GENERAL INTRODUCTION TO HYPERTENSION

DEFINITION
Hypertension is also called as High blood pressure, is a common
condition in which the force of blood on the walls of your arteries is
often too high.
Arteries are the blood vessels that carry blood away from the heart to
supply your tissues with oxygen and nutrients.In your heart, two
chambers, called ventricles,contract with each heartbeat to push blood to
your lungs and through the arteries to the whole body.

FACTORS AFFECT THE PRESSURE

As blood flows through, the three main factors affect the pressure on the
artery walls.

The first is cardiac output, or the amount of blood your ventricles push
out of your heart each minute.

The blood pressure increase[goes up] as cardiac output increases.

The second factor affecting the blood pressure is blood volume,

or the total amount of blood in the body.
Blood pressure also goes up as blood volume increases.

The third factor that affects the blood pressure is resistance, which is
anything working against the blood flow through your arteries.

Several factors contribute to resistance.

One resistance factor is the flexibility of the artery wall.

Healthy arteries expand with each heartbeat

to help reduce blood pressure on the wall.
Another resistance factor is the diameter of the arteries.

The body is able to increase the diameter of the arteries to lower the
blood pressure, or reduce the diameter to raise the blood pressure.

A third resistance factor is blood viscosity, or thickness.

In your blood, more particles, such as proteins and fat, increase

viscosity.
If the blood is thicker, the blood pressure goes up as the heart works
harder to push it through the arteries.

The blood pressure can be measured with a device called a

sphygmomanometer, or blood pressure cuff.

When the heart beats, the pressure of blood on the walls of your arteries
is called systolic pressure.

When the heart relaxes between beats, pressure on the artery wall is
called diastolic pressure.

While the blood pressure may change throughout the day, it should
normally be less than 120 millimeters of mercury for systolic pressure,
and less than 80 millimeters of mercury for diastolic pressure.

If the systolic pressure frequently stays above 140, or your diastolic

pressure frequently stays above 90, have high blood pressure.

Over time, high blood pressure will damage the walls of the arteries.

The artery wall may become weak and form an enlargement called an
aneurysm.
Or the wall may burst and bleed into the surrounding tissue.
Small tears in your artery wall may attract certain substances in your
blood, such as cholesterol, fat, and calcium, to form a build-up called a
plaque.

Blood flow through the artery decreases as the plaque enlarges.

Blood cells can stick to the plaque and form solid clumps, called
clots,further reducing, or completely blocking, your blood flow.

Damage to your arteries raises your blood pressure even more by

making your heart beat more forcefully.

Artery damage and reduced blood flow lead to conditions such as:
 a stroke,
 heart attack,
 or kidney disease.

CAUSES OF HIGH BLOOD PRESSURE

The exact causes of high blood pressure are not known, but several things
may play a role, including:

 Smoking
 Being overweight or obese
 Lack of physical activity
 Too much salt in the diet
 Too much alcohol consumption (more than 1 to 2 drinks per day)
 Stress
 Older age
 Genetics
 Chronic kidney disease
TYPES

Mainly high blood pressure divided into two type firstly primary, or
essential hypertension and secondly Secondary Hypertension.

Firstly Let discuss about primary, or essential hypertension

The essential hypertension remains somewhat mysterious, but it has been

linked to certain risk factors like

 Blood plasma volume

 Hormonal imbalance
 Lifestyle factors include stress smoking, drinking too much
alcohol, being overweight, eating too much salt, and not getting
enough exercise.

Next lets discuss about Secondary Hypertension

Secondary hypertension (or, less commonly, inessential hypertension)
is a type of hypertension which by definition is caused by an identifiable
underlying primary cause.  [ Secondary hypertension is when there’s an
identifiable— and potentially reversible— cause of the hypertension.]

The underlying causes of secondary hypertension include:

 Narrowing of the arteries that supply blood to your kidneys

 Adrenal gland disease
 Side effects of some medications, including birth control pills, diet
aids, stimulants, antidepressants, and some over-the-counter
medications
 Obstructive sleep apnea
  Hormone abnormalities
 Thyroid abnormalities
 Constriction of the aorta

SIGNS AND SYMPTOMS

[are abnormalities that can indicate a potential medical condition.

Whereas a symptom is subjective, that is, apparent only to the patient
(for example back pain or fatigue), a sign is any objective evidence of a
disease that can be observed by others (for example a skin rash or
lump).]

If the blood pressure is extremely high, there may be certain

symptoms to look out for, including:
 Severe headaches.
 Nosebleed.
 Fatigue or confusion.
 Vision problems.
 Chest pain.
 Difficulty breathing.
 Irregular heartbeat.
 Blood in the urine.

PATHOPHYSIOLOGY
The cause of hypertension is unknown but these unknown causes like
precipitating factor and predisposing leads to pathophysiology of HT.
First talk about predisposing factors. This predispoing factors means
these are the factors which are already present in the body like age,
gender, genetic, race. Coming to the other hand is the precpitating
factors like stress, obesity, kidney disorder etc..

