Hypertension

BY DR. SIDRA BATOOL

M.PHIL. PHARMACOLOGY
Contents
Introduction (Definition)
Categories/types of hypertension
Pathogenesis(Mechanism &factors inducing HTN)
Risk factors
Clinical presentation
Control of blood pressure
Complications
COMPOSITIO
N OF BLOOD
VESSELS
Composition of Blood
vessels
Structure of vascular wall varies along the length of
vasculature

Arteries are thicker than veins to accommodate more

pressure (As aorta has more pressures than vena cava.

Ratio between wall thickness and lumen decreases in

capillaries for more sustained and smooth flow and pressure.
Pressure
Pressure is the force applied perpendicular to the surface
of an object per unit area over which that force is
distributed.
Composition of Blood
vessels
Different vasculatures are more prone to particular diseases
hence:

Atherosclerosis occurs mainly in larger, muscular arteries

Hypertension affects small arterioles, and specific forms of

vasculitis selectively involve vessels of only a certain caliber.
Composition of Blood
vessels
Intima

Media

Adventia
Vascular organization
Large elastic arteries

Medium-sized muscular arteries

Small arteries

Capillaries

Veins
Large elastic arteries
Smooth muscle and elastic tissues in media

These muscles and elastic tissues contract and relax during

systole and diastole, respectively

With the passage of age these muscles decrease their

contractility and transmits higher B.P to other organ.
Large elastic arteries
Aorta, arch vessels, iliac and pulmonary arteries
Small arteries
The velocity of blood flow is sharply reduced, and flow
becomes steady rather than pulsatile.

More smooth muscles, very few elastic fibers

More resistance due to less diameter

Blood pressure (BP)
A lateral pressure exerted by the blood on the walls of the blood vessels while flowing
through them.

Blood pressure in a blood vessel depends upon two things.

1) Distance from the heart

2) Nature of the blood vessel.

Blood pressure is more in blood vessels close to the heart.

Blood pressure is more in arterial system than in the venous system. This is because;
◦ walls of arteries are thicker and less elastic

◦ the walls of the veins are thinner and more elastic.

Normal blood pressure is 120/80 mmHg,

Systolic BP (SBP) is the maximum BP during the ventricular systole- 120

mmHg.
◦ Range: 110-130 mmHg.

Diastolic BP (DBP) is the minimum pressure during the ventricular diastole. It is

80 mmHg.
◦ Range: 70-90 mmHg
 Physiological Variations Age:
BP more in adult than in children.

Sex: BP more in male than females.

Pregnancy: During the later stages of pregnancy BP usually increase.

Altitude: BP is higher in people living at higher altitude.

Exercise: Systolic BP increases during exercise.

Emotion: BP rises during emotional expressions.

Sleep: BP falls during sleep

 Terminologies

Hypotension:
◦ Low BP may lead to hypoperfusion of organs which may lead to organ
dysfunction or even tissue death

Hypertension:
◦ High BP leads to damage of blood vessels, organ failure and
atherosclerosis
Factor Effecting Blood
Pressure
Volume of blood.

Force of contraction of the heart.

Heart rate and BP are inversely proportional.

Viscosity of blood.

Nature of the blood.

Elasticity of blood vessel

BP Determination
Blood pressure (BP) is determined by
◦ cardiac output (CO)
◦ total peripheral resistance (TPR),
BP = CO x TPR.
Cardiac output (CO) is affected by two factors,
◦ the heart rate (HR)- no. of beat/min
◦ the stroke volume (SV), the volume of blood pumped from one ventricle of the heart
with each beat
CO = HR x SV,
BP = HR x SV x TPR
In reflex bradycardia, blood pressure is reduced by decreasing cardiac output (CO) via a
decrease in heart rate (HR).
Cardiac output
 It is a function of stroke volume (amount of blood ejected from ventricles per
beat) and heart rate

