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NIKHIL VAISHNAV
M.SC.(NURSING)
PARUL UNIVERSITY
 Introduction
 Definition
As per new 2017 ACC/AHA
definition
“ Hypertension is defined as a
persistent systolic BP(SBP) of
130 mm Hg or more, diastolic
BP(DBP) of 80 mm Hg or more” .
1.13 billion people worldwide have
hypertension .
HTN is present in 25-30 % of urban & 10-20 % of
rural population.
Approx. 100-110 million persons have HTN in
India.
HTN is the attributable cause for 57 % of stroke
and 24.5 % of coronary heart disease in India.
 Malignant Hypertension.
 Hypertensive urgency.
 Hypertensive emergency.
 White coat HTN.
 Pseudohypertension.
 Transient HTN.
 Paradoxical HTN
 Hypertensive crisis.
 Isolated systolic HTN
 Accelerated HTN
 Masked HTN
 Resistant hypertension
 Extremely high blood pressure( >180/120
mm Hg) that develops rapidly .
 It should be treated as medical
emergency.
 S/S are changes in vision , kidney failure,
grade IV retinopathy(papillidema) etc.
 It is clinical situation where blood
pressure is elevated without
evidence of target organ damage.
 Blood pressure readings at 180/120
or higher .
 BP can be controlled safely within
a few hours with medications.
Condition where blood pressure is
elevated with evidence of target
organ damage.
 BP is > 180 / 120 mm Hg.
 Blood pressure must be reduced
immediately to prevent imminent
organ damage.
 White coat syndrome is a
phenomenon in which people exhibit
a blood pressure level above the
normal range, in a clinical setting.
 They do not exhibit it in other
settings.
 It may be due
to anxiety experienced during a
clinic visit
 It is an uncommon phenomenon
seen in elderly clients.
 Intra –arterial BP is lower than the
BP measured by sphygmomanometer.
 It is caused by stiff and non
compliant vessels due to thickened
wall of arteries with aging.
An increased BP for a particular
period of time and then droping
back to normal.
 It is seen in Acute stroke, Acute MI,
pregnancy, Acute
glomerulonephritis.
 Paroxysmal hypertension is episodic
and volatile high blood pressure,
which may be due to stress of any
sort, or from a pheochromocytoma.
 There is a sudden increase in BP
even on anti hypertensive drugs.
 A hypertensive crisis is a severe increase
in blood pressure that can lead to a
stroke.
 BP is 180 /120 mm of Hg.
 It is an umbrella term includes
hypertensive urgency & emergency.
 S/S are severe chest pain, severe
headache, confusion, Shortness of breath
etc.
 Systolic BP > 130 mm Hg , but
Diastolic BP < 80 mm of Hg.
 Common type of HTN in older
people.
 Caused by artery stiffness,
diabetes, and overactive thyroid.
 When blood pressure reading is normal at
the doctor's office but high at home—is
known as masked hypertension .
 Resistant hypertension is high blood pressure that
does not respond well to aggressive medical
treatment.
 Hypertension is considered resistant when all of the
following are true:
1) Someone is taking three* different blood pressure
medications at their maximally tolerated doses.
2) One of the blood pressure medications is
a diuretic (removes fluid and salt from the body).
3) Blood pressure remains above goal—(usually
130/80 mmHg) .
4) If hypertension requires four or more medications
to be controlled it is also called resistant
hypertension.
 Hypertension is defined as resistant when BP
remains > 160/100 mm Hg despite use of 3
different antihypertensive drugs with
complementary mechanisms of action (one of
which being a diuretic).
PRIMARY
HYPERTENSION
SECONDARY
HYPERTENSION
 Also referred to as essential or
idiopathic HTN.
 There is elevated BP without an
identified cause.
 Accounts for 90-95%. Of all cases of
HTN.
 Since primary HTN has unknown
cause, there are several contributing
factors.
 Increased SNS activity.
 Obesity.
 Diabetes mellitus.
 Insulin resistance.
 Stress
 Excessive alcohol consumption.
 Increased Sodium intake.
 Vasoconstriction(Endothelium).
 Tobacco use.
 Dysfunction in RAAS system.
 Dyslipidemia
➢ Age
➢ Alcohol
➢ Tobacco use.
➢ Diabetes mellitus
➢ Elevated serum
lipids
➢ Excess dietary
sodium.
➢ Ethnicity
➢ Gender
➢ Family history.
➢ Obesity.
➢ Sedentary
lifestyle.
➢ Stress
➢ Socioeconomic
status
 SBP rises
progressively with
increasing age.
 DBP may decrease
with age.
 After age 50,
SBP>140 mm Hg is
more important
cardiovascular risk
factor than DBP.
