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HYPERTENSION
By-Kifle Alamirew(MD)
1
DEFINITION OF HYPERTENTION
īļ The following definitions were suggested in 2003 by the
seventh report of the Joint National Committee (JNC
7) based upon the average of two or more properly
measured readings at each of two or more visits after an
initial screen:
ī‚ĸ Normal blood pressure: systolic <120 mmHg and
diastolic <80
ī‚ĸ Prehypertension: systolic 120-139 or diastolic 80-89
ī‚ĸ Hypertension:
īƒ˜ Stage 1: systolic 140-159 or diastolic 90-99
īƒ˜ Stage 2: systolic >=160 or diastolic >=100
2
CONT’Dâ€Ļ..
īļ Based on 2017GC guidelines the definition of HTN is
changed:
ī‚ĸ Normal blood pressure: systolic <120 mmHg and
diastolic <80
ī‚ĸ Elevated: systolic 120-129 or diastolic < 80
ī‚ĸ Hypertension:
īƒ˜ Stage 1: systolic 130-139 or diastolic 80-89
īƒ˜ Stage 2: systolic >=140 or diastolic >=90
īļ These definitions apply to adults on no antihypertensive
medications and who are not acutely ill. If there is a
disparity in category between the systolic and diastolic
pressures, the higher value determines the severity of the
hypertension 3
CONTâ€Ļ
īąEpidemiology
ī‚§ HTN is the most prevalent risk factor for
cardiovascular diseases (CVD).
ī‚§ ~30 % at age >18 yr;> 50 % at age >60.
ī‚§ As age increases SBP increases but diastolic
BP tends to decrease after age 55 resulting
in wide pulse pressure & isolated systolic
HTN
ī‚§ BP is greater for males until menopause 4
CONTâ€Ļ
īąMechanism of HTN
o Determinant
ī‚§ Intravascular volume
ī‚§ Vascular resistance
īƒŧ Autonomic nervous System
īƒŧ Renin -Angiotensin-Aldosterone system
īƒŧ Vascular system(stiffness/elasticity)
5
CONTâ€Ļ
ī‚§ Intra vascular volume
īƒŧ Is based on ECF Na+ content
īƒŧ Slow but its effect lasts long.
īƒŧ ↑ECF Na+ → ↑ ECF volume → This leads to
↑BP initially by increasing CO but later by
increasing TPR in order to decrease tissue flow
of blood. The final effect is to increase
natriuresis to balance for gain in Na+.
īƒŧ If kidney fails or has low sensitivity to pressure
diuresis the BP will remain high to decrease the
Na+ load.
6
CONTâ€Ļ
o ANS(SNS)
īƒŧ For minute to minute control of BP
īƒŧ Stimulated by baroreflex(carotid & aortic arch)
īƒŧ Adrenergic neurons(NE and Dopamine) and
adrenal medulla(Epinephrine)
īƒŧ Act on their receptors(a1,a2,B1,and B2)
7
CONTâ€Ļ
o RAAS
ī‚ĸ Renin from kidneys(Juxtaglomerlar) is released
in response to ↓renal plasma flow, low Na
states.
