Hypertension is defined as high blood pressure that is linked to increased long-term health risks. The document discusses guidelines for classifying blood pressure levels and outlines the prevalence, awareness, treatment, and control of hypertension worldwide. It also summarizes the risks and complications of hypertension if left untreated, including heart, brain, kidney, and eye damage, and emphasizes the importance of lifestyle modifications and drug therapy to reduce complications.

1. 1

2. Hypertension

3. Definition of Blood Pressure
The pressure exerted by blood against the artery
through which it flows
Blood pressure =
cardiac output X systemic vascular resistance
CO X SVR = BP
3

4. Hypertension is defined:
 As the level of blood pressure
linked with a doubled increased
long-term risk for adverse events
OR
Hypertension is ... “the level of
blood pressure at which the
benefits of action (i.e. therapeutic
intervention) exceed those of
inaction.”
4
Evans and Rose Brit Med Bull

5. 5

6. 6

7. Definition of Hypertension
JNC - VII BHS
Normal <120/<80 Optimal <120/<80
Prehypertension 120-139/80-89 Normal <130/<85
Stage 1 140-159/90-99 High Normal 130-139/85-89
Stage 2 >160/>100 Hypertension
Chobnian JAMA 2003;289:2560 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
7

8. What guidelines are used to
categorize HTN?
The Joint Committee on Prevention,
Evaluation, and Treatment of High
Blood Pressure (JNC 7) guidelines
provide the most current guidelines
http://www.nhlbi.nih.gov/hbp/detect/categ.htm
8

9. 9

10. JNC 6 Report
10

11. 11

12. 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
12

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

14. Prevalence of Hypertension
14

15. Awareness, Treatment and Control of
Hypertension is Rather Low Worldwide
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
* BP < 140/90 mmHg
Wolf-Maier et al. Hypertension. 2004;43:10–17; 15
15 Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912.

16. 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 II
II (Phase 1) (Phase 2)
1976–80 1988–91 1991–94 1999–2000
Awareness 51 73 68 70
Treatment 31 55 54 59
Control 10 29 27 34
16

17. 17

18. 18

19. Benefits of Lowering BP
Average Percent Reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%
19

20. 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-fold
8
relative CV risk
Fold increase in
6
4-fold
4
2-fold
2
1-fold
0
115/75 135/85 155/95 175/105
SBP/DBP (mmHg) 20

21. Each 2 mmHg Decrease in SBP
Reduces CV Risk by 7–10%
• Meta-analysis of 61 prospective, observational studies
• 1 million adults aged 40–69 y with BP > 115/75 mmHg
• 12.7 million person-years
7% reduction
in risk of IHD
and other
2 mmHg vascular disease
decrease in mortality
mean SBP
10% reduction
in risk of stroke
mortality
21
21 Lewington et al. Lancet. 2002;360:1903–1913.

22. 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.
22

23. 23

24. 24

25. Factors contribute to the
development of primary HTN
1. Sympathetic nervous system
hyperactivity
2. Renin-angiotensin-aldosterone system
hyperactivity
3. Endothelial dysfunction
25

26. 26

27. Types of HTN?
Primary Secondary
• ?? ‘essential’idiopathic • Caused by some other
• Most common type medical problem or
found in 90-95% of condition:
those with HTN • High-dose estrogen
• Cause not well • Renal artery stenosis
understood • Pregnancy (PET)
• Salt sensitive
• Cushing’s syndrome
• RAAS dependent
• pheochromocytoma
• Others?
27

28. 28

29. ABPM ?
Renin level ??
29

30. 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
30

31. 31

32. 32

33. 33

34. BP measurement
Physical assessment • Proper size cuff
• Height & weight applied 1 inch above
• Blood pressure brachial artery
Measuring BP • Inflate cuff to 30
accurately: mmHg above initial
• No smoking or caffeine radial pulse check If
30 minutes before BP elevated, wait 2
• Rest for 5 minutes prior minutes, recheck
to BP
• Check BP in other arm
• Apply cuff to bare arm
34

35. 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 Indicated for evaluation of “white-
monitoring 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
35

36. 36

37. White Coat and Ambulatory BP monitoring ABPM
37

38. 38

39. 39

40. Key Messages
 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.
40

41. 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.
41

42. 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.
42

43. 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
43

44. 44

45. 45

46. Complications of Hypertension
Heart
 resistance  
workload  left
ventricular
hypertrophy
• CAD, angina, MI
• Heart failure
46