 Excessive alcohol
intake is strongly
associated with HTN.
 Moderate intake of
alcohol has
cardioprotective
properties.
 Hypertensive males
should limit their
daily alcohol intake to
2 drinks.
 Hypertensive females
should limit 1 drink
per day .
 Smoking tobacco greatly increases
risk of cardiovascular disease.
 Hypertensive people who smoke
tobacco are at greater risk for
cardiovascular disease.
 HTN is more common in
patient with DM.
 When HTN and DM coexist,
complications such as target
organ disease are more severe.
 Increased level of
Cholesterol &
triglycerides are
primary risk factor
in atherosclerosis.
 Hyperlipidemia is
more common in
hypertensive
people
 High sodium
intake can lead to
HTN in salt
sensitive patients.
 Decreases the
effectiveness of
certain
antihypertensive
drugs.


 HTN is more prevalent in men in
young adulthood and early middle
age.
 After the age 64, HTN is more in
women.
 History of a close blood
relative(parents, sibling) with HTN is
associated with an increasing risk of
HTN.
 Regular physical activity can
control weight & reduce
cardiovascular risk.
 Physical activity may
decrease BP
HTN is more prevalent in lower
socioeconomic groups and among the
less educated.
Social isolation.
Lack of support.
 Repeated stress
may develop HTN
more frequently
than others.
 Weight gain is associated
with increased frequency of
HTN.
 Central abdominal obesity
has more risk .
 Secondary HTN is elevated BP with
a specific cause .
 It can be identified and corrected.
 It accounts for 5-10 % of HTN cases.
 Contributing factor to hypertensive
crisis.
 Treatment aimed at treating the
underlying cause.
❑ Renal disease( renal artery stenosis,
glomerulonephritis, renal parenchymal
disease).
❑ Coarctation or congenital narrowing of
aorta.
❑ Cirrhosis of liver.
❑ Endocrine disorders(
pheochromocytoma, Cushing syndrome,
thyroid disease, primary
hyperaldosteronism) .
❑ Pregnancy induced hypertension.
❑ Sleep apnea.
❑ Drugs: Oral contraceptives , estrogen
replacement therapy, NSAIDs, sympathetic
stimulants ( cocaine, monoamine oxidase) ,
corticosteroids.
❑ Neurologic disorders( brain tumors, head
injury, quadriplegia, GBS) .
Heredity.
water & sodium retention
Altered Renin –angiotensin –aldosterone mechanism.
Stress & Increased SNS activity.
Insulin resistance & Hyperinsulinemia
Endothelial dysfunction
. Hypertension is a complex multifactorial disorder
with genetic, environmental and demographic
factors contributing to its prevalence.
Several genetic variations influence the body’s
sensitivity to salt lead to HTN.
Endothelial surface proteins activated , stimulates
proinflammatory properties, impairs vasodilatory
effects leads to HTN.
Excessive sodium intake is linked to the
HTN development.
Only 1 in 3 develop HTN, Though most
people consume a high sodium diet.
Effect of sodium on BP has a strong
genetic component.
Effect of sodium is greater in middle
aged & older adults.

Impair nitrous
oxide mediated
vasodilatation
Stimulates SNS
activity
High insulin
level in blood
Insulin resistance is a risk factor
in the development of HTN &
CVD.
Additional effects of insulin
include vascular hypertrophy &
increased renal sodium
absorption.
It is recognized as a marker of CVD(
primary HTN)
Vasodilator( Nitric oxide) &
Vasoconstrictor( Endothelin) are
produced in endothelial cells.
Therefore endothelial dysfunction
affects BP.
High levels of
Endothelin
prolonged
vasoconstriction
HTN
Oxygen free
radicals
Impair the Nitrous
oxide availability
Altered
Vasodilation
HTN
Renal parenchymal disease
Renovascualar disease
Primary hyperaldosteronism.
Pheochromocytoma
Liver cirrhosis
Sleep apnea
Due to loss of nephrons .
Retention of salt & water.
Decreased release of nitric oxide.
Activation of renin angiotensin
mechanisms.
Renal artery stenosis
Renal ischemia
Release of renin from JG cells
RAAS process
increased blood pressure
❑ Hyperaldosteronism is characterized by
excessive secretion of aldosterone.
Excessive aldosterone secretion
Retention of sodium , water &
chloride
Increased ECF
Increased venous return to
heart
CO increased thus BP increased
PCC is a rare tumor of
adrenal gland
Excessive release of
adrenaline & nor adrenaline
Increased HR, CO
Increased BP

Due to liver cirrhosis
Scarring in liver
Blockage of portal vein blood flow through
the liver.
Increased pressure in portal vein
Large veins( Varices) in esophagus
Varices bleed easily.
