Hypertension is another name for high blood pressure. It can lead to severe complications and increases the risk of heart disease, stroke, and death.

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Management of Hypertension
Project
Submitted to;
I.K Gujral Punjab Technical University, Jalandhar
IN PARTIAL FULFILMENT OF REQUIREMENT FOR THE AWARD OF DEGREE
Bachelor in Pharmacy
By – Pawan
(Enrolment number – 1438306)
CT Institute of Pharmaceutical Sciences
Jalandhar, Punjab (India) – 144020
(Approved by AICTE, PCI and affiliated by I.K Gujral Punjab Technical University)

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CERTIFICATE
This is certify hereby certify that the work which is being presented in this project entitled
"Management of Hypertension", in partial fulfilment of the requirements for the award of
degree of Bachelor of Pharmacy Submitted to Punjab Technical University (Jalandhar), is an
authentic record of my own work carried out at CT Institute of Pharmaceutical Sciences,
Jalandhar during a period from August 2017 to November 2017 under the supervision of Mr.
Narinder.
The matter embodied in this project report has not been submitted by me for the award of any
other degree/diploma project of this any other University/Institute.
Pawan
(Enrolment No: 1438306)
This is to certify that the above statement made by the candidate is correct to the best of our
knowledge.
Mr. Narinder
Assistant Professor
CT Institute Of Pharmaceutical Sciences, Jalandhar
Forwarded By:
Prof. Dr. Surya Prakash Gautam
Principal
CT Institute Of Pharmaceutical Science, Jalandhar

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Acknowledgement
No research is ever the outcome of single individuals, talent of efforts. This project work would
not have been possible without the hearted encouragement, support and co- operation of my
parents, guide, teacher, friends and well wishers. This project is a fruit of infinite
encouragement, infallible guidance and unstinted cooperation received from multidirectional
aiming for a un directional goal. With heartiness I take opportunity to pen down few words of
heartfelt expression for all involved directly or indirectly in making this project a success. This
work was carried out at the department of pharmaceutics and Pharmaceutical Technology, C.T
Institute of Pharmaceutical Science, Jalandhar during the year 2017-2018. I am indebted for
same. At the heart of every event lie causes, reason and a motivating force organ inspiration.
To a student, in whatever walk of life he may be, this inspiration is always through a guide a
mentor. With a deep sense of gratitude and the respect, I thank my esteemed guide and
preceptor Mr. Narinder, Assistant Professor, C.T Institute of Pharmaceutical Sciences, Jalandhar
for inestimable guidance, valuable suggestions and consent encouragement during the course
of study. To work under such personality has been a great and inexplicable that will go along a
way my memory in my life. I consider myself fortunate for being his student. It is with affection
and reverence that I acknowledge my in debt ness to his outstanding dedication, often for
beyond the call of duty. I consider myself extremely fortunate to have a chance to work under
his guidance. I am in debted to Dr. Surya Prakash Gautam, Director of CT Institute of
Pharmaceutical Sciences for consent inspiration, encouragement and support to carry out this
work. Words do not suffice to express my sincere thanks.

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ABSTRACT
Hypertension is a major risk factor for cardiovascular disease and is present in 69% of patients
with a first myocardial infarction, in 77% of patients with a first stroke, in 74% of patients with
chronic heart failure, and in 60% of patients with peripheral arterial disease. Double-blind,
randomized, placebo-controlled trials have found that antihypertensive drug therapy reduces
cardiovascular events in patients aged younger than 80 years and in patients aged 80 years and
older in the Hypertension in the Very Elderly Trial. Although the optimal blood pressure
treatment goal has not been determined, existing epidemiologic and clinical trial data suggest
that a reasonable therapeutic blood pressure goal should be <140/90 mm Hg in patients
younger than 80 years and a systolic blood pressure of 140-145 mm Hg if tolerated in patients
aged 80 years and older. Non-pharmacologic lifestyle measures should be encouraged both to
prevent development of hypertension and as adjunctive therapy in patients with hypertension.
Angiotensin - converting enzyme inhibitors, angiotensin receptor blockers, beta blockers,
calciumchannel blockers, and diuretics have all reduced cardiovascular events in randomized
trials. The choice of specific drugs depends on efficacy, tolerability, presence of specific
comorbidities, and cost.

