Why is there bradycardia in complete heart block?

AI Thread Summary
The discussion centers on the independent contraction of the atria and ventricles in the heart and the reasons for the slower heart rate associated with this phenomenon. The lower intrinsic rate of the accessory pacemaker in the ventricles, typically around 40 beats per minute, is identified as a key factor. This slower rate can lead to ectopic beats, which are extra heartbeats that can originate from either the conducting system or the myocardium itself. Ectopic beats may be triggered by factors such as hypoxia, stimulants, or lack of sleep. In cases of complete heart block, the SA node does not communicate with the AV node, resulting in P waves that do not correspond with QRS complexes. The QRS complex reflects a bradycardic rate due to the slower pacemaker activity in the absence of SA node influence. Sustained runs of ectopic beats can lead to ventricular tachycardia, which poses significant health risks.
sameeralord
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Ok I know that atria and ventricles contract independently and it makes sense heart would beat slower but what is the exact reason. The accesssory pacemaker that activates ventricles, is is lot slower than AV node is that the reason? Thanks :smile:
 
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sameeralord said:
Ok I know that atria and ventricles contract independently and it makes sense heart would beat slower but what is the exact reason. The accesssory pacemaker that activates ventricles, is is lot slower than AV node is that the reason? Thanks :smile:

Yes. The lower parts of the atrioventricular conducting fibers have a lower intrinsic rate, typically about 40 bpm. This sets up a situation where other parts the left ventricular myocardium may "take over" with a higher rate. This is called "ectopy". While it sometimes can be lifesaving, it can also be dangerous. Single ventricular ectopic beats are common, and can occur in healthy persons. When they occur in runs, they can be life threatening and often require emergency cardioversion, either with IV drugs or electrically. Untreated, they can degenerate into ventricular fibrillation with no effective beats.
 
SW VandeCarr said:
Yes. The lower parts of the atrioventricular conducting fibers have a lower intrinsic rate, typically about 40 bpm. This sets up a situation where other parts the left ventricular myocardium may "take over" with a higher rate. This is called "ectopy". While it sometimes can be lifesaving, it can also be dangerous. Single ventricular ectopic beats are common, and can occur in healthy persons. When they occur in runs, they can be life threatening and often require emergency cardioversion, either with IV drugs or electrically. Untreated, they can degenerate into ventricular fibrillation with no effective beats.

Hey thanks again :smile: So ectopic beats do they originate from the conducting system of heart or outside the heart? Also if there is ectopic heart beats in complete heart block, does that mean there is tachycardia?
 
sameeralord said:
Hey thanks again :smile: So ectopic beats do they originate from the conducting system of heart or outside the heart? Also if there is ectopic heart beats in complete heart block, does that mean there is tachycardia?

Ectopic beats can arise within or outside the conducting system. Virtually any cell of the myocardium (heart muscle) can potentially initiate a depolarization wave which then spreads across the entire ventricular myocardium. Ectopic beats usually originate in the left ventricular myocardium and may be initiated by hypoxia (low tissue oxygen), drugs (stimuants like caffeine) or lack of sleep among other things. In normal hearts they are just single extra beats, but with heart disease they can occur in runs. A run of three or more is called ventricular tachycardia (VT), but it's the sustained VT that is (usually) life threatening.
 
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sameeralord said:
Ok I know that atria and ventricles contract independently and it makes sense heart would beat slower but what is the exact reason. The accesssory pacemaker that activates ventricles, is is lot slower than AV node is that the reason? Thanks :smile:

Just a quick note in addition to what SW said, in a complete block (as you guessed) the SA node doesn't relay to the AV node.

So on an electrocardiogram the P waves don't correspond to the QRS complex. The P waves can actually have a normal frequency and sinus rhythm (that is they occur at a normal frequency and are upright in leads II, III and VF).

The QRS complex is what would be bradycardic, occurring 40-55 tpm because as you and SW discussed the slower rate of pacemaker ability further along the conducting pathways.

Remember in terms of pacemaker ability it goes SA node>AV nodal fibers>Purkinje fibers. So its the increased speed of the SA node's depolarization that keeps AV/Purkinje fibers from setting the pace ( because they get depolarized before their threshold for selfexcitation is reached), but in a block the next fastest pacemaker tends to take over.
 
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