It is usually asymptomatic so called” silent
killer” .
When HTN becomes severe & target organ
disease occurs.
Severe hypertension effects blood vessels in
various organs & increases workload on heart.
So secondary symptoms include fatigue,
dizziness, palpitations, angina and dyspnea.
What are the complications
of Hypertension?
Hypertensive
heart disease
Cerebrovascular
disease
Peripheral
vascular disease
Nephrosclerosis
Eye disease
Sexual
dysfunction
Coronary
artery disease
Left
ventricular
hypertrophy
Heart
failure
Hypertension disrupts
coronary artery endothelium.
Atheroma formation
Stiffed arterial wall with a
narrowed lumen
CAD, MI & ANGINA
Sustained HTN
Increased cardiac workload
LVH to increase cardiac
output & cardiac contraction
Increased Myocardial
workload and oxygen demand
Progressive LVH with CAD
Heart failure
Due to increased preload &
After load
Heart compensatory
mechanism failed
Contractility diminished
CO diminished
Fatigue, dyspnoea, Shortness of
breath
Cerebral
atherosclerosis
Hypertensive
encephalopathy
Atherosclerosis is the most common cause of
Cerebrovascular disease.
HTN is a major risk factor for cerebral
atherosclerosis & stroke.
Plaque is found at the bifurcation of the common
carotid artery.
Portion of plaque or blood clot may break off and
travel to coronary vessels causes thromboembolism.
Hypertensive encephalopathy (HE) is general brain
dysfunction due to significantly high blood pressure.
Generally the blood pressure is greater than
200/130 mmHg
Symptoms may include headache, vomiting, trouble
with balance, and confusion.
It occurs after a marked rise in BP if cerebral
blood flow is not decreased by auto regulation.
Elevated Blood pressure
Autoregulation of cerebral flow
decreased
Cerebral blood vessels dilate
increased capillary
permeability
cerebral edema
Increased
intracranial pressure
Brain damage
Death
HTN speeds up the process of
atherosclerosis in PVD.
It leads to PVD, aortic
aneurysm, aortic dissection .
Intermittent claudication is a
classic symptom of PVD.
 Hypertension is the second
leading cause of kidney failure
 Some degree of renal disease is
usually present in hypertensive
patient.
Eventually renal failure.
Atrophy of renal tubules, glomeruli destruction & death of nephrons.
Renal ischemia
Narrowing of renal blood vessels
Uncontrolled HTN
 Eyes contain tiny blood vessels . Due to long
term effects of HTN, following conditions
occur:
1. Blood vessel damage (retinopathy).
2. Fluid buildup under the retina
(choroidopathy).
3. Nerve damage (optic neuropathy)
 Retinopathy: A lack of blood flow to the retina
leads to blurred vision or the complete loss of
sight.
 Fluid buildup under the retina
(choroidopathy) This buildup of fluid under the
retina, the light-sensitive layer of tissue at the
back of the eyeball, results in distorted vision or,
in some cases, scarring that impairs vision.
 Nerve damage (optic neuropathy): The result of
blocked blood flow that damages the optic
nerve, it can kill nerve cells in eyes, which may
cause temporary or permanent vision loss.
HTN damages blood vessels causes
reduced blood flow to the pelvis. It leads
to sexual dysfunction in both gender.
In Male it causes Erectile dysfunction.
In Women it leads to decreased libido &
less interest in sex.
ASSESSMENT
Known duration of HTN & previously recorded BP.
Any history or symptoms of coronary artery disease, heart
failure, sleep apnea or loud snoring .
History or symptoms of other relevant coexisting
disorders (eg, stroke, renal dysfunction, peripheral
arterial disease, dyslipidemia, diabetes, gout).
Family history .
Social history includes exercise
levels and use of tobacco, alcohol,
and stimulant drugs (prescribed
and illicit).
A dietary history focuses on intake
of salt and stimulants (eg, tea,
coffee, caffeine-containing sodas,
energy drinks).
Measurement of height, weight, and waist
circumference . ( Central obesity)
Funduscopic examination for retinopathy .
Auscultation for bruits in the neck and abdomen(
Renal artery stenosis) .
Abdomen palpation for kidney enlargement and
abdominal masses ( Polycystic kidney disease) .
A full cardiac, respiratory, and neurologic
examination.
Diminished or delayed femoral
pulses suggest aortic
Coarctation.
A unilateral renal artery bruit
may be heard in slim patients
with Renovascualar
hypertension.
Routine urinalysis & spot urine
albumin:creatinine ratio .
BUN , serum creatinine level , urinalysis to
screen for renal involvement .
Decreased Creatinine clearance indicates
renal insufficiency.
Serum electrolytes: potassium (Hypokalemia)
is important to detect hyperaldosteronism.
