quick diastolic bp question

[Thego2guy]

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Hi guys,

I have difficulty understanding what happens physiologically when a pt has acute elevation of diastolic bp. For example, a 60 y/o pt has acute bp of 130/108 following a food poisoning/stomach flu. What happens physiologically, and what are common causes for that acute bp elevation?

I searched here on SDN, and elsewhere, and I couldn't get any physiologic explanations.

Thanks in advance! (hope this is the right forum to post this in)

 

[CaptainSSO]

What happens? Increased blood flow. Q = P/R. Increased MAP, increase flow.

An increase in MAP is caused by increases in cardiac output (heart rate and/or stroke volume) and/or total peripheral resistance.

MAP = Cardiac output * TPR

As far as why a bug will initiate these responses, one reason is that the inflammatory cytokines released via the immune response will cause vasodilation and subsequent drop in BP, so this must be compensated for. Fever will increase heart rate, except for in the case of typhoid fever.

 

[Thego2guy]

Thanks for your reply!

I get what you are saying, and I also thought that it was a compensatory effect. What I just don't understand is why the diastolic bp affected more than the systolic? And would the compensatory effect be that great? I mean, a 130/108 relationship just seems a little off to me. If the diastole is that large, then I would expect the systole to be much larger. Physiologically, is the aorta not dilating enough to create a lower diastolic bp?

What happens? Increased blood flow. Q = P/R. Increased MAP, increase flow.

An increase in MAP is caused by increases in cardiac output (heart rate and/or stroke volume) and/or total peripheral resistance.

MAP = Cardiac output * TPR

As far as why a bug will initiate these responses, one reason is that the inflammatory cytokines released via the immune response will cause vasodilation and subsequent drop in BP, so this must be compensated for. Fever will increase heart rate, except for in the case of typhoid fever.

 

[PMPMD]

Thanks for your reply!

I get what you are saying, and I also thought that it was a compensatory effect. What I just don't understand is why the diastolic bp affected more than the systolic? And would the compensatory effect be that great? I mean, a 130/108 relationship just seems a little off to me. If the diastole is that large, then I would expect the systole to be much larger. Physiologically, is the aorta not dilating enough to create a lower diastolic bp?

In a very simplistic sense, diastolic BP reflects SVR and pulse pressure reflects SV. In the clinical vignette provided, the patient is likely hypovolemic (dehydrated) so their SV is decreased - hence the decreased PP. The SVR increase is compensatory to maintain MAP and vital organ perfusion.

 

[dr zaius]

In a very simplistic sense, diastolic BP reflects SVR and pulse pressure reflects SV. In the clinical vignette provided, the patient is likely hypovolemic (dehydrated) so their SV is decreased - hence the decreased PP. The SVR increase is compensatory to maintain MAP and vital organ perfusion.

Beat me to it. At least I was thinking correctly 😳.

 

[Thego2guy]

In a very simplistic sense, diastolic BP reflects SVR and pulse pressure reflects SV. In the clinical vignette provided, the patient is likely hypovolemic (dehydrated) so their SV is decreased - hence the decreased PP. The SVR increase is compensatory to maintain MAP and vital organ perfusion.

Thank you! I never thought of it that way, it makes sense now. So physiologically there is a compensatory peripheral vasoconstriction which maintains perfusion to organs via elevating diastolic bp. SVR = Diastolic. Gotcha.

 

[PMPMD]

Thank you! I never thought of it that way, it makes sense now. So physiologically there is a compensatory peripheral vasoconstriction which maintains perfusion to organs via elevating diastolic bp. SVR = Diastolic. Gotcha.

There are other factors that determine DBP but SVR is a big one.

 

[Thego2guy]

There are other factors that determine DBP but SVR is a big one.

The issue that I had was understanding why something can affect DBP and not SBP aside from the obvious reasons (ie: Aorta, ventricle relaxation). For example, I thought that SVR affects both DBP and SBP equally (hence when you said DBP is mostly SVR it cleared things up). To my knowledge blood viscosity, blood volume, constriction/dilation, and general CO equally affect both DBP and SBP.

What specific variables affect one more than the other?

Once again, thank you for clearing this up!!

 

[CaptainSSO]

^TPR will affect both, but not equally. Systolic pressure is by definition MAP during systole, so its largest determinant will be the force and volume
of the contraction of the heart.

Same reason when you exercise systolic will increase and diastolic will drop. The force of the heart's contractions have increased, but there is vasodilation resulting in decreased diastolic pressure.

 

[Thego2guy]

^TPR will affect both, but not equally. Systolic pressure is by definition MAP during systole, so its largest determinant will be the force and volume
of the contraction of the heart.

Same reason when you exercise systolic will increase and diastolic will drop. The force of the heart's contractions have increased, but there is vasodilation resulting in decreased diastolic pressure.

Right, TPR = SVR? I now know that SVR is one of those variables that affects DBP more than SBP.

There are other factors that determine DBP but SVR is a big one.

So my question is, what are the other factors? Unless TPR is =/= SVR and TPR is another separate factor. 😕

 

[PMPMD]

TPR and SVR are the same thing. I've never heard TPR used clinically.

 

[CaptainSSO]

Other factors are things like increased osmolality of the blood, which will draw fluid into the blood vessels, increasing pressure.

 

[Thego2guy]

Other factors are things like increased osmolality of the blood, which will draw fluid into the blood vessels, increasing pressure.

I thought increased oncotic/osmotic pressure will affect both SBP and DBP equally.

 

[kaleerkalut]

What happens? Increased blood flow. Q = P/R. Increased MAP, increase flow.

An increase in MAP is caused by increases in cardiac output (heart rate and/or stroke volume) and/or total peripheral resistance.

MAP = Cardiac output * TPR

As far as why a bug will initiate these responses, one reason is that the inflammatory cytokines released via the immune response will cause vasodilation and subsequent drop in BP, so this must be compensated for. Fever will increase heart rate, except for in the case of typhoid fever.

Why not in typhoid fever? TIA 🙂

 

[CaptainSSO]

I thought increased oncotic/osmotic pressure will affect both SBP and DBP equally.

Not necessarily equally. Few things in biology are as cut and dried as that. For example, if you cut your sodium intake by half, it tends to lower systolic pressure by about 7 mmHg and diastolic by about 1 mmHg.

 

[CaptainSSO]

Why not in typhoid fever? TIA 🙂

As far as I know, a specific mechanism for this phenomenon (it is referred to as relative bradycardia) has not been elucidated. There are a couple other infectious diseases where relative bradycardia tends to occur as well, such as Legionnaire's disease and chlamydia.

http://www.ncbi.nlm.nih.gov/m/pubmed/8945708/

 

[Thego2guy]

Not necessarily equally. Few things in biology are as cut and dried as that. For example, if you cut your sodium intake by half, it tends to lower systolic pressure by about 7 mmHg and diastolic by about 1 mmHg.

Thanks man, I appreciate it!

I was also wondering about the relative bradycardia, perhaps they secrete some toxin which affects the parasympathetic nervous system? Naive answer, but its the best one I have 😳