I started this thread by thinking this question but I developed it further below

What is the mechanism maintaining refractory period of pacemakers?

My conjecture is that the mechanism is the simultaneous depolarisation of at least SA node and AV node. I am not convinced yet about the Purkinje fibers' participation.

Bigger question from this is:

How do pacemakers work under threshold without action potential? There are continually leaking Funny channels (Na+) in pacemakers. There has to be chemical changes intrinsic changes

  • change in the permeability of Funny channels or
  • active pumping of Na+ out OR pumping something negative inside the cell (probably Cl-, not sure) and

extrinsic changes

  • reflex arch blocking the action potential of pacemakers when enough preceeding sensitisation of AV node
    • I have no evidence for that this kind of sensitisation would happen in SA node or in Purkinje fibers.

which all seem to be working together in firing recovery mechanism through AV node without specific SA node stimulation. Example logic tree for a myocardial infarction patient of 68 years old:

  • R wave of atrial fibrillation and flutter
  • extrinsic stimulus to start sensitisation of AV node
  • intrinsic sensitisation of AV node
  • extrinsic stimulus through reflex arch
  • systole and upper-systole of AV node starting
  • lower-systole of AV node
    • intersection of upper- and lower-systoles
  • unstable end of lower-systole
  • unstable systole
  • extrinsic firing simultaneous SA and AV node (similar extrinsic regulation as in the beginning of this logic tree)
  • prolonged and stable refractory period and long compensatory pause

It is debated whether the pathophysiology of IST and POTS results from abnormal autonomic regulation or abnormal sinus node function.

My conjectures based on my logic tree

  • Pathophysiology of IST results from normal extrinsic (recovery) mechanism of autonomic regulation which body uses to recover from abnormal stimuli (etc atrial fibrillation and flutter)
  • Pathophysiology of POTS results from abnormal extrinsic mechanism of autonomic regulation when there is no stimuli after abnormal stimuli

What is causing the abnormal autonomic mechanism in POTS? I would say that IST precedes POTS. Prolonged IST seems to be going to POTS. Physical explanation is that the body cannot last regular IST so it goes to POTS, since losing its normal extrinsic regulation. What is this (apparently cumulative, not necessarily long-term) trigger of disabling the extrinsic autonomic regulation of the heart?


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