isolated systolic hypertension

[txhorn]

can someone help me understand isolated systolic htn? this seems like a silly concept to struggle with...

why exactly do you get systolic htn with aortic stiffening? i understand that aortic stiffening --> greater contraction force required by the LV to maintain an adequate blood pressure, but wouldn't the LV contract just hard enough to maintain a BP of 120/80? why would it contract so hard that you end up with a BP of 180/70?

thanks

---

Members don't see this ad.

 

[Malpractice]

had this same question in Uworld this morning. the way i look at it:

aorta is a big elastic artery that can act like a shock-absorber. when it becomes stiff, you lose some of this ability, and instead the "shock" is transmitted to the rest of the arteries --> increased systolic pressure.

 

[txhorn]

hmm, okay i think i get it now. so instead of the aorta transmitting the shock/pressure to the rest of the body gradually throughout diastole, it does so immediately --> increased initial systolic pressure?

 

[Handinhand]

I'd like to bump this because I just had this question and I think it's flawed.

We measure blood pressure peripherally, usually from the brachial artery. I do not understand how a stiffening of the aorta could cause hypertension distal to it. In my head I liken to this to an aortic valve stenosis, which results in a narrowed pulse pressure (think of kinking a water hose, you get lowered pressure distal to the narrowing).

The only literature I can find on this associated aortic stiffening with high blood pressure, but not as the cause of the hypertension.

 

[Donald Juan]

I think if the aorta is not able to stretch, then it is is not able to increase its volume during systole. This would mean that blood is shooting through it faster and at higher pressure than it would normally.

 

[alicealicealice]

Simple way to look at it
Compliance = Volume/Pressure AKA C=V/P
Solving for V:
V=CP
Now if the stiffness of the aorta increases, the compliance C decreases. However the heart must put out the same volume V of blood into that aorta. So by the above equation, holding V constant and decreasing C, P must increase.

In other words:
"Hearts ejecting into a stiffer arterial system must generate higher end-systolic pressures for the same net stroke volume. The result is a greater energy requirement for a given level of ejected flow." http://atvb.ahajournals.org/content/25/5/932.long

Things are more complicated of course, because lack of distension means lack of normal endothelial feedback regulation (vasodilator release etc) as described in the paper