What would be 2 factors that affects the stroke volume of the heart?

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TheKitty.x
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What would be 2 factors that affects the stroke volume of the heart?
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username5064508
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Given that stroke volume is linked to the equation stroke volume x heart rate = cardiac output, I'd imagine that heart rate can affect the stroke volume.

To that end cardiac output will too, but since that is based on other factors it may not be the best answer. I would hazard a guess on something like blood pressure.
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Jpw1097
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(Original post by TheKitty.x)
What would be 2 factors that affects the stroke volume of the heart?
There are 3 factors that affect stroke volume: preload, afterload and inotropy (or contractility).

Preload refers to the volume of blood in the heart before it contracts (end-diastolic volume). The more blood that enters the heart, the more the heart stretches and this causes it to contract with more force, increasing stroke volume. This is known as the Frank-Starling law.

Contractility refers to the force of contraction that is independent of how much it is stretched - it is length-independent. This is essentially driven by the sympathetic nerve fibres that innervate the heart as well as circulating adrenaline.

Afterload refers to the load that the heart must overcome to eject blood into the aorta - this is essentially the pressure in the aorta (blood pressure). High blood pressure (hypertension) will increase afterload, decreasing the stroke volume. Valvular heart disease (e.g. a stiff aortic valve) will also decrease the stroke volume.
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macpatgh-Sheldon
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(Original post by Jpw1097)
There are 3 factors that affect stroke volume: preload, afterload and inotropy (or contractility).

Preload refers to the volume of blood in the heart before it contracts (end-diastolic volume). The more blood that enters the heart, the more the heart stretches and this causes it to contract with more force, increasing stroke volume. This is known as the Frank-Starling law.

Contractility refers to the force of contraction that is independent of how much it is stretched - it is length-independent. This is essentially driven by the sympathetic nerve fibres that innervate the heart as well as circulating adrenaline.

Afterload refers to the load that the heart must overcome to eject blood into the aorta - this is essentially the pressure in the aorta (blood pressure). High blood pressure (hypertension) will increase afterload, decreasing the stroke volume. Valvular heart disease (e.g. a stiff aortic valve) will also decrease the stroke volume.
Hi young man - now you are a 3rd year med student, or am I losing track of time (?) - you have as always given a brilliant answer here - just a small comment to make on your last paragraph if I may - although you are right that high blood pressure would be associated with a greater afterload, the inherent factor that results in the increased afterload is actually increased arteriolar resistance against which the ventricular muscle has to force the blood. This (indirectly) fits in with your description in that "blood pressure = cardiac output X peripheral resistance", so that a higher peripheral resistance [primarily due to relative vasoconstriction through increased alpha-adrenergic activity {via the actions of both adrenaline (both alpha and beta) AND noradrenaline (mainly alpha)}] results in BOTH higher blood pressure AND a reduced stroke volume, assuming that heart rate is kept constant.

Please correct me if this viewpoint of mine is out of date .

M
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Jpw1097
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(Original post by macpatgh-Sheldon)
Hi young man - now you are a 3rd year med student, or am I losing track of time (?) - you have as always given a brilliant answer here - just a small comment to make on your last paragraph if I may - although you are right that high blood pressure would be associated with a greater afterload, the inherent factor that results in the increased afterload is actually increased arteriolar resistance against which the ventricular muscle has to force the blood. This (indirectly) fits in with your description in that "blood pressure = cardiac output X peripheral resistance", so that a higher peripheral resistance [primarily due to relative vasoconstriction through increased alpha-adrenergic activity {via the actions of both adrenaline (both alpha and beta) AND noradrenaline (mainly alpha)}] results in BOTH higher blood pressure AND a reduced stroke volume, assuming that heart rate is kept constant.

Please correct me if this viewpoint of mine is out of date .

M
Fourth year now
It’s an interesting point. I think you’re probably right that in hypertension (essential hypertension that is), it’s the increased total peripheral/systemic vascular resistance that increases the afterload, rather than the high blood pressure directly. It’s not something I’ve really considered before, I just know that longstanding hypertension will cause left ventricular hypertrophy due to the increased afterload. But now you mention it, I suppose the mechanism driving essential hypertension is increased total peripheral resistance.
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nexttime
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This sounds like its meant to be a heart rate/cardiac output related question, but i wouldn't say those factors affect stroke volume... I'd say stroke volume affects cardiac output. The other way around.

What determines how big your heart is... well, what species you are, how big you are, sex, conditioning, those sorts of things

(Original post by Jpw1097)
But now you mention it, I suppose the mechanism driving essential hypertension is increased total peripheral resistance.
Circulating volume can also affect it though. Hence why diuretics decrease BP, and why renal function is so linked to BP.

If you work out what the underlying cause of hypertension is and how to treat it just let me know via PM. Then when I get my Nobel prize don't worry, it'll be pure coincidence I promise.
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Jpw1097
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(Original post by nexttime)
This sounds like its meant to be a heart rate/cardiac output related question, but i wouldn't say those factors affect stroke volume... I'd say stroke volume affects cardiac output. The other way around.

What determines how big your heart is... well, what species you are, how big you are, sex, conditioning, those sorts of things


Circulating volume can also affect it though. Hence why diuretics decrease BP, and why renal function is so linked to BP.

If you work out what the underlying cause of hypertension is and how to treat it just let me know via PM. Then when I get my Nobel prize don't worry, it'll be pure coincidence I promise.
Yes of course circulating volume affects blood pressure, however, I’m not too sure this is necessarily what cause essential hypertension, it’s certainly involved in secondary causes of hypertension. To be honest, I’m not really sure what the mechanism of essential hypertension is, it’s probably a combination of circulating volume and peripheral resistance. I’ll be sure to let you know when I find out though
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TheKitty.x
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(Original post by Jpw1097)
There are 3 factors that affect stroke volume: preload, afterload and inotropy (or contractility).

Preload refers to the volume of blood in the heart before it contracts (end-diastolic volume). The more blood that enters the heart, the more the heart stretches and this causes it to contract with more force, increasing stroke volume. This is known as the Frank-Starling law.

Contractility refers to the force of contraction that is independent of how much it is stretched - it is length-independent. This is essentially driven by the sympathetic nerve fibres that innervate the heart as well as circulating adrenaline.

Afterload refers to the load that the heart must overcome to eject blood into the aorta - this is essentially the pressure in the aorta (blood pressure). High blood pressure (hypertension) will increase afterload, decreasing the stroke volume. Valvular heart disease (e.g. a stiff aortic valve) will also decrease the stroke volume.
Thank you so much x
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nexttime
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(Original post by Jpw1097)
Yes of course circulating volume affects blood pressure, however, I’m not too sure this is necessarily what cause essential hypertension, it’s certainly involved in secondary causes of hypertension. To be honest, I’m not really sure what the mechanism of essential hypertension is, it’s probably a combination of circulating volume and peripheral resistance. I’ll be sure to let you know when I find out though
There were lots of old experiments on dogs regarding this - chop bits out and give cruel doses of drugs to see of you can mimick chronic htn. I was told (in a lecture, a long time ago) that their conclusion was that it was very difficult to actually make a healthy dog hypertensive deliberately, except in you started messing with kidney fluid balance. Don't have a citation.

But how that reflects naturally occurring htn is anyone's guess I suppose!
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