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Table of contents
Sr. No. Contents Page no.
1 Introduction of Hypertension 5 - 7
2 Types 7 - 8
3 Classification 9
4 Causes 9 - 13
5 Pathogenesis 13 - 22
6 Diagnosis 23 - 25
7 Management 25 - 31
8 Risk management 32
9 Conclusion 33

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Introduction Of Hypertension
The World Health Organization (WHO) has identified India as one of those nations that is going
to have most of the lifestyle disorders in the near future. As per World Health Organization
report, about 40% of people aged more than 25 years had hypertension in 2008[2]. Danaei et al.
Studied secular trends in the age-adjusted mean systolic blood pressure (SBP) worldwide. Their
findings revealed mean age-adjusted SBP declined by approximately 2mmHg from 1980 to 2008.
The age-adjusted SBP was highest in low-income and middle-income countries. In the same
period, mean age-adjusted SBP declined in economically developed regions such as Australia,
North America, and Western Europe and increased in economically developing regions such as
Oceania, East Africa, and South and South-east Asia. Additionally, due to the growth and aging
of the population around the world, the number of people with uncontrolled hypertension was
reported to have increased between 1980 and 2008[3].
 About one third of adults in most communities in the developed and developing
world have hypertension.
 Hypertension is the most common chronic condition default with by primary care
physicians and other health practitioners.
 Most patients with hypertension have other risk factors as well, including lipid
abnormalities , glucose intolerance, or diabetes; a family history of early
cardiovascular events
 Obesity ; and cigarette smoking.
 The success of treating hypertension has been limited, and despite well-established
approaches to diagnosis and treatment, in many communities fewer than half of all
hypertensive patients have adequately controlled blood pressure.
Essential hypertension (also called primary hypertension or idiopathic hypertension) is the most
common type of hypertension, affecting 95% of hypertensive patients,[1][2][3][4] it tends to be
familial and is likely to be the consequence of an interaction between environmental and
genetic factors. Prevalence of essential hypertension increases with age, and individuals with
relatively high blood pressure at younger ages are at increased risk for the subsequent
development of hypertension and it makes them suffer a lot. Hypertension increases the risk of
cerebral, cardiac, and renal events.[5]

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Fig 1 - Automated Arm Blood Pressure Meter
Hypertension refers to increase in arterial pressure above the normal limit of blood pressure.
Blood pressure is the pressure exerted by blood column per unit area of arterial wall during
pumping of heart. The line of demarcation between normal and raised blood pressure is
obscure and depends on individual circumstances. However, most doctors agree that the ideal
blood pressure for a physically healthy person is around 120/80 mmHg.[1] Hypertension is a
major risk factor for cardiovascular diseases, stroke and kidney diseases. About 2.3 million
deaths in India was attributed to cardiovascular diseases in the year 1990 and is projected to
double by the year 2020.[2] Hypertension is directly accounted for 57% of all stroke deaths and
24% of all coronary heart disease deaths in India. Epidemiological studies show that
hypertension is present in 25% urban and 10% rural subjects in India. At an underestimate,
there are 31.5 million hypertensive in rural and 34 million in urban populations.
TYPES OF HYPERTENSION
• Primary or essential hypertension - The hypertension is of unknown origin. Primary or
essential hypertension (97-98%) has no clear underlying cause but appears to be the result of
inter play of complex genetic and environmental factors
• Secondary hypertension - Hypertension with an identifiable cause secondary to another
disease such as renal disease or tumour .Secondary hypertension (2-3%) is caused by a specific

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underlying mechanism usually involving kidneys or endocrine system.
Fig 2 - Types Of Hypertension
CAUSES OF HYPERTENSION
Primary Hypertension About 95% of adults with high blood pressure have primary
hypertension. The cause of primary hypertension is not known, although genetic and
environmental factors that affect blood pressure regulation are now being studied.
Environmental factors include excess intake of salt , obesity, and perhaps sedentary lifestyle.
Some genetically related factors could include inap-inap propriately high activity of the renin-
angiotensin-aldosterone system.
Secondary Hypertension This pertains to the relatively small number of cases about 5% of all
hypertension, where the cause of the high blood pressure can be identified and sometimes
treated. The main types of secondary hypertension are chronic kidney disease, renal artery
stenosis, excessive aldosterone secretion, pheochromocytoma, and sleep apnoea. A simple
screening approach for identifying secondary hypertension is given later.
Classification Of Hypertension
Category Systolic (mm of Hg) Diastolic (mm of Hg)
Optimal <120 <80
Normal 120 - 129 80 - 84
High Normal 130 - 139 85 - 89
Grade 1 HTN (Mild) 140 - 159 90 - 99