Renin ACE(lung)
↓ ↓
Angiotensinogen (liver)→Angio.I →Angio.II
Angiotensin II : Potent vasoconstrictor, tropics for
adrenal medulla (zona glomerulosa),and
stimulate adrenergic nervous system 8
ETIOLOGY OF HTN
īƒ˜ Essential(idiopathic, primary)
ī‚§ Accounts 80-95%
ī‚§ Has no identifiable cause(even though extensive
investigations)
īƒ˜ Secondary
ī‚§ Accounts 5-15%
ī‚§ Causes are known
9
CONTâ€Ļ
īƒ˜Essential HTN
īƒŧ Tends to be familial and is likely to be the
consequence of an interaction between
environmental and genetic factors
10
RISK FACTORS FOR ESSENTIAL HYPERTENSION
ī‚ĸ Family histroy of hypertension
ī‚ĸ Hypertension tends to be both more common and more
severe in blacks
ī‚ĸ Evidence for a relationship between sodium intake and
essential hypertension continues to mount
ī‚ĸ Multiple studies show a clear association between excess
alcohol intake and the development of hypertension
ī‚ĸ Obesity is associated with an increased prevalence and
incidence of hypertension
ī‚ĸ Dyslipidemia may also be associated with the
development of hypertension, and is independent of
obesity
ī‚ĸ Hypertension may be more common among those with
certain personality traits, such as hostile attitudes and
11
COUSE OF SECONDARY HYPERTENSION
īƒ˜ Renal paranchymal disease
īƒ˜ Renovascular hypertension
īƒ˜ Primary aldosteronism
īƒ˜ Cushing’s syndrome
īƒ˜ Pheochromocytoma
īƒ˜Miscellaneous causes of secondary hypertension:
īƒŧObstructive sleep apnea
īƒŧCoarctation of the aorta: the most common
congenital cardiovascular cause of hypertension
īƒŧthyroid diseases and acromegaly
īƒŧHypercalcemia
īƒŧHypertension may also be related to a number of
prescribed or over-the-counter medications:
ex.steroids
12
DIAGNOSIS OF HYPERTENSION
ī‚ĸ Office blood pressure measurement
īƒŧ Draw backs: white coat and masked hypertensions
ī‚ĸ Ambulatory bood pressure measurement
ī‚ĸ Home blood pressure measurement
13
GUIDELINES FOR THE MEASUREMENT OF BLOOD
PRESSURE TO DIAGNOSE AND TREAT HYPERTENSION
ī‚ĸ Allow the patient to sit quietly for 5 minutes before measuring
blood pressure
ī‚ĸ No caffeine during the hour preceding the reading and no smoking
during the preceding 30 minutes
ī‚ĸ No exogenous adrenergic stimulants, such as phenylephrine in
decongestants or eye drops for pupillary dilatation
ī‚ĸ The patient should be seated comfortably with the back supported
and the upper arm bared without constrictive clothing
ī‚ĸ The legs should not be crossed
ī‚ĸ The arm should be supported at heart level, and the bladder of the
cuff should encircle at least 80% of the arm circumference
ī‚ĸ Neither the patient nor the observer should talk during the
measurement
ī‚ĸ Take at least two readings on each visit, separated by as much time
as possible; if readings vary by more than 5 mmHg, take additional
reading until two consecutive readings are close
ī‚ĸ For the diagnosis of hypertension, take measurement on atleast two visits
14
CONT’Dâ€Ļâ€Ļ
â€ĸ Initially, take blood pressure in both arms; if pressures differ, use
the higher arm
ī‚ĸ If the arm pressure is elevated, take the pressure in one leg,
particularly in patients under age 30
ī‚ĸ Inflate the bladder quickly to 20 mmHg above the systolic pressure
as estimated from loss of radial pulse and then deflated it at a rate of 2
to 3 mm/sec, and the first and last audible sounds should be taken
as systolic and diastolic pressure. The column should be read to the
nearest 2 mm Hg
ī‚ĸ Check for postural changes by taking readings after five minutes
supine, then immediately and two minutes after standing - this is
particularly important in patients over age 65, diabetics, or those
taking antihypertensive drugs
īƒŧ For monitoring of therapy, the BP should be measured before
antihypertensive medications are taken to estimate the trough or
nadir effect. If the BP is taken soon after drug ingestion, the BP may
be normal or even below normal and then will gradually increase to
potentially hypertensive levels until the next dose is taken
15
CONT’Dâ€Ļ..
īƒŧ Mercury sphygmomanometers provide the most accurate
measurement of BP. Aneroid sphygmomanometers, which are
used in many offices, should be checked against a mercury
device since the air gauge may be in error .However, this may
become increasingly impossible as mercury is removed from
circulation due to concerns of environmental toxicity
īƒŧ Automated oscillometric BP measuring devices are
increasingly being used in medical offices, and for home
monitoring. The readings are typically lower than BP obtained
with the auscultatory method. The disadvantages are that the
oscillometric method has somewhat greater inherent error
and epidemiologic data are based on auscultatory methods.
However, advantages are that observer error and training are
minimal. Proper timing, patient positioning, cuff size and
placement are still necessary, as is evaluation of machine
accuracy at periodic intervals
16
CONTâ€Ļ
īąEffects of HTN
ī‚§ Target Organ Damage(Brain, Heart, Kidney &
Peripheral vessels)
ī‚§ They are directly related to increased risk of
atherosclerosis or direct effect of the elevated
BP.
