Hypertension is a major public health problem that significantly increases the risk of heart disease, stroke, and kidney disease. While medications can effectively treat hypertension, lifestyle modifications like following the DASH diet, reducing sodium intake, regular exercise, weight management, and limiting alcohol and tobacco use are important first steps to help prevent and control high blood pressure. The guidelines recommend treating hypertension with medications if lifestyle changes do not lower blood pressure enough, with a goal of reducing blood pressure to under 140/90 mmHg to minimize complications.

1. 1

2. HHyyppeerrtteennssiioonn

3. The Importance of
Hypertension
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4. DDeeffiinniittiioonn ooff BBlloooodd PPrreessssuurree
The pressure exerted by blood against the artery
4
through which it flows
Blood pressure =
cardiac output X systemic vascular resistance
CO X SVR = BP

5. 5
Hypertension is defined as:
 the level of blood pressure lliinnkkeedd wwiitthh aa
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aaddvveerrssee eevveennttss
OR
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bbeenneeffiittss ooff aaccttiioonn ((ii..ee.. tthheerraappeeuuttiicc
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EEvvaannss aanndd RRoossee BBrriitt MMeedd BBuullll 11997711;;2277::3377--4422

6. 6

7. 7

8. 8
Definition of Hypertension
JNC - VII BHS
Normal <120/<80
Prehypertension 120-139/80-89
Stage 1 140-159/90-99
Stage 2 >160/>100
Chobnian JAMA 2003;289:2560
Optimal <120/<80
Normal <130/<85
High Normal 130-139/85-89
Hypertension
Grade 1 140-159/90-99
Grade 2 160-179/100-109
Grade 3 >180/>110
Isolated syst.
hypertension
Grade 1 140-159/<90
Grade 2 >160/<90
Williams BMJ 2004;328;634

9. 9
Definitions ooff hhyyppeerrtteennssiioonn bbyy ooffffiiccee
aanndd oouutt--ooff--ooffffiiccee bblloooodd pprreessssuurree lleevveellss

10. 10
Pulse Pressure
PP = SBP – DBP
Increase in pulse pressure (PP)
indicates greater stiffness in large
conduit arteries, primarily the thoracic
aorta.
PP, therefore, is a surrogate measure
of dynamic, cyclic stress during
systole.
PP may be a better marker of
increased CV risk than either systolic
BP or diastolic BP alone in older
persons.

11. 11
What clinical guidelines are
used to categorize HTN?
The Joint Committee on
Prevention, Evaluation, and
Treatment of High Blood
Pressure (JNC 8) guidelines
provide the most current
guidelines

13. 13

14. 14
JNC 6 Report

15. 15

16. JNC 8 Report
In patients 60 years or over, start treatment in blood pressures
>150 mm Hg systolic or >90 mm Hg diastolic and treat to under
those thresholds. (Strong Recommendation–Grade A)
In patients <60 years, treatment initiation and goals should be
140/90 mm Hg, the same threshold used in patients >18 years with
either chronic kidney disease (CKD) or diabetes. (Expert
Opinion–Grade E)
In nonblack patients with hypertension, initial treatment can be a
thiazide-type diuretic, CCB, ACE inhibitor, or ARB, while in the
general black population, initial therapy should be a thiazide-type
diuretic or CCB. (Moderate Recommendation–Grade B)
In patients >18 years with CKD, initial or add-on therapy should
be an ACE inhibitor or ARB, regardless of race or diabetes status.
(Moderate Recommendation–Grade B)
16

17. 17
Prevalence
>65 million Americans have
hypertension (HTN)
Of those diagnosed with HTN <
50% have their blood pressure
under control
Lack of treatment leads to
serious complications

18. 18
High Prevalence of Hypertension
Worldwide
28
38
42
47 49 49
55
38
60
40
20
0
Italy Sweden England Spain Finland Germany
USA Japan*
Prevalence of hypertension (%)
Adults aged 35–64 y (data are age- and sex-adjusted), except* (adults aged ≥ 30 y)
Hypertension defined as BP ³ 140/90 mmHg or on treatment
Wolf-Maier et al. JAMA. 2003;289:2363-2369;
Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912.

19. 19
Prevalence of Hypertension

20. Proportion of patients in the population (%)
Country Aware Treated Controlled*
Japan 16.0 – 4.1
England 35.8 24.8 10.0
Germany 36.5 26.1 7.8
Spain 38.9 26.8 5.0
Sweden 48.0 26.2 5.5
Italy 51.8 32.0 9.0
USA 69.3 52.5 28.6
20
20
Awareness, Treatment and Control of
Hypertension is Rather Low Worldwide
* BP < 140/90 mmHg
Wolf-Maier et al. Hypertension. 2004;43:10–17;
Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912.

