2. Overview
Blood pressure measurement
Definition of hypertension
Epidemiology
Mechanism & etiology
Effects of Hypertension
Approach to patients with hypertension
Management of Hypertension
3. BP Measurement
Use auscultatory method with a properly calibrated and validated
instrument.
Patient should be seated quietly for 5 minutes in a chair
(not on an exam table), feet on the floor, and arm supported at heart
level.
Appropriate-sized cuff should be used to ensure accuracy.
At least two measurements should be made.
Clinicians should provide to patients, verbally and in writing, specific BP
numbers and BP goals.
4. BP Measurement Techniques
Method Brief Description
In-office Two readings, 5 minutes apart,
sitting in chair. Confirm elevated
reading in contralateral arm.
Ambulatory BP
monitoring
Indicated for evaluation of “white-
coat” HTN. Absence of 10–20% BP
decrease during sleep may indicate
increased CVD risk.
Self-measurement Provides information on response to
therapy. May help improve
adherence to therapy and evaluate
“white-coat” HTN.
5. Blood Pressure Classification(JNC 7)
Normal <120 and <80
Prehypertension 120–139 or 80–89
Stage 1
Hypertension
140–159 or 90–99
Stage 2 Hypertension >160 or >100
BP Classification SBP mmHg DBP mmHg
6. European society of HTN
BP classification Systolic Diastolic
Optimal <120 <80
Normal 120-129 80-84
High normal 130-139 85-89
HTN Grade 1 140-159 90-99
Grade 2 160-179 100-109
Grade 3 >180 >110
Isolated systolic HTN >140 <90
8. Epidemiology
HTN is the most prevalent risk factor for
cardiovascular diseases (CVD).
~30 % at age >18 yr;> 50 % at age >60.
As age increases SBP increases but diastolic BP tends
to decrease after age 55 resulting in wide pulse
pressure & isolated systolic HTN
BP is greater for males until menopause.
9. Ethiopia
Addis Ababa
32 % male and 30% female adults with BP >140/90 or
on anti hypertensive.
20 % of males and 38% females are overweight.
10. Mechanisms of HTN
Determinants of BP
Intravascular volume
Autonomic nervous System
Renin -Angiotensin-Aldosterone sytem
Vascular system(stiffness/elasticity)
11. Intravascular volume
Is based on ECF Na content
Slow but its effect lasts long.
↑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.
If kidney fails or has low sensitivity to pressure diuresis
the BP will remain high to decrease the Na load.
12. Adrenergic system
For minute to minute control of BP
Stimulated by baro reflex(carotid & aortic arch)
Includes :adrenergic neurons(mainly NE &dopamine)
& adrenal medula(mainly epinephrine)
Receptors :
Receptors Sites Effects
ά1 Vas sm muscle Constriction
ά2 Presynaptic
neurons
Decrease release
of NE-
Vasodilattion
β1 Cardiac muscle ↑contarction & HR
β2 Vasc sm mus vasodilatation
13. Renin-angiotensin-aldosterone
Renin from kidneys(Juxtaglomerlar & macula densa) is
released in response to↓ renal plasma flow, low Na states.
Renin ACE(lung)
↓ ↓
Angiotensinogen(liver)→Angio.I →Angio.II
Angiotensin II :potent vasoconstrictor, trophic for adrenal medula
(zona glomerulosa),& stimulate adrenergic nervous system
14. Etiology of HTN
Based on extent of investigation HTN in about 80-95%
has no identifiable cause
Essential/Idiopathic/Primary HTN
• 5-15 % etilogy can be identifed
Secondary hypertension
Essential HTN
tends to be familial and is likely to be the consequence
of an interaction between environmental and genetic
factors
15. Risk factors for essential HTN
Age, family history, race
Obesity, metabolic syndrome, insulin, dyslipidemia,
resistance
Alcohol intake
Diet :excess salt intake
Certain personality trait(hostile attitudes and time
urgency/impatience )
16. Identifiable
Causes of Hypertension
Renovascular disease: most common secondary cause.
