Consequences of abnormal blood pressure unrelated to cardiac output?

Question

A question from Kaplan's MCAT Biology Review asks:

In bacterial sepsis (overwhelming bloodstream infection), a number of capillary beds throughout the body open simultaneously. What effect would this have on the blood pressure? Besides the risk of infection, why might sepsis be dangerous for the heart?

The answer is:

Opening up more capillary beds (which are in parallel) will decrease the overall resistance of the circuit. The cardiac output will therefore increase in an attempt to maintain constant blood pressure. This is a risk to the heart because the increased demand on the heart can eventually tire it, leading to a heart attack or a precipitous drop in blood pressure.

I had always viewed blood pressure as a means to achieve appropriate blood flow, and a system with lower resistance would simply operate with lower pressure (via Ohm's Law). However, the answer implies that maintaining normal blood pressure is a goal in itself, such that the body would naturally raise cardiac output to dangerous levels in order to maintain it.

Can someone help explain:

1. Does blood pressure play a role in blood circulation that makes it more important than just a means towards appropriate cardiac output?

2. What are health consequences of abnormal blood pressure unrelated to cardiac output from a biochemical perspective? If I search for "abnormal blood pressure" I'll get broad symptoms like "dizziness" that don't explain its effect on different tissues that cause the symptoms.

Answer 1

Blood pressure, as you noted, is just a means to an end: the flow of blood through tissues. The trouble is, many of the body's regulatory systems use blood pressure (rather than flow) as an index of cardiovascular status. A key example is the baroreceptor system, which senses changes in blood pressure and tries to correct them by effects on the heart, blood vessels and kidneys.

In sepsis with decreased blood pressure, baroreceptor firing increases in an attempt to increase cardiac output $^1$. This increased demand on the heart can be counterproductive and cause the heart to fail. But this phenomenon is not unique to sepsis. There are many other conditions where a hyperdynamic circulation leads to heart failure: such as anaemia, thyrotoxicosis and thiamine deficiency $^2$.

All of these examples highlight a basic principle in pathophysiology: adaptations can sometimes turn maladaptive.

Note: The effects of sepsis on the cardiovascular system are complex and go beyond vasodilation. For more details, you could read a textbook of pathophysiology/medicine. Or go through any of the review articles on this topic, such as the one by Lelubre & Vincent $^3$.

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References:

1. Gattinoni L, Carlesso E. Supporting hemodynamics: what should we target? What treatments should we use? Crit Care [Internet]. 2013 Mar 12 [cited 2020 Aug 24]:17(Suppl 1):Article S4 [8 p.]. Available from: https://ccforum.biomedcentral.com/articles/10.1186/cc11502
2. Mehta PA, Dubrey SW. High output heart failure. QJM. 2009 Apr;102(4):235–41. https://doi.org/10.1093/qjmed/hcn147
3. Lelubre C, Vincent J. Mechanisms and treatment of organ failure in sepsis. Nat Rev Nephrol. 2018;147(7):417–27. https://doi.org/10.1038/s41581-018-0005-7