L26 Flashcards
what are they 2 types of hypertension and what % of people with hypertension have each type
primary hypertension = 95% of people
secondary = 5%
what causes primary hypertension
the cause is unknown = idiopathic essential
it happens with stiffer arteries with ageing
what causes secondary hypertension
this has specific causes
the 2 main causes of primary hypertension are an increase in arterial blood volume and a decrease in arterial compliance
which is the most important factor
we don’t know between these 2
Salt retention in kidney = increase in blood volume
autoregulation result in arteriolar vasoconstriction
arterial compliance decrease = increase in total peripheral resistance (TPR)
how do these processes relate to each other
Sympathetic activation of the arterioles (hypothalamus-medulla oblongata) = arteriolar vasoconstriction -> arterial compliance decrease -> increase TPR
this causes less blood flow to kidney = release of vasoactive substances and salt retention which increase blood volume
These are not mutual inclusive or inclusive
This indicates the important of the kidney and arterial compliance and sympathetic activation pathway in hypertension. therefore they are both as important as each other
Sympathetic is being activated during moderate exercise
what does this cause
In the vessels we have vasodilation is some vascular beds to that the tissues get more O2 but constriction in other vascular beds
As a consequences of sympathetic activation and excerise means that TPR decreases. This means that during moderate exercise arterial pressure is kept constant. It increases slightly during intense exercise
The increase in overall sympathetic activity then HR goes up SV goes up and MAP goes up
BP is very similar in all mammals
what is an example where this is not the case
a giraffe
their MAP is 172-200mmHg
giraffes are not born hypertensive (they are born normotensive)
why do they develop high blood pressures
because of their neck
As giraffe grows, blood flow to cardiovascular brainstem reduces, due to effects of gravity
Sympathetic nerve outflow increases to cause nerve-mediated hypertrophy of vessel wall (G-suit)
Increase in TPR, and thereby MAP, to preserve cerebrovascular flow
tibbia artery will have massive wall and small luman
carotid artery will have huge luman
giraffes have to put thei heads down to drink
how do they overcome this problem
Minimise blood flowing back into head:
Upper neck - rete mirabile
Jugular veins - seven valves
Lower legs - great pressures
Very tight sheath of thick skin over lower limbs
maintain high extravascular pressure
what are some consequences of hypertension
- Kidney disease
- Development of Atherosclerosis – Stroke
- Atrial Fibrillation
- Myocardial Infarction / Coronary artery disease
- Cardiac Remodelling (Hypertrophy - Heart Failure)
why do you get cardiac remodelling of the heart in hypertrophy
Increases workload (afterload) of the heart because of the stiffer tube (aorta) to eject blood into causing a faster returning reflected pulse wave
it is also because of higher resistance to the output
what ae the 2 ways of cardiac remodelling
there is remodelling at the cellular level
OR
remodelling at the organ level
what is cellular remodelling of the heat
hypertrophy of the cardiac myocytes
or hypertrophy because of fibrosis (this passably could be organ remodelling)
describe hypertrophy of the cardiac myocytes
Increase in number of sarcomeres in the cardiomyocytes (size)
NOT in number of cardiomyocytes or the size of the sarcomeres (might even be less cardio myocytes because of apoptosis)
what causes fibrosis in the heart
If the hearts is under increased load there are tiggers to make more fibrosis
This is because you are the making the cells bigger but you also need to make the scaffolding bigger to support them
hypertrophy cased by fibrosis causes an increase in the extracellular matrix
what does this contain
Collagen type I + III Elastin Proteoglycans Laminin Fibronectin
what collagen type increases first in fibrosis
type 3 and then type 1
i think type 3 is the stiff one
what is the difference between concentric and eccentric remodelling
concentric = wall thicker
eccentric = luman bigger
does pressure overload cause concentric or eccentric remodelling
concentric
does volume overload cause concentric or eccentric remodelling
eccentric
what does pressure overload cause
thickening of the LV and no dealation in early stages of disease
what does volume overload cause
thinning of the LV and significant dilation
this is usually because there is something wrong with the valve
what is hypertrophic cardiomyopathy caused by
predominantly genetic mutations
what does hypertrophic cardiomyopathy cause
gross thickening of the LV walls with no dilation/decrease in LV chamber size
cardiac dilation in heart failure is because of
increase in myocyte length»_space; and width
leads to…..