ī‚§ Genetic, racial factors, presence of other CVD
risk factors and control of the HTN influence
development of Target Organ Damage(TOD).
17
CLINICAL PRESENTATION OF HTN
ī‚§ Most patients are asymptomatic
ī‚§ diagnosed on routine evaluation or when they
come for other illnesses
ī‚§ Others come with symptoms or signs of TOD
ī‚§ Few will come symptoms directly related to
elevated BP
īƒŧ Headache, Epitasis, Hematuria
18
1. HEART(HHD) â€Ļ
ī‚§ Heart disease is the most common cause of
death in hypertensive patients.
ī‚§ Is the result of structural and functional
adaptations leading to left ventricular
hypertrophy(LVH), diastolic dysfunction, CHF,
atherosclerotic coronary artery and
microvascular disease, and cardiac arrhythmias.
19
2. BRAIN
ī‚§ Both types of stroke(accounts 50%)
ī‚§ Hypertensive Encephalopathy
ī‚§ Cognitive impairment/dementia
3 Kidney
ī‚§ Leads to glomerulosclerosis & tubular
ischemia & atrophy.
ī‚§ Primary renal disease is the most common
aetiology of secondary hypertension.
ī‚§ Conversely, hypertension is a risk factor for
renal injury and ESRD
20
CONTâ€Ļ
ī‚§ Renal risk appears to be more closely related to
systolic than to diastolic blood pressure
ī‚§ Black men are at greater risk than white men for
developing ESRD at every level of blood
pressure.
ī‚§ Clinically albuminuria is early marker of renal
injure
4: Peripheral arteries
ī‚§ Increased risk of atherosclerosis(PDA)
ī‚§ Intermittent claudication or gangrene
5. Eye: hypertensive retinopathy
21
PATIENT EVALUATION
ī‚§ History, Exam, appropriate lab tests are done with
objectives of:
1. Defining the Blood pressure levels
2. Assess lifestyle and identify other CV risk factors or
concomitant CV disorders that affects prognosis and
guides treatment
3. Assess the presence or absence of target organ
damage
4. Identifying secondary forms of hypertension.
22
HISTORY
ī‚ĸ Duration of hypertension
ī‚ĸ Previous therapies: responses and side effects
ī‚ĸ Family history of hypertension and cardiovascular disease
ī‚ĸ Dietary and psychosocial history
ī‚ĸ Other risk factors: weight change, dyslipidemia, smoking,
diabetes, physical inactivity
ī‚ĸ Evidence of secondary hypertension: history of renal disease;
change in appearance; muscle weakness; spells of sweating,
palpitations, tremor; erratic sleep, snoring, daytime
somnolence; symptoms of hypo- or hyperthyroidism; use of
agents that may increase blood pressure
ī‚ĸ Evidence of target organ damage: history of TIA, stroke,
transient blindness; angina, myocardial infarction, congestive
heart failure; sexual function
ī‚ĸ Other comorbidities
23
PHYSICAL EXAMINATION AND LABORATORY TESTS TO BE DONE
ROUTINELY
24
WORK UP OF SECONDARY FORMS OF
HYPERTENSION(INDICATED)
25
CONTâ€Ļ
īƒ˜ Finally what we do is:
ī‚§ Determine Stage of HTN
ī‚§ Determine the presence and/or absence of
associated risk factors
ī‚§ Determine presence or absence of
TOD/associated clinical condition
ī‚§ Decide on the nature of treatment of the HTN
and other risk factors and plan the follow up
ī‚§ Set goal of the treatment
26
CONTâ€Ļ
īƒ˜ Who should be treated?
ī‚§ Those with BP levels known to cause risk
ī‚§ Levels of BP known to expose to risks are
different in different conditions
ī‚§ Stratification of patients and their risk profile
need definition
27
CONTâ€Ļ
īƒ˜Goal of therapy
ī‚§ BP <130/80 mmHg
ī‚§ Control other risk factors
īƒŧBMI, quitting smoking, cholesterol, moderation on
alcohol consumption, and exercise
ī‚§ Achieve SBP goal especially in persons >50 years of age.