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Table 1 - Classification Of Hypertension
Causes Of Hypertension
Hypertension represents a major public health problem affecting more than one billion
individuals worldwide [1]. The advent of antihypertensive therapy has substantially reduced the
occurrence of cardiovascular events. However, antihypertensive therapy failed to achieve blood
pressure control in all patients, with hypertension control rates remaining in general
disappointingly low. Blood pressure goals are not attained in some patients despite the
simultaneous use of several antihypertensive medications. Several terms have been used to
define this condition: “refractory hypertension”, “difficult-to-treat hypertension”, “difficult-to-
control hypertension”; however, the term “resistant hypertension” seems to prevail.
Resistant hypertension is currently defined as uncontrolled blood pressure despite the use of
optimal doses of three antihypertensive medications, of which one is a diuretic [2]. Several
factors have been identified as contributors to resistant hypertension. Poor patient adherence,
physician inertia, inadequate doses or inappropriate combinations of antihypertensive drugs,
excess alcohol intake, and volume overload are some of the most common causes of resistance
[2–10]. Secondary forms of hypertension represent another very important contributor to drug
resistance.
 High intake of cholesterol
 High intake of caffeine
 High salt of fat containing diet
 inactiveness
Grade 2 HTN (Moderate) 160 - 179 100 - 109
Grade 3 HTN (Severe) >Or = 180 > Or = 110
Isolated Systolic HTN > Or = 140 < 80

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Fig 3 - Causes Of Hypertension
1. Prevalence and Prognosis of Resistant Hypertension
The exact prevalence of resistant hypertension in the general population remains unknown.
Data from small observational studies show a wide variation (from 5% to 50%) according to the
studied populations [2–10]. Data from large clinical trials point towards a relatively high
prevalence of resistant hypertension (20–35%). It has to be noted, however, that atypical drug
combinations have been used in most of these studies as required by study protocols.
Therefore, the evaluation of the prevalence of resistant hypertension requires a large,
prospective, population-based study, specially designed for this aim.
Similarly, the prognosis of resistant hypertension is currently unknown [2–10]. Available
evidence addressing the prognosis of resistant hypertension is scarce, since virtually no
longitudinal study has addressed this topic. Data from small clinical studies point towards an
increased cardiovascular risk in patients with resistant hypertension. In addition, patients with
resistant hypertension frequently have comorbidities that are known to increase cardiovascular
morbidity and mortality, such as chronic kidney disease, diabetes, and obesity. Moreover,

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patients with resistant hypertension have higher rates of target organ damage than the general
hypertensive population and are thus at increased cardiovascular risk.
2. Lifestyle Factors
Resistance to antihypertensive treatment is affected by several lifestyle factors. Excessive
dietary salt intake is common in patients with resistant hypertension and contributes to
treatment resistance by blunting the blood pressure reduction of most antihypertensive drugs,
including diuretics and inhibitors of the renin-angiotensin axis [2–10].
Obesity can also contribute to treatment resistance [2–10]. It has been shown that blood-
pressure control is more difficult to be achieved in obese than lean hypertensive patients.
Several lines of evidence indicate a graded positive correlation between body mass index and
blood pressure levels, while weight loss results in blood pressure reduction. Insulin resistance,
sympathetic nervous system over activity, sodium retention, and activation of the renin-
angiotensin system have been implicated in the pathogenesis of obesity-induced hypertension.
Alcohol consumption is another important factor [2–10]. Large alcohol consumption (>3 drinks
per day) has been shown to result in blood pressure elevation. In addition, blood pressure
control might be achieved more difficult in heavy drinkers due to poor adherence in
antihypertensive therapy. The role of physical inactivity in patients with resistant hypertension
has not been adequately studied.
3. Drug-Induced Hypertension
A variety of prescription or over the counter medicines as well as other exogenous substances
may induce hypertension or contribute to treatment resistance. Drug-induced hypertension is
among the most common causes of secondary hypertension and is frequently encountered in
everyday clinical practice. However, despite the frequent occurrence of drug-induced
hypertension, primary care physicians frequently miss the opportunity to detect and
appropriately manage this iatrogenic form of secondary hypertension. Therefore, a detailed
and meticulous medical history is of utmost importance in patients with resistant hypertension,
since the identification and subsequent withdrawal of the offending drug may alleviate
treatment resistance. However, withdrawal of the responsible agent is not always possible; in
such cases, dose reduction and/or search for alternate treatment may substantially improve or
even control blood pressure levels. Another very important aspect relates to the great
variability of the effects of administered drugs on blood pressure. The administration of
offending drugs can result in excessive blood pressure elevation in some individuals, while most