Blood glucose level to detect DM.
Chest X ray to detect cardiomegaly, Coarctation
of aorta.
Lipid profile to identify atherosclerosis and CVD.
ECG to identify Left ventricular hypertrophy(LVH)
, previous MI .
Thyroid function test : To rule out
hypothyroidism , hyperthyroidism.
Echocardiography to detect LVH .
Uric acid level : Rises with diuretic therapy.
Renal ultrasound : To detect possible renal
disease.
Renal angiography: To detect or confirm renal
artery stenosis.
Ambulatory BP recording : To assess white coat
HTN & masked HTN .
Plasma free metanephrines : To rule out
pheochromocytoma
Urinary cortisol test : To detect possible
cushing’s disease.
Plasma renin activity & aldosterone: To
detect primary aldosteronism .
Sleep study : people with sleep apnea.
 The goal of treatment includes achieve
and maintain goal BP, reduce
cardiovascular risk and target organ
disease.
 Primary hypertension has no cure, but
some causes of secondary hypertension
can be corrected.
 Treatment targets for the general
population, including all those with a
kidney disorder or diabetes: BP < 130/80
mm Hg regardless of age up to age 80.
Lifestyle
modifications
Medications
Devices & Physical
interventions
Weight reduction
DASH eating plan
Physical activity
Dietary sodium reduction
Avoidance of tobacco products
Moderation of alcohol intake
Management of Psychosocial risk factors
Weight reduction has a significant effect on
lowering Blood pressure.
For overweight hypertensive patinets a combination
of dietary calories restriction and moderate physical
activity is recommended to reduce weight .
A weight loss of 22 lb may decrease SBP by approx. 5
to 22 mm Hg
Dietary approaches to stop hypertension(
DASH) diet emphasizes fruits, vegetables ,
low fat milk , whole grains, fish , poultry ,
been , seeds & nuts .
DASH diet plan lowers BP and LDL
cholesterol.
AHA & ACSM recommended that all
adults perform regular physical activity
(brisk walking) at least 30 minutes per
day more than 5 days per week .
Moderate intense activity such as brisk
walking, jogging, swimming can lower
BP, control body weight.
Healthy adults should restrict sodium intake
to less than or equal to 2.3 gram/day.
Hypertensive person should limit sodium to
less than 1.5 gram/day.
Avoid foods known to high in sodium(
canned soups) .
Do not add salt in the preparation of foods
or at meals.
The patient , Family & person who
prepare meals should be taught about
sodium restricted diet.
Foods high in sodium should be identified
Sodium restriction may be enough to
control BP in some patients with HTN.
Nicotine causes vasoconstriction and
increases BP.
Smoking tobacco is a major risk
factor for CVD.
The benefits of tobacco cessation are
seen within 1 year in all age groups.
Drinking three or more alcoholic drinks daily
is a risk factor for CVD & Stroke.
Men should limit alcohol not more than 2
drinks per day.
Women and lighter weight men to no more
than 1 drink per day.
Liver cirrhosis due to excessive alcohol intake
is the frequent cause of secondary HTN.
Psychosocial risk factors have direct effects on CVS by
activating SNS and stress hormone.
It can lead to HTN , tachycardia etc.
Screening for Psychosocial risk factors should be done.
Relaxation therapy, guided imagery , biofeedback ,
support groups, exercise training may be useful in patient
with HTN.

Percutaneous
catheter-based
radiofrequency
ablation .
Carotid
baroreceptor
stimulation
Aka renal denervation .
Used to control Resistant Hypertension.
There is reduction of renal sympathetic activity by Percutaneous
catheter-based radiofrequency ablation via the renal arteries .
Renal sympathetic nerve signals are interrupted by radiofrequency
ablation.
It is approved in Europe and Australia for resistant hypertension.
 https://www.msdmanuals.com/en-
in/professional/cardiovascular-disorders/hypertension/overview-
of-hypertension
 Lewis medical surgical nursing 3rd edition .
 https://www.heart.org/en/health-topics/high-blood-pressure
 https://www.heartandstroke.ca/heart/risk-and-
prevention/condition-risk-factors/high-blood-pressure
 https://www.acc.org/latest-in-
cardiology/articles/2017/11/08/11/47/mon-5pm-bp-guideline-
aha-2017
 Bhatt DL, Kandzari DE, O'Neill WW, et al, for the SYMPLICITY
HTN-3 Investigators: A controlled trial of renal denervation for
resistant hypertension. N Engl J Med 370:1393–1401, 2014. DOI:
10.1056/NEJMoa1402670.
 https://www.hopkinsmedicine.org/health/conditions-and-
diseases/high-blood-pressure-hypertension/resistant-
hypertension
Hypertension
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Hypertension

  • 3.