 Stroke volume is dependent upon filling pressure which Is regulated by

sodium homeostasis and its effect on blood volume

 Heart rate and heart contractility are regulated by adrenergic receptors

 Peripheral Resistance

o It is regulated predominantly at the level of arterioles by neural and humoral inputs

o Vascular tone reflects a balance between vasoconstrictors (Ang II, catecholamines and
endothelin) and vasodilators (NO, kinins and prostaglandins

o BP is also affected by local factors like vasoconstriction in tissue due to higher blood flow,
tissue pH and hypoxia

o Kidneys, adrenal gland and myocardium interact to influence vascular tone and to regulate
blood volume by adjusting sodium reabsorption
Regulation of Blood Pressure
BP Regulation
Nervous mechanism

Renal mechanism

Hormonal mechanism

Local mechanism
POTENTIAL MECHANISMS
Several mechanisms are involved in short-term and long-term regulation of BP for
adequate tissue perfusion; these include the following:
1) Neuronal regulation.
2 ) Hormonal mechanisms.
a) RAAS system
b) Natriuretic hormone
c) Hyperinsulinemia
d) Local mechanism
3) Vascular endothelial mechanism.
4) Electrolytes and other chemicals.
 Control of Blood pressure
Short term control
Baroreceptors (Baroreflex)
ANS
-Other stretch receptors
Long-term control
◦ Renin/ angiotensin/ aldosterone system
◦ Vasopressin (ADH)
◦ Atrial natiuretic peptide
Neural control of BP-Short term
regulation
oThe nervous system regulates blood pressure in the short term through a
feedback loop involving baroreceptors, chemoreceptors the brainstem, and
the autonomic nervous system.
oThis system allows the body to quickly adapt to changes in blood pressure
by adjusting heart rate, vascular tone, and cardiac output to maintain stable
blood pressure.
Neural control of BP-Short term
regulation
oBaroreceptors are pressure-sensing receptors in the carotid sinus and aortic
bodies (walls of heart and blood vessels).
o Baroreceptors sense stretch and rate of stretch by generating action potential.
o An increase in the blood vessel pressure increases action potential generation
rates and provides information to CNS via the Glossopharyngeal nerve and
Vagus nerve.
o These action potentials get transmitted to the solitary nucleus that signals to
autonomic neurons secrete hormones to affect the cardiovascular system.
o Activation of the aortic baroreceptor during increases in blood pressure
effectively inhibits the efferent sympathetic nerve response.
Baroreceptors (Baroreflex)
 Sensory information is used primarily in autonomic reflexes that in turn
influence the cardiac output and vascular smooth muscle to influence Total
peripheral resistance.
Baroreceptors act immediately as a part of a –ve feedback system called a
baroreflex as soon as there is a change from the usual mean atrial blood pressure
returning the pressure toward a normal level.
 Activation of these receptors reflexly increases parasympathetic and decreases
sympathetic activity in the heart, arterioles, and kidneys, which decreases blood
pressure through peripheral vasodilatation and bradycardia.
Increased B.P= ↑ Parasympathetic activity-by releasing Acetylcholine
Decreased B.P= ↑ Sympathetic activity-by releasing Nor-epinephrine
 Neuronal mechanisms :
- Stimulation of α1 (arterioles and venules) : vasoconstrictions.
- Stimulation of α2 : decrease sympathetic outflow.
- Stimulation of β1 (heart, JG cells in kidney) : increase in heart rate and
contractility, renin release.
- Stimulation of β2 (lungs, liver, arteriolar smooth muscles, pancreas) :
vasodilation, bronchodilation.
- Baroreceptor reflex system
BR: nerve endings lying in the walls of large arteries, especially in
carotid arteries and aortic arch.
Transmit impulse through 9 th cranial nerve and vagus nerves.
 Baroreceptor reflex
Blood pressure falls

Sensors Aortic arch Carotid sinus

Neural integration Medulla Ob.

