Thank you very much. This AVNRT was very hard for me to understand.

@ECGwithReid

4 ай бұрын

💪Keep up the strong work!

Good video explaining the concept of AVNRT. Any simplified ECG criteria for assessment of accessory pathway. Will be a great help

@ECGwithReid

4 ай бұрын

Thanks for your kind words!! Glad you enjoyed 😁

Good video, thank you! Although similar in concept, I hope you do one explaining the pathophysiology of fast-slow and slow-slow AVNRT!

@ECGwithReid

4 ай бұрын

Surely will, in the future! I figured that, since Slow-Fast AVNRT is the case in ~90% of AVNRT that this would be the highest yield for viewers! 👍👍 Once I get all the basic foundational content down, I will be adding more nuanced/advanced videos on some of these topics that you mentioned. Stay tuned, my friend! 💪

@davidstern3526

4 ай бұрын

And how the vagal maneuvers affect the AV node to terminate them! Thank you

@ECGwithReid

4 ай бұрын

@@davidstern3526the AV node is innervated by the Autonomic Nervous system (parasympathetic and sympathetic fibers). Vagal maneuvers are those that increase intrathoracic pressure (bearing down, blowing into a syringe, etc.). Increase in intrathoracic pressure worsens venous return to the thorax/ heart by worsening the pressure gradient within the venous system. Less return to the heart ➡️ less myocardial filling/stretching, which is sensed by sensory fibers organic to the myocardium. They sense this signal, and our autonomic response is to increase the ratio of parasympathetic:sympathetic tone, effectively slowing the heart down since less return means less needed to pump out. Essentially telling the heart to “chill out.” This results in an increase in parasympathetic innervation to the SA and AV node. Remember that the Vagus nerve (cranial nerve X) is responsible for parasympathetic innervation of the heart. Parasympathetic fibers release ACh, binding to muscarinic receptors. M2 receptors are G inhibitory protein coupled receptors, and their activation will ultimately decrease intracellular cAMP and lead to a decreased expression of voltage gated Ca channels and increase K channels. This means that the AV node will be in a more “hyperpolarized” state and be unable continue propagating the reentry signal that is traveling through the fast and slow pathways. This is how the rhythm terminates!

@davidstern3526

4 ай бұрын

@@ECGwithReid Wow - what a clear and detailed response! BTW what I intended for with my initial comment was following on the other users comment who was asking for more videos, so I thought id throw in a topic for future videos on the mechanism of stopping the tachycardia. But you were kind enough to type it all out to me! Thank you

@ECGwithReid

4 ай бұрын

@@davidstern3526 👍👍. Physiology is fun! I never pass up an opportunity to chat about it 😁

Thank you sir, If sir can clarify me on this two Questions. 1. How can we know that the rhythm is triggered by PAC? Any clue we can observe in ECG with AVNRT. 2. What happens to normal P waves coming from SA node? Is it block or conducts?

@ECGwithReid

4 ай бұрын

Great questions! 1. It is rare that we will get to see the initiation of AVNRT on a full day 12 lead ECG. However, if you are analyzing a wearable Holter monitor or a cardiac monitor you can see the onset of the arrhythmia. ECG features are 1) short RP tachycardia, 2) Pseudo R’ in V1 and sometimes aVR, 3) Pseudo S in leads II, III, aVF, 4) narrow QRS (unless there is a preexisting bundle branch block). 2. You can’t have normal P waves from the SA node during AVNRT. Because there are retrograde P waves coming from the reentry circuit within the AV node. They travel retrograde and depolarize the atria, they also will depolarize the SA node, suppressing it. Hope this helps!

@sangaydorji4731

4 ай бұрын

@@ECGwithReid thank you for the prompt clarification sir, 🙏