Control of hypertension is of utmost target in clinical practice for the community benefit.. Some little efforts can make big differences..

1. By: Dr./ SAHAR H. MOSTAFA
Consultant of internal medicine
El-MatariaTeaching Hospital-Cairo- Egypt
November,2016

2. Persistent elevation of BP above
normal values ≥ (140 / 90), on three
different occasions, under mental and
physical rest

3. Question: Why above these values..?
Answer:  Because this the value above which the
benefits of treating hypertension(HTN), appear to
outweigh the risks

4.  Normal BP: < (130 / 80)
 Pre-Hypertension: 130 – 139 / 85 - 89
 Hypertension: ≥(140/90)
Normal BP:
<(130 / 80)
Pre-
Hypertension:
130–139/85-89
Hypertension:
≥(140/90)

5. 29 % of the world’s adult population will be
projected to develop hypertension(HTN), by
the year 2025

6. Stages of HTN Systolic BP Diastolic BP
Stage I (mild) 140 – 159 90 – 99
Stage II (moderate) 160 – 179 100 – 109
Stage III (severe) ≥ 180 ≥ 110

7.  Question: when a person’s systolic and diastolic BP fall
into different categories, which stage would be
defined..?
 Answer:The higher one

8.  Focusing on 3 Goals:
• Accurate assessment of BPGoal 1
• Cardiovascular risk
stratificationGoal 2
• Identification of 2ry causesGoal 3

9.  Goals would be achieved through:

10.  Personal History:
• Age
• Smoking
• Alcohol
• Job
 Present History:
• Co morbid disease(diabetes, gout, bronchial asthma, depression, migraine, ..)
• Diet
• Drugs
• Lifestyle
• Ask for 2ry causes
• Search forTOD (target organ damage)
 Past History: Record last BP and last treatment
 Family History:
• Hypertension
• Renal disease
• Premature stroke

12.  Asymptomatic:
HTN may be termed the silent killer
 Alerting symptoms:
Headache, fatigue, blurring of vision, ..

14.  Face
 Pulse
 BMI
 BP
 Chest examination
 Heart examination
 Abdominal examination
 Neurological examination

16.  Face:
Cushingoid ?steroids, ?Cushing’s
Lid edema Nephrotic syndrome
Staring look Thyrotoxic
Bloated Myxedema
Acromegalic Acromegaly

17.  Pulse: ------> Radial
• Equality
• Volume
• Special character
• Femoral: radio-femoral delay in coarctation of aorta
• Trousseau Sign: Carpopedal spasm when BP is increased above
systolic for > 3 min. due to hypokalemia (Conn’s syndrome)

18.  BMI: Normally < 25
BMI = WEIGHT ( Kg) / HEIGHT (m2)
NORMAL 18.5 – 25
OVERWEIGHT 25 – 30
OBESE 30 – 40
MORBID OBESITY > 40

19.  BP:
• Supine: arm same level as heart
• Sitting: back supported, feet on ground
• Standing: after 5 min of standing; to elucidate autonomic
insufficiency, as in:
• Diabetes
• Parkinsonism
• Old age
---------------------------------------------------------
N.B. : At 1st visit, document BP in both arms

20.  Home BP monitoring:
• It engages the patient in his own heath care
• Persistent nocturnal hypertension will increase the BP burden on
cardiovascular system
• The morning surge in BP is associated with increased incidence of stroke,
myocardial infarction as well as sudden cardiac death
• Elimination of over treatment(if the office readings are persistently elevated)
 Ambulatory BP monitoring:
• It measures the time integral BP burden on cardiovascular system
• It also provides better correlation than office readings of BP, especially those
withTOD(target organ damage)
• Prevention of under treatment(if the office readings are less than the
ambulatory ones, due to sympathetic overactivity in daily life)

