This document discusses hypertension (high blood pressure) including: - Classifications of blood pressure and treatment approaches based on blood pressure levels. - Methods for measuring blood pressure. - Risk factors and complications of hypertension. - Types of hypertension including essential, secondary, malignant, and white coat hypertension. - Mechanisms involved in blood pressure regulation. - Lifestyle modifications and pharmacological treatments for lowering blood pressure.

1. HYPERTENSION
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2. BP classification
BP Classification SBP mmHg* DBP mmHg
Lifestyle
Modification
Drug
Therapy**
Normal <120 and <80 Encourage No
Prehypertension 120-139 or 80-89 Yes No
Stage 1
Hypertension
140-159 or 90-99 Yes
Single
Agent
Stage 2
Hypertension
≥ 160 or ≥ 100 Yes Combo
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3. BP RECORDING
Method Brief Description
In-office
Two readings, 5 minutes apart. Sitting in chair.
Confirm elevated reading in contralateral arm.
Self-measurement
Provides information on response to therapy.
May help improve adherence to therapy and
evaluate “white-coat” HTN.
Ambulatory BP
monitoring
Indicated for evaluation of “white-coat” HTN.
Can be used to confirm self-measurement when
inconsistent with in-office measurement.
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4.  Risk factors
 Hypertensive and normotensive
 Complications of hypertension
 Myocardial infarction
 Stroke
 Hypertensive encephalopathy
 Dissecting aortic aneurysem
 Hypertensive nephrosclerosis
 Peripheral vascular disease
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5. Types
1. Essential hypertension: genetic
factors
2. Secondary hypertension
 Renal disease
 Endocrine disease: Conn’s
syndrome (hyperaldosteronism),
Cushing’s syndrome
(hyperglucocorticoidism)
 Vascular disease: renal artry
stenosis, coarctation of aorta 11/14/2022
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6. 3. Malignant hypertension
 Accelerated hypertension is characterized by
greatly elevated BP with evidence of vessel
damage.
 Damage to optic fundus
 Renal damage: haemeturia, proteinuria and
impaired renal function
 Hypertensive encephalopathy: confusion,
headache, visual loss and coma.
4. White coat hypertension
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7. Regulation of BP
 MAP is the average of blood pressure over a cardiac
cycle and is determined by the cardiac output
(CO), systemic vascular resistance (SVR), and central
venous pressure (CVP)):
 MAP= CO × SVR
 Baro receptor reflex
 NO
 ANP
 Bradykinin,
 ADH,
 Endothelins-vasoconstriction-
bosentan, sitaxentan or ambrisentan.
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 Bradykinin is an inflammatory mediator. It is
a peptide that causes blood vessels to dilate
(enlarge), and therefore causes blood
pressure to fall.
 ACE inhibitors, which are used to lower blood
pressure, increase bradykinin (by inhibiting its
degradation), further lowering blood pressure.
Bradykinin dilates blood vessels via the
release of prostacyclin, nitric oxide,
and Endothelium-Derived Hyperpolarizing
Factor.

10. Management of hypertension
 Diagnosis of BP
 Assessment of hypertensive patient can be
done by physical examination of patient eg
abdominal bruits, palpable kidneys.
 Lab analysis
 Contributory factors: salt intake, smoking,
alcohol, obesity etc
 End organ damage: examination of optic fundi
to detect retinal changes, ECG analysis.
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11. BP Classification SBP mmHg* DBP mmHg
Lifestyle
Modification
Drug
Therapy**
Normal <120 and <80 Encourage No
Prehypertension 120-139 or 80-89 Yes No
Stage 1
Hypertension
140-159 or 90-99 Yes
Single
Agent
Stage 2
Hypertension
≥ 160 or ≥ 100 Yes Combo
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12. Life style
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13. Impact of a 5 mmHg Reduction
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14. Treatment
 Nonpharmacological
 Pharmacological
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15. Dietary Approaches to
Stop Hypertension
 Lowers systolic BP
 in normotensive
patients by an
average of 3.5 mm
Hg
 In hypertensive
patients by 11.4 mm
Hg
http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/
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16. Pharmacological treatment
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18. Class Examples Major adverse
effects
Notes
Diurteics Thiazide, loops Hypokalemia,
gout, glucose
intolerance,
uremia,
dehydration
Cheap, , long term
metabolic effects,
especially for elderly and
patient that had cardiac
failure. first line therapy
β-blockers Atenelol,
propranolol,
metoprolol
Tiredness, reduced
exercise tolerance,
bradycardia,
wheezing, cardiac
failure, impotence
Cheap, effective,
adverse effects common,
first line therapy
Calcium
antagonists:
dihydroperidine
s
Nifedipine,
amolodipine
Flushing, edema,
postural
hypotension,
headache
More expensive, not well
tolerated, low incidences
of MI and stroke, used
for patient with ischemic
heart disease or
diabetes
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19. Class Examples Major adverse
effects
Notes
Calcium channel
antagonists
Veapamil,
diltiazem
Bradycardia, heart
block
Well tolerated, for
patient who cant
tolerate β
blockers. Caution
needed when
used with β
blockers
ACE inhibitors Captopril, enalpril,
lisinopril, ramipril
Cough, rash, taste
disturbance, renal
failure,
angioedema
Expensive, cough,
limit to those with
diabetes and
cardiac failure.
Angiotensin II
antagonists
Losartan ,
valsartan
irbesartan
Renal failure,
headache
More expensive,
especially for
patients in whom
ACE inhibitor
indicated is not
tolerated.
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20. Class Examples Major adverse
effects
Notes
α blockers Prazocin,
doxazocin
Edema, postural
hypotension
More expensive, adv
effects common, long
term efficacy is poor,
less effective than
thiazide in preventing
heart failure and
combined
cardiovascular out
comes. Second line
Centrally acting
vasodilators
Methyl dopa,
moxonidine
Tiredness,
depression
Poorly tolerated, used
in severe
hypertension, third
line
Direct acting vaso
dilators
Monoxidil,
nitro
prusside,
Edema, postural
hypotension ,
headache
Poorly tolerated. used
in severe
hypertension, third
line
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21. Thiazide Diuretics
• Drug of choice for last 3 decades
• Normotensive: no effect
• Mechanism: inhibit Na- /K/Cl- pumps in the distal tubule
• Examples: Hydrocholorthiazide 12.5-25 mg daily, Chlorthalidone 12.5-50 mg daily
• Reduces plasma and ECF vol.
• Compensatory mechanisms develop.
• Fall in BP is maintained by slowly developing reduction in tpr.
• BP fall happens over 4 weeks (10 mm Hg). Chronic treatment has no effect on CO or HR,
but tpr is reduced.
• No postural hypotension.
• Effective first line agent and provides synergistic benefit
• As single agent more effective (in 30% cases)
• Uses- Edema, HT, Dibetes insipedus, Hypercalciurea.
• Contra- Diabetes, Hypokalemia, Hearing loss, Hyperuricaemia.
• Not useful in low GFR pateints