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individuals will experience little or no increases of blood pressure. This variability represents a
rule without exception. Therefore, it would be very important to identify predictors of blood
pressure elevation, in order to individualize drug treatment. Up to now, however, no such
reliable predictors have been identified.
Pathogenesis Of Hypertension
Many pathophysiologic factors have been implicated in the genesis of essential hypertension:
increased sympathetic nervous systemactivity, perhaps related to heightened exposure or
response to psychosocial stress; overproduction of sodium-retaining hormones and
vasoconstrictors; long-term high sodium intake; inadequate dietary intake of potassium and
calcium; increased or inappropriate renin secretion with resultant increased production of
angiotensin II and aldosterone; deficiencies of vasodilators, such as prostacyclin, nitric oxide
(NO), and the natriuretic peptides; alterations in expression of the kali krein–kinin system that
affect vascular tone and renal salt handling; abnormalities of resistance vessels, including
selective lesions in the renal microvasculature; diabetes mellitus; insulin resistance; increased
activity of vascular growth factors; alterations in adrenergic receptors that influence heart rate,
inotropic properties of the heart, and vascular tone; and altered cellular ion transport.
The novel concept that structural and functional abnormalities in the vasculature, including
endothelial dysfunction, increased oxidative stress, vascular remodeling, and decreased
compliance, may antedate hypertension and contribute to its pathogenesis has gained support
in recent years. Although several factors clearly contribute to the pathogenesis and
maintenance of blood pressure elevation, renal mechanisms probably play a primary role, as
hypothesized by Guyton (5) and reinforced by extensive experimental and clinical data. As
discussed in this paper, other mechanisms amplify (for example, sympathetic nervous system
activity and vascular remodeling) or buffer (for example, increased natriuretic peptide or kali
krein–kinin expression) the pressure effects of renal salt and water retention. These interacting
pathways play major roles in both increasing blood pressure and mediating related target organ
damage.
Although several factors clearly contribute to the pathogenesis and maintenances of blood
pressure elevation renal mechanism probably play a primary role as hypothesized by Guyton(5)
and reinforced by extensive experimental and clinical data. As discussed, other mechanisms
amplify or buffer the pressor effects of renal salt and water retention. Understanding these
complex mechanisms has important implications for the targeting of antihypertensive therapy
to achieve benefits beyond lowering blood pressure

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Fig 3 - Pathophysiologic Mechanism Of Hypertension
 Genetic
Evidence for genetic influence on blood pressure comes from various sources. Twin studies
document greater concordance of blood pressures in mono zygotic than dizygotic twins (6), and
population studies show greater similarity in blood pressure within families than between
families (7). The latter observation is not attributable to only a shared environment since
adoption studied demonstrate greater concordance of blood pressure among biological siblings
than adoptive siblings living in the same household (8). Furthermore, single genes can have
major effects on blood pressure, accounting for the rare Mendelian forms of high and low
blood pressure (3). Although identifiable single-gene mutations account for only a small
percentage of hypertension cases, study of these rare disorders may elucidate pathophysiologic
mechanisms that predispose to more common forms of hypertension and may suggest novel
therapeutic approaches (3). Mutations in 10genes that cause Mendelian forms of human
hypertension and 9 genes that cause hypotension have been described to date, as reviewed by
Lifton and colleagues (3, 9).These mutations affect blood pressure by altering renal salt
handling, reinforcing the hypothesis of Guyton (5) that the development of hypertension
depends on genetically determined renal dysfunction with resultant salt and water retention (2).

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In most cases, hypertension results from a complex interaction of genetic, environmental, and
demographic factors. Improved techniques of genetic analysis, especially genome-wide linkage
analysis, have enabled a search for genes that contribute to the development of primary
hypertension in the population. Application of these techniques has found statistically
significant linkage of blood pressure to several chromosomal regions, including regions linked
to familial combined hyper lipidemia (10–13).These findings suggest that there are many
genetic loci, each with small effects on blood pressure in the general population. Overall,
however, identifiable single-gene causes of hypertension are uncommon, consistent with a
multi factorial cause of primary hypertension (14).
Fig – Mutation altered blood pressure in humans
A diagram of a nephron, the filtering unit of the kidney, is shown. The molecular pathways
mediating sodium chloride (NaCl) reabsorption in individual renal cells in the thick ascending
limb (TAL) of the Henle’s loop, distal convoluted tubule (DCT), and the cortical collecting tubule
(CCT) are indicated, along with the pathway of the renin–angiotensin system, the major
Regulator of renal salt reabsorption. Inherited diseases affecting these pathways are indicated
(hypertensive disorders [red] and hypotensive disorders [blue]). 11-HSD2 11-hydroxysteroid
dehydrogenase-2; ACE angiotensin-converting enzyme; AME apparent mineralo corticoid