22. Both Home and ambulatory BP monitoring are useful in:
• Diagnosis of labile hypertension
• Diagnosis of white coat hypertension
• Diagnosis of intermittent hypertension(Fluctuations in
pheochromocytoma)

23.  Chest examination:
• For possible chronic airway obstruction

24.  Heart Examination:
• Sustained apical impulse
• Pulsation at 2nd aortic area(A2)
• Accentuated S1 in left ventricular hypertrophy(LV H)
• S3 gallop, at mitral area in LVH
• S4 gallop, at mitral area in diastolic dysfunction
• Ejection systolic click, at 1st aortic area in sclerotic valve
• Soft Ejection systolic murmur of low intensity, at 1st aortic area(A1) in aortic
valve ring dilatation
• Accentuated aortic component of S2 with wide splitting, at 2nd aortic
area(A2)

26.  Abdominal Examination:
• Renal mass in polycystic kidney disease(PKD)
• Audible bruits in: renal artery stenosis or abdominal aortic aneurysm

28.  Neurological Examination:
• Speech
• Gait
• Reflexes
• Sensory and Motor affections

29.  Routine blood tests:
• Complete blood count(CBC)
• Erythrocyte sedimentation rate(ESR)
• Random blood sugar(RBS) ± Hb A1c
• Blood Urea
• Serum Creatinine
• Serum uric acid
• Liver enzymes(ALT / AST)
• Serum albumin
• Serum lipids(cholesterol and triglycerides)
 Urine analysis (?proteinuria)
 Resting 12- ECG leads ± Ecchocardiography
 Fundus examination
 Renal (ultrasonograhy ± isotope scanning)

33. MAJOR RISK FACTORS
 Age (>55 in males and >65 in
females)
 Cigarette smoking
 Obesity (BMI>30kg/m2)
 Dyslipidemia
 Chronic kidney disease: CKD, with
urine protein: >150 mg/dl and
GFR: <60 ml/min
 Family history of premature
stroke
TARGET ORGAN DAMAGE(TOD)
 Heart:
• left ventricular hypertrophy:
LVH/ or failure: LVF
• Ischemic heart disease: IHD
 Brain:
• Stroke
• Transient ischemic attacks:
TIAs
 Retinopathy: Grade I -to- IV
 Peripheral vascular disease: PVD
 Hypertensive nephrosclerosis

34. Low-risk Group
{ 2 % }
Moderate-risk
Group { 60 % }
High-risk Group
{ 1/3 of cases }
Clinical cardiovascular
disease
No No +
TOD No No +
Risk factors No 1 0r 2
(other than diabetes)
1 or more
(including diabetes or
CKD)
Target BP Control < (140 / 90) < (135 / 85) < (125 / 75)
Treatment Stage I HTN:
Lifestyle
modifications, for up
to 12 months
Stage II or III HTN:
Add medications
•Lifestyle
modifications
•Medications
•Add low-dose aspirin
•Add lipid-lowering
agents
•Lifestyle
modifications
•Medications
•Add low-dose aspirin
•Add lipid-lowering
agents

35. 1ry (Essential) HTN 2ry HTN
Age (years) Young (35-55) <35 -or- >55
Apparent cause No +
Family history + -
Course Benign
(slowly progressive, with long-
term complications
Malignant
(rapidly progressive, with
early complications)

36.  Theories of pathogenesis:
• ↑activity of vasomotor center(VMC)  ↑sympathetic discharge
• ↑activity of adrenals  ↑aldosterone secretion
• ↑cardiac output(COP)  ↑peripheral resistance(PR)
• ↑renin activity
• Insulin resistance and obesity  metabolic syndrome
• Alcohol
• Excess salt intake  Na sensitivity
• Impaired pressure natriuresis
• Impaired baroreceptors  baroreceptor resetting
• Genetic
• Obstructive sleep apnea: OSA