22. Loop diuretics
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 Furosemide: strong diuretic but weaker
antihypertensive than thiazide.
 Short duration: 4-6.
 The tpr is not reduced.
 Electrolyte imbalance
 Indicated in hypertension when thiazide are
ineffective, CHF is present, resistance in co
regime, marked fluid retention.

23. Advantages of diuretics
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 Once a day dosing
 No fluid retention
 Low postural hypotension
 Low cost

24. Disadvantages
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 Hypokalemia
 Carbohydrate intolerance
 hyperlipedemia
 Hyperuricaemia
 Dose dependent increase risk of death

25. Diuretic treatment for
hypertensives
 Elderly
 Low renin
hypertension
 Systolic BP
 Obese
 Renal disease with
Na+ retention
 Low cost
 Young active
 Diabetic
 Gout or family
history of gout
 Abnormal lipid
profile
 Pregnancy induced
hypertension
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Suitable for To be avoided

26. Beta blockers: With/without internal
sympathomimetic activity
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 Mild hypertensives
 Effect is maintained over 24 hrs
 Nonselective (β1+ β2)
 Without intrinsic sympathomimetic activity eg
propranolol, sotalol, nadolol and timolol.
 Some blockers exhibit internal sympathomimetic
activity eg oxprenolol, pindolol and alprenolol.
 With additional α blocking property: Labetalol
 Cardioselective (β1): atenolol, metoprolol,
acebutolol

27. Effect on heart
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B1 selective
Without sympathomimetic activ
Rate, force, C.O, CHF, O2, ang
With sympathomimetic activity,
bradycardia is not seen

28. Effect on blood vessels
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B1 selective
Without sympathomimetic activity
(Re reversal of vasomotor reversal),
Increased TPR ,
With sympathomimetic activity

29. Effect on respiratory tract/
bronchi
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Ppnl contraindicated

30. Metabolic effects
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 Effect on lipid metabolism: Ppnl blocks
lipolysis
 Effect on blood glucose: Ppnl inhibits
glycogenolysis, long-term induces
carbohydrate intolerance by reducing insulin
release

31. Disadvantages: prototype-Ppnl
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 Can precipitate CHF
 Can complicate asthma
 Worsens chronic obstructive lung disease
 Plasma lipid profile is altered on long term use
 Carbohydrate tolerance is impaired in prediabetics
 Withdrawal should be gradual
 Is contraindicated in sick sinus or partial heart
block
 Cold hands and feet worsening of peripheral
vascular disease
 Night mares, forgetfulness and rarely
hallucinations

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 Ppnl: well absorbed after oral administration,
but has low BA due to high first pass
metabolism in liver. Lipophilic and penetrates
into brain.T1/2: 3-6 hrs
 Dose: 10 -160 mg BD

33. Cardioselective beta blockers
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 Atenolol, metoprolol, acebutolol
 More specific for β1 than β2.
 Less interference with carbohydrate
metabolism,
 Low incidence of cold hands and feet
 No deleterious effect on blood lipid profile
 Less liable to impair exercise capacity.

