Transcript Hypertension

1
Hypertension
The Importance of Hypertension
Prevalence data
The first killer
Silent killer
Masked killer
Financial burden
Preventable
Treatable
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
4
Hypertension is defined as:
 the level of blood pressure linked with a doubled
increased long-term risk for adverse events
OR
The level of blood pressure at which the benefits
of action (i.e. therapeutic intervention) exceed
those of inaction.”
Evans and Rose Brit Med Bull 1971;27:37-42
5
6
7
Definitions of hypertension by office
and out-of-office blood pressure levels
8
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
9
11
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
High Prevalence of Hypertension
Worldwide
Prevalence of hypertension (%)
60
55
38
40
38
47
49
Spain
Finland
42
28
20
0
USA
Italy
Sweden England
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
13
49
Wolf-Maier et al. JAMA. 2003;289:23632369;
Sekikawa, Hayakawa. J Hum Hypertens. 2004; 2004;18:911–912.
Japan* Germany
Prevalence of Hypertension
14
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
15
Wolf-Maier et al. Hypertension. 2004;43:10–17;
Sekikawa, Hayakawa. J Hum Hypertens. 2004;18:911–912.
15
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
Awareness
Treatment
Control
II
1976–80
51
II
(Phase 1)
1988–91
73
II
(Phase 2)
1991–94
68
1999–2000
70
31
10
55
29
54
27
59
34
16
Awareness, Treatment and Control of
Blood Pressure 1976-2000 (NHANES)
80
70
60
50
Awareness
Treatment
Control
40
30
20
10
0
1976-1980 1988-1991 1991-1994 1999-2000
17
18
19
Benefits of Lowering BP
Average Percent Reduction
Stroke incidence
35–40%
Myocardial infarction
20–25%
Heart failure
50%
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
Fold increase in
relative CV risk
10
8-fold
8
6
4-fold
4
2
2-fold
1-fold
0
115/75
135/85
155/95
SBP/DBP (mmHg)
175/105
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
2 mmHg
decrease in
mean SBP
22
Lewington et al. Lancet. 2002;360:1903–1913.
7% reduction
in risk of IHD
and other
vascular disease
mortality
10% reduction
in risk of stroke
mortality
22
23
Factors contribute to the
development of primary HTN
1.
2.
3.
Sympathetic nervous system
hyperactivity
Renin-angiotensin-aldosterone system
hyperactivity
Endothelial dysfunction
24
25
Types of HTN?
Primary
• ?? ‘essential’idiopathic
• Most common type
found in 90-95% of
those with HTN
• Cause not well
understood
• Salt sensitive
• RAAS dependent
Secondary
• Caused by some other
medical problem or
condition:
•
•
•
•
•
•
High-dose estrogen
Renal artery stenosis
Pregnancy (PET)
Cushing’s syndrome
pheochromocytoma
Others?
26
27
ABPM ?
Renin level ??
28
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
29
30
31
32
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
33
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 “whitecoat” 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
34
35
36
37
38
White Coat and Ambulatory BP monitoring ABPM
39
40
41
Key Messages
 For persons over age 50, SBP is a more important than DBP as
CVD risk factor, likewise wide pulse pressure
 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.
42
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.
43
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.
44
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
45
46
47
Complications of Hypertension
Heart
•  resistance  
workload  left
ventricular
hypertrophy
• CAD, angina, MI
• Heart failure
48
Complications of Hypertension
Brain
• Atherosclerosis,
stroke
49
Complications of Hypertension
Peripheral vascular
disease
• Aortic aneurysm or
dissection
Retinal damage
• damage to blood
vessels of the eye
Kidney disease
• vessels less elastic
 decreased
perfusion renal
failure
50
Acute Complications
Hypertensive
Crisis:
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
51
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
Hypertensive urgency:
BP is elevated but there
is no evidence of target
organ damage
• Especially brain
52
GOAL: Reduce Complications
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
53
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
54
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
55
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
56
DASH Diet
http://www.nhlbi.nih.gov/health/publi
c/heart/hbp/dash/
Dietary Approaches to Stop
Hypertension = DASH
• A diet rich in fruits, vegetables and lowfat dairy products with reduced fat
content
• Limits sodium intake to 2.4 g/day
57
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
58
59
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 alphabeta-blockers
60
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
61
Bakris et al. Am J Med. 2004;116(5A):30S–38S;
Dahlöf et al. Lancet. 2005;366:895–906.
2
3
4
Average number of antihypertensive medications
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)
62
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)
63
Pharmacologic Management of
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
64
Why don’t some patients respond
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
65
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
66
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
67
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
68
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)
69
Pheo: Signs & Symptoms
The five P’s:
•
•
•
•
•
Pressure (HTN)
Pain (Headache)
Perspiration
Palpitation
Pallor
90%
80%
71%
64%
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
70
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 -blockade, anesthesia induction,
histamine, ACTH, glucagon, metoclopramide)
• Strenuous exercise, movement that increases intra-abdo
pressure (lifting, straining)
• Micturition (bladder paraganlgioma)
71
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
72
Plasma Metanephrines
Not postural dependent: can draw
normally
Secreted continuously by pheo
SEN 99% SPEC 89%
False Positive: acetaminophen
Assay not widely available yet
73
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%
74
75
Renovascular Hypertension
76
77
Endocrine Hypertension
Catecholamine producing tumours
Mineralocorticoid hypertension
Renin-dependent hypertension
Hyperthyroidism and hypothyroidism
Acromegaly
Hyperparathyroidism
78
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?
79
80
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
81
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
82
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
83
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
84
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
85
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
86
Renin
Aldo
Liddle
low
low
Licorice
low
low
RAS
high
high
Conn’s
low
high
87
Renin-AngiotesninAldosterone System
A drop in BP or blood
volume causes kidneys to
secrete renin, a
precursor to
angiotensin I
Angiotensin-converting
enzyme turns
angiotensin I into
angiotensin II, a potent
vasoconstrictor
Stimulates adrenal
glands to release
aldosterone
This prompts the
kidneys to retain sodium
and water
The increased volume
and vasoconstriction
raise BP
88
89
90