21. 21
BP Control Rates
Trends in awareness, treatment, and control of high
blood pressure in adults ages 18–74
National Health and Nutrition Examination Survey,
Percent
II
1976–80
II
(Phase 1)
1988–91
II
(Phase 2)
1991–94 1999–2000
Awareness 51 73 68 70
Treatment 31 55 54 59
Control 10 29 27 34

22. 22
Awareness, Treatment and
Control of
Blood Pressure 1976-2000
(NHANES)
80
70
60
50
40
30
20
10
0
1976-1980 1988-1991 1991-1994 1999-2000
Awareness
Treatment
Control

23. 23

24. 24

25. 25
Benefits of Lowering
BP
Average Percent Reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%

26. 26
Risk of CV Mortality Doubles With
Each 20/10 mmHg BP Increase
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 y with BP > 115/75 mmHg
• 12.7 million person-years
10
8
6
4
2
0
Fold increase in
relative CV risk
1-fold
2-fold
4-fold
8-fold
115/75 135/85 155/95 175/105
SBP/DBP (mmHg)

27. Each 2 mmHg Decrease in SBP
Reduces CV Risk by 7–10%
7% reduction
in risk of IHD
and other
vascular disease
mortality
27
27
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 y with BP > 115/75 mmHg
• 12.7 million person-years
2 mmHg
decrease in
mean SBP
10% reduction
in risk of stroke
mortality
Lewington et al. Lancet. 2002;360:1903–1913.

28. 28
Preventable CHD Events from Control of
Hypertension in US Adults
(Wong et al., Am Heart J 2003; 145: 888-95)
19
37
31
56
21
11
39
21
60
50
40
30
20
10
0
PAR% / NNT
Men PAR% Women PAR% Men NNT Women NNT
Treatment to <140/90 mmHg Treatment to <120/80 mmHg
PAR% = population attributable risk (proportion of CHD events
preventable), NNT = number needed to treat to prevent 1 CHD event ;
<0.01 comparing men and women for PAR%

29. 29
CVD Risk
 HTN prevalence ~ 50 million people in the United States.
 The BP relationship to risk of CVD is continuous, consistent, and
independent of other risk factors.
 Each increment of 20/10 mmHg doubles the risk of CVD across the
entire BP range starting from 115/75 mmHg.
 Prehypertension signals the need for increased education to reduce
BP in order to prevent hypertension.

30. 30

31. 31

32. 32
Factors contribute to the
development of primary HTN
1. Sympathetic nervous system
hyperactivity
2. Renin-angiotensin-aldosterone system
hyperactivity
3. Endothelial dysfunction

33. 33

34. 34
Types of HTN?
PPrriimmaarryy
• ?? ‘essential’idiopathic
• Most common type
found in 90-95% of
those with HTN
• Cause not well
understood
• Salt sensitive
• RAAS dependent
SSeeccoonnddaarryy
• Caused by some other
medical problem or
condition:
• High-dose estrogen
• Renal artery stenosis
• Pregnancy (PET)
• Cushing’s syndrome
• pheochromocytoma
• Others?

35. 35

36. Renin level ??
36
ABPM ?

37. 37
What are the Symptoms?
Symptoms may or may not be present
• Dizziness (unsteadiness)
• Early morning headache
activity tolerance
• Malaise, fatigue
• Blurring of vision
• Spontaneous nosebleed
• Palpitations, angina, dyspnea
• Early signs/symptoms are often missed

38. 38

39. 39

40. 40

41. 41
BP measurement
Physical assessment
• Height & weight
• Blood pressure
Measuring BP
accurately:
• No smoking or caffeine
30 minutes before
• Rest for 5 minutes prior
to BP
• Apply cuff to bare arm
• Proper size cuff
applied 1 inch above
brachial artery
• Inflate cuff to 30
mmHg above initial
radial pulse check If
BP elevated, wait 2
minutes, recheck
• Check BP in other arm

42. 42
BP Measurement Techniques
Method Brief Description
In-office Two readings, 5 minutes apart, sitting
in chair. Confirm elevated reading in
contralateral arm. 140/90
Ambulatory BP
monitoring
Indicated for evaluation of “white-coat”
HTN. Absence of 10–20% BP
decrease during sleep may indicate
increased CVD risk. 130/80
Self-measurement Provides information on response to
therapy. May help improve
adherence to therapy and evaluate
“white-coat” HTN. 135/85

