Why does your cardiac output increase in a warm environment? Is it due to increased blood flow to the skin to dissipate the heat?
Thanks.
Thanks.
cardiac output vs temperature question
- Thread starter mossyfiber12
- Start date
i thought it was because the heat is acting as a catalyst and is thus increasing the rate of our rxns, making them faster. This would mean that our heart rate will increase in order to provide more O2 to cells as metabolism increases.
i'm just a premed though... take this with a grain of salt
CO increases in warm environments due to an increased autonomic sympathetic: parasympathetic ratio with regards to the heart.
To clarify:
Increased blood flow to the periphery (as a means to dissipate heat) leads to lowered stroke volume. In order to maintain CO, heart rate will have to be increased--> achieved by net cardiac ANS sympathetic stimulation. Overall CO change will depend on the level of heart rate and stroke volume change.
Increased blood flow to the periphery (as a means to dissipate heat) leads to lowered stroke volume. In order to maintain CO, heart rate will have to be increased--> achieved by net cardiac ANS sympathetic stimulation. Overall CO change will depend on the level of heart rate and stroke volume change.
I had a different take on it.
Peripheral vasodilation to dissipate heat would lead to decreased total peripheral resistance (Poiseuille's equation). In order to maintain blood pressure, cardiac output would have to increase.
The decrease in peripheral resistance leads to a decrease in afterload, so stroke volume would increase. Heart rate would probably also increase in order to maintain blood pressure.
That sounds correct, SV and HR both increase. Iincreased sympathetic output (decreased inhibition at baroreceptors due to low bp) resulting in increased chrontropy and inotropy at the cardiac level, combined with decreased afterload due to peripheral vasodilation should increase both HR and SV.
This part doesn't make any sense. I think those other two guys have it right, or at least part of the equation.
Isnt the parasymp system that causes skin blood vessels to vasodilate? An increase in vasodilation of periperhial BVs will lead to a lower TPR and a lowered BP. The lowered BP will signal via the baro-rcs to increase cardiac output via the symp system...?
The superficial vessels receive their autonomic innervation via gray rami communicantes off the sympathetic chain (along with arrector pili and sweat glands), so it's like having your foot on the gas. You decrease vascular tone in the skin by taking your foot a little off the accelerator instead of putting on the brakes, i.e. parasympathetics. That leads to vasodilation.
The response in your skin is locally controlled, just like your muscles get increased blood supply when they are exercising due to a local response. But yes, this leads to a lower TPR (and thus lower afterload)---> in order to maintain BP, your CO is going to increase via symapthetic outflow to your heart (a more central response), driven by baroreceptor reflexes.
Our professor talked about how people go out drinking and die due to hypthermia in certain cold areas..bc alcohol in high doses increases parasymp outflow and causes vasodilation which inappropriate causes heat loss.
I would imagine at the skin it is a combination of parasymp flow and local intrinsic control (hyperemia) that regulates the blood flow to the skin. Either way it is the drop in TPR due to the vasodilation that leads to the increased C.O. to maintain BP.
Do any text books address this?
I think it bears mentioning that there is no parasympathic innervation at cutaneous blood vessels....
This is my explanation
[1] HR increases due to hypothalamic input
The warm temperature sensors of the hypothalamus stimulate not only the Muscarinic sweat receptors, but the adrinergic receptors of the heart as well. So I think the heart rate increase comes more from a higher-up signal.
[2] Periphearal dilation has a mild effect
Peripheral dilation will induce a mild drop in BP, which will be picked up by baroreceptors. The baroreceptors will then relay this to brainstem, which will stimulate the pressor center to increase HR.
A correction needs to be made here:
Afterload -> This is the load that the heart works against in systole when pumping into the aorta. This is mostly a material property of the aortic wall. This explains why artherosclerosis of aorta leads to increased Systolic pressure (i.e. you develop a higher afterload).
Baroreceptor function -> these receptors are pure sensors. As blood rushes over them, stretching occurs and this signal is sent to the brain stem. Low blood pressure is picked up by baroreceptors due to lower stretch and this is sent to the brainstem. The brainstem responds by inhibiting sympathetic center and stimulating the vagal center. The baroreceptors are NOT inhibited/disinhibited directly, they are sensors nothing more.
Last edited:
It's partly a property of the aortic wall.
The other part is systemic vascular resistance. Excessive peripheral vasodilation to transmit heat and inability to maintain blood pressure can lead to syncope.
Your post essentially suggests that afterload can't really change unless you modify the properties of the aortic wall. There's smooth muscle there, but the major modifications of systemic resistance are at the arterioles.