28
TREATMENT
īƒ˜Non pharmacologic
ī‚§ For all
ī‚§ Therapeutic life style change
īƒŧ Modifying diet(DASH plan)
īƒŧ Exercise
īƒŧ Secession of smoking
īƒŧ Moderate alcohol
īƒŧ Salt restriction
īƒŧ Wt reduction
29
CONTâ€Ļ
īƒ˜Pharmacologic
ī‚§ Indicated for those failed to achieve goal BP
after 2-3 months of TLC .
ī‚§ At beginning in those with hypertensive
crisis OR in those with TOD & BP not in
target.
ī‚§ Drug classes
ī‚ĸ Diuretics .ARBs
ī‚ĸ CCBs .Vasodilators
ī‚ĸ BBs .ACEIs
30
FOLLOW UP AND MONITORING
ī‚§ Patients should return for follow up and
adjustment of medications until the BP goal is
reached.
ī‚§ More frequent visits for stage 2 HTN or with
complicating comorbid conditions.
ī‚§ Serum potassium and creatinine monitored
1–2 times per year. After BP at goal and
stable, follow up visits at 3- to 6-month
intervals.
ī‚§ Co morbidities, such as heart failure,
associated diseases, such as diabetes, and the
31
HYPERTENSIVE EMERGENCY
ī‚§ severe symptomatic hypertension (often defined as systolic blood
pressure 180 mmHg and/or diastolic blood pressure 120 mmHg
A. Malignant hypertension
ī‚§ Is marked hypertension with retinal haemorrhages,
exudates, or papilledema
ī‚§ Is usually associated with a diastolic pressure above
120 mmHg.
B. Hypertensive encephalopathy
ī‚§ Refers to the presence of signs of cerebral oedema
caused by breakthrough hyper perfusion from severe
and sudden rises in blood pressure
ī‚§ Characterized by the insidious onset of headache,
nausea, and vomiting, followed by non localizing
neurologic symptoms such as restlessness, confusion,
and, if the hypertension is not treated, seizures and
coma
32
CONTâ€Ļ
īƒ˜ Hypertensive Urgency
ī‚§ Severe hypertension (as defined by a diastolic
blood pressure above 120 mmHg) in
asymptomatic patients. .
ī‚§ No evidence of organ damage
33
CRISIS(EMERGENCY AND
URGENCY)
ī‚§ In hypertensive urgency oral agents are
used to reduce BP over 24 hour then to
target level over two to three months.
ī‚§ Captopril
34

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9 htn

  • 2. DEFINITION OF HYPERTENTION īļ The following definitions were suggested in 2003 by the seventh report of the Joint National Committee (JNC 7) based upon the average of two or more properly measured readings at each of two or more visits after an initial screen: ī‚ĸ Normal blood pressure: systolic <120 mmHg and diastolic <80 ī‚ĸ Prehypertension: systolic 120-139 or diastolic 80-89 ī‚ĸ Hypertension: īƒ˜ Stage 1: systolic 140-159 or diastolic 90-99 īƒ˜ Stage 2: systolic >=160 or diastolic >=100 2
  • 3. CONT’Dâ€Ļ.. īļ Based on 2017GC guidelines the definition of HTN is changed: ī‚ĸ Normal blood pressure: systolic <120 mmHg and diastolic <80 ī‚ĸ Elevated: systolic 120-129 or diastolic < 80 ī‚ĸ Hypertension: īƒ˜ Stage 1: systolic 130-139 or diastolic 80-89 īƒ˜ Stage 2: systolic >=140 or diastolic >=90 īļ These definitions apply to adults on no antihypertensive medications and who are not acutely ill. If there is a disparity in category between the systolic and diastolic pressures, the higher value determines the severity of the hypertension 3
  • 4. CONTâ€Ļ īąEpidemiology ī‚§ HTN is the most prevalent risk factor for cardiovascular diseases (CVD). ī‚§ ~30 % at age >18 yr;> 50 % at age >60. ī‚§ As age increases SBP increases but diastolic BP tends to decrease after age 55 resulting in wide pulse pressure & isolated systolic HTN ī‚§ BP is greater for males until menopause 4
  • 5. CONTâ€Ļ īąMechanism of HTN o Determinant ī‚§ Intravascular volume ī‚§ Vascular resistance īƒŧ Autonomic nervous System īƒŧ Renin -Angiotensin-Aldosterone system īƒŧ Vascular system(stiffness/elasticity) 5
