Step I How does hypertension lead to an increased workload for the heart?

[warriorinthemaking]

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Here's what I don't understand:

Hypertension --> increased afterload --> decreased stroke volume, cardiac output.... --> decreased blood pressure? normalized blood pressure. --> no problem

or maybe this train of thought

Hypertension --> increased afterload --> decreased stroke volume, cardiac output --> compensatory increase in heart contractility by the symp ns --> maintained stroke volume, cardiac output, exacerbates hypertension. positive feedback loop --> malignant hypertension in like 5 minutes

How does the heart know it must contract harder in response to hypertension-induced increased afterload? Wouldn't parasympathetic tone be increased instead, rather than sympathetic?

Please, my head is spinning in circles.
Thank you in advance!

 

[ciucia53]

So, I am no expert on cardiac physiology, but this is my thought - when you have an increased afterload, this will increase wall tension by the law of Laplace (where tension is proportional to pressure * radius / thickness and in this case the increased afterload leads to increased LV pressure). When you have increased wall tension, the O2 demand increases, which is an indicator of increased workload.

 

[AnatomyGrey12]

Higher systemic pressure means the heart must pump harder (see post above about wall tension) to get the same output against the greater resistance. This leads to greater workload as referenced above.

 

[Lnsean]

Here's what I don't understand:

Hypertension --> increased afterload --> decreased stroke volume, cardiac output.... --> decreased blood pressure? normalized blood pressure. --> no problem

or maybe this train of thought

Hypertension --> increased afterload --> decreased stroke volume, cardiac output --> compensatory increase in heart contractility by the symp ns --> maintained stroke volume, cardiac output, exacerbates hypertension. positive feedback loop --> malignant hypertension in like 5 minutes

How does the heart know it must contract harder in response to hypertension-induced increased afterload? Wouldn't parasympathetic tone be increased instead, rather than sympathetic?

Please, my head is spinning in circles.
Thank you in advance!

Baroreceptors that line the aorta/carotids sense drop in MAP and activates compensatory mechanism to increase contractility. Kidneys will also see less CO and activate RAAS. The LV can compensate by pumping harder but there is a price.

 

[JooceMan137]

So, I am no expert on cardiac physiology, but this is my thought - when you have an increased afterload, this will increase wall tension by the law of Laplace (where tension is proportional to pressure * radius / thickness and in this case the increased afterload leads to increased LV pressure). When you have increased wall tension, the O2 demand increases, which is an indicator of increased workload.

Pretty much nailed the heart workload thing.