extensive fibrosis
myocyte death
advanced cardiac disfunction
pathological hypertrophy in heart failure is because of
increase in myocyte length «_space;and width
fibrosis
maybe some cardiac dysfunction
hypertrophy in cardiac failure leads to
you have an increase in MAP which leads to..
increase wall thickness to
normalise wall stress. this further increase in MAP
(vicious circle)
You get a increase in wall thickness and MAP to normalise the stress within the wall. You need this increase in pressure because you need to increase the afterload. If you didn’t change the wall thickness then the stress in th cardiomyocytes would be very increased
This then goes into a deadly cycle and eventually leads to thinned ventical
what % of cardiac failure is because of either concentric or eccentric hypertrophy
concentric = 50-60%
eccentric = 40-50%
describe concentric heart failure
Heart failure with preserved ejection fraction (HFpEF)
this is also known as diastolic heart failure
describe eccentric heart failure
Heart failure with reduced ejection fraction (HFrEF)
also known as systolic HF
what are the 2 types of heart failure
concentric/diastolic HF
eccentric/systolic HF
what kind of heart failure are males and females more likely to get
male = eccentric/systolic
female = concentric/diastolic
factors influencing form of remoderling/transition
these show that the heart can respond in many ways to hypertension
Blood pressure (Hypertension) = Concentric
Old age = Concentric
Coronary Artery Disease = Concentric
Valve leaks = Eccentric
Obesity = Eccentric / concentric (predominantly eccentric)
Diabetes = Concentric / eccentric (predominantly concentric)
Familiar Dilated Cardiomyopathy = Eccentric
in systemic hypertension what is the effect on the right ventricle
ealt stage = mo effect
late stage = hypertrophy of RV
what causes right ventricular hypertrophy
Increase LV filling pressure translates into pulmonary circulation
Hypertrophied LV interacts
with the RV
the above means that When the septum gets really thick (because of left ventricular hypertrophy) it will push into the right ventricle which will then cause the right vertical to get bigger to compensate
In the early stages of hypertension the right ventricle does not remodel
BECAUSE
the development of atherosclerosis in the aorta increases afterload.
both statments are correct but not causally related
what are some risk factors for developing hypertension
- Age
- Ethnicity
- Family History
- Smoking
- Lack of activity/exercise
- Diet (Lipids, salt, alcohol)
- Overweight/obesity
- Diabetes
- Stress
- Medications
what are the 2 main types of treatments for hypertension
change in life sytel and pharmacological
what are some lifestyle changes that can decrease hypertension
- Change Diet (less salt & lipids, more fish, fruit & vegetables)
- Reduce Alcohol consumption
- Stop Smoking
- Perform Physical activity - Exercise training
- Loose Weight
what is the role of diuretics on hypertension
Thiazides, decrease blood volume
therefore decrease hypertension
what is an example of and what do β-adrenergic receptor blockers do
carvedilol, decreases CO and baroreceptor sensitivity
therefore decreasing hypertension
(it effects the heart)
what do Calcium channel blockers, Angiotensin II receptor blockers and Angiotensin converting enzyme (ace) inhibitors all have in common
they also decrease TPR
what are Calcium channel blockers, Angiotensin II receptor blockers and Angiotensin converting enzyme (ace) inhibitors often used along side of
diuretics (decrease in blood volume)
together these would decrease TPR and blood volume = dramatic effect
why is renal denervation an alternative treatment for hypertension
The kidney has sympathetic nerves that are innovated and signals are send from the brain to the kidney altering its function
The kidney also has afferent nerves to send signals back to the brain about how the kidney is functioning
This system usually works but when it doesn’t it is because the sympathetic drive from the brain to the kidney and from the kidney back to the brain is increase
Therefore one of the suggested treatment to to stop this communication
what does renal denervation involve
Radiofrequency ablation of efferent and afferent nerves
how does renal denervation use Radiofrequency ablation of efferent and afferent nerves
The tip is brought up the aorta into the renal arteriy and then by radial oblation they oblate (cut) both the afferent and efferent nerves
In animals this works really well
What do you need to be human and qualify to have a renal denervation
Hypertensive patients (160-180 mmHg) taking >2 antihypertensive drugs
Nerves can potentially grow back. what test can we do to see if they have
they measured muscle sympathetic nerve activity to skeletal muscles. The graph shows an overall activation of skeletal muscle (sympathetic activation)
After 12 months of renal deprivation then you can see that also the sympathetic drive is decreases as well to the muscle showing a over body decrease in sympathetic activation
you can look at the muscles to see if they have less sympathetic nerve activity, if they do then the nerves haven’t grown back