  • 6. CONTâ€Ļ ī‚§ Intra vascular volume īƒŧ Is based on ECF Na+ content īƒŧ Slow but its effect lasts long. īƒŧ ↑ECF Na+ → ↑ ECF volume → This leads to ↑BP initially by increasing CO but later by increasing TPR in order to decrease tissue flow of blood. The final effect is to increase natriuresis to balance for gain in Na+. īƒŧ If kidney fails or has low sensitivity to pressure diuresis the BP will remain high to decrease the Na+ load. 6
  • 7. CONTâ€Ļ o ANS(SNS) īƒŧ For minute to minute control of BP īƒŧ Stimulated by baroreflex(carotid & aortic arch) īƒŧ Adrenergic neurons(NE and Dopamine) and adrenal medulla(Epinephrine) īƒŧ Act on their receptors(a1,a2,B1,and B2) 7
  • 8. CONTâ€Ļ o RAAS ī‚ĸ Renin from kidneys(Juxtaglomerlar) is released in response to ↓renal plasma flow, low Na states. Renin ACE(lung) ↓ ↓ Angiotensinogen (liver)→Angio.I →Angio.II Angiotensin II : Potent vasoconstrictor, tropics for adrenal medulla (zona glomerulosa),and stimulate adrenergic nervous system 8
  • 9. ETIOLOGY OF HTN īƒ˜ Essential(idiopathic, primary) ī‚§ Accounts 80-95% ī‚§ Has no identifiable cause(even though extensive investigations) īƒ˜ Secondary ī‚§ Accounts 5-15% ī‚§ Causes are known 9
  • 10. CONTâ€Ļ īƒ˜Essential HTN īƒŧ Tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors 10
  • 11. RISK FACTORS FOR ESSENTIAL HYPERTENSION ī‚ĸ Family histroy of hypertension ī‚ĸ Hypertension tends to be both more common and more severe in blacks ī‚ĸ Evidence for a relationship between sodium intake and essential hypertension continues to mount ī‚ĸ Multiple studies show a clear association between excess alcohol intake and the development of hypertension ī‚ĸ Obesity is associated with an increased prevalence and incidence of hypertension ī‚ĸ Dyslipidemia may also be associated with the development of hypertension, and is independent of obesity ī‚ĸ Hypertension may be more common among those with certain personality traits, such as hostile attitudes and 11
  • 12. COUSE OF SECONDARY HYPERTENSION īƒ˜ Renal paranchymal disease īƒ˜ Renovascular hypertension īƒ˜ Primary aldosteronism īƒ˜ Cushing’s syndrome īƒ˜ Pheochromocytoma īƒ˜Miscellaneous causes of secondary hypertension: īƒŧObstructive sleep apnea īƒŧCoarctation of the aorta: the most common congenital cardiovascular cause of hypertension īƒŧthyroid diseases and acromegaly īƒŧHypercalcemia īƒŧHypertension may also be related to a number of prescribed or over-the-counter medications: ex.steroids 12
  • 13. DIAGNOSIS OF HYPERTENSION ī‚ĸ Office blood pressure measurement īƒŧ Draw backs: white coat and masked hypertensions ī‚ĸ Ambulatory bood pressure measurement ī‚ĸ Home blood pressure measurement 13
  • 14. GUIDELINES FOR THE MEASUREMENT OF BLOOD PRESSURE TO DIAGNOSE AND TREAT HYPERTENSION ī‚ĸ Allow the patient to sit quietly for 5 minutes before measuring blood pressure ī‚ĸ No caffeine during the hour preceding the reading and no smoking during the preceding 30 minutes ī‚ĸ No exogenous adrenergic stimulants, such as phenylephrine in decongestants or eye drops for pupillary dilatation ī‚ĸ The patient should be seated comfortably with the back supported and the upper arm bared without constrictive clothing ī‚ĸ The legs should not be crossed ī‚ĸ The arm should be supported at heart level, and the bladder of the cuff should encircle at least 80% of the arm circumference ī‚ĸ Neither the patient nor the observer should talk during the measurement ī‚ĸ Take at least two readings on each visit, separated by as much time as possible; if readings vary by more than 5 mmHg, take additional reading until two consecutive readings are close ī‚ĸ For the diagnosis of hypertension, take measurement on atleast two visits 14