43. 43

44. 44

45. 45

46. 46

47. 47
White Coat and Ambulatory BP monitoring ABPM

48. 48

49. 49

50.  For persons over age 50, SBP is a more important than DBP as
CVD risk factor.
 Starting at 115/75 mmHg, CVD risk doubles with each increment
of
20/10 mmHg throughout the BP range.
 Persons who are normotensive at age 55 have a 90% lifetime risk
for developing HTN.
 Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be
considered prehypertensive who require health-promoting
lifestyle modifications to prevent CVD.
50
KKeeyy MMeessssaaggeess

51. 51
Key Messages (Continued)
 Thiazide-type diuretics should be initial drug therapy for most,
either alone or combined with other drug classes.
 Certain high-risk conditions are compelling indications for
other drug classes.
 Most patients will require two or more antihypertensive drugs
to achieve goal BP.
 If BP is >20/10 mmHg above goal, initiate therapy with two
agents, one usually should be a thiazide-type diuretic.

52. 52
Key Messages
(Continued)
 The most effective therapy prescribed by the
careful clinician will control HTN only if
patients are motivated.
 Motivation improves when patients have
positive experiences with, and trust in, the
clinician.
 Empathy builds trust and is a potent motivator.
 The responsible physician’s judgment remains
paramount.

53. 53
Complications of HTN
The higher the BP and the
longer an individual has
hypertension, the higher the
risk of complications which
include:
• Hypertensive heart disease
• Cerebrovascular disease
• Peripheral vascular disease
• Kidney disease
• Retinal damage

54. 54

55. 55

56. Complications of Hypertension
Heart
56
 resistance  
workload  left
ventricular
hypertrophy
• CAD, angina, MI
• Heart failure

57. Complications of Hypertension
BBrraaiinn
57
• Atherosclerosis,
stroke

58. Complications of Hypertension
PPeerriipphheerraall vvaassccuullaarr
ddiisseeaassee
58
• Aortic aneurysm or
dissection
RReettiinnaall ddaammaaggee
• damage to blood
vessels of the eye
KKiiddnneeyy ddiisseeaassee
• vessels less elastic
 decreased
perfusion renal
failure

59. 59
Acute Complications
HHyyppeerrtteennssiivvee
CCrriissiiss::
Severe and abrupt
elevation of BP
Diastolic over
120mm hg
High Mortality
Sx: papilledema,
progressive renal
failure,
encephalopathy
Most common
cause is untreated
hypertension
Goal: slowly
decrease BP

60. 60
Classifications
Hypertensive Crisis
Hypertensive crisis is
categorized by the
degree of organ damage
Hypertensive
emergency:
BP is severely elevated
and there is evidence of
target organ damage
• Especially brain
Hypertensive urgency:
BP is elevated but there
is no evidence of target
organ damage

61. GOAL: Reduce Complications
61
JNC 8 guidelines
recommend a
target BP of less
than 140/90
Except elderly
above 60 150/90
Patients with renal
disease or
diabetes need BP
less than 140/90

62. 62
What Reduces Risk of
Complications?
REDUCING MMOODDIIFFIIABBLLEE RRIISSKK
FFACCTTOORRSS IISS A KKEEYY
IINNTTEERRVVEENNTTIIOONN
Goal = Patient teaching to
reduce risk factors
Drug therapy is initiated if
lifestyle changes are not
effective to control BP

63. 63
Management of
Hypertension
Depends on risk group
Lifestyle modifications
Drug therapy is initiated if
lifestyle modifications do not
achieve goal
Add or change drugs if goal not
achieved

64. 64
Lifestyle Modification
Lose excess weight
Cut back on salt
Exercise regularly
Cease alcohol intake
Adopt the DASH eating plan to decrease
cholesterol intake
STOP smoking

65. 65
DASH Diet
http://www.nhlbi.nih.gov/health/public/Dietary Approaches to Stop
Hypertension = DASH
• A diet rich in fruits, vegetables and low-fat
dairy products with reduced fat
content
• Limits sodium intake to 2.4 g/day

66. Non-pharmacologic Management
of Hypertension
Weight management
• DASH
Low sodium-low fat
diet
Smoking cessation
Restrict alcohol and
caffeine
Regular aerobic
exercise
Stress management
• bio-feedback, relaxation,
66
yoga, Tai Chi

67. 67

68. 68
Drug Therapy for HTN
Diuretics
• Flush excess water
and sodium from the
body
• Thiazide diuretics
• Loop diuretics:
furosemide (Lasix)
• Potassium sparing:
Aldactone
Beta adrenergic
blockers
Three classes:
• Cardioselective
• Non-selective
• Combined alpha-beta-
blockers