34. Acting on both alpha and beta
receptor
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 Labetalol
 There are 4 stereoisomers of labetalol each of
which has a distinct profile of action on subtypes α
and β receptors.
 Agonist on β 2, antagonist on β1and α1.
 It has 1/3 less potency than Ppnl for β1and 5 times
more potent in blocking β than α.
 It has less agonistic activity on β1 but is β 2 agonistic
activity.
 Side effect is postural hypotension.
 Start with 50 mg BD

35. Alpha blockers
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 egs Prazosin, Terazosin
 It is a competitive antagonist of α1 receptor.
 Dilates both resistance and capacitance vessels.
 Initiating dose is 0.5 mg at bedtime followed by 10 mg
(max). An oral dose produces peak fall in BP after 4-5
hrs and effect lasts for 12 hr.
 It improves carbohydrate metabolism
 Has favorable effect on lipid profile
 Helps left ventricular failure by reducing preload and
afterload.

36. Beta adrenergic blockers
 Angina or post MI
 Co-existing
tachycardia
 Tense young patients
 Non obese, high renin
hypertensive
 Low cost
 pregnancy
 CHF
 Bradycardia
 Asthma
 Diabetic
 Abnormal lipid
profile
 elderly
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Suited for To be avoided

37. Combinations of beta blockers with
diuretic
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 Atenolol-chlorthalidone (50/25, 100/25) Tenoretic
 Bisoprolol-hydrochlorothiazide (2.5/6.25, 5/6.25,
10/6.25) Ziac
 Metoprolol-hydrochlorothiazide (50/25, 100/25)
Lopressor HCT
 Nadolol-bendroflumethiazide (40/5, 80/5) Corzide
 Propranolol LA-hydrochlorothiazide (40/25, 80/25)
Inderide LA
 Timolol-hydrochlorothiazide (10/25)

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 Symp blockers
 Renin inhibitory peptides
 ACE inhibitors
 AT1 antagonist
 Aldosterone antagonists

40. Angiotensin inhibitors
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 First choice in all grades of essential hypertension
 20% of high BP cases has high plasma renin
 ACE inhibitors: Captopril, enalapril, lisinopril etc.
 They mainly act by inhibiting the peripheral
resistance.
 Does not have any sympathomimetic activity.
 Used in nephropathy (with or with out BP).
 Captopril dose : 75-150 mg tab, T1/2: 2.2, BA:
65%.
 Enalpril T1/2: 11hrs, lisinopril T1/2: 12 hr

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 Severe hypotension may occur in patients with
hypovolemia,
 hyperkalemia,
 dry cough
 rashes
 Contraindicated in pregnancy due to
hypotensive effect on fetus, anuria and renal
failure.

42. Angiotensin receptor inhibitors
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 Losartan and Valsartan were the first marketed
blockers of AT1 receptors.
 Candesartan, eposartan, telmisartan,
irbesartan
 They do not have any effect on bradykinin.
 More selective for angiotensin effects than
ACEI.
 Side effects similar as ACEI
 Dose : losartan: 50mg/day. Peak effect at 3-6
weeks.

43. Treatment choice
 High renin release
 Young pateints
 Diabetes
 Angina and post MI
cases
 CHF
 gout
 Renal stenosis
 Pregnancy
 High salt intake
 With diuretic therapy
 Preexisting dry
cough
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Suited for
Avoided

44. Calcium Channel blockers
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 They decrease peripheral resistance.
 No effect on heart.
 Onset is quick.
 Monotherapy is effective
 Do not impair physical capacity.
 No sedation or other CNS effect.
 Not contraindicated in asthma, angina.
 Do not affect male sexual function.
 No deleterious effect on plasma lipid profile
 No effect on fetus.
 Tend to increase HR and CO by reflex mechanism
 Nifidipine exhibits short half life therefore used for emergency
treatment

45. Vasodilators
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 Hydralazine, diazoxide, minoxidil
 Vasodilatation , reduces TPR, significant
decrease in diastolic BP,
 Reflex rise in BP observed.
 Hydralazine, Well absorbed orally, peak occurs
in 1-2 hrs. Hypotensive effect lasts for 12 hrs

46. Special patient groups
 Diabetes: ACE inhibitors along with calcium
channel blockes, β blockers, α blockers and
thiazides.
 Target BP < 130/80 or 125/75 < in diabetic
nephropathy.
 Renal disease: ACE Inhibitors, diuretics should
not be used.
 Pregnancy: Pre-eclampsia, BP above 135/85
 Drugs contraindicated: diuretics, ACE Inhibitors,
Reserpine, Non Selective β Blockers: Ppnl
 Safer drugs: Hydralazine, methyldopa,
dihydropyridine CCB, prazosin, clonidine,
atenolol, pindolol
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47. Treatment for hypertensive
management
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 Admission to ICU
 Continuous recording of BP, bodyweight and
fluid intake and output.
 Parental preparations are used to lower BP
(within few hrs) followed by oral
antihypertensive therapy.
 Sodium nitroprusside, nitroglycerin, labetalol,
calcium channel blockers, hydralazine.