Vasoconstriction Cardiac stimulation Cardiac inhibition

Constriction
Increased stroke Increased heart
Effectors of veins &
volume rate
arterioles

Increased R Increased CO

Increased BP
Nervous mechanism (Baroreceptor mechanism)
Increased BP Decrease BP

Stimulation
Dilation of blood Bradycardia and
Baroreceptors vessels dec. CO

Decrease Increase vagal

vasomotor tone tone

Inhibition of Stimulation of
vasoconstrictors vasodilators area
area

Impulse via IX and Nucleus of tractus

X cranial nerves solitarius
 Chemoreceptors
Chemoreceptors are specialized sensory receptors that detect changes in the chemical
composition of the blood, such as levels of oxygen (O₂), carbon dioxide (CO₂), and pH
(acidity).
ANS Control Model

Cross-section of a blood vessel. In general

each vessels is divided in three layers
called tunicas.
BP is also affected in this efferent
pathways of the ANS. The sympathetic
system innervates the smooth muscle
tissue, providing different lumen
diameters according to the stimuli
received by the baroreceptors.
Renal mechanism-to regulate BP
Kidneys play an important role in blood pressure regulation as
follows:
• Renin-angiotensin system - Both regulate peripheral resistance and
sodium homeostasis (direct action on vessels, increase blood volume
producing aldosterone secretion).
• The kidney produces vascular relaxing factors produces vascular
relaxing factors or antihypertensive substances(PG, NO) or
antihypertensive substances(PG, NO)
• When BV reduces—GFR leading to increased absorption of sodium
by the increased absorption of sodium by the proximal tubules.
Role of kidney in regulating normal
blood pressure
RAAS (Renin-Angiotensin Aldosterone
system)
 The kidneys play an important role the regulation of arterial pressure,
especially through RAAS.
 Decrease in BP & renal blood flow, volume depletion or decreased
sodium concentration, & activation of the sympathetic nervous system
can all trigger an increased secretion of the enzyme renin from cells of
the juxtaglomerular apparatus in the kidney.
 Renin excreted from the kidney acts on plasma angiotensinogen to
catalyze the formation of angiotensin-1. Angiotensin-converting enzyme
(ACE) converts angiotensin-1 to angiotensin-2.
RAAS (Renin-Angiotensin Aldosterone
system)
Angiotensin-2 is potent vasoconstrictor that acts directly on arteriolar smooth
muscle & also stimulates the production of aldosterone by adrenal glands.
Aldosterone causes sodium & water retention & the excretion of potassium. which
ultimately results into:
•Increase Peripheral resistance
•Increase Blood Volume
•Increase Blood pressure
-Angiotensin II infusion causes hypertension.
-Hypertensive patients drop BP much more significantly than euvolemic
normotensive patients when angiotensin II is blocked.
Renin Angiotensin
System
Activities of renal system
Aldosterone & Anti-diuretic hormone
 The release of antidiuretic hormone (ADH) release from the posterior pituitary
gland
 The release of aldosterone from the zona glomerulosa of the adrenal cortex
within the adrenal gland.
 Aldosterone functions to increase the arterial pressure through the upregulation
of Na+/K+ pumps of the distal convoluted tubule and collecting duct within the
nephron
 This activity is the distal convoluted tubule leads to increased reabsorption of
sodium, as well as increased secretion of potassium
 The increase in sodium reabsorption leads to passive reabsorption of water and
an increase in blood pressure
Natriuretic hormones
ANP promote natriuresis (loss of sodium).
Atrial myocytes synthesize, store and release ANP in response to
stretch (low P volume sensor).
 The major effect is renal vasodilation.↑ blood flow=Increased GFR
Thus more Na+ reaches macula densa.
More Na+ excreted.
May inhibit action of renin, and generally opposes the effects of
angiotensin II.
Natriuretic hormone inhibits sodium and potassium ATPase and thus
interferes with sodium transport across cell membranes.
Inherited defects in the kidney’s ability to eliminate sodium can cause
an increase in blood volume. A compensatory increase in concentration
of circulating natriuretic hormone theoretically could increase urinary
excretion of sodium and water.
However, this same hormone is also thought to block the active
transport of sodium out of arteriolar smooth muscle cells. The increased
intracellular concentration of sodium ultimately would increase
vascular tone and BP.
 Hyperinsulinemia
•Also known as metabolic syndrome.
•Increased insulin concentration may lead to hypertension because of
increased renal Na retention, and enhanced sympathetic nervous system
activity.
•Moreover, insulin has growth hormones-like actions that can induce
hypertrophy of vascular smooth muscles.
•Insulin also may elevate BP by increasing intracellular calcium which leads
to increased intravascular resistance.
•The exact mechanism by which insulin resistance and hyperinsulinemia is
occur in liver and kidney.
Hormonal mechanism
Hormone that increase BP
Hormonal mechanism
Hormone that decrease BP
Local Mechanism
Local constriction (EDCF)
Local vasodilation (NO)
Vascular Endothelium