37. Diet
• Liquorice
• Tyramine-rich food
• Chewable tobacco
Drugs
• Corticosteroids / Oral contraceptive pills
• NSAIDs
• Erythropoeitin / Cyclosprine A
• Cocaine / Amphetamine
Renal
• Glomerulonephritis / Interstitial nephritis
• Diabetic nephropathy
• PKD
• Renal artery stenosis
• Obstructive uropathy

38. Blood:
polycythemia
Cardiovascular:
Coarctation of aorta
Neurological:
Increased ICT
Endocrinal
• Cushing’s and Conn’shypokalemic HTN
• Acromegaly
• Pheochromocytoma
• Myxedema
• Hyperparathyroidism
• Hyperthyroidism isolated systolic HTN
• Congenital adrenal hyperplasia

39.  Any hospitalization for urgent or emergent HTN
 Recurrent “flash” pulmonary edema
 Refractory HTN, especially if in a young or after age of 50
 Precipitous worsening of renal function after treatment with
ACE-Is
 Unilateral small kidney by any radiographic study
 Extensive peripheral atherosclerosis
 Flank bruit

40. ?The surgical/ pharmacological reversibility of the 2ry
type of HTN..
 RenalA. stenosis:
• Renal angioplasty for fibromuscular dysplasia
• Renal stenting for bilateral artery stenosis
 Cushing’s:
• Surgical removal of tumor
• Metyrapone
 Acromegaly:
• Trans-sphenoidal hypophysectomy
• Yttrium implantation
 Pheochromocytoma:
• Laparoscopic adrenalectomy
 Coarctation of aorta:
• Surgical repair

41.   When BP is often, but not always, in the hypertensive
range..
It is usually border-line HTN

42.  Cushing’s disease
 Conn’s syndrome
 Renal artery stenosis
 Glucocorticoid-remediable aldosteronism(GRA)
 Liddle’s syndrome
 Bartter’s syndrome
 Gitelman’s syndrome
 Congenital adrenal hyperplasia

43. Plasma aldosterone Plasma renin
Liddle’s syndrome Decreased Decreased
2ry
hyperaldosteronism
(renal artery stenosis)
Increased Increased
Conn’s syndrome Increased Decreased
GRA Increased Decreased

44.   Isolated rise in systolic BP(SBP) with normal diastolic BP
(< 90 mmHg) also called: Isolated systolic hypertension
(ISH)
 Grades:
• Grade I: SBP = 140 – 159 mmHg
• Grade II: SBP = ≥ 160 mmHg
 Causes:
• Fever / anxiety
• Atherosclerosis
• Thyrotoxicosis
• Aortic regurge(AR)
• Coarctation of aorta
• Patent ductus arteriosus(PDA)
• Complete heart block(CHB)

45.   BP ≥ 200 / 120 mmHg
 Classification:
• Hypertensive urgency (accelerated HTN):
o With noTOD
o Gradual control of BP within 24-28 Hs
• Hypertensive emergency:
o In the form of: encephalopathy, LVF, aortic dissection, cerebrovascular stroke,
or malignant HTN
o Micro-angiopathic hemolytic anemia may be present
o TOD is present
o Rapid control of BP within 1-2 Hs, only by 25 % (target BP ~ 160/100)

46.  Patient dialogue and patient
education
▪Lifestyle modifications
Medications

47.  Patient dialogue and Patient education:
• HTN is not episodic and not symptomatic
• Understanding medications cost
• Trying for moderation of life stressful conditions
(home/job)
• Understanding that “almost” control isn’t good enough;
hence the importance to achieve the “target” BP control
• To < (140/90), in low-risk patients
• To < (140/90), in moderate- and high-risk patients

48.  Lifestyle modifications:
• Weight reduction:Target BMI <25 Kg/m2
• Aerobic exercises / RelaxationTechniques(± anxiolytics)
• Avoid Alcohol
• Avoid smoking: Major risk for coronary ischemia, nephrosclerosis
• Moderate dietary Na intake: in processed food as well as salt
shaker, reduce from 10 to 6 gm/d, will show full benefits in 5Wks
• Advise balanced meals:
• Encourage fresh vegetables/fruits(rich in K supplements)
• Allow low-fat dairy milk products and low-fat diet(mainly
of polyunsaturated fatty acids)