  • 4.
  • 5. As per new 2017 ACC/AHA definition “ Hypertension is defined as a persistent systolic BP(SBP) of 130 mm Hg or more, diastolic BP(DBP) of 80 mm Hg or more” .
  • 6.
  • 7. 1.13 billion people worldwide have hypertension . HTN is present in 25-30 % of urban & 10-20 % of rural population. Approx. 100-110 million persons have HTN in India. HTN is the attributable cause for 57 % of stroke and 24.5 % of coronary heart disease in India.
  • 8.
  • 9.  Malignant Hypertension.  Hypertensive urgency.  Hypertensive emergency.  White coat HTN.  Pseudohypertension.  Transient HTN.  Paradoxical HTN  Hypertensive crisis.  Isolated systolic HTN  Accelerated HTN  Masked HTN  Resistant hypertension
  • 10.  Extremely high blood pressure( >180/120 mm Hg) that develops rapidly .  It should be treated as medical emergency.  S/S are changes in vision , kidney failure, grade IV retinopathy(papillidema) etc.
  • 11.  It is clinical situation where blood pressure is elevated without evidence of target organ damage.  Blood pressure readings at 180/120 or higher .  BP can be controlled safely within a few hours with medications.
  • 12. Condition where blood pressure is elevated with evidence of target organ damage.  BP is > 180 / 120 mm Hg.  Blood pressure must be reduced immediately to prevent imminent organ damage.
  • 13.  White coat syndrome is a phenomenon in which people exhibit a blood pressure level above the normal range, in a clinical setting.  They do not exhibit it in other settings.  It may be due to anxiety experienced during a clinic visit
  • 14.
  • 15.  It is an uncommon phenomenon seen in elderly clients.  Intra –arterial BP is lower than the BP measured by sphygmomanometer.  It is caused by stiff and non compliant vessels due to thickened wall of arteries with aging.
  • 16. An increased BP for a particular period of time and then droping back to normal.  It is seen in Acute stroke, Acute MI, pregnancy, Acute glomerulonephritis.
  • 17.  Paroxysmal hypertension is episodic and volatile high blood pressure, which may be due to stress of any sort, or from a pheochromocytoma.  There is a sudden increase in BP even on anti hypertensive drugs.
  • 18.  A hypertensive crisis is a severe increase in blood pressure that can lead to a stroke.  BP is 180 /120 mm of Hg.  It is an umbrella term includes hypertensive urgency & emergency.  S/S are severe chest pain, severe headache, confusion, Shortness of breath etc.
  • 19.  Systolic BP > 130 mm Hg , but Diastolic BP < 80 mm of Hg.  Common type of HTN in older people.  Caused by artery stiffness, diabetes, and overactive thyroid.
  • 20.
  • 21.  When blood pressure reading is normal at the doctor's office but high at home—is known as masked hypertension .
  • 22.
  • 23.  Resistant hypertension is high blood pressure that does not respond well to aggressive medical treatment.  Hypertension is considered resistant when all of the following are true: 1) Someone is taking three* different blood pressure medications at their maximally tolerated doses. 2) One of the blood pressure medications is a diuretic (removes fluid and salt from the body). 3) Blood pressure remains above goal—(usually 130/80 mmHg) . 4) If hypertension requires four or more medications to be controlled it is also called resistant hypertension.
  • 24.  Hypertension is defined as resistant when BP remains > 160/100 mm Hg despite use of 3 different antihypertensive drugs with complementary mechanisms of action (one of which being a diuretic).
  • 25.
  • 26.
  • 28.  Also referred to as essential or idiopathic HTN.  There is elevated BP without an identified cause.  Accounts for 90-95%. Of all cases of HTN.  Since primary HTN has unknown cause, there are several contributing factors.
  • 29.  Increased SNS activity.  Obesity.  Diabetes mellitus.  Insulin resistance.  Stress  Excessive alcohol consumption.  Increased Sodium intake.  Vasoconstriction(Endothelium).  Tobacco use.  Dysfunction in RAAS system.  Dyslipidemia
  • 30. ➢ Age ➢ Alcohol ➢ Tobacco use. ➢ Diabetes mellitus ➢ Elevated serum lipids ➢ Excess dietary sodium. ➢ Ethnicity ➢ Gender ➢ Family history. ➢ Obesity. ➢ Sedentary lifestyle. ➢ Stress ➢ Socioeconomic status
  • 31.  SBP rises progressively with increasing age.  DBP may decrease with age.  After age 50, SBP>140 mm Hg is more important cardiovascular risk factor than DBP.
  • 32.  Excessive alcohol intake is strongly associated with HTN.  Moderate intake of alcohol has cardioprotective properties.  Hypertensive males should limit their daily alcohol intake to 2 drinks.  Hypertensive females should limit 1 drink per day .