47. Complications of Hypertension
Brain
• Atherosclerosis,
stroke
47

48. Complications of Hypertension
Peripheral vascular Kidney disease
disease
• vessels less elastic
• Aortic aneurysm or
 decreased
dissection
perfusion renal
Retinal damage
failure
• damage to blood
vessels of the eye
48

49. Acute Complications
Hypertensive Sx: papilledema,
Crisis: progressive renal
Severe and abrupt failure,
elevation of BP encephalopathy
Diastolic over Most common
120mm hg cause is untreated
hypertension
High Mortality
Goal: slowly
decrease BP
49

50. Classifications Hypertensive Crisis
Hypertensive crisis is Hypertensive urgency:
categorized by the BP is elevated but there
degree of organ damage is no evidence of target
Hypertensive organ damage
emergency:
BP is severely elevated
and there is evidence of
target organ damage
• Especially brain
50

51. GOAL: Reduce Complications
JNC 7 guidelines
recommend a target
BP of less than
140/90
Patients with renal
disease or diabetes
need BP less than
130/80
51

52. What Reduces Risk of
Complications?
REDUCING MODIFIABLE RISK
FACTORS IS A KEY INTERVENTION
Goal = Patient teaching to reduce risk
factors
Drug therapy is initiated if lifestyle
changes are not effective to control BP
52

53. 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
53

54. TREATMENT: 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
54

55. DASH Diet
http://www.nhlbi.nih.gov/health/public/heart/h
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
55

56. 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,
yoga, Tai Chi
56

57. 57

58. Drug Therapy for HTN
Diuretics Beta adrenergic
• Flush excess water blockers
and sodium from the Three classes:
body
• Cardioselective
• Thiazide diuretics
• Non-selective
• Loop diuretics:
• Combined alpha-
furosemide (Lasix)
beta-blockers
• Potassium sparing:
Aldactone
58

59. The Majority of Hypertensive Patients Need
Combination Therapy to Achieve BP Goals
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)
1 2 3 4
Bakris et al. Am J Med. 2004;116(5A):30S–38S;
Average number of antihypertensive medications
59 Dahlöf et al. Lancet. 2005;366:895–906.

60. 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)
60

61. Pharmacologic Management
of Hypertension
Angiotensin Angiotensin II
converting enzyme receptor blockers
(ACE) inhibitors (ARB)
• Decrease effect of • Prevent action of
RAA system: angiotensin II and
Capoten, Lisinopril produce vasodilation
• Diabetes mellitus • losartan (Cozaar)
w/proteinuria, heart
failure
61

62. Pharmacologic Management of
Hypertension
Vasodilators Alpha-receptor
• Direct arterial agonists
vasodilation • Clonidine
• Sodium nitroprusside • Acts on central
(Nipride) nervous system
• Often used in • Lowers peripheral
hypertensive crisis vascular resistance
62

63. Why don’t some patients respond
to therapy?
Non-adherence to Drug related causes
therapy Other conditions
• Patients don’t take
Secondary
their HTN meds →
complications!!!
hypertension
• Cost, inadequate Volume overload
teaching, side effects,
inconvenient dosing
63

64. 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 64

65. 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
65

66. 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
66

67. 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)
67

68. 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
68

69. 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 β-blockade, anesthesia induction,
histamine, ACTH, glucagon, metoclopramide)
• Strenuous exercise, movement that increases intra-abdo
pressure (lifting, straining)
• Micturition (bladder paraganlgioma)
69

70. 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 70

71. Plasma Metanephrines
Not postural dependent: can draw
normally
Secreted continuously by pheo
SEN 99% SPEC 89%
False Positive: acetaminophen
Assay not widely available yet
71

72. 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%
72

73. 73

74. Renovascular Hypertension
74

75. 75

76. Endocrine Hypertension
Catecholamine producing tumours
Mineralocorticoid hypertension
Renin-dependent hypertension
Hyperthyroidism and hypothyroidism
Acromegaly
Hyperparathyroidism
76

77. 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?
77

78. 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
78

79. 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
79

80. 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
80

81. 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
81

82. 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
82

83. 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
83

84. Renin Aldo
Liddle low low
Licorice low low
RAS high high
Conn’s low high
84

85. Renin-Angiotesnin-
Aldosterone System
A drop in BP or blood Stimulates adrenal
volume causes kidneys to glands to release
secrete renin, a
renin aldosterone
precursor to This prompts the
angiotensin I kidneys to retain sodium
Angiotensin-converting and water
enzyme turns The increased volume
angiotensin I into and vasoconstriction
angiotensin II, a potent raise BP
vasoconstrictor
85

86. 86

87. 87