50.  Medications:
Some Considerations:
• Use long-acting preparations
• Use combinations (synergism)
• Avoid dose-dependent side effects

51. Drug categories used in HTN:
• Diuretics
• Angiotensin-converting-enzyme inhibitors(ACE- Is)
• Angiotensin-receptor blocker(ARBs)
• Calcium-channel Blockers(CCBs): Dihydropyridines( DHP), and
Non-Dihydropyridines(Non-DHP)
• Beta Blockers(BBs)
• Alpha Blockers
• Alpha and Beta Blockers
• Central Sympatholytics
• Vasodilators

52.  Diuretics:
A. Loop Diuretics:
• Frusemide(Lasix:20, 40mg) ( +Spironolactone= Lasilactone)
• Bumetanide(Burinex:1mg)
• Torsemide(Torseretic:5, 10mg)
B. Thiazides:
• Hydroclorothiazides: HCT(Hydrex:25mg)
• Indapamide(Natrilix:2.5mg)
• Chlorthalidone(Hygroton:50mg)
C. K-sparing Diuretics:
• Spironolactone(Aldactone:25, 100mg) ( +HCT= Aldactazide)
• Amiloride( +HCT= Moduretic:5/50mg)
• Tiamterene( +Xipamide= Epitens:30/10mg)

53. Site and mechanism of
action
Indications in HTN Unwanted Effects
LOOP Block Na+/K+/Cl- transport in
thick ascending limb of loop of
Henle
(Large filtered Na-load)
•HTN with renal
impairment
•HTN with congestive
heart failure
•↓K+ (dose-dependent)
•↓Na+
THIAZIDES Block Na+/Cl- Co-transport in
distal convoluted tubule
(Low-filtered Na load)
•Isolated systolic HTN
(ISH)
•Long-Term treatment
of HTN
•Not if GFR<30 ml/min
•↑blood glucose
•↑plasma lipids
•Precipitate gout
•Erectile dysfunction
K-SPARING Blocking ENac-receptors, in
collecting duct:
•Directly(Triamterene and
amiloride
•Via inhibiting aldosterone
activity on receptors
(Spironolactone)
•Amiloride in Liddle’s
Syndrome
•Spironolactone in:
oConn’s
o2ry
hyperaldosteronism
, as heart failure or
liver cirrhosis
•↑K+
•C.I. in:
oRenal failure
oDiabetes with
↓↓(renin&aldosterone)
•Sexual
dysfunction(spironolactone)
•Painful gynecomastia
(spironolactone)

54.  ACE- Is:
• Captopril(Capoten)
• Enalapril(Ezapril)
• Ramipril(Tritace:1.25, 2.5, 5, 10mg)
• Lisinopril(Sinopril:5, 10mg)
• Fosinopril(Monopril:10, 20mg)
• Quinapril
 ARBs:
• Olmesartan(Erastapex:20, 40mg)
• Valsartan(Tareg:80, 160mg)
• Irbesartan(Approvel:150, 300mg)
• Candesartan(Atacand:8, 16, 32mg)
• Telmisartan(Micardis:40, 80mg)

55. Site and mechanism of action Indications in HTN Unwanted Effects
ACE- Is •Block conversion of angiotensin III
•Block metabolism of bradykinin
•HTN with diabetic
nephropathy(Type1)
•HTN with renal
impairement
•HTN with congestive
heart failure, or LV-
dysfunction
•HTN with
hyperuricemia
•After myocardial
infarction
•Dry cough(bradykinin-
mediatedshift to use ARBs)
•↑K+
•Acute renal failure, in bilateral
renal artery stenosis and in
hypovolemia
•Angioedema(rare)
•Teratogenic
ARBs Block interaction of angiotensin II on
AT1-receptors
•HTN with diabetic
nephropathy(Type2)
•HTN with congestive
heart failure, or LV-
dysfunction
•Acute renal failure, in bilateral
renal artery stenosis and in
hypovolemia
•Angioedema(rare)
•Teratogenic