69. 69
The Majority of Hypertensive Patients Need
Combination Therapy to Achieve BP Goals
1 2 3 4
Average number of antihypertensive medications
Trial (SBP achieved)
ASCOT-BPLA (137 mmHg)
ALLHAT (138 mmHg)
IDNT (138 mmHg)
RENAAL (141 mmHg)
UKPDS (144 mmHg)
ABCD (132 mmHg)
MDRD (132 mmHg)
HOT (138 mmHg)
AASK (128 mmHg)
Bakris et al. Am J Med. 2004;116(5A):30S–38S;
Dahlöf et al. Lancet. 2005;366:895–906.

70. 70
Pharmacologic Management
of Hypertension
Alpha-adrenergic blockers
• Suppress nerve impulses to blood vessels, which
allows blood to pass more easily so BP goes ↓
• prazosin (Minipress)
Calcium channel blockers
• decrease the influx of Ca++ into muscle cells
• Act on vascular smooth muscles (primary arteries) to
decrease spasm and promote vasodilation
• Amlodipine (Norvasc); felodipine (Plendil)

71. 71
Pharmacologic Management
of Hypertension
Angiotensin
converting enzyme
(ACE) inhibitors
• Decrease effect of
RAA system:
Capoten, Lisinopril
• Diabetes mellitus
w/proteinuria, heart
failure
Angiotensin II
receptor blockers
(ARB)
• Prevent action of
angiotensin II and
produce vasodilation
• losartan (Cozaar)

72. Pharmacologic Management of
72
Hypertension
Vasodilators
• Direct arterial
vasodilation
• Sodium nitroprusside
(Nipride)
• Often used in
hypertensive crisis
Alpha-receptor
agonists
• Clonidine
• Acts on central
nervous system
• Lowers peripheral
vascular resistance

73. Why don’t some patients respond
73
to therapy?
Non-adherence to
therapy
• Patients don’t take
their HTN meds →
complications!!!
• Cost, inadequate
teaching, side effects,
inconvenient dosing
Drug related causes
Other conditions
Secondary
hypertension
Volume overload

74. 74
Causes of
Resistant Hypertension
 Improper BP measurement
 Excess sodium intake
 Inadequate diuretic therapy
 Medication
• Inadequate doses
• Drug actions and interactions (e.g., nonsteroidal anti-inflammatory
drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives)
• Over-the-counter (OTC) drugs and herbal supplements
 Excess alcohol intake
 Identifiable causes of HTN

75. 75
Summary Key Points
Two types of HTN: primary & secondary
Inadequate BP control leads to serious
complications including STROKE
Key point: risk factor modification
Treatment focuses on lifestyle management and
drug therapy
JNC 7 provides the most current treatment
guidelines for hypertension

76. 76
Identifiable
Causes of Hypertension
 Sleep apnea
 Drug-induced or related causes
 Chronic kidney disease
 Primary aldosteronism
 Renovascular disease
 Chronic steroid therapy and Cushing’s syndrome
 Pheochromocytoma
 Coarctation of the aorta
 Thyroid or parathyroid disease

77. 77
Pheochromocytoma
0.01-0.1% of HTN population
• Found in 0.5% of those screened
M = F
3rd to 5th decades of life
Rare, investigate only if clinically suspicion:
• Signs or Symptoms
• Severe HTN, HTN crisis
• Refractory HTN (> 3 drugs)
• HTN present @ age < 20 or > 50 ?
• Adrenal lesion found on imaging (ex. Incidentaloma)

78. 78
Pheo: Signs & Symptoms
The five P’s:
• Pressure (HTN) 90%
• Pain (Headache) 80%
• Perspiration 71%
• Palpitation 64%
• Pallor 42%
• Paroxysms (the sixth P!)
The Classical Triad:
• Pain (Headache), Perspiration, Palpitations
• Lack of all 3 virtually excluded diagnosis of pheo in a series of
> 21,0000 patients

79. 79
Pheo: Paroxysms, ‘Spells’
10-60 min duration
Frequency: daily to monthly
Spontaneous
Precipitated:
• Diagnostic procedures, I.A. Contrast (I.V. is OK)
• Drugs (opiods, unopposed b-blockade, anesthesia induction,
histamine, ACTH, glucagon, metoclopramide)
• Strenuous exercise, movement that increases intra-abdo
pressure (lifting, straining)
• Micturition (bladder paraganlgioma)

