Lecture 26 Flashcards
What are the two types of hypertension and what causes them? What percentage do each of these make up?
- primary hypertension (95%)
the cause is unknown (stiffer arteries with age) - secondary hypertension (5%) specific cause
What are the two general hypotheses for the causes of primary hypertension?
- arterial blood volume increases
- arterial compliance decreases
Describe how an increase in the arterial blood volume comes about and how that affects the compliance
There is increased salt retention and water retention in the kidney which leads to an increase in blood volume. Via autoregulation, there is arteriolar vasoconstriction. This leads to a decrease in arterial compliance and an increase in the TPR
Describe how an decrease in the arterial compliance comes about and how that affects the blood volume
There is ___________ activation of the ________ (from the _________ and medulla __________) which leads to arteriolar ___________. This leads to a decrease in arterial _________ and increased ________. There is less blood flow to the ___________ so it releases vasoactive substances and then we get salt ________. This leads to an ________ in blood volume
There is sympathetic activation of the arterioles (from the hypothalamus and medulla oblongata) which leads to arteriolar vasoconstriction. This leads to a decrease in arterial compliance and increased TPR. There is less blood flow to the kidney so it releases vasoactive substances and then we get salt retention. This leads to an increase in blood volume
How can Ohm’s Law be used to describe MAP?
MAP = CO (HR x SV) x TPR
How is MAP effected by moderate exercise?
During exercise, there is a balanced increase in sympathetic activity. In the heart, it causes an increase in CO due to an increase in both HR and SV. It also causes vasodilation in some beds to promote O2 delivery, constriction in other vascular beds but overall TPR will decrease.
How is MAP effected by a systemic increase in overall sympathetic activity (hypertension)? What is an exception to this?
In the heart, it causes an increase in CO due to an increase in both HR and SV. TPR will increase so MAP increases. The exception is in giraffes
What is wrong with giraffes?
Giraffes have sever hypertension (175 - 200 mmHg). In their neck there are valves in the vain that stop backflow to their head to prevent it from bursting when they are drinking. There is also great pressures in their lower legs and so they have a very high sheath of thick skin over the lower limbs to maintain high extravascular pressure.
Are giraffe’s born hypertensive?
no
What happens to giraffes as they grow?
As giraffe grows, blood flow to cardiovascular brainstem reduces, due to effects of gravity. If there were no adaptations, the blood flow to the brain would be too low. So, there is a huge sympathetic outflow. Sympathetic nerve outflow increases to cause nerve-mediated hypertrophy of vessel wall (G-suit) so there is a thicker wall. This causes an
increase in TPR, and thereby MAP, to preserve cerebrovascular flow
The cause of primary hypertension is thought to be due to:
A. an increase in arterial compliance and/or an increase in arterial blood volume.
B. an increase in arterial compliance and/or a decrease in arterial blood volume.
C. a decrease in arterial compliance and/or an increase in arterial blood volume.
D. a decrease in arterial compliance and/or a decrease in arterial blood volume.
C. a decrease in arterial compliance and/or an increase in arterial blood volume.
How does hypertension affect afterload? Why is this?
It increases the afterload. This is because the stiffer the aorta means that there is a faster returning pulse wave and the force required to pump stuff out of the heart (increased afterload).
What is the effect on the heart when there is an increase in afterload?
When there is higher resistance to output during hypertension, the heart remodels to eject enough blood
How does the heart remodel to keep up with the increased afterload?
- at a cellular level: the cardiomyocytes get bigger and increase their CSA, there are more sarcomeres in each cardiomyocyte (not more cardiomyocytes or increased size of sarcomeres)
- at the organ level
What is fibrosis that occurs during hypertrophy?
This is when there is an increased load triggers the formation of more ECM (the scaffold for the myocyte to have the bigger contraction)