Vascular endothelium produces several factors that affect vascular

tone and influence platelets and mononuclear cell functions.

The endothelium derived factors, generally classified as endothelium

derived relaxing factors (EDRF) and endothelium derived contracting
factors (EDCF) include nitric oxide (NO), prostacyclin, endothelium
dependant hyperpolarizing factors (EDHF) and endothelin .
Electrolytes and other chemicals
- Excess sodium Intake
- Potassium depletion --- increase peripheral VR.
HYPERTENSION
 Introduction
•Definition:
Hypertension also called silent killer is a chronic medical
condition characterized by persistent elevation of the systolic or
diastolic pressure above 140/90mmHg.
-In hypertension arterial blood vessels constricted, Hence increase
the Resistance to blood flow, causing an increase in blood pressure
against vessel walls.
 SYSTEMIC HYPERTENSION
Hypertension (HT) = pathologically  blood pressure
Blood pressure : Systolic /diastolic pressure
Normal blood pressure (adults) : < 140 mm Hg/90 mm Hg

Borderline HT : 140 - 160 mm Hg/90 - 95 mm Hg

Definite HT : > 160 mm Hg/95 mm Hg
Classification of blood
pressure/Hypertension
Blood pressure classifications proposed by the European
Society of Hypertension/ European Society of Cardiology
(ESH/ESC), World Health Organization (WHO) and in The
Seventh Report of the United States Joint National
Committee on Prevention, Detection, Evaluation, and
Treatment of High Blood Pressure (JNC 7) are
Classification of
Hypertension in adults-JNC 7
Types
It is divided into two types
1) Primary hypertension (Essential hypertension)
2) Secondary hypertension (Non-essential hypertension)
 Primary hypertension
o Essential, primary, or idiopathic hypertension is defined as high BP in which secondary
causes such as renovascular disease, renal failure, pheochromocytoma, aldosteronism, or
other causes of secondary hypertension are not present.
o Essential hypertension accounts for 95% of all cases of hypertension.
o Essential hypertension is a heterogeneous disorder, with different patients having different
causal factors that lead to high BP.

oIt results when arterial blood pressure is increased due to increased peripheral resistance.

oIt is further divided in to two types namely:

◦ benign hypertension

◦ malignant hypertension
 Multifactorial genetic and
environmental factors of primary HTN
1) Sympathetic NS hyper-reactivity
2) Hyper-reactivity of RAAA
3) Defects in Natriuresis
4) Intracellular sodium and calcium
5) Obesity
6) Sodium intake
7) Low potassium intake
8) High alcohol intake
9) Smoking
10) Sedentary lifestyle
11) Aging
Benign hypertension
o There is a moderate increase in blood pressure with systolic pressure of 200 mm Hg
and the diastolic pressure of above 100 mm Hg.

o In resting condition and sleep, the blood pressure returns to normal level.

o Later, if there is increase in blood pressure it will not come back to normal level in
resting conditions.
 Malignant hypertension
o Malignant hypertension is the term used to describe high blood pressure that

causes damage to your organs.