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excess; ANG angiotensin; DOC deoxycorticosterone; GRA gluco corticoid-remediable
aldosteronism; MR mineralocorticoid receptor; PHA1 pseudo hypo aldosteronism type 1; PT
proximal tubule. Reproduced from Lifton et al. (3), with permission from Elsevier Science.
 Inherited Cardiovascular Risk Factor
Cardiovascular risk factors, including hypertension , tend to cause segregate more commonly
than would be expected by chance. Approximately 40% of persons with essential hypertension
also have hypercholesterolemia. Genetic studies have established a clear association between
hypertension and dyslipidemia (25). Hypertension and type 2 diabetes mellitus also tend to
coexist. Hypertensionis approximately twice as common in persons with diabetes’s in persons
without diabetes, and the association is even stronger in African Americans and Mexican
Americans(26). The leading cause of death in patients with type 2diabetes is coronary heart
disease, and diabetes increases the risk for acute myocardial infarction as much as a previous
myocardial infarction in a non diabetic person (26).Since 35% to 75% of the cardiovascular
complications of diabetes are attributable to hypertension, diabetic patients need aggressive
antihypertensive treatment, as well as treatment of dyslipidemia and glucose control.
Hypertension, insulin resistance, dyslipidemia, and obesity often occur concomitantly (27).
Associated abnormalities include micro albuminuria, high uric acid levels, hyper coagulability,
and accelerated atherosclerosis. This cause segregation of abnormalities, referred to as the
insulin resistance syndrome or the metabolic syndrome, increases cardiovascular disease (CVD)
risk. Physicians must assess and treat these risk factors individually, recognizing that many
hypertensive patients have insulin resistance, dyslipidemia, or both.
The leading cause of death in patients with type 2diabetes is coronary heart disease, and
diabetes increases the risk for acute myocardial infarction as much as a previous myocardial
infarction in a non diabetic person (26).Since 35% to 75% of the cardiovascular complications of
diabetes are attributable to hypertension, diabetic patients need aggressive antihypertensive
treatment, as well as treatment of dyslipidemia and glucose control.
Hypertension, insulin resistance, dyslipidemia, and obesity often occur concomitantly (27).
Associated abnormalities include micro albuminuria, high uric acid levels, hyper coagulability,
and accelerated atherosclerosis. This cause segregation of abnormalities, referred to as the
insulin resistance syndrome or the metabolic syndrome, increases cardiovascular disease (CVD)
risk. Physicians must assess and treat these risk factors individually, recognizing that many
hypertensive patients have insulin resistance, dyslipidemia, or both.

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Fig 5 - Role of the sympathetic nervous systemin the pathogenesis of cardiovascular diseases.
 Vascular Remodeling
Peripheral vascular resistance is characteristically elevated in hypertension because of
alterations in structure ,mechanical properties, and function of small arteries. Remodeling of
these vessels contributes to high blood pressure and its associated target organ damage.
Peripheral resistance is determined at the level of the pre capillary vessels, including the
arterioles (arteries containing a single layer of smooth-muscle cells) and the small arteries
(lumen diameters 300 m). The elevated resistance in hypertensive patients is related to
rarefaction (decrease in number of parallel-connected vessels) and narrowing of the lumen of
resistance vessels. Examination of gluteal skin biopsy specimens obtained from patients with
untreated essential hypertension has uniformly revealed reduced lumen areas and increased
media–lumen ratios without an increase in medial area in resistance vessels ( inward ,eutropic
remodeling)