Precipitating factors are nothing but environmental factors that affect the
human body leads to hypertension.
Due to the above causes disturbances in

 Renin-angiotensin aldosterone system

 Autonomic nervous system &
 Endothelial dysfunction

Firstly we discuss on Renin-angiotensin aldosterone system in this

video.
Before getting into all the complex stuff let's have an overview of the

system .so whenever your blood pressure falls known as hypotension the
kidneys are able to sense it and they activate the renin-angiotensin-
aldosterone system which acts on kidney as well as the blood vessels to
restore the blood pressure to the normal most of you know the kidneys
are supplied by a set of renal arteries which supply almost 20 to 25
percent of whole cardiac output two kidneys this blood reaches the
glomeruli through the efferent arteriol leaves the glomerular through the

afferent arterioles. These cells you see are the juxtaglomerular cells the
word juxta means near and these cells are located near the glomerulus
.These cells secrete a substance known as pro rennin and hypotension is
a main stimulator of converting pro renin into rennin. Renin is an
enzyme which acts on angiotensinogen.The word angio means vessels
the word Tennyson hojin means a substance which constricts the vessels
it is a plasma protein which is synthesized in the liver.Renin converts
angiotensinogen into angiotensin one the next step takes place in the
lungs when the enzyme angiotensin converting enzyme acts on
angiotensin 1 and converts it into angiotensin 2. The angiotensin 2 is a
powerful way so constructor which mediates the effects of renin-
angiotensin-aldosterone system.

let's look at the effects of angiotensin 2 on blood vessels as I said

angiotensin II is a very potent ways to constrictor it constricts both the
arteries as well as the veins the constriction of the arteries leads to a total
peripheral resistance.

Increase and the constriction of veins lead to increase in the venous

return to the heart both these mechanisms increase the blood pressure of
the person. This effect is rapid and takes a fewminutes now let's look at
the effects of angiotensin ii on the kidneys. These effects are slow and
take a few days to have their maximum effect angiotensin ii acts on
kidney in two ways .The first is the direct mechanism as most of you
know the GFR of the kidney is directly proportional to the blood flow
through the kidneys. The blood enters the glomerular through the
afferent arterioles and angiotensin ii being a powerful vasoconstrictor
constricts.These afferent arterioles mainly and decreases the blood flow
through the Kidneys. This results in a decrease in the GFR of the kidney
which results in a decrease in the urine output through the kidney .
Now second is the indirect effect in which the angiotensin ii acts on the
adrenal gland and releases aldosterone. Aldosterone in turn acts on the
kidney and increases the sodium reabsorption as well as the water
reabsorption. so we have a decreased urine output increase in the water
reabsorption and increase in the sodium reabsorption all theseeffects
lead to an increase in the extracellular fluid of the body and increase in
the capillary pressure and a long-term increase in the arterial pressure.

so to summarize let's suppose a person gets stabbed and he loses a lot of

blood this will lead to a decrease in the blood pressure of the person
known as hypotension which is a potent trigger of activation of renin-
angiotensin-aldosterone system.The RAS further acts on the blood
vessels as well as the kidneys and normalizes the blood pressure . so this
was all about the renin-angiotensin-aldosterone system .
secondly we discuss on Autonomic nervous systemlt
[let us discuss about the Key Terms content
 autonomic nervous system: The part of the nervous system that regulates the involuntary
activity of the heart, intestines, and glands. These activities include digestion, respiration,
perspiration, metabolism, and blood pressure modulation.
 norepinephrine: A catecholamine with multiple roles including as a hormone and
neurotransmitter. Areas of the body that produce or are affected by this substance are described
as noradrenergic.
 sympathetic: Of or related to the part of the autonomic nervous system that under stress raises
blood pressure and heart rate, constricts blood vessels, and dilates the pupils.
 baroreceptor: A nerve ending that is sensitive to changes in blood pressure.
 parasympathetic: Of or relating to the part of the autonomic nervous system that inhibits or
opposes the effects of the sympathetic nervous system.]

Hypertension is related to abnormalities inans.once the bp get decreased the

sympathetic neverous sydtem get activated.due to this activation adrenaline and
noradrenaline are released from the………………this adrenaline and
noradrenaline stimulates SA node by this number of heart impluses get increased
which leads to increased in the heart rate which manifest hypertension.

Mean while the arterial baroreceptors  produce baroreflexes which also manifest
greater vasoconstrictor responses. Due to this Constriction of the blood vessels
will result in an increase in the blood pressure also alters the cardiac Output.