o This is an emergency condition characterized by elevated blood pressure

usually at >180 mm Hg systolic or >120-130 mm Hg diastolic, plus damage to
multiple organs. (The blood pressure elevated to a great extends of about 250
mm Hg of systolic pressure and 150 mm Hg of diastolic pressure. )

o It produces severe symptoms like renal disease, retinal disease, and being a
fatal disease, it causes death within few years.
Characteristics
Some of the characteristics of primary or essential hypertension are,

1) The mean arterial pressure is increased 40-60 %.

2) The renal blood flow in the later stages is decreased about one half of normal.

3) The resistance to blood flow through the kidney is increased 2-4 fold.

4) The kidneys will not excrete adequate amounts of salt and water unless the
arterial pressure is high.
 Mechanism of Essential
hypertension

Reduced renal sodium excretion in the presence of normal arterial pressure probably is
a key pathogenic feature; indeed, this is a common etiologic factor in most forms of
hypertension. Decreased sodium excretion causes an obligatory increase in fluid volume
and increased cardiac output, thereby elevating blood pressure
 Mechanism of Essential
hypertension
Reduced renal sodium excretion
i) Increasing blood volume

When the kidneys are less effective at excreting sodium, more sodium remains in the
bloodstream. Sodium attracts and holds water, so the retention of sodium leads to an
increase in blood volume. The expanded blood volume requires the heart to pump more
blood through the circulatory system, which increases the pressure on the walls of the
arteries, leading to higher blood pressure.
 Mechanism of Essential
hypertension
Increasing vascular resistance

- These are not necessarily an independent factor, as chronic vasoconstriction may result
in permanent thickening of the wall of the blood vessels.

Sodium retention can also cause the smooth muscles in the blood vessel walls to contract,
narrowing the vessels (a process known as vasoconstriction). Narrower blood vessels
increase resistance to blood flow, which further elevates blood pressure. Additionally,
high sodium levels can impair the function of endothelial cells that line the blood vessels,
reducing their ability to produce nitric oxide, a substance that helps blood vessels relax
and dilate. This reduced vasodilation contributes to sustained high blood pressure.
Secondary hypertension
•Secondary hypertension has an identifiable cause, such as renal artery stenosis or
pheochromocytoma, and is managed as part of the primary condition.
Causes of Secondary Hypertension:
CARDIOVASCULAR RENAL

Coarctation of aorta Acute glomerulonephritis

Chronic renal disease Chronic renal disease

Polyarteritis nodosa Polycystic disease

Increased intravascular volume Renal artery stenosis

Increased cardiac output Renin producing tumor

 Causes
ENDOCRINE NEUROLOGIC

Adrenocortical hyperfunction (Cushing syndrome, Psychogenic

primary aldosteronism, congenital adrenal hyperplasia)

Exogenous hormones (glucocorticoids, estrogen Increased intracranial pressure

[including pregnancy-induced and oral contraceptives],
sympathomimetics and tyramine-containing foods,
monoamine oxidase inhibitors)

Pheochromocytoma Sleep apnea

Acromegaly Acute stress, including surgery

Hypothyroidism (myxedema) &

Hyperthyroidism (thyrotoxicosis)
 Secondary hypertension
Most of the remaining cases (secondary hypertension) are due to primary renal disease, renal
artery narrowing (renovascular hypertension), or adrenal disorders. Several relatively rare
single-gene disorders cause hypertension (and hypotension) by affecting renal sodium
resorption. Such disorders include
• Gene defects in enzymes involved in aldosterone metabolism(e.g., aldosterone synthase,
11β-hydroxylase, 17α-hydroxylase), leading to increased aldosterone secretion, increased salt
and water resorption, and plasma volume expansion
• Mutations in proteins that affect sodium resorption (as in Liddle syndrome, which is
caused by mutations in ENaC, leading to increased distal tubular resorption of sodium-induced
by aldosterone)
Secondary hypertension
The different forms of secondary hypertension are
◦ Cardiovascular hypertension