56.  CCBs:
A. DHPs:
• Nifedipine(Epilat-Retard:20mg)
• Amlodipine(Norvasc:5, 10mg)
• Felodipine(Plendil:2.5, 5, 10mg)
• Nimodipine(Nimotop)
B. Non-DHPs:
• Deltiazem(Altiazem:60, 90, 120mg)
• Verapamil(Isoptin:80, 240mg)

57. Site and mechanism of action Indications in HTN Unwanted Effects
CCBs:
DHPs
Non-DHPs
•Block voltage-gated Ca+ channels, in:
•Cardiac myocytes
•Vascular smooth muscle cells
•Prevention of Ca+influx V.D.
•HTN with stroke
•HTN with dementia
•HTN in elderly,
especially if diabetics
•ISH
•HTN with angina
•DHPs: headache,
flushing and ankle
edema
•Non-DHPs:C.I. in LV
dysfunction and in
heart block
•Both can precipitate
myocardial infarction;
due to ↓BP but with
↑reflex sympathetic
activity(RSA)
•Both have –ve
inotropic effect
•Verapamil causes
severe constipation

58.  Beta Blockers(BBs):
A. Non-cardioselective:
• Propranolol(Inderal:10, 40mg)
• Sotalol(Betacor:80mg)
B. Cardioselective:
• Atenolol(Tenormin:50, 100mg)
• Metoprolol(Betaloc:100mg)
• Bisoprolol(Concor:5, 10mg)
• Nebivolol(Nevilob:5mg)

59. Site and mechanism of
action
Indications in HTN Unwanted Effects
BBs •-ve inotropic
•-ve chronotropic
•↓ COP
•HTN with coronary
ischemia
•HTN with anxiety
•After M.I.
•HTN with CHF
•HTN with
tachyarrhythmia
•Raynaud’s phenomenon
•Bronchospasm
•Hyperglycemia
•Non-selective:
oheart block
oHeart failure
oMask hypoglycemic
symptoms
oNight mares
oDepression

60.  Alpha Blockers:
• Prazosin(Minipress:1, 2mg)
• Doxazocin(Dosin:1, 2mg)
• Terazocin(Itrin)
• Phenoxybenzamine
 Alpha and Beta Blockers:
• Carvedilol(Dilatrend or Carvid:6.25, 12.5, 25mg)
• Labetalol

61. Site and mechanism of action Indications in HTN Unwanted Effects
Alpha
Blockers
Combined
Alpha and
Beta
Blockers
•Alpha-1 blockade: Prazocin,
Doxazosin
•Alpha-1+Alpha-2 blockade:
Phenoxybenzamine
•Vasodilator effect
•Dilatation of urethral smooth
muscles
•Prazocin and Doxazosin
in: HTN with prostatism
•Phenoxybenzamine in:
Preoperative treatment
of pheochromocytoma,
followed by BBs
•Carvedilol in: HTN with
heart failure
Orthostatic hypotension
(Except: Carvedilol)

62.  Central Sympatholytics:
• Alpha-methyl dopa(Aldomet:250, 500mg)
• Reserpine(Brinerdin)
 Vasodilators:
• Hydralazine(Apresoline)