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Fig 5 - Vascular remodeling can modify the cross-sections of blood vessels.
 Salt - Sensitive Hypertension
The development of salt-sensitive hypertension is proposed to occur in 3 phases. In the first
phase, the kidney is structurally normal and sodium is excreted normally. However, the kidney
may be exposed to various stimuli that result in renal vasoconstriction, such as hyperactivity of
the sympathetic nervous system or intermittent stimulation of the renin–angiotensin system.
During this phase, the patient may have either normal blood pressure or borderline
hypertension, which (if present) is salt-resistant. In the second phase, subtle renal injury
develops, impairing sodium excretion and increasing blood pressure. This phase is initiated by
ischemia of the tubules, which results in interstitial inflammation (involving mononuclear-
leukocyte infiltration and oxidant generation), which in turn leads to the local generation of
vasoconstrictors, such as angiotensin II, and a reduction in the local expression of vasodilators,
especially nitric oxide. In addition, renal vasoconstriction leads to the development of pre
glomerular arteriolopathy, in which the arterioles are both thickened (because of smooth-
muscle cell proliferation) and constricted. The resulting increase in renal vascular resistance and
decrease in renal blood flow perpetuate the tubular ischemia, and the glomerular
vasoconstriction lowers the single-nephron glomerular filtration rate (GFR) and the glomerular
ultra filtration coefficient (Ki). These changes result in decreased sodium filtration by the

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glomerulus. The imbalance in the expression of vasoconstrictors and vasodilators favouring
vasoconstriction also leads to increased sodium reabsorption by the tubules; together, these
changes lead to sodium retention and an increase in systemic blood pressure. In the third phase,
the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium
handling. Specifically, as the blood pressure increases, there is an increase in renal perfusion
pressure across the fixed arterial lesions. This increase helps to restore filtration and relieve the
tubular ischemia, thereby correcting the local imbalance in vasoconstrictors and vasodilators
and allowing sodium excretion to return toward normal levels. However, this process occurs at
the expense of an increase in systemic blood pressure and hence a rightward shift in the
pressure–natriuresis curve
Fig – Pathway for salt sensitive hypertension
Diagnosis of Hypertension
 Blood pressure can be measured by either a conventional sphygmomanometer using a
stethoscope or by an automated electronic device. The electronic device, if available, is
preferred because it provide more reproducible results than the older method and is
not influenced by variations in technique or by the bias of the observers. If the
auscultatory method is used, the first and fifth Korotkoff sounds (the appearance and
disappearance of sounds) will correspond to the systolic and diastolic blood pressures.
 Arm cuffs are preferred. Cuffs that fit on the finger or wrist are often inaccurate and
should, in general, not be used.

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 It is important to ensure that the correct size of the arm cuff is used (in particular, a
wider cuff in patients with large arms [>32 cm circumference]).
 The blood pressure should be taken after patients have emptied their bladders. Patients
should be seated with their backs supported and with their legs resting on the ground
and in the uncrossed position for 5 minutes.
 The patient’s arm being used for the measurement should be at the same level as the
heart, with the arm resting comfortably on a table.
 It is preferable to take 2 readings, 1 to 2 minutes apart, and use the average of these
measurements.
 It is useful to also obtain standing blood pressures (usually after 1 minute and again
after 3 minutes) to check for postural effects, particularly in older people.
 In general, the diagnosis of hypertension should be confirmed at an additional patient
visit, usually 1 to4 weeks after the first measurement. On both occasions, the systolic
blood pressure should be ≥140 mmHg or the diastolic pressure ≥90 mmHg, or both, in
order to make a diagnosis of hypertension.
 If the blood pressure is very high (for instance, a systolic blood pressure ≥180 mm Hg),
or if available resources are not adequate to permit a convenient second visit, the
diagnosis and, if appropriate ,treatment can be started after the first set of readings that
demonstrate hypertension.
 For practitioners and their staff not experienced in measuring blood pressures, it is
necessary to receive appropriate training in performing this important technique.
Some patients may have blood pressures that are high in the clinic or office but are
normal elsewhere. This is often called white-coat hypertension. If it is suspected,
consider getting home blood pressure readings to check this possibility. Another
approach is to use ambulatory blood pressure monitoring, if it is available. In this
procedure, the patient wears an arm cuff connected to a device that automatically
measures and records blood pressures at regular interval is usually over a 24-hour
period.
 It can be helpful to measure blood pressures at home. If available ,the electronic device
is simpler to use and is probably more reliable than the sphygmomanometer. The
average of blood pressures measured over 5 to 7 days, if possible in duplicate at each
measurement, can be a useful guide for diagnostic and treatment decisions.
Management of Hypertension
 In low- and medium-risk condition