  • 33.  Smoking tobacco greatly increases risk of cardiovascular disease.  Hypertensive people who smoke tobacco are at greater risk for cardiovascular disease.
  • 34.
  • 35.
  • 36.  HTN is more common in patient with DM.  When HTN and DM coexist, complications such as target organ disease are more severe.
  • 37.
  • 38.  Increased level of Cholesterol & triglycerides are primary risk factor in atherosclerosis.  Hyperlipidemia is more common in hypertensive people
  • 39.  High sodium intake can lead to HTN in salt sensitive patients.  Decreases the effectiveness of certain antihypertensive drugs. 
  • 40.
  • 41.  HTN is more prevalent in men in young adulthood and early middle age.  After the age 64, HTN is more in women.
  • 42.  History of a close blood relative(parents, sibling) with HTN is associated with an increasing risk of HTN.
  • 43.  Regular physical activity can control weight & reduce cardiovascular risk.  Physical activity may decrease BP
  • 44. HTN is more prevalent in lower socioeconomic groups and among the less educated. Social isolation. Lack of support.
  • 45.  Repeated stress may develop HTN more frequently than others.
  • 46.
  • 47.  Weight gain is associated with increased frequency of HTN.  Central abdominal obesity has more risk .
  • 48.
  • 49.
  • 50.  Secondary HTN is elevated BP with a specific cause .  It can be identified and corrected.  It accounts for 5-10 % of HTN cases.  Contributing factor to hypertensive crisis.  Treatment aimed at treating the underlying cause.
  • 51. ❑ Renal disease( renal artery stenosis, glomerulonephritis, renal parenchymal disease). ❑ Coarctation or congenital narrowing of aorta. ❑ Cirrhosis of liver. ❑ Endocrine disorders( pheochromocytoma, Cushing syndrome, thyroid disease, primary hyperaldosteronism) .
  • 52. ❑ Pregnancy induced hypertension. ❑ Sleep apnea. ❑ Drugs: Oral contraceptives , estrogen replacement therapy, NSAIDs, sympathetic stimulants ( cocaine, monoamine oxidase) , corticosteroids. ❑ Neurologic disorders( brain tumors, head injury, quadriplegia, GBS) .
  • 53. Heredity. water & sodium retention Altered Renin –angiotensin –aldosterone mechanism. Stress & Increased SNS activity. Insulin resistance & Hyperinsulinemia Endothelial dysfunction
  • 54.
  • 55.
  • 56. . Hypertension is a complex multifactorial disorder with genetic, environmental and demographic factors contributing to its prevalence. Several genetic variations influence the body’s sensitivity to salt lead to HTN. Endothelial surface proteins activated , stimulates proinflammatory properties, impairs vasodilatory effects leads to HTN.
  • 57.
  • 58. Excessive sodium intake is linked to the HTN development. Only 1 in 3 develop HTN, Though most people consume a high sodium diet. Effect of sodium on BP has a strong genetic component. Effect of sodium is greater in middle aged & older adults.
  • 59.
  • 60.
  • 61.
  • 62.
  • 63. Impair nitrous oxide mediated vasodilatation Stimulates SNS activity High insulin level in blood
  • 64. Insulin resistance is a risk factor in the development of HTN & CVD. Additional effects of insulin include vascular hypertrophy & increased renal sodium absorption.
  • 65. It is recognized as a marker of CVD( primary HTN) Vasodilator( Nitric oxide) & Vasoconstrictor( Endothelin) are produced in endothelial cells. Therefore endothelial dysfunction affects BP.
  • 66. High levels of Endothelin prolonged vasoconstriction HTN Oxygen free radicals Impair the Nitrous oxide availability Altered Vasodilation HTN
  • 67. Renal parenchymal disease Renovascualar disease Primary hyperaldosteronism. Pheochromocytoma Liver cirrhosis Sleep apnea
  • 68. Due to loss of nephrons . Retention of salt & water. Decreased release of nitric oxide. Activation of renin angiotensin mechanisms.
  • 69.
  • 70.
  • 71. Renal artery stenosis Renal ischemia Release of renin from JG cells RAAS process increased blood pressure
  • 72.
  • 73.
  • 74. ❑ Hyperaldosteronism is characterized by excessive secretion of aldosterone.
  • 75. Excessive aldosterone secretion Retention of sodium , water & chloride Increased ECF Increased venous return to heart CO increased thus BP increased
  • 76. PCC is a rare tumor of adrenal gland Excessive release of adrenaline & nor adrenaline Increased HR, CO Increased BP
  • 77.
  • 78.
  • 79.