63. Site and mechanism of
action
Indications in HTN Unwanted Effects
Central
Sympatholytics
Stimulation of Alpha-2 receptors
in CNS  ↓Central sympathetic
outflow
Stimulation of Alpha-2 receptors,
presynaptic  Inhibiting NE
release ↓sympathetic drive to
heart and peripheral circulation 
o↓Heart rate
o↓Cardiac Output
o↓Peripheral resistance
Alpha-methyl-dopa
in: HTN with
pregnancy
•Autoimmune hemolytic
anemia
•SLE
•Rebound HTN
•Orthostatic hypotension
•NOT with BBs; for fear of
bradycardia
•C.I. in depression
Vasodilators Opening of ATP/K+ Channels
V.D.
Acute severe HTN
with Pregnancy
•Tachycardia
•Peripheral edema
•Hydralazine:
oIV  ↓↓BP
oOral  SLE

64.  Some Selected Combinations:
• Captopril + HCT Capozide
• Enalapril + HCT Ezapril-Co
• Lisinopril + HCT Sinopril-Co
• Ramipril + HCTTritace-Comb
• Valsartan + HCT Co-Tareg
• Irbesartan + HCT Co-Approvel
• Candisartan + HCT Atacand-Plus
• Bisoprolol + HCT Concor-Plus
• Atenolol + ChlorthalidoneTenodone:50, 100mg
• Atenolol + NifedipineTenolat
• Amlodipine + BenazeprilAlkapress-Plus:5, 10mg
• Amlodipine + PerindoprilCoviram:5/5mg

65.  Consider Some Precautions:
• Initial treatment Low-dose combination therapy, then additional drug
for every 10mmHg(SBP) above the target goal
• Medications-induced sexual dysfunction, as:Thiazides,BBs
• Ankle edema of CCBs (DHPs), can be treated by addition of venodilators as:
ACE-Is or ARBs, not a diuretic
• CCBs, better not to be combined with a diuretic in coronary ischemia
• Grapefruit juice increase bioavailability of CCBs
• BBs shouldn’t be combined with non-DHPs, for fear of bradycardia,
especially in elderly
• NSAIDs and ASA >325mgDecrease effect of ACE-Is based treatment
• Consider HTN in Special Situations

66. YES NO
ACE-Is
(especially in type-1
DM)
Thiazides; because:
High
dosesHyperglycemia
ARBs
(especially in type-2
DM)
BBs; because:
•Mask hypoglycemic
symptoms
•↑Hyperlipidemia
Diuretic (Loop)
CCBs (DHPs)
&/OR
BBs
(cardioselective)

67. YES NO
ACE-Is
(with monitoring)
Thiazides
ARBs
CCBs (DHPs)
BBs
&/OR
Diuretic (Loop)

68. YES NO
CCBs BBs; because:
Alpha receptors ill b
unopposed Severe
V.C.
Carvedilol
Prazosin

69. YES NO
ACE-Is Thiazides
CCBs BBs
Alpha-methyl
dopa

70. YES NO
BBs
(cardioselective)
CCBs
(Except
NifedipineRefl
ex tachycardia
ACE- Is

71. YES NO
ACE- Is CCBs
( -ve
inotropes)
ARBs
Diuretics
BBs
(Cardioselective:
Nebivolol, metoprolol,
bisoprolol)
Alpha & Beta Blocker
(Carvedilol)

72. YES NO
BBs
(Non-selective, which
pass BBB)
CCBs
(Cinnarizine)

73. YES NO
Alpha-methyl dopa ACE- Is
(Teratogenic)
Labetalol ARBs
(Teratogenic)
Atenolol Diuretics
(↓placental blood
flow)
Hydralazine Propranolol
(Fetal bradycardia)
CCBs

74. YES NO
Alpha-methyl
dopa
Diuretics
BBs
Labetalol

75. YES NO
ACE- Is Thiazides
CCBs BBs

76. YES NO
CCBs (DHPs) ACE- Is
ARBs BBs
Diuretics
Alpha & Beta Blockers

77. YES NO
BBs

78. YES NO
Prazocin
Doxazocin
Tetrazocin

79. YES NO
Thiazides BBs
ACE-Is

80. YES NO
CCBs
Thiazides
ACE- Is
ARBs