◦ Renal hypertension

◦ Endocrine hypertension

◦ Neurogenic hypertension
Cardiovascular hypertension
It is produced due to
a) Atherosclerosis- hardening and narrowing of blood vessels
b) Coarctation of aorta- narrowing of aorta.
Renal hypertension
It is produced due to

a) Stenosis renal arteries- narrowing of one or both renal arteries, so that the renal
function is impaired.

b) Glomerulonephritis- nephritis with inflammation of the capillary loops in the

renal glomeruli.
Endocrine hypertension
It occurs due to

a) Pheochromocytoma- tumor in adrenal medulla

b) Hyperaldosteronism- excess secretion of aldosterone from adrenal cortex -

Conn’s syndrome.

c) Cushing’s syndrome- excess secretion of cortisone.

d) Gigantism or Acromegaly- excess secretion of growth hormone.

Neurogenic hypertension
Acute hypertension can be caused by strong stimulation of the sympathetic nervous
system.

a) Section of the baroreceptors nerves.

b) Lesions in tractus solitarius.

c) Increased intracranial pressure

 Other Categories of
Hypertension
White coat hypertension
•White coat hypertension, more commonly known as white coat
syndrome, is a phenomenon in which patients exhibit elevated blood
pressure in a clinical setting but not in other settings. It is believed
that this is due to the anxiety some people experience during a clinic
visit.
•The term "masked hypertension" can describe the contrasting
phenomenon, where blood pressure is elevated during daily living,
but not in an office setting.
Resistant hypertension
•Resistant hypertension is the name given to high blood pressure that’s
difficult to control and requires multiple medications.
•Hypertension is considered resistant when your blood pressure stays
above your treatment target, even though you’re taking three different
types of blood pressure lowering medications, including a diuretic.
•It may have secondary hypertension which cause hasn’t identified and
treated by multiple medication.
Isolated systolic hypertension
o Isolated systolic hypertension is defined as systolic blood pressure
above 140 mm Hg and diastolic blood pressure under 90 mmHg. It’s
the most frequent type of hypertension in older adults.
o An estimated, 15 percent trusted source of people 60 years or older
have isolated systolic hypertension. The cause is thought to be the
stiffening of arteries with age.
Gestational hypertension
o Gestational hypertension or pregnancy-induced hypertension (PIH) is the
development of new in a pregnant woman after 20 weeks' gestation without the
presence of protein in the urine or other signs of pre-eclampsia.

oGestational hypertension is defined as having a blood pressure greater than

140/90 on two separate occasions at least 6 hours apart.
 Hypertensive crises
Hypertensive crises can present as hypertensive urgency or as a hypertensive emergency.
Hypertensive urgency:
Hypertensive urgency is a situation where the blood pressure is severely elevated [SBP 180 or
higher or DBP 110 or higher, but there is no associated organ damage.
Those experiencing hypertensive urgency may or may not experience one or more of these
symptoms
◦ Severe headache
◦ Shortness of breath
◦ Nosebleeds
◦ Severe anxiety
Hypertensive Emergency
•A hypertensive emergency exists when blood pressure reaches levels that are
damaging organs.
•Hypertensive emergencies generally occur at blood pressure levels exceeding
180 systolic OR 120 diastolic, but can occur at even lower levels in patients
whose blood pressure had not been previously high.
•The consequences of uncontrolled blood pressure in HTN Emergency range can
be severe and include
Stroke,LOC,Memory loss, Heart attack, Damage to eyes and kidney
functions, Aortic dissection, pulmonary edema,Angina and Eclampsia.
Etiology &
Pathophysiology
 Etiology of hypertension
o Genetic Factors

o Environmental factors  stress, obesity, smoking, physical inactivity and high levels of
salt consumption modify the impact of genetic determinants.