  • 80. Due to liver cirrhosis Scarring in liver Blockage of portal vein blood flow through the liver. Increased pressure in portal vein Large veins( Varices) in esophagus Varices bleed easily.
  • 81.
  • 82.
  • 83.
  • 84.
  • 85. It is usually asymptomatic so called” silent killer” . When HTN becomes severe & target organ disease occurs. Severe hypertension effects blood vessels in various organs & increases workload on heart. So secondary symptoms include fatigue, dizziness, palpitations, angina and dyspnea.
  • 86.
  • 87. What are the complications of Hypertension?
  • 88.
  • 91.
  • 92. Hypertension disrupts coronary artery endothelium. Atheroma formation Stiffed arterial wall with a narrowed lumen CAD, MI & ANGINA
  • 93.
  • 94.
  • 95.
  • 96. Sustained HTN Increased cardiac workload LVH to increase cardiac output & cardiac contraction Increased Myocardial workload and oxygen demand Progressive LVH with CAD Heart failure
  • 97.
  • 98.
  • 99. Due to increased preload & After load Heart compensatory mechanism failed Contractility diminished CO diminished Fatigue, dyspnoea, Shortness of breath
  • 100.
  • 101.
  • 103. Atherosclerosis is the most common cause of Cerebrovascular disease. HTN is a major risk factor for cerebral atherosclerosis & stroke. Plaque is found at the bifurcation of the common carotid artery. Portion of plaque or blood clot may break off and travel to coronary vessels causes thromboembolism.
  • 104.
  • 105. Hypertensive encephalopathy (HE) is general brain dysfunction due to significantly high blood pressure. Generally the blood pressure is greater than 200/130 mmHg Symptoms may include headache, vomiting, trouble with balance, and confusion. It occurs after a marked rise in BP if cerebral blood flow is not decreased by auto regulation.
  • 106.
  • 107. Elevated Blood pressure Autoregulation of cerebral flow decreased Cerebral blood vessels dilate increased capillary permeability cerebral edema
  • 109. HTN speeds up the process of atherosclerosis in PVD. It leads to PVD, aortic aneurysm, aortic dissection . Intermittent claudication is a classic symptom of PVD.
  • 110.
  • 111.  Hypertension is the second leading cause of kidney failure  Some degree of renal disease is usually present in hypertensive patient.
  • 112. Eventually renal failure. Atrophy of renal tubules, glomeruli destruction & death of nephrons. Renal ischemia Narrowing of renal blood vessels Uncontrolled HTN
  • 113.
  • 114.  Eyes contain tiny blood vessels . Due to long term effects of HTN, following conditions occur: 1. Blood vessel damage (retinopathy). 2. Fluid buildup under the retina (choroidopathy). 3. Nerve damage (optic neuropathy)
  • 115.  Retinopathy: A lack of blood flow to the retina leads to blurred vision or the complete loss of sight.  Fluid buildup under the retina (choroidopathy) This buildup of fluid under the retina, the light-sensitive layer of tissue at the back of the eyeball, results in distorted vision or, in some cases, scarring that impairs vision.  Nerve damage (optic neuropathy): The result of blocked blood flow that damages the optic nerve, it can kill nerve cells in eyes, which may cause temporary or permanent vision loss.
  • 116. HTN damages blood vessels causes reduced blood flow to the pelvis. It leads to sexual dysfunction in both gender. In Male it causes Erectile dysfunction. In Women it leads to decreased libido & less interest in sex.
  • 118. Known duration of HTN & previously recorded BP. Any history or symptoms of coronary artery disease, heart failure, sleep apnea or loud snoring . History or symptoms of other relevant coexisting disorders (eg, stroke, renal dysfunction, peripheral arterial disease, dyslipidemia, diabetes, gout). Family history .
  • 119. Social history includes exercise levels and use of tobacco, alcohol, and stimulant drugs (prescribed and illicit). A dietary history focuses on intake of salt and stimulants (eg, tea, coffee, caffeine-containing sodas, energy drinks).
  • 120. Measurement of height, weight, and waist circumference . ( Central obesity) Funduscopic examination for retinopathy . Auscultation for bruits in the neck and abdomen( Renal artery stenosis) . Abdomen palpation for kidney enlargement and abdominal masses ( Polycystic kidney disease) . A full cardiac, respiratory, and neurologic examination.
  • 121. Diminished or delayed femoral pulses suggest aortic Coarctation. A unilateral renal artery bruit may be heard in slim patients with Renovascualar hypertension.
  • 122. Routine urinalysis & spot urine albumin:creatinine ratio . BUN , serum creatinine level , urinalysis to screen for renal involvement . Decreased Creatinine clearance indicates renal insufficiency. Serum electrolytes: potassium (Hypokalemia) is important to detect hyperaldosteronism.