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Lifestyle modification is started initially and frequently reassessed. If blood pressure target is
not achieved, pharmacologic therapy is initiated.
 In high- and very high-risk conditions
Lifestyle modification and drug therapy are initiated
simultaneously to achieve rapid control of blood pressure.
 Hypertension management includes lifestyle modification and drug therapy.
 Annual follow-up of patients with high normal blood pressure is recommended as 10%
develop hypertension each year.
1. Life Style Modification
 Weight reduction: Significant decrease in blood pressure is observed following weight
reduction in obese or over weight individuals with hypertension.
 Physical exercise: Aerobic physical exercise for 20–30 minutes per day for at least 5 days
per week improves blood pressure and reduces cardiovascular morbidity.
 Quit smoking: Tobacco abuse in any form is found to increase blood pressure.
 Decrease alcohol use: Moderation of alcohol consumption is advised
2. Dietary Modification
 Low sodium diet: No added salt diet is usually advocated in hypertensive. Typical Indian
food provides 4–5 gm of sodium per day. Pickles, salted vegetables and canned fish are
rich in sodium and should be avoided. Intake of 2.3 gm of sodium or less is
recommended as per dietary approaches to stop hypertension(DASH)
 Diet rich in vegetables and fruits: These are rich in potassium content and improve blood
pressure
 Low fat content. Diet low in saturated fats should be used,

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Fig - Dietary approaches to stop Hypertension
3. Drug Therapy
Lifestyle modification alone is not sufficient to achieve the target blood pressure. Rapid control
of blood pressure is needed as in urgencies and emergencies.
 Angiotensin Converting Enzyme Inhibitor
These agents reduce blood pressure by blocking the renin-angiotensin system. They do this by
preventing conversion of angiotensin I to the blood pressure-raising hormone angiotensin II.
They also increase availability of the vasodilator brady kinin by blocking its breakdown.
Angiotensin-converting enzyme inhibitors are well tolerated. Their main side effect is cough
(most common in women and in patients of Asian and African background). Angioedema is an
uncommon but potentially serious complication that can threaten airway function, and it
occurs most frequently in black patients.
These drugs can increase serum creatinine by as much as 30%, but this is usually because they
reduce pressure within the renal glomerulus and decrease filtration. This is a reversible change
in function and is not harmful. An even greater increase in creatinine sometimes occurs when
angiotensin-converting enzyme inhibitors are combined with diuretics and produce large blood
pressure reductions. Again, this change is reversible, although it may be necessary to reduce
doses of one or both drugs. If creatinine levels increase substantially this can be caused by

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concomitant treatment with non steroidal anti-inflammatory drugs or it may indicate the
presence of renal artery stenosis
 Calcium Channel Blocker
These agents reduce blood pressure by blocking the inward flow of calciumions through the L
channels of arterial smooth muscle cells. There are two main types of calcium channel blockers:
dihydropyridines, such as amlodipine andnifedipine, which work by dilating arteries; and non
dihydropyridines, such as diltiazem and verapamil, which dilate arteries somewhat less but also
reduce heart rate and contractility.
Most experience with these agents has been with the dihydropyridines, such as amlodipine and
nifedipine ,which have been shown to have beneficial effects on cardiovascular and stroke
outcomes in hypertension trials. The main side effect of calcium channel blockers is peripheral
oedema, which is most prominent at high doses; this finding can often be attenuated by
combining these agents with angiotensin-converting enzyme inhibitors or angiotensin receptor
blockers. Non dihydropyridine calciumchannel blockers are not recommended in patients with
heart failure, butamlodipine appears to be safe when given to heart failure patients receiving
standard therapy (including angiotensin-converting enzyme inhibitors) for this condition.
 Beta - Blockers
b-blockers reduce cardiac output and also decrease the release of renin from the kidney. They
have strong clinical outcome benefits in patients with histories of myocardial infarction and
heart failure and are effective in the management of angina pectoris. They are less effective in
reducing blood pressure in black patients than in patients of other ethnicities. b-blockers may
not be as effective as the other major drug classes in preventing stroke or cardio vascular
revents in hypertensive patients, but they are the drugs of choice in patients with histories of
myocardial infarction or heart failure. Many of these agents have adverse effects on glucose
metabolism and therefore are not recommended inpatients at risk for diabetes, especially in
combination with diuretics. They may also be associated with heart block in susceptible
patients. The main side effects associated with b-blockers are reduced sexual function, fatigue,
and reduced exercise tolerance.
 Angiotension Receptor Blocker
Angiotensin receptor blockers, like angiotensin-converting enzyme inhibitors, antagonize the
renin-angiotensin system. They reduce blood pressure by blocking the action of angiotensin II
on its AT1receptor and thus prevent the vasoconstrictor effects of this receptor. The

