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Blood pressure is the product of cardiac output and total peripheral resistance:

$\text{BP} = \text{CO} \times \text{TPR}$

Since cardiac output is the product of heart rate and stroke volume, we have:

$\text{BP} = \text{HR} \times \text{SV} \times \text{TPR}$

Stroke volume is determined by preload, contractility, and afterload. An increase in afterload leads to a reduction in stroke volume and thus a decrease in blood pressure. [1]

However, it then seems that hypertension, which increases afterload, would lead to a decrease in blood pressure and form a negative feedback loop. Is this in fact what happens in the human body?

Also, when total peripheral resistance increases, it seems to me that afterload should increase, leading again to a reduction in blood pressure. Nonetheless, peripheral resistance also directly determines blood pressure ($\text{BP} = \text{CO} \times \text{TPR}$). Which of these has a stronger effect?

1: http://pie.med.utoronto.ca/CA/CA_content/CA_cardiacPhys_strokeVolume.html

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However, it then seems that hypertension, which increases afterload, would lead to a decrease in blood pressure and form a negative feedback loop. Is this in fact what happens in the human body?

Yes and no. If the only parameters affecting cardiac output were peripheral vascular resistance, then yes, a resultant decrease in blood pressure would occur initially with hypertension. And yes, that is what happens. However, it is quite temporary because there are numerous modulators of "blood pressure", as blood flow, especially to the head, is critical to survival.

There are baroreceptors located at points in the arterial vasculature which, upon sensing a fall in blood pressure, cause the sympathetic nervous system to release positive inotropes, causing the heart to contract more forcefully to push out that increased afterload. There are cordioreceptors assessing the effect of every heartbeat; decreased BP causes an increase in heart rate. Sensors in kidney arterial vasculature sense decreased blood pressure and preserve water and electrolytes to increase intravascular fluid volume. Etc, etc.

Which in the end boils down to

BP = CO x TPR

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  • $\begingroup$ Thank you, can't upvote yet but I would. Is there a way to predict with any accuracy what the effect of changing one of these parameters (as in a pathological condition or upon administering a drug) would be? Right now, I feel like the answer is just "it depends on many variables", but I assume that wouldn't be of much help in a clinical setting. $\endgroup$
    – Quin
    Jan 20 at 18:13
  • $\begingroup$ Of course! These things are studied extensively in disease and drug trials. If we couldn't predict their effects, drug dosage recommendations and therapies for diseases would not be possible. I don't need mine to be the accepted answer, but if it was/is helpful, you certainly should upvote it. $\endgroup$
    – anongoodnurse
    Jan 20 at 18:59
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Not really following your logic at all, but maybe it helps to think that the parameter that needs to be held constant to deliver sufficient/constant blood to tissues is cardiac output.

All you need is your first equation:

$\text{BP} = \text{CO} \times \text{TPR}$

to see that an increase in peripheral resistance will mean an increase in (mean) BP if CO is constant.

Anything else you argue from subsequent steps has to conform to this, or you've made an error someplace.

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  • $\begingroup$ I agree that this would be the case if there were no feedback loops and the cardiovascular system could be modeled in a linear manner. However, why do you consider that first equation to be the 'primal' equation? For example, if you agree that increasing TPR increases afterload, which decreases SV and subsequently decreases CO, then surely increasing TPR both increases and decreases BP. I don't think we can simply assume that CO is constant. $\endgroup$
    – Quin
    Jan 20 at 16:21
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    $\begingroup$ @Quin No, you can't assume anything at all; for many possible parameters, the outcome is death and then you can simply assume everything drops to zero. I'm saying that what the body cares about is how much blood it gets, so generally that's the reference point it makes sense to consider from a perspective of homeostasis. From a perspective of illness, all bets are off, but it doesn't make any sense to assume homeostasis is absent, either. $\endgroup$
    – Bryan Krause ♦
    Jan 20 at 16:35

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