  • 123. Blood glucose level to detect DM. Chest X ray to detect cardiomegaly, Coarctation of aorta. Lipid profile to identify atherosclerosis and CVD. ECG to identify Left ventricular hypertrophy(LVH) , previous MI . Thyroid function test : To rule out hypothyroidism , hyperthyroidism.
  • 124. Echocardiography to detect LVH . Uric acid level : Rises with diuretic therapy. Renal ultrasound : To detect possible renal disease. Renal angiography: To detect or confirm renal artery stenosis. Ambulatory BP recording : To assess white coat HTN & masked HTN .
  • 125. Plasma free metanephrines : To rule out pheochromocytoma Urinary cortisol test : To detect possible cushing’s disease. Plasma renin activity & aldosterone: To detect primary aldosteronism . Sleep study : people with sleep apnea.
  • 126.  The goal of treatment includes achieve and maintain goal BP, reduce cardiovascular risk and target organ disease.  Primary hypertension has no cure, but some causes of secondary hypertension can be corrected.  Treatment targets for the general population, including all those with a kidney disorder or diabetes: BP < 130/80 mm Hg regardless of age up to age 80.
  • 128. Weight reduction DASH eating plan Physical activity Dietary sodium reduction Avoidance of tobacco products Moderation of alcohol intake Management of Psychosocial risk factors
  • 129.
  • 130. Weight reduction has a significant effect on lowering Blood pressure. For overweight hypertensive patinets a combination of dietary calories restriction and moderate physical activity is recommended to reduce weight . A weight loss of 22 lb may decrease SBP by approx. 5 to 22 mm Hg
  • 131.
  • 132. Dietary approaches to stop hypertension( DASH) diet emphasizes fruits, vegetables , low fat milk , whole grains, fish , poultry , been , seeds & nuts . DASH diet plan lowers BP and LDL cholesterol.
  • 133.
  • 134.
  • 135.
  • 136. AHA & ACSM recommended that all adults perform regular physical activity (brisk walking) at least 30 minutes per day more than 5 days per week . Moderate intense activity such as brisk walking, jogging, swimming can lower BP, control body weight.
  • 137.
  • 138.
  • 139.
  • 140. Healthy adults should restrict sodium intake to less than or equal to 2.3 gram/day. Hypertensive person should limit sodium to less than 1.5 gram/day. Avoid foods known to high in sodium( canned soups) . Do not add salt in the preparation of foods or at meals.
  • 141. The patient , Family & person who prepare meals should be taught about sodium restricted diet. Foods high in sodium should be identified Sodium restriction may be enough to control BP in some patients with HTN.
  • 142.
  • 143.
  • 144.
  • 145. Nicotine causes vasoconstriction and increases BP. Smoking tobacco is a major risk factor for CVD. The benefits of tobacco cessation are seen within 1 year in all age groups.
  • 146.
  • 147. Drinking three or more alcoholic drinks daily is a risk factor for CVD & Stroke. Men should limit alcohol not more than 2 drinks per day. Women and lighter weight men to no more than 1 drink per day. Liver cirrhosis due to excessive alcohol intake is the frequent cause of secondary HTN.
  • 148.
  • 149.
  • 150. Psychosocial risk factors have direct effects on CVS by activating SNS and stress hormone. It can lead to HTN , tachycardia etc. Screening for Psychosocial risk factors should be done. Relaxation therapy, guided imagery , biofeedback , support groups, exercise training may be useful in patient with HTN.
  • 151.
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  • 158. Aka renal denervation . Used to control Resistant Hypertension. There is reduction of renal sympathetic activity by Percutaneous catheter-based radiofrequency ablation via the renal arteries . Renal sympathetic nerve signals are interrupted by radiofrequency ablation. It is approved in Europe and Australia for resistant hypertension.
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  • 170.  https://www.msdmanuals.com/en- in/professional/cardiovascular-disorders/hypertension/overview- of-hypertension  Lewis medical surgical nursing 3rd edition .  https://www.heart.org/en/health-topics/high-blood-pressure  https://www.heartandstroke.ca/heart/risk-and- prevention/condition-risk-factors/high-blood-pressure  https://www.acc.org/latest-in- cardiology/articles/2017/11/08/11/47/mon-5pm-bp-guideline- aha-2017  Bhatt DL, Kandzari DE, O'Neill WW, et al, for the SYMPLICITY HTN-3 Investigators: A controlled trial of renal denervation for resistant hypertension. N Engl J Med 370:1393–1401, 2014. DOI: 10.1056/NEJMoa1402670.  https://www.hopkinsmedicine.org/health/conditions-and- diseases/high-blood-pressure-hypertension/resistant- hypertension