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angiotensin receptor blockers are well tolerated. Because they do not cause cough and only
rarely cause angioedema, and have effects and benefits similar to angiotensin-converting
enzyme inhibitors, they are generally preferred over angiotensin-converting enzyme inhibitors
if they are available and affordable. Like angiotensin-converting enzyme inhibitors, angiotensin
receptor blocker scan increase serum creatinine (see comments about angiotensin-converting
enzyme inhibitors), but usually this is a functional change that is reversible and not harmful.
These drugs do not appear to have dose-dependent side effects, so it is perfectly reasonable to
start treatment with medium or even maximum approved doses. These drugs have the same
benefits on cardio vascular and renal outcomes as angiotensin-converting enzyme inhibitors.
Like angiotensin-converting enzyme inhibitors, they tend to work better in white and Asian
patients than in black patients, but, when combined with either calcium channel blockers or
diuretics, they become equally effective in all patient groups.
 Thiazide and thiazide like diuretics
These agents work by increasing excretion of sodium by the kidneys and additionally may have
some vasodilator effects. Clinical outcome benefits (reduction of strokes and major
cardiovascular events) have been best established with chlorthalidone, indapamide, and
hydrochlorothiazide, although evidence for the first two of these agents has been the strongest.
Chlorthalidone has more powerful effects on blood pressure than hydrochlorothiazide (when
the same doses are compared) and has a longer duration of action. The main side effects of
these drugs are metabolic (hypokalemia, hyperglycemia, and hyperuricemia).
The likelihood of these problems can be reduced by using low doses (e.g, 12.5 mg or 25 mg of
hydro-chlorothiazide or chlorthalidone) or by combining these diuretics with angiotensin-
converting enzyme inhibitors or angiotensin receptor blockers, which have been shown to
reduce these metabolic changes. Combining diuretics with potassium-sparing agents also helps
prevent hypokalemia. Diuretics are most effective in reducing blood pressure when combined
with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, although they
are also effective when combined with calciumchannel blockers.
Risk Management
As well as pharmacological measures for the control of blood pressure, there should be active
treatment of those factors known to increase the risk of hypertension. There are two distinct
measures. First, those that lower blood pressure, for example weight reduction, reduced salt
intake, limitation of alcohol consumption, physical exercise, increased fruit and vegetable
consumption, and reduced total and saturated fat intake. Second, those that that reduce

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cardiovascular risk, for example stopping smoking; replacing saturated with polyunsaturated
and monounsaturated fats; increased oily fish consumption; and reduced total fat intake.
Because hypertensive patients are at very high risk of coronary artery disease, other
therapeutic measures include aspirin and statin therapies. Lose-dose aspirin is effective in the
prevention of thrombotic events such as stroke and myocardial infarction ;this is also true in
hypertensive patients whose blood pressure is well controlled. The risk of severe bleeding is
very low provided blood pressure is reduced to below 150/90 mm Hg. The benefits of lipid-
lowering drug treatment with statins are well established in coronary heart disease and in
cerebro vascular disease, two conditions frequently associated with arterial hypertension.
CONCLUSION
It is important to note that this evidence-based guideline has not redefined high BP, and the
panel believes that the 140/90mmHg definition from JNC 7 remains reasonable. The
relationship between naturally occurring BP and risk is linear down to very low BP, but the
benefit of treating to these lower levels with antihypertensive drugs is not established. For all
persons with hypertension, the potential benefits of a healthy diet, weight control, and regular
exercise cannot be overemphasized. These lifestyle treatments have the potential to improve
BP control and even reduce medication needs. Although the authors of this hypertension
guideline did not conduct an evidence review of lifestyle treatments in patients taking and not
taking antihypertensive medication, we support the recommendations of the 2013 Lifestyle
Work Group.
The recommendations from this evidence-based guideline from panel members appointed to
the Eighth Joint National Committee (JNC 8) offer clinicians an analysis of what is known and
not known about BP treatment thresholds, goals, and drug treatment strategies to achieve
those goals based on evidence from RCTs. However, these recommendations are not a
substitute for clinical judgment, and decisions about care must carefully consider and
incorporate the clinical characteristics and circumstances of each individual patient. We hope
that the algorithm will facilitate implementation and be useful to busy clinicians. The strong
evidence base of this report should inform quality measures for the treatment of patients with
hypertension.