Sleep apnea
Drug-induced or related causes
Chronic kidney disease
Primary aldosteronism
Chronic steroid therapy and Cushing’s syndrome
Pheochromocytoma
Coarctation of the aorta
Thyroid or parathyroid disease
17. Effects of HTN
Target organs : brain, Heart, kidney & peripheral
vessels. They are directly related to increased risk of
atherosclerosis or direct effect of the elevated BP.
Genetic , racial factors, presence of other CVD risk
factors & control of the HTN influence development of
Target organ damage(TOD).
18. Clinical presentation:
Most patients are asymptomatic : diagnosed on
routine evaluation or when they come for other
illnesses
Others come with symptoms or signs of TOD
Few will come sxs directly related to elevated BP
Headache
Epistaxis, hematuria
19. Effects of Hypertension.
1. Heart→HHD
Heart disease is the most common cause of death in
hypertensive patients.
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.
21. Effects ...
3 .Kidney leads to glomerulosclerosis & tubular
ischemia & atrophy.
Primary renal disease is the most common etiology of
secondary hypertension. Conversely, hypertension is a
risk factor for renal injury and ESRD
22. Effects….Renal
Renal risk appears to be more closely related to systolic
than to diastolic blood pressure, and black men are at
greater risk than white men for developing ESRD at
every level of blood pressure.
Clinically albuminuria is early marker of renal injury
24. Patient Evaluation
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.
26. Laboratory Tests
Routine Tests
• Blood glucose
• Lipid profile, after 9- to 12-hour fast, that includes high-density and
low-density lipoprotein cholesterol, and triglycerides
• serum potassium, hematocrit
• Urinalysis
• Serum creatinine
• Electrocardiogram
Optional tests
• Measurement of urinary albumin excretion or albumin/creatinine ratio
More extensive testing to identify secondary forms is not generally
recommended unless indicated
27. Patient profile
Determine Stage of HTN
For the stage of HTN determine the presence and/or
absence of associated risk factors
Determine presence or absence of TOD/associated clinical
condition
Based on the findings decide on the nature of treatment of
the HTN and other risk factors and plan the follow up
Set goal of the treatment
28. Who should be treated?
Those with BP levels known to cause risk
Levels of BP known to expose to risks are different in
different conditions
Stratification of patients and their risk profile need
definition
29. Goals of Therapy
Uncomplicated hypertension BP <140/90 mmHg
Hypertension with risks other than diabetes <140/90
Hypertension with diabetes BP <130/80 mmHg
Hypertension with chronic kidney disease, CVD, CAD, PVD BP
<130/80
Control other risk factors
BMI, quitting smoking, cholesterol, moderation on alcohol
consumption, and exercise
Achieve SBP goal especially in persons >50 years of age.
30. Treatment
A. Non pharmacologic
Indicated for all hypertensive
Include: -Therapeutic life style change(TLC)
-Modification of diet
-Exercise
31. Lifestyle Modification
Modification Approximate SBP reduction
Weight reduction 5–20 mmHg/10 kg weight loss
Adopt DASH eating
plan
8–14 mmHg
Dietary sodium
reduction
2–8 mmHg
Physical activity 4–9 mmHg
Moderation of alcohol
consumption
2–4 mmHg
32. Physical activity
Increase gradually to 30 minutes brisk walking or
cycling Salt - < 5 gm (1 teaspoon) a day
DIET
Fruits and vegetables
5 servings of fruit and vegetable
1 serving – 1 banana or apple, orange, mango
33. Diet….
Fatty Food
Limit fatty meat, dairy fat replace with chicken
Cooking oil to less than 2 tablespoon
Avoid palm or coconut oil
Replace with olive, soya, corn, safflower oil
Eat fish
Avoid heavy alcohol
Men 2 or less drinks
Women 1 or less drinks
35. Life style management
If found effective in controlling HTN, life style
intervention should be re-enforced
If life style is in-effective drug (s) should be added
Drug choices made
Other risk factors managed
36. B. Pharmacoogic trea....
Indicated for those failed to achieve goal BP after 2-3
months of TLC .
