Lecture 26 Flashcards

1
Q

What are the two types of hypertension and what causes them? What percentage do each of these make up?

A
  • primary hypertension (95%)
    the cause is unknown (stiffer arteries with age)
  • secondary hypertension (5%) specific cause
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2
Q

What are the two general hypotheses for the causes of primary hypertension?

A
  • arterial blood volume increases

- arterial compliance decreases

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3
Q

Describe how an increase in the arterial blood volume comes about and how that affects the compliance

A

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

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4
Q

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

A

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

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5
Q

How can Ohm’s Law be used to describe MAP?

A

MAP = CO (HR x SV) x TPR

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6
Q

How is MAP effected by moderate exercise?

A

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.

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7
Q

How is MAP effected by a systemic increase in overall sympathetic activity (hypertension)? What is an exception to this?

A

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

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8
Q

What is wrong with giraffes?

A

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.

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8
Q

Are giraffe’s born hypertensive?

A

no

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9
Q

What happens to giraffes as they grow?

A

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

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10
Q

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.

A

C. a decrease in arterial compliance and/or an increase in arterial blood volume.

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11
Q

How does hypertension affect afterload? Why is this?

A

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).

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12
Q

What is the effect on the heart when there is an increase in afterload?

A

When there is higher resistance to output during hypertension, the heart remodels to eject enough blood

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13
Q

How does the heart remodel to keep up with the increased afterload?

A
  • 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
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14
Q

What is fibrosis that occurs during hypertrophy?

A

This is when there is an increased load triggers the formation of more ECM (the scaffold for the myocyte to have the bigger contraction)

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15
Q

What things make up the ECM?

A

Collagen type I + III

Elastin Proteoglycans Laminin Fibronectin

16
Q

What is the difference between physiological remodelling and pathophysiological remodelling?

A

Pathophysiological remodelling occurs with fibrosis and is irreversible. Physiological remodelling is reversible

17
Q

What are three examples of pathophysiological remodelling?

A
  • thickening of LV walls during hypertension
  • thinning of LV walls and LV dilation during heart failure
  • gross thickening of LV walls during hypertrophic cardiomyopathy
18
Q

What causes the thickening of the LV walls during hypertension. What sort of remodelling is this?

A

caused by a pressure overload
this is concentric remodelling (lumen gets smaller
(this can further increase the MAP which leads to a vicious circle)

19
Q

What causes the thinning of the LV walls during heart failure. What sort of remodelling is this?

A

volume overload
- eccentric remodelling (lumen has become smaller)
this is due to a valve problem

20
Q

Hypertension lead to ________ _______ which leads to burned out ________ which leads to _______ _________

A

compensated hypertrophy
LV
cardiac failure

21
Q

Do all changes lead to cardiac failure?

A

No

22
Q

What happens during pathological hypertrophy?

A

There is concentric remodelling as a result of the pressure overload. The myocyte length increases but the myocyte width increases even more. There is fibrosis and maybe cardiac dysfunction.

23
Q

What happens during cardiac dilation?

A

There is eccentric contraction as a result of volume overload. The myocyte length increases much more than the myocyte width increases. There is extensive fibrosis, myocyte death and advanced cardiac dysfunction

23
Q

One diagram suggests that all remodelling will lead to heart failure. Is this true?

A

no

24
Q

Describe the newer models of cardiac failure

A
  • diastolic heart failure which results from concentric hypertrophy (there is preserved ejection fraction)
  • systolic heart failure due to eccentric hypertrophy (there is reduced ejection fraction)
25
Q

What are some factors affecting whether there will be concentric or eccentric remodeling?

A
  • age (older = concentric)
  • sex (male = eccentric, female = concentric)
  • medical conditions (eg. coronary heart disease = concentric, valve leaks = eccentric)
  • genetic factors (normally eccentric)
26
Q

How is the right ventricle affected by systemic hypertension?

A
  • early stage, there is no effect on RV

- late stage, you can get hypertrophied RV

27
Q

Why does the RV hypertrophy during systemic hypertension?

A

The systemic circulating factors that affect the left ventricle also affect the right ventricle.
In addition, some of the LV pressure can translate into the pulmonary circulation so if the left side remodels, this might have an effect on the pulmonary circulation
The hypertrophied LV interacts with the RV (eg. the septum thickens)

28
Q

In the early stages of hypertension the right ventricle does not remodel BECAUSE the development of atherosclerosis in the aorta increases afterload.

A

B. Both statements are correct and NOT causally related.

29
Q

What are some rick factors for the development of hypertension?

A
age
ethnicity
family history
smoking
lack of exercise
diet
obesity
diabetes
stress
medications
30
Q

How can we treat hypertension?

A
  • change diet (less salt and fat, more fish and fruit and veges)
  • less alcohol
  • stop smoking
  • do exercise
  • loose weight
  • take medications (one or combination of the two)
31
Q

What are alternative treatments to hypertension?

A

The kidneys talk to the brain and talk to each other. Because the sympathetic drive increases during hypertension, we can try and cut off the connection between the brain and the kidney to stop the nerves in the kidney