o Reduced renal sodium excretion in the presence of normal arterial pressure probably is
a key pathogenic feature.

o Increased vascular resistance

oSympathetic nervous system hyperactivity

o Other factors (polycythemia, low K+ intake, excessive use of alcohols and NSAIDs)
Pathophysiology
Pathophysiology
Inappropriate Sympathetic nervous system
oAn increase renal sympathetic nerve activity is known to be a
factor capable of decreasing renal excretory function that leads to
sodium reabsorption which in turn leads to renal Na retention that
causes renal vasoconstriction which in turn leads to renal vascular
resistanceincrease renin release which causes angiotensin-II
production.
o Increased production of catecholamines (epinephrine and
norepinephrine) results in SNS overactivity.
Sympathetic nervous system

oThis results in an increased heart rate, increased peripheral vascular

resistance due to systemic vasoconstriction, and hypertension.

o Additionally, an overactive SNS effects insulin resistance, and

vascular remodeling has procoagulant effects, which can lead to
neoplasm and narrowing of the blood vessels.
 Peripheral resistance
Elevated peripheral resistance is the hallmark of primary hypertension.
The increase in peripheral resistance is typically due to reduction in the
arterial lumen size as a result of vascular remodeling.
This remodeling, or change in vascular tone, may be modulated by
various endothelium-derived vasoactive substances, growth factors &
cytokines. This increase in arterial stiffness results in elevated systolic
blood pressure.
 Vascular endothelial
dysfunction (stiff vessel walls)
o The vascular endothelium is a single cell layer that lines the blood
vessels.
o It will produce vasoactive substance and growth factors like nitric acid,
endothelin etc, that affect vascular tone and influence platelets and
mononuclear cell functions.
o These substances are potent vasoconstrictors and causes increases blood
pressure level.
Vascular endothelial
dysfunction (stiff vessel walls)
• The endothelium-derived factors, generally classified as endothelium-derived relaxing
factors (EDRF) and endothelium-derived contracting factors (EDCF) include nitric oxide
(NO), prostacyclin, endothelium-dependant hyperpolarizing factors (EDHF) and
endothelin.
•- Deficiency in the local synthesis of vasodilating substances (eg: prostacyclin and
bradykinin)
•- Excess vasoconstricting substances (eg: angiotensin 2 and endothelin 2 )
•- Deficiency in NO release (from endothelium )
 Effects of HTN
CVS:
Increased myocardial work leads to concentric hypertrophy of left ventricle,
angina pectoris
accelerated coronary artery diseases.
There is systolic as well as diastolic dysfunction.
Kidneys:
Progressive arteriosclerosis involves both the efferent and afferent renal arterioles and
capillaries of glomerular tuft.
This leads to compromise in renal function, shrinkage of kidneys, proteinuria.
CNS:

Hypertension may cause microaneurysms (localized outpouching or dilation of blood

vessels), which may rupture and cause cerebral hemorrhage.

Accelerated atherosclerosis may cause cerebral thrombosis, embolism, and infection.

Cerebral arteriolar spasm may cause hypertensive encephalopathy.

CARDIOVASCUL
AR RISK
FACTORS
 Cardiovascular risk factors
not modifyable
◦ Ethnic-genetic risk (black people)
◦ Age
◦ Gender
modifyable
◦ Hypertension
◦ Hyperlipidemia (Cholesterol, TGs)
◦ Smoking
◦ Diabetes
◦ Overweight
◦ Inactivity (physical)
◦ Stress
Specific hypertension risks
not modifyable
◦ Ethnic-genetic risk (black people)
◦ Age
◦ Gender
modifyable
◦ Diabetes
◦ Overweight
◦ Alcohol
◦ Salt intake
◦ combination
 Overweight
oThough the exact mechanism of how obesity is a cause for hypertension is
unknown. but the neuroendocrine mechanism and also the factor resulting from
adipose tissue are considered to be a cause .
oObesity worst affects the RAAS and sympathetic nervous system.
Overweight
 Clinical presentation
SIGN & SYMPTOMS:
Mild to moderate essential hypertension
- asymptomatic
 Secondary hypertension
- Hyperthyroidism : weight loss, tremors, heart rate abnormalities,
reddening of the palms and increased sweating.
- Hyperaldosteronism : numbness, excessive urination, excessive
sweating, electrolytes imbalance , dehydration and elevated blood
alkalinity.
In pregnancy
- Pre Eclampsia, Eclampsia.
 In newborns and neonates - Failure to thrive, seizures, irritability, lack of
energy and difficulty breathing.
 In children - Headache, fatigue, blurred vision, nosebleeds, and facial
paralysis.
Essential hypertension is usually symptomless and detected by GP during
regular medical exam