  • 15. CONT’Dâ€Ļâ€Ļ â€ĸ Initially, take blood pressure in both arms; if pressures differ, use the higher arm ī‚ĸ If the arm pressure is elevated, take the pressure in one leg, particularly in patients under age 30 ī‚ĸ Inflate the bladder quickly to 20 mmHg above the systolic pressure as estimated from loss of radial pulse and then deflated it at a rate of 2 to 3 mm/sec, and the first and last audible sounds should be taken as systolic and diastolic pressure. The column should be read to the nearest 2 mm Hg ī‚ĸ Check for postural changes by taking readings after five minutes supine, then immediately and two minutes after standing - this is particularly important in patients over age 65, diabetics, or those taking antihypertensive drugs īƒŧ For monitoring of therapy, the BP should be measured before antihypertensive medications are taken to estimate the trough or nadir effect. If the BP is taken soon after drug ingestion, the BP may be normal or even below normal and then will gradually increase to potentially hypertensive levels until the next dose is taken 15
  • 16. CONT’Dâ€Ļ.. īƒŧ Mercury sphygmomanometers provide the most accurate measurement of BP. Aneroid sphygmomanometers, which are used in many offices, should be checked against a mercury device since the air gauge may be in error .However, this may become increasingly impossible as mercury is removed from circulation due to concerns of environmental toxicity īƒŧ Automated oscillometric BP measuring devices are increasingly being used in medical offices, and for home monitoring. The readings are typically lower than BP obtained with the auscultatory method. The disadvantages are that the oscillometric method has somewhat greater inherent error and epidemiologic data are based on auscultatory methods. However, advantages are that observer error and training are minimal. Proper timing, patient positioning, cuff size and placement are still necessary, as is evaluation of machine accuracy at periodic intervals 16
  • 17. CONTâ€Ļ īąEffects of HTN ī‚§ Target Organ Damage(Brain, Heart, Kidney & Peripheral vessels) ī‚§ They are directly related to increased risk of atherosclerosis or direct effect of the elevated BP. ī‚§ Genetic, racial factors, presence of other CVD risk factors and control of the HTN influence development of Target Organ Damage(TOD). 17
  • 18. CLINICAL PRESENTATION OF HTN ī‚§ Most patients are asymptomatic ī‚§ diagnosed on routine evaluation or when they come for other illnesses ī‚§ Others come with symptoms or signs of TOD ī‚§ Few will come symptoms directly related to elevated BP īƒŧ Headache, Epitasis, Hematuria 18
  • 19. 1. HEART(HHD) â€Ļ ī‚§ Heart disease is the most common cause of death in hypertensive patients. ī‚§ Is the result of structural and functional adaptations leading to left ventricular hypertrophy(LVH), diastolic dysfunction, CHF, atherosclerotic coronary artery and microvascular disease, and cardiac arrhythmias. 19
  • 20. 2. BRAIN ī‚§ Both types of stroke(accounts 50%) ī‚§ Hypertensive Encephalopathy ī‚§ Cognitive impairment/dementia 3 Kidney ī‚§ Leads to glomerulosclerosis & tubular ischemia & atrophy. ī‚§ Primary renal disease is the most common aetiology of secondary hypertension. ī‚§ Conversely, hypertension is a risk factor for renal injury and ESRD 20
  • 21. CONTâ€Ļ ī‚§ Renal risk appears to be more closely related to systolic than to diastolic blood pressure ī‚§ Black men are at greater risk than white men for developing ESRD at every level of blood pressure. ī‚§ Clinically albuminuria is early marker of renal injure 4: Peripheral arteries ī‚§ Increased risk of atherosclerosis(PDA) ī‚§ Intermittent claudication or gangrene 5. Eye: hypertensive retinopathy 21
  • 22. PATIENT EVALUATION ī‚§ History, Exam, appropriate lab tests are done with objectives of: 1. Defining the Blood pressure levels 2. Assess lifestyle and identify other CV risk factors or concomitant CV disorders that affects prognosis and guides treatment 3. Assess the presence or absence of target organ damage 4. Identifying secondary forms of hypertension. 22
