bradycardia in response to hypoxemia in kids

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ether_screen

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I may be missing something completely obvious, but can someone give an IN-DEPTH physiologic explanation why kids immediately respond to hypoxemia with bradycardia? Thanks in advance.
 
ether_screen said:
I may be missing something completely obvious, but can someone give an IN-DEPTH physiologic explanation why kids immediately respond to hypoxemia with bradycardia? Thanks in advance.

This is not in-depth, but the sympathetic nervouse system is still developing in younger children.
 
It's not just in response to bradycardia. When I was intubating on the NICU, I was pretty surprised that these kids didn't tach away as I approached the trachea (these kiddo's weren't always sedated). Moreover, the signal that a particular attempt was OVER was the kiddo's bradycardia, not desat. Now, I know that a kid's CO is principally derived from their HR, but there is usually room to go up...

I read somewhere about the "dive" reflex of neonates. That is, with hypoxemia/airway stimulation, the cardio-respiratory stim is centrall shutdown, that to a brain-stem-level reflex present in neonates of other species as well. Seems to share similarities with the dive-reflex of sea-mammals who need to conserve O2 underwater. Furthermore, could be an exageration of vagal reflexes seen in older kids/adults. Perhaps then in kiddos the dive reflex simply outperforms the sympathetic response...
 
ether_screen said:
I may be missing something completely obvious, but can someone give an IN-DEPTH physiologic explanation why kids immediately respond to hypoxemia with bradycardia? Thanks in advance.

but just couldnt help sharing my thoughts....
In kids especially neonates the parasympathetic nervous system is at a higher level of development that the sympathetic.The heart is prone to cardiodepression in cases of stress,thus hypoxemia leads to bradycardia very soon.
The sympathetic nervous system and baroreceptor reflexes are not mature enough to deal with the stress.
 
Hence pretreatment with atropine prior to laryngoscopy in kids (RSI).
 
In the neonate the following studies were done (mainly on fetal sheep/rabbits)... if the carotid bodies were denervated or the vagal efferent to the heart was removed, hypoxia would not lead to bradycardia. Hence this is a carotid body mediated event: the carotid body is triggered by the hypoxic blood. It appears that the response is mediated by activation of ADO A2a receptors (that is a sub-type of adenosine receptors) and this reflex seems to be more apparent in neonates for possibly a few reasons: 1) increased expression of ADO A2a receptor mRNA 2) increased adenosine levels in the neonate 3) the area postrema in the neonate seems to be more intrinsically tied into cardiac reflex arcs along with the carotid bodies, and that over time, other reflexes start superimposing themselves over this reflex.

I don't know what the genetic advantage would be of bradycardia in the setting of hypoxia....
 
Tenesma and everyone else,

Thanks so much.
 
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