More raised BP may cause headaches, tiredness, nose bleeds

Malignant hypertension characterized by very high BP causes severe headaches

and hypertensive encephalopathy (headache, vomiting, imbalance, confusion).
 Diagnostic Investigation
To assess target organ damage:
◦ X-ray of chest for heart size ,

◦ ECG for LV hypertrophy and evidence of IHD., Echocardiogram for LV systolic

and diastolic functions., Urinalysis- proteinuria > 200 mg/ day and hematuria
suggest renal involvement.

To detect the cause of hypertension

◦ X-ray chest Rib notching suggests coarctation of aorta,

◦ Imaging of abdomen (Sonography, CT scan, MRI)

 Complications
Chronic elevated BP causes various complications in the body which leads other dangerous health
conditions
These complications depend on extent of raised BP
If BP is greatly raised:
There will be direct vascular damage and/or organ damage e.g.
◦ heart failure,
◦ renovascular damage,
◦ aneurysm (dilation and thinning of blood vessel),
◦ aortic dissection,
◦ hypertensive encephalopathy,
◦ retinal damage,
◦ neuropathy,
◦ hemorrhagic stroke (Brain hemorrhage)
If BP is moderately raised:

Complications are mainly indirect by precipitation of atherosclerosis which

may be enhanced by smoking and hyperlipidemia (High cholesterol levels).

Atherosclerosis greatly increase the chance of angina, myocardial infarction,

pulmonary embolism and Stroke.

Morbidity and Mortality:

By causing these complications of vital body organs hypertension greatly

enhance the risk of death. Careful management of BP can reduce these risks.
Non-pharmacological management of hypertension
Reduction of Body Weight
Sodium Restriction
Alcohol Restriction
Physical Exercise
Proper diet
Management
It depends upon BP of the patient

Severe Hypertension (210/120 mmHg):

◦ It is a medical emergency which can cause renal damage, hemorrhagic stroke,
encephalopathy
◦ But BP is reduced progressively, abrupt decrease in BP may compromise cerebral
blood supply but if there is encephalopathy abrupt vasodilation by Na nitroprusside
is required
◦ ACE inhibitors, hydralazine, labetalol are used to gradually decrease BP
Moderate hypertension (160-180/100-110 mmHg):
◦ Treated with antihypertensive drugs and BP is monitored closely and therapy is
adjusted accordingly

Mild Hypertension (140-160/90-100:

◦ BP is managed with lifestyle changes and drug therapy is normally reserved for
increased risk of complications
◦ In elderly patients up to 139/89 mmHg is considered normal BP
Reference
Robbins Basic Pathology, 9th Edition, by Kumar Abbas Aster
Textbook of Pathology by Harsh Mohan 7th edition

Pathophysiology, Dr. S.L. Bodhankar and Dr. N.S.Vyawahare,

Lippincott’s Illustrated Reviews, Pharmacology, 2nd Edition

Pathophysiology, Dr. Prakash Ghadi

 Assignment
Q1. Define Pre-hypertension and hypertension, its symptoms, diagnosis,
causative factors, its treatment options and combination available in
market. (10)

Q2. Discuss etiology, pathophysiology and management of

hypertension. (10)