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I have a question: What physiological controls (if any) does the body have on heart rate post-heart transplant?


I'm not sure...but I guess the autonomic control would go and since in the heart it favours more towards sympathetic therefore there may be bradycardia and less contractility of the cardiac muscles....only a guess


With autonomic control removed, wouldn't the intrinsic characteristics favour tachy (intrinisic rate ~ 100 bpm). Any increase in heart rate up to 100 bpm in normal individuals is manifested by parasympathetic withdrawal.


very good qs
iam reading this from harrison's pg=1330(15th ed)
during procedure folllowing happens:diseased heart is removed but following parts are not dissected:1)posterior wall of the right atrium. 2)superior and inferior vena cava. 3) posterior wall of the left atrium along with pulmonary vein intact
following parts are dissected from donor's heart
1)posterior wall of right and left atrium
after transplantatiion following occurs
increased heart rate due to intact donor sinus node which is under autonomic control.


These patients are 'pre-load dependent' meaning that their acute needs for increased CO are met by increased SV. Increased HR can be accomplished (remember catecholamines), but it takes longer, and it also takes longer to return to baseline, because of no vagal input. So SANS can still affect heart but PANS cannot. However, I believe the baseline HR for these patients is closer to brady than tachy, due to intrinsic nodal activity.
Many of them are paced, for this reason, I think.


Idiopath and the others.......
I think that's right; baseline would change to the intrinsic rate of 100 bpm, and PANS would bot be possible due to the lack of vagal innervation. I'm pretty sure that you're right about SANS possibly having some effect, but why? would it be from blood-borne sympathomimetic NT's? Sorry, I have a limited knowledge of this stuff, I'm not in medical school yet but I think I will be within a year. Once again thanks everyone.

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