80. 80
Pheo: ‘Rule of 10’
10% extra-adrenal (closer to 15%)
10% occur in children
10% familial (closer to 20%)
10% bilateral or multiple (more if
familial)
10% recur (more if extra-adrenal)
10% malignant
10% discovered incidentally

81. 81
Plasma Metanephrines
Not postural dependent: can draw
normally
Secreted continuously by pheo
SEN 99% SPEC 89%
False Positive: acetaminophen
Assay not widely available yet

82. 82
Localization: Imaging
CT abdomen
• Adrenal pheo SEN 93-100%
• Extra-adrenal pheo SEN 90%
MRI
• > SEN than CT for extra-adrenal pheo
MIBG Scan
• SEN 77-90% SPEC 95-100%

83. 83

84. 84
Renovascular Hypertension

85. 85

86. 86
Endocrine Hypertension
Catecholamine producing tumours
Mineralocorticoid hypertension
Renin-dependent hypertension
Hyperthyroidism and hypothyroidism
Acromegaly
Hyperparathyroidism

87. 87
Typical clinical scenarios
Difficult hypertension with hypokalaemia,
on polypharmacy- referred to
endocrinologist for exclusion of 2ary
hypertension
Coincidentaloma of adrenal with
hypertension, on polypharmacy
Which drugs are permissible, and after how
much delay should there be before
investigation?

88. 88

89. Mineralocorticoid hypertension- in
whom should it be suspected?
Diagnosis should be suspected in patient with
hypertension, spontaneous hypokalaemia
(<3.5mmol/l), and alkalosis.
Severe hypokalaemia (<3.0) on diuretics
Investigate patient hypertension refractory to
conventional therapy, or adrenal coincidentaloma
Recent onset of hypertension
Normokalaemia present in >35% patients on low
salt diet
89

90. 90
Clinical features of
hyperaldosteronism
Mild to severe hypertension
Sodium retention + intravascular vol exp
®mineralocorticoid escape
Resetting of osmostat (thirst provoked at higher [Na+])
K+ loss (kaliuresis) +/- low serum K+ (unprovoked: rule out
diuretics, laxatives, vomiting, herbal supplements)
Suppression of renin generation (rule out drugs,excessive
dietary sodium intake)
Polyuria, nocturia,fatigue,cramps, Mg++↓
Exclude liquorice abuse / carbenoxolone therapy
NB minor mineralocorticoids DOC, compound B

91. Imaging in 1ary hyperaldosteronism
High resolution CT scanning with thin (2-3mm)
slices
Bilateral adrenal venous catheter (measure cortisol,
adrenaline + aldosterone) remains gold standard –
operator dependent: right adrenal notoriously
difficult to cannulate. Give iv ACTH (2μg/min)
during sampling to magnify difference between
tumour and non-tumorous side
Non-tumorous side PAC = peripheral value
because of suppressed PRA
91

92. Glucocorticoid remediable
hyperaldosteronism GRA (FH1)
Due to aberrant expression of chimeric gene
formed by unequal recombination of promoter
and initial parts of CYP11B1 and section of
CYP11B2 with aldosterone synthase activity
Aldosterone under ACTH control
Autosomal dominant: FH of early onset BP↑ with
CVA ,K+↓
High levels of 18-hydroxy and 18-oxocortisol
Rx : chronic administration of low dose GC,
spironolactone, or amiloride
92

93. 93
Liddle syndrome
Familial BP↑, unprovoked K+↓, PRA↓, and
undetectable PAC
Autosomal dominant, caused by constitutive
activation of distal renal epithelial sodium
channel (β,γ C-terminal subunit mutations
prevent trafficking of channel)
Treated by amiloride

94. 94
Liddle's – low renin, low aldo
Licorice and SAME -- low renin, low aldo
Renal artery stenosis and renin-secreting
tumors -- high renin, high aldo
Adrenal hyperfunction -- low renin, high
aldo

95. 95
Renin Aldo
Liddle low low
Licorice low low
RAS high high
Conn’s low high

96. 96
Renin-Angiotesnin-
Aldosterone System
A drop in BP or blood
volume causes kidneys to
secrete rreenniinn, a
precursor to
angiotensin I
Angiotensin-converting
enzyme turns
aannggiiootteennssiinn II iinnttoo
aannggiiootteennssiinn IIII,, a potent
vasoconstrictor
Stimulates adrenal
glands to release
aallddoosstteerroonnee
This prompts the
kidneys to retain sodium
and water
The increased volume
and vasoconstriction
raise BP

97. 97

98. 98