  • 23. HISTORY ī‚ĸ Duration of hypertension ī‚ĸ Previous therapies: responses and side effects ī‚ĸ Family history of hypertension and cardiovascular disease ī‚ĸ Dietary and psychosocial history ī‚ĸ Other risk factors: weight change, dyslipidemia, smoking, diabetes, physical inactivity ī‚ĸ Evidence of secondary hypertension: history of renal disease; change in appearance; muscle weakness; spells of sweating, palpitations, tremor; erratic sleep, snoring, daytime somnolence; symptoms of hypo- or hyperthyroidism; use of agents that may increase blood pressure ī‚ĸ Evidence of target organ damage: history of TIA, stroke, transient blindness; angina, myocardial infarction, congestive heart failure; sexual function ī‚ĸ Other comorbidities 23
  • 24. PHYSICAL EXAMINATION AND LABORATORY TESTS TO BE DONE ROUTINELY 24
  • 25. WORK UP OF SECONDARY FORMS OF HYPERTENSION(INDICATED) 25
  • 26. CONTâ€Ļ īƒ˜ Finally what we do is: ī‚§ Determine Stage of HTN ī‚§ Determine the presence and/or absence of associated risk factors ī‚§ Determine presence or absence of TOD/associated clinical condition ī‚§ Decide on the nature of treatment of the HTN and other risk factors and plan the follow up ī‚§ Set goal of the treatment 26
  • 27. CONTâ€Ļ īƒ˜ Who should be treated? ī‚§ Those with BP levels known to cause risk ī‚§ Levels of BP known to expose to risks are different in different conditions ī‚§ Stratification of patients and their risk profile need definition 27
  • 28. CONTâ€Ļ īƒ˜Goal of therapy ī‚§ BP <130/80 mmHg ī‚§ Control other risk factors īƒŧBMI, quitting smoking, cholesterol, moderation on alcohol consumption, and exercise ī‚§ Achieve SBP goal especially in persons >50 years of age. 28
  • 29. TREATMENT īƒ˜Non pharmacologic ī‚§ For all ī‚§ Therapeutic life style change īƒŧ Modifying diet(DASH plan) īƒŧ Exercise īƒŧ Secession of smoking īƒŧ Moderate alcohol īƒŧ Salt restriction īƒŧ Wt reduction 29
  • 30. CONTâ€Ļ īƒ˜Pharmacologic ī‚§ Indicated for those failed to achieve goal BP after 2-3 months of TLC . ī‚§ At beginning in those with hypertensive crisis OR in those with TOD & BP not in target. ī‚§ Drug classes ī‚ĸ Diuretics .ARBs ī‚ĸ CCBs .Vasodilators ī‚ĸ BBs .ACEIs 30
  • 31. FOLLOW UP AND MONITORING ī‚§ Patients should return for follow up and adjustment of medications until the BP goal is reached. ī‚§ More frequent visits for stage 2 HTN or with complicating comorbid conditions. ī‚§ Serum potassium and creatinine monitored 1–2 times per year. After BP at goal and stable, follow up visits at 3- to 6-month intervals. ī‚§ Co morbidities, such as heart failure, associated diseases, such as diabetes, and the 31
  • 32. HYPERTENSIVE EMERGENCY ī‚§ severe symptomatic hypertension (often defined as systolic blood pressure 180 mmHg and/or diastolic blood pressure 120 mmHg A. Malignant hypertension ī‚§ Is marked hypertension with retinal haemorrhages, exudates, or papilledema ī‚§ Is usually associated with a diastolic pressure above 120 mmHg. B. Hypertensive encephalopathy ī‚§ Refers to the presence of signs of cerebral oedema caused by breakthrough hyper perfusion from severe and sudden rises in blood pressure ī‚§ Characterized by the insidious onset of headache, nausea, and vomiting, followed by non localizing neurologic symptoms such as restlessness, confusion, and, if the hypertension is not treated, seizures and coma 32
  • 33. CONTâ€Ļ īƒ˜ Hypertensive Urgency ī‚§ Severe hypertension (as defined by a diastolic blood pressure above 120 mmHg) in asymptomatic patients. . ī‚§ No evidence of organ damage 33
  • 34. CRISIS(EMERGENCY AND URGENCY) ī‚§ In hypertensive urgency oral agents are used to reduce BP over 24 hour then to target level over two to three months. ī‚§ Captopril 34