2. DEFINITION OF HYPERTENTION
īļ 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:
īĸ Normal blood pressure: systolic <120 mmHg and
diastolic <80
īĸ Prehypertension: systolic 120-139 or diastolic 80-89
īĸ Hypertension:
ī Stage 1: systolic 140-159 or diastolic 90-99
ī Stage 2: systolic >=160 or diastolic >=100
2
3. CONTâDâĻ..
īļ Based on 2017GC guidelines the definition of HTN is
changed:
īĸ Normal blood pressure: systolic <120 mmHg and
diastolic <80
īĸ Elevated: systolic 120-129 or diastolic < 80
īĸ Hypertension:
ī Stage 1: systolic 130-139 or diastolic 80-89
ī Stage 2: systolic >=140 or diastolic >=90
īļ 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. CONTâĻ
īąEpidemiology
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. CONTâĻ
īąMechanism of HTN
o Determinant
ī§ Intravascular volume
ī§ Vascular resistance
īŧ Autonomic nervous System
īŧ Renin -Angiotensin-Aldosterone system
īŧ Vascular system(stiffness/elasticity)
5
6. CONTâĻ
ī§ Intra vascular volume
īŧ Is based on ECF Na+ content
īŧ Slow but its effect lasts long.
īŧ âECF Na+ â â ECF volume â This leads to
âBP 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+.
īŧ If kidney fails or has low sensitivity to pressure
diuresis the BP will remain high to decrease the
Na+ load.
6
7. CONTâĻ
o ANS(SNS)
īŧ For minute to minute control of BP
īŧ Stimulated by baroreflex(carotid & aortic arch)
īŧ Adrenergic neurons(NE and Dopamine) and
adrenal medulla(Epinephrine)
īŧ Act on their receptors(a1,a2,B1,and B2)
7
8. CONTâĻ
o RAAS
īĸ Renin from kidneys(Juxtaglomerlar) is released
in response to ârenal plasma flow, low Na
states.
Renin ACE(lung)
â â
Angiotensinogen (liver)âAngio.I âAngio.II
Angiotensin II : Potent vasoconstrictor, tropics for
adrenal medulla (zona glomerulosa),and
stimulate adrenergic nervous system 8
9. ETIOLOGY OF HTN
ī Essential(idiopathic, primary)
ī§ Accounts 80-95%
ī§ Has no identifiable cause(even though extensive
investigations)
ī Secondary
ī§ Accounts 5-15%
ī§ Causes are known
9
10. CONTâĻ
īEssential HTN
īŧ 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
īĸ Family histroy of hypertension
īĸ Hypertension tends to be both more common and more
severe in blacks
īĸ Evidence for a relationship between sodium intake and
essential hypertension continues to mount
īĸ Multiple studies show a clear association between excess
alcohol intake and the development of hypertension
īĸ Obesity is associated with an increased prevalence and
incidence of hypertension
īĸ Dyslipidemia may also be associated with the
development of hypertension, and is independent of
obesity
īĸ Hypertension may be more common among those with
certain personality traits, such as hostile attitudes and
11
12. COUSE OF SECONDARY HYPERTENSION
ī Renal paranchymal disease
ī Renovascular hypertension
ī Primary aldosteronism
ī Cushingâs syndrome
ī Pheochromocytoma
īMiscellaneous causes of secondary hypertension:
īŧObstructive sleep apnea
īŧCoarctation of the aorta: the most common
congenital cardiovascular cause of hypertension
īŧthyroid diseases and acromegaly
īŧHypercalcemia
īŧHypertension may also be related to a number of
prescribed or over-the-counter medications:
ex.steroids
12
13. DIAGNOSIS OF HYPERTENSION
īĸ Office blood pressure measurement
īŧ Draw backs: white coat and masked hypertensions
īĸ Ambulatory bood pressure measurement
īĸ Home blood pressure measurement
13
14. GUIDELINES FOR THE MEASUREMENT OF BLOOD
PRESSURE TO DIAGNOSE AND TREAT HYPERTENSION
īĸ Allow the patient to sit quietly for 5 minutes before measuring
blood pressure
īĸ No caffeine during the hour preceding the reading and no smoking
during the preceding 30 minutes
īĸ No exogenous adrenergic stimulants, such as phenylephrine in
decongestants or eye drops for pupillary dilatation
īĸ The patient should be seated comfortably with the back supported
and the upper arm bared without constrictive clothing
īĸ The legs should not be crossed
īĸ The arm should be supported at heart level, and the bladder of the
cuff should encircle at least 80% of the arm circumference
īĸ Neither the patient nor the observer should talk during the
measurement
īĸ 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
īĸ For the diagnosis of hypertension, take measurement on atleast two visits
14
15. CONTâDâĻâĻ
âĸ Initially, take blood pressure in both arms; if pressures differ, use
the higher arm
īĸ If the arm pressure is elevated, take the pressure in one leg,
particularly in patients under age 30
īĸ 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
īĸ 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
īŧ 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. CONTâDâĻ..
īŧ 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
īŧ 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. CONTâĻ
īąEffects 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
īŧ Headache, Epitasis, Hematuria
18
19. 1. HEART(HHD) âĻ
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. CONTâĻ
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
īĸ Duration of hypertension
īĸ Previous therapies: responses and side effects
īĸ Family history of hypertension and cardiovascular disease
īĸ Dietary and psychosocial history
īĸ Other risk factors: weight change, dyslipidemia, smoking,
diabetes, physical inactivity
īĸ 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
īĸ Evidence of target organ damage: history of TIA, stroke,
transient blindness; angina, myocardial infarction, congestive
heart failure; sexual function
īĸ Other comorbidities
23
25. WORK UP OF SECONDARY FORMS OF
HYPERTENSION(INDICATED)
25
26. CONTâĻ
ī 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. CONTâĻ
ī 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. CONTâĻ
īGoal of therapy
ī§ BP <130/80 mmHg
ī§ Control other risk factors
īŧBMI, quitting smoking, cholesterol, moderation on
alcohol consumption, and exercise
ī§ Achieve SBP goal especially in persons >50 years of age.
28
29. TREATMENT
īNon pharmacologic
ī§ For all
ī§ Therapeutic life style change
īŧ Modifying diet(DASH plan)
īŧ Exercise
īŧ Secession of smoking
īŧ Moderate alcohol
īŧ Salt restriction
īŧ Wt reduction
29
30. CONTâĻ
īPharmacologic
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
īĸ Diuretics .ARBs
īĸ CCBs .Vasodilators
īĸ 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
1â2 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. CONTâĻ
ī 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