As I learn about heart failure in medical school, we are consistently taught that one of the compensatory responses to heart failure (and the accompanying reduction in cardiac output) is for the sympathetic nervous system (SNS) to activate. While this has myriad effects, one that is described in most cardiac pathophysiology textbooks (eg, Lilly) is that the activation of the SNS causes peripheral vasoconstriction, raising the systemic vascular resistance (SVR).

However, I don't understand why the body would do this. The underlying problem in HF is a reduction in cardiac output (either due to diastolic or systolic failure). Raising SVR (using the cardiac equivalent of Ohm's Law: Pressure = CO x SVR) would either a) cause cardiac output to drop, holding pressure constant or b) force the heart to generate more pressure to generate to maintain a constant CO. Both seem like poor responses to a failing heart. So why does the body do this?

Put otherwise, if I had independent control over every hemodynamic parameter in the body and I was confronted by a failing heart, my solution would be to increase HR and contractility (which the SNS does), but to vasodilate the systemic arterioles to lower resistance and thus (by Ohm;s Law once again) reduce the pressure the heart would need to generate in order to drive the same amount of flow as prior to the heart failure. Why is this a bad idea?

I think there are some preliminary questions that might help clear up my confusion. They are probably very basic, but I think they will help clear up the confusion I face.

A. Why is blood pressure (specifically mean arterial pressure, measured at the aorta) important to maintain? The goal of the heart is to maintain tissue perfusion, which seems to me to be function of the volume of blood which gets to a certain organ.

B. Does the body regulate blood pressure or cardiac output? If both, which takes priority?

I think if I understand these two questions, I might be able to better understand why the body reacts the way it does to heart failure.

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    $\begingroup$ Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer. $\endgroup$
    – Community Bot
    May 2, 2022 at 19:01
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    $\begingroup$ This is basic physiology. The human body doesn't "think" or know/reason; it reacts to stimuli. If the CO is low, it basically reacts the same way in an attempt to normalize BP regardless of the cause (e.g. hemorrhage vs. CHF). This is also why ACE-inhibitors are used in CHF, because the body doesn't "know" why BP is lower than normal. $\endgroup$ May 3, 2022 at 21:59
  • $\begingroup$ Perhaps it's related to the physiological results of drowning, which also causes cardiac arrest, which appear to be of the same type. In that case, you can research the reasons for the physiology of conservation of oxygen in response to drowning, which is an ancient nervous pathway that exists in nearly all terrestrial vertebrates. Perhaps there is some research to do on the specifics of that. $\endgroup$ May 4, 2022 at 22:55
  • $\begingroup$ Best try a medical forum, this is generalist so a lot of genetics/ecology/microbiology folk here. $\endgroup$ May 5, 2022 at 9:09
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    $\begingroup$ @LifeInTheTrees - Nit-picky, but there are also a lot of medical people here, including physicians and people who teach medical students (I've been both). This kind of question is very basic and will likely not be answered by a medical professional. A medical forum might be better, but a medical student forum might be best. $\endgroup$ May 5, 2022 at 11:25


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