sdadam
DialedMedics.com
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I suspect that the amount of adenosine required to effect a PT's rhythm has a correlation to the degree of damage in the heart.
Adenosine is endogenously released in response to ischemia in the heart and has what appear to be impressive cardio-protective effects. It's seen some promising use in the topical treatment of diabetic ulcers in fact.
My theory is that the degree of ischemia and disease in the heart correlates to interstitial adenosine levels. The increased level of adenosine could then through several known mechanisms such as down regulation of A2a receptors in the effected areas (in this case AV node, hopefully AVNRT if we are looking to treat it with adenosine.)
That down regulation and the existence of endogenous adenosine already occupying receptor sites at the time of administration could easily explain why there would be a correlation. It would also explain why in my anecdotal experience, although I would love to gather some data, lower doses are very effective at causing systolic pauses in PSVT's that are not AVNRT (pathologies out of the AV node) to display the underlying rhythm but why it seems most of us only see sustained conversion at the higher doses. I would postulate that the fact that you need a hire dose to effect the AV node is an indication that you should advance the dose to full effect. If the AV node responds immediately to a low dose then I suspect pathology outside the AV node. This all boils down to researching the genetic expression of adenosine receptor sub-types through the body. If you want to understand how and why the dosing of adenosine works the way it does (or any drug for that matter) it's in the receptor / ligand relationship.
Adenosine is endogenously released in response to ischemia in the heart and has what appear to be impressive cardio-protective effects. It's seen some promising use in the topical treatment of diabetic ulcers in fact.
My theory is that the degree of ischemia and disease in the heart correlates to interstitial adenosine levels. The increased level of adenosine could then through several known mechanisms such as down regulation of A2a receptors in the effected areas (in this case AV node, hopefully AVNRT if we are looking to treat it with adenosine.)
That down regulation and the existence of endogenous adenosine already occupying receptor sites at the time of administration could easily explain why there would be a correlation. It would also explain why in my anecdotal experience, although I would love to gather some data, lower doses are very effective at causing systolic pauses in PSVT's that are not AVNRT (pathologies out of the AV node) to display the underlying rhythm but why it seems most of us only see sustained conversion at the higher doses. I would postulate that the fact that you need a hire dose to effect the AV node is an indication that you should advance the dose to full effect. If the AV node responds immediately to a low dose then I suspect pathology outside the AV node. This all boils down to researching the genetic expression of adenosine receptor sub-types through the body. If you want to understand how and why the dosing of adenosine works the way it does (or any drug for that matter) it's in the receptor / ligand relationship.