Cause and Effects of an AV Heart Block
A normal heartbeat is initiated by an electrical signal which starts in the sinoatrial (SA) node, the heart’s natural pacemaker located in the right atrium. The impulse travels through the atria, moving down to the atrioventricular (AV) node, located in the center of the heart between the atria and ventricles. The AV node functions as a critical delay in the conduction system, preventing the atria & ventricles from contracting at the same time, which would cause an ineffective flow of blood through the heart. The electrical current travels from the AV node to the ventricles, causing the ventricles to contract and pump blood out to the body.
In a patient with an AV heart block, the electrical signal controlling the heartbeat is partially or completely blocked from reaching the ventricles.
Common causes of heart block
Heart blocks may be congenital, they may occur secondary to medications, or be caused by disease that results in tissue death affecting a portion of the conduction system.
As a person ages, the risk of acquired heart block increases, along with the incidence of heart disease. The most common cause of acquired heart block is a heart attack, but may also be caused by an enlarged heart, heart failure, and rheumatic fever.
AV blocks are identified by their severity… First-degree, second-degree, which can be subdivided into type 1 and type 2, and then third-degree heart block.
Organizing heart blocks by constant vs. variable P-R interval can help you separate one heart block from another. The heart blocks with a constant P-R interval include the First degree & Second degree Type II (Mobitz II). The heart blocks with a variable P-R interval include Second degree Type I (Wenckebach) & Third degree.
First degree AV block is the most common heart block. It occurs when the electrical impulses are slowed down, but they still successfully reach the ventricles. On the EKG, the PR interval represents the measurement of conduction time between the atria & ventricles. First degree heart block will look like a typical sinus rhythm, with a constant PR interval; however, it will measure >0.20 second, when it should normally be 0.12-0.20 second. This indicates a conduction delay in the AV node. The rhythm is always stated in the interpretation – for example, ‘sinus rhythm with a 1st degree AV block’ or ‘sinus bradycardia with a 1st degree AV block.’
First degree heart block is often seen in highly trained athletes, and when occurring in isolation, the patient is usually asymptomatic & no treatment is necessary. It may also be found in association with rheumatic fever, acute inferior MI, increased vagal tone, and AV nodal blocking drugs, such as digoxin & beta-blockers.
Second degree AV block exists when there is intermittent conduction failure & can be broken down into two categories – Type I (also called Mobitz I or Wenckebach) & Type II (also called Mobitz II).
In Mobitz I (Wenckebach), the electrical impulses are delayed further & further until conduction fails to reach the ventricles entirely. Malfunctioning AV node cells progressively fatigue until they fail to conduct an impulse. This is characterized by a P-R interval that progressively gets longer & longer until the P wave is not followed by a QRS complex – the QRS has dropped off after the P wave – essentially the heart has skipped a beat.
Any drug that slows AV conduction may cause a Type I block, such as beta-blockers, calcium channel blockers, digoxin, or amiodarone. However, these blocks are most often seen in patients with an inferior MI, increased vagal tone, electrolyte imbalance, myocarditis, or following cardiac surgery.
Mobitz I blocks are usually transient & reversible, not requiring treatment unless the patient becomes symptomatic. Atropine may be effective in increasing cardiac output in symptomatic patients.
Mobitz II is usually due to structural damage to the conducting system below the AV node, in the His-Purkinje system. This may be seen with myocardial infarction, fibrosis of the conducting system, inflammatory conditions, cardiac surgery (esp. when close to the septum), autoimmune disease, hyperkalemia, as well as drugs (such as beta-blockers, calcium channel blockers, digoxin, & amiodarone).
Mobitz II is likely to be associated with hemodynamic compromise which may be sudden & unexpected, causing syncope or sudden cardiac death. If cardiac output is decreased, a temporary pacemaker can be inserted until the conduction stabilizes, however, if the block is persistent, the patient will benefit from a permanent pacemaker.
Third-degree heart block is a complete heart block in which none of the electrical impulses from the atria reach the ventricles, so the atria & ventricles beat independently. The ventricles may generate some impulses on their own, called junctional or ventricular escape beats, but at a rate much slower than normal. On the EKG, the P waves & QRS complexes are seen regularly, but at two distinctly different rates, because the atria & ventricles are beating independently of each other.
The causes of third-degree heart block are the same as for Mobitz I and Mobitz II – the most important ones including inferior MI, AV-nodal blocking drugs (such as calcium-channel blockers, beta-blockers, & digoxin), and degeneration of the conducting system due to unknown cause. Complete heart block is essentially the endpoint of either Mobitz I or Mobitz II AV block. It may be due to the progressive fatigue of AV nodal cells (as in Mobitz I), or it may be the result of a sudden onset of complete conduction failure throughout the His-Purkinje system (as in Mobitz II).
Patients with third degree heart block feel poorly, with lightheadedness & fatigue, with a high risk for sudden cardiac death, especially if it is accompanied with an anterior MI. Urgent backup temporary pacing is required as well as the insertion of a permanent pacemaker or defibrillator.
A heart block is a partial delay or complete interruption
in the conduction pathway between the atria & ventricles.
The electrical signals telling the heart to contract
are partially or totally blocked between the
atria & ventricles – an atrioventricular (AV) block.
AV blocks are identified by their severity:
First-degree is not a true block, but a consistent delay of conduction in the AV node, resulting in a P-R interval longer than 0.20 second. The electrical impulses are slowed as they pass through the conduction system, but they all successfully reach the ventricles. This type is relatively common & treatment is generally not needed.
Second-degree Mobitz I (Wenckebach) is an intermittent block at the AV node. The electrical impulses are delayed further & further with each heartbeat until an impulse fails to reach the ventricles entirely. This is seen on the EKG as a P-R interval that progressively lengthens until a QRS complex is dropped, therefore there are more P waves than QRS complexes.
Second-degree Mobitz II is an intermittent block at the bundle of His or bundle branches resulting in some of the electrical impulses not transmitted from the atria to the ventricles at all. There is a constant P-R interval, but random QRS complexes are missing. This condition is more serious and will likely require a pacemaker.
Third-degree heart block is a complete block at or below the AV node in which none of the electrical impulses from the atria reach the ventricles – the atria & ventricles beat independently of each other. Urgent treatment is required – ultimately a permanent pacemaker or defibrillator will need to be inserted.