when first degree heart block coexists with a bundle-branch block, the cause is more likely to be a conduction delay in the His-Purkinje system.
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. Drugs which increase calcium concentration such as Digitalis, decrease AVN conduction time.
In normal individuals, the AV node slows the conduction of electrical impulse through the heart. This is manifest on a surface ECG as the PR interval. The normal PR interval is from 120 ms to 200 ms in length. This is measured from the initial deflection of the P wave to the beginning of the QRS complex.
In first degree heart block, the diseased AV node conducts the electrical activity more slowly. This is seen as a PR interval greater than 200 ms in length on the surface ECG. It is usually an incidental finding on a routine ECG.
First degree heart block does not require any particular investigations except for electrolyte and drug screens especially if an overdose is suspected.
The management includes identifying and correcting electrolyte imbalances and withholding any offending medications. This condition does not require admission unless there is an associatedmyocardial infarction
. Even though it usually does not progress to higher forms of heart block, it may require outpatient follow up and monitoring of theECG
especially if there is a comorbidbundle 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 theECG
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.
There are two distinct types of second degree AV block, called Type 1 and Type 2. The distinction is made between them because type 1 second degree heart block is considered a more benign entity than type 2 second degree heart block.
Mobitz I heart block is characterized by progressive prolongation of the PR interval on the electrocardiogram (ECG) on consecutive beats followed by a blocked P wave (i.e. a 'dropped' QRS complex). After the dropped QRS complex, the PR interval resets and the cycle repeats.
One of the baseline assumptions when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be regular. If the atrial rhythm is not regular, there could be alternative explanations as to why certain P waves do not conduct to the ventricles.
This is almost always a benign condition for which no specific treatment is needed.
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. 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.
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.
Most people with Wenckebach (Type I Mobitz) do not show symptoms. However, those that do usually display one or more of the following:
Third degree AV block, also known as complete heart block, is a defect of the electrical system of the heart, in which the impulse generated in the atria (typically the SA node on top of the right atrium) does not propagate to the ventricles.
Because the impulse is blocked, an accessory pacemaker below the level of the block will typically activate the ventricles. This is known as an escape rhythm. Since this accessory pacemaker activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG).
One of the most important character of this block is the absolute absence of the opportunity for atrial impulse to enter and capture the ventricles.It means that in the scene of this block we never seen any fusion or capture beats(Dr.Nader Ahmad Exeer).
Patients with third degree AV block typically experience a lower overall measured heart rate (as low as 28 beats per minute during sleep), low blood pressure, and poor circulation. In some cases, exercising may be difficult, as the heart cannot react quickly enough to sudden changes in demand or sustain the higher heart rates required for sustained activity.
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, and the AV node may recover. Studies have shown that third degree heart block in the setting of an inferior wall myocardial infarction typically resolves within 2 weeks[citation is needed]. 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.
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 and sends a pulse to the AV node at an appropriate interval, essentially completing the connection between the two nodes. 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.
Treatment in emergency situations is an external pacer. Atropine is generally not given because of the complete block in the AV node and the complete disassociation between the atria and ventricles. Atropine is only useful in increasing the conductivity through the AV node. Therefore, with no pathway through the AV node to strengthen, atropine would have little and most likely no effect at all on a 3rd degree heart block. However American Heart Association does state that giving a trial of atropine while waiting for the pacer to be set up is accetable.