Lastly we discuss on Endothelial dysfunction as I mentioned in

the above explaination
 Endothelial dysfunction also starts with decreased in bp leads
to increased in blood vasculation which stimulates the
vasoconstricting substances like superoxides. the substances
produce increased pressured on the walls of the heart which
finially manifest hypertension. [ endothelial dysfunction means
An imbalance of reduced production of nitric oxide (NO) or increased production of reactive
oxygen species (ROS), mainly superoxide, may promote endothelial dysfunction. due to this
large blood vessels on the heart's surface constrict (narrow) instead of dilating (opening).]
 CHF
Same as above video
 Renin-angiotensin aldosterone system
 Autonomic nervous system

FRANK STARLING MECHANISM

In this video we're going
to discuss starlings law of the heart
otherwise known as the frank-starling
mechanism to begin we need to have a
foundational understanding of three
important terms those terms are end
diastolic volume or edv preload and
stroke volume let's start with end
diastolic volume first edv is the amount
of blood in the ventricles just before
contraction or systole as the name
implies it is the volume of blood in the
ventricle at the end of the loading
phase or diastole so as we look to our
diagram here and diastolic volume is
this amount of blood that fills the
ventricle after the heart has contracted
next let's go over preload with preload
we're talking about the physiological
event that occurs during the cardiac
cycle the contracting and relaxing of
the heart the physiological event were
examining with preload is how the end
diastolic volume that amount of blood
left in the heart after diastole
stretches the walls of the ventricle
priming the pump to perform its duty of
pumping blood to the lungs or to the
body tissues so as we see here on our
diagram preload is shown by these arrows
that represent the stretching of the
ventricle walls that the blood inside
that chamber is causing lastly let's
look at stroke volume this is simply the
amount or the volume of blood that is
pumped from the ventricle each time the
heart contracts for our diagram here
let's assume we have a healthy adult
male heart depending on weight this will
usually be around 70 to 80 milliliters
now that we have an idea of these
fundamental components let's look at
what the frank-starling mechanism is
really getting at by definition the law
states that stroke volume increases as a
response to an increase in the volume of
blood in the ventricles before the heart
contracts so
more blood in the ventricle equals
creator stretching of the ventricular
walls which equals a more forceful
contraction during systole going one
step further and looking at the
important terms we've learned more end
diastolic volume equals more preload
which equals more stroke volume which in
the end gives us a more forceful
contraction during .
one of the ways where that is controlled

we've looked at muscle contraction and

 we said that the functional unit of
06:58
contraction is the sarcomere and this is
07:01
one sarcomere here and
we have
07:13
this that we call myosin. this is the
07:17
myosin filament and the blue hair we
07:20
call actin so this is a for actin and
07:24
this is M for myosin on the myosin we
07:27
have myosin heads and those myosin heads
07:30
associate with the actin and they pull
07:33
the actin so that this process can
07:36
happen where we have the sliding
07:38
filaments . the filaments slide against
07:40
each other the muscle contracts and then
07:45
the muscle relaxes. this is the exact
07:48
same process that happens in the heart
now the way the structure
07:58
of this sarcomere is set up in order for
08:01
us to have the maximum amount of
08:03
contraction we have to have optimum
08:06
overlap . here we have overlapping between
 08:09
the myosin heads and the actin and in
08:14
order to get the best contraction the
08:16
strongest contraction we have to have
08:18
maximum overlap this is how this works
08:22
when the heart gets filled with blood
08:24
this stretches out more so the end of
08:28
this sarcomere might be over here
08:31
because there's more blood in the heart
08:34
that stretching of the muscle causes an
08:37
increase in contraction for a number of
08:40
Reasons.
08:41
imagine if the end of this actin was
08:44
over here. there's an increased distance
08:47
between these two points so that it has
08:50
a further distance to travel
08:54
the sarcomere gets shorter that's gonna
08:57
cause a stronger contraction and if you
09:00
have a stronger contraction it's gonna
09:02
send more blood out of the heart leaving
09:05
less blood in the heart. in addition to
 09:08
this we've spoken about how calcium is
09:11
involved in this process
but calcium is released CA 2 plus
09:20
calcium ions are released from the
09:23
sarcoplasmic reticulum that binds to
09:26
troponin which is on here blocking the
09:30
binding sites for the myosin head when
09:33
calcium comes that exposes the binding
09:36
site so that the myosin heads can bind
09:38
freely and the stretching of the heart
09:43
increases the affinity of this troponin
09:46
for calcium ions now if you have an
09:50
increased affinity for calcium ions
09:53
you're gonna have more myosin heads
09:56
being able to bind to the binding sites
09:59
on the actin and that is also gonna
10:02
increase the contraction this is called
10:04
the frank-starling mechanism.
VENTRICULAR HYPERTROPHY AND REMODELING

 Ventricular hypertrophy is a term used to describe an increase in

ventricular muscle mass. 
 Ventricular remodeling is described as the changes in both
myocardial cells and extracellular matrices, resulting in change of 
size, shape, structure, and functions of the heart.
 These progressive changes in ventricular structure and function
ultimately results in a change in shape of the left ventricle from an
ellipse to a sphere.
 This results in more space available to accommodate more blood and
thus increase the cardiac output.