At beginning in those with hypertensive crisis OR in
those with TOD & BP not in target.
39. Initial drug choice
In the absence of compelling evidences
Least expensive of the following
Thiazide
Calcium channel blockers (SR-formulations)
Beta-blockers
ACEI/ARBs
40. Compelling evidence for the use of specific drugs
Compelling indications Preferred drug
Elderly, SH Diuretic, calcium channel blocker
Renal disease –diabetic
nephropathy
- non-diabetic
ACEI
Cardiac diseases
-Post MI
- Angina
- LV dysfunction
- CHF
-LVH
-Cerebro-VD
ACEI
B-blocker
B-Blocker
B-blocker, ACEI, ARB, Diuretic,
aldactone
ARB
ACEI, DIURETIC
41. Algorithm for Treatment of Hypertension
Not at Goal Blood Pressure (<140/90 mmHg)
(<130/80 mmHg for those with diabetes or chronic kidney disease)
Initial Drug Choices
Drug(s) for the compelling
indications
Other antihypertensive drugs
(diuretics, ACEI, ARB, BB, CCB)
as needed.
With Compelling
Indications
Lifestyle Modifications
Stage 2 Hypertension
(SBP >160 or DBP >100 mmHg)
2-drug combination for most (usually
thiazide-type diuretic and
ACEI, or ARB, or BB, or CCB)
Stage 1 Hypertension
(SBP 140–159 or DBP 90–99 mmHg)
Thiazide-type diuretics for most.
May consider ACEI, ARB, BB, CCB,
or combination.
Without Compelling
Indications
Not at Goal
Blood Pressure
Optimize dosages or add additional drugs
until goal blood pressure is achieved.
Consider consultation with hypertension specialist.
42. Followup and Monitoring
Patients should return for followup and adjustment of
medications until the BP goal is reached.
More frequent visits for stage 2 HTN or with complicating
comorbid conditions.
Serum potassium and creatinine monitored 1–2 times per year.
43. Followup and Monitoring
(continued)
After BP at goal and stable, follow up visits at 3- to 6-month
intervals.
Co morbidities, such as heart failure, associated diseases, such
as diabetes, and the need for laboratory tests influence the
frequency of visits.
44. Hypertensive emergencies
A.Malignant hypertension — is marked hypertension
with retinal hemorrhages, exudates, or papilledema . – is
usually associated with a diastolic pressure above 120
mmHg.
B.Hypertensive encephalopathy refers to the presence of
signs of cerebral edema caused by breakthrough
hyperperfusion from severe and sudden rises in blood
pressure
characterized by the insidious onset of headache, nausea,
and vomiting, followed by nonlocalizing neurologic
symptoms such as restlessness, confusion, and, if the
hypertension is not treated, seizures and coma
45. Hypertensive urgency
. — Severe hypertension (as defined by a diastolic
blood pressure above 120 mmHg) in asymptomatic
patients. .
No evidence of organ damage
46. Management of hypertensive crisis
The initial aim of treatment in is to rapidly lower the
diastolic pressure to about 100 to 105 mmHg by
parenteral agents; within two to six hours, with the
maximum initial fall in BP not exceeding 25 percent of
the presenting value .
Once the BP is controlled, switch to oral therapy, with
the diastolic pressure being gradually reduced to 85 to
90 mmHg over two to three months.
In hypertensive urgency oral agents are used to reduce
BP over 24 hour then to target level over two to three
months.
47. Black Populations
In general, treatment is similar for all demographic groups.
Socioeconomic factors and lifestyle important barriers to BP
control.
Prevalence, severity of HTN increased in African Americans.
African Americans demonstrate somewhat reduced BP
responses to monotherapy with BBs, ACEIs, or ARBs compared
to diuretics or CCBs.
These differences usually eliminated by adding adequate doses
of a diuretic.
