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RIA BANDIARA dr. Sp.

PD

SUBDIVISION NEPHROLOGY AND HYPERTENSION


DEPT. INTERNAL MEDICINE
FACULTY OF MEDICINE UNIVERSITY PADJADJARAN
HASAN SADIKIN GENERAL HOSPITAL
BANDUNG
Reference

 Kaplan’s Clinical Hypertension, Norman M.K, 8th


Edition, 2002
 1999 World Health Organization International
Society of Hypertension Guidelines for the
Management of Hypertension
 The Sixth Report of The Joint National
Committee on Prevention, Detection, Evaluation
and Treatment of High Blood Pressure
 The Seventh Report of The Joint National
Committee on Prevention, Detection, Evaluation
and Treatment of High Blood Pressure
Lecture Content

 Introduction
 Definition
 Pathophysiology
 Pathogenesis
 Pathophysiology of T.O.D
 Measurement of blood pressure
 History, Physical examination
 Treatment
What is the JNC VII?
 Seventh Report of the Joint National
Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood
Pressure
 Uses evidence-based medicine and consensus
 Updates approaches to hypertension control
including diagnosis, evaluation, lifestyle
modification, and drug therapy
Objective
 “The objective of identifying and treating high
blood pressure is to reduce the risk of
cardiovascular disease and associated morbidity
and mortality”

 JNC VII
Why Control Hypertension?
 Heart disease and stroke are the 1st and 3rd
leading causes of death in the U.S.

 More than $259 billion in direct and indirect


costs
Epidemiology
 2 million new cases of hypertension diagnosed
each year in the U.S.
 23% of men and 25% of women over the age
of 18 in the U.S. have HTN
 The prevalence of HTN among African
Americans is increased 30-50% in each age
group compared to persons of European
descent
Epidemiology cont.
 The prevalence of HTN increases steadily with
age; over 70% of women and 50% of men in
the U.S. over the age of 70 have HTN
 Linear relationship between the degree of HTN
and the risk for CV and renal disease
Hypertension
 Hypertension is not a disease
 It is an arbitrarily defined disorder to which
both environmental and genetic factors
contribute
 Major risk factor for:
 cerebrovascular disease
 myocardial infarction

 heart failure

 peripheral vascular disease

 renal failure
 Blood pressure is a continuous variable which
fluctuates widely during the day
 physical stress
 mental stress

 The definition of hypertension has been


arbitrarily set as:
That blood pressure above which the
benefits of treatment outweigh the risks
in term of morbidity and mortality
At what blood pressure is a patient
hypertensive?
 BHS 140/90
 JNC-VII 140/90 Opt <120/<80
 WHO-ISH 140/90
 The current recommendation in the UK is
140/90
 However risk is important and in diabetes
130/80
Definition
Based on recommendation JNC VII, The
Classification of BP for adult  18 years :
Normal : systolic lower than 120
diastolic lower than 80
Pre-hypertension : systolic 120 – 139
diastolic 80 – 99
Stage-1 : systolic 140 – 159 or
diastolic 90 – 99
Stage-2 : systolic equal to or more than 160 or
diastolic equal to or more than 100
New (1999) WHO-ISH Definitions
and Classification of BP Levels
Category Systolic BP Diastolic BP
(mm Hg) (mm Hg)

Optimal BP <120 <80


Normal BP <130 <85
High-Normal 130-139 85-89

Grade 1 Hypertension (mild) 140-159 90-99


Subgroup: Borderline 140-149 90-94
Grade 2 Hypertension (moderate) 160-179 100-109
Grade 3 Hypertension (severe) >180 >110

Isolated Systolic Hypertension >140 <90


Subgroup: Borderline 140-149 <90
Guidelines for Measurement of Blood
Pressure

1. Patient conditions
1.1. Posture
Initialy, particularly in patients over age 65,
diabetic, or receiving antihypertensive therapy,
check for postural changes by taking readings after
5 minutes supine, then immediately and 2 minutes
after they stand

For routine follow-up, sitting pressures are


recommended. The patient should sit quietly with
the back supported for 5 minutes and the arm
supported at the level of the heart.
Guidelines for Measurement of Blood
Pressure (continued)

1.2. Circumstances
No caffeine during the hour preceeding the reading
No smoking during the 15 minutes precding the
reading
No exogenous adrenergic stimulants (e.g.
phenylephrine in nasal decongestants or eye drops
for pupillary dilation)
A quiet, warm setting.
Home readings taken under varying circumstances
and 24 hours ambulatory recordings may be
preferable and more accurate in predicting
subsequent cardiovascular disease.
Guidelines for Measurement of Blood
Pressure (continued)
2. Equipment :

 Cuff size : the bladder should encircle and cover


two - thirds of the length of the arm; if it does
not, place the bladder over the brachial artery. If
bladder is too small, high readings may result.
 Manometer : Aneroid gauges should be
calibrated every 6 months against a mercury
manometer.
 For infants, use ultrasound equipment (e.g. the
Doppler method)
Guidelines for Measurement of Blood
Pressure (continued)
3. Technique
3.1. Number of readings
On each occasion, take at least two readings,
separated by as much time as is practical. If
readings vary by more than 5 mmHg, take
additional readings until two are close.
For diagnosis, obtain three sets of readings at
least 1 week apart.
Initially, take pressure in both arms; if the
pressures differ, use arm with the higher
pressure.
If the arm pressure is elevated, take pressure in
one leg, particularly in patients younger than
30.
Guidelines for Measurement of Blood
Pressure (continued)
3.2. Performance
Inflate the bladder quickly to a pressure 20 mmHg
above the systolic pressure, as recognized by
disappearance of the radial pulse.
Deflate the bladder 3 mmHg every second
Record the Korotkoff phase V (disappearance),
except in children, in whom ose of phase IV
(muffling) may be preferable.
If the Korotkoff sounds are weak, have the patient
raise the arm, open and close the hand.

4. Recordings
Note the pressure, patient position, the arm, cuff
size ; e.g. 140/90, seated, right arm, large adult
cuff.
Bladder Length

Centre of bladder
must be over Children > 5 years  12 cm
artery

Usually supplied 23 cm

Strongly
recommended Normal and lean arms 35 cm
for routine use

Muscular and Obese arms 42 cm


2.
The cuff must be level with the
heart. If Arm Circumference
exceeds 33 cm, a large cuff must
be used. Place stethoscope
diaphragm over brachial artery
3.
The column of
1. mercury must be
vertical. Inflate to
The patient should acclude the pulse.
be relaxed and the Deflate at 2 to 3
arm must be mm/sec. Measure
supported. Ensure systolic (first sound)
no tight clothing and diastolic
constricts the arm (disappearance) to
nearest 2 mmHg.
Control of blood pressure
 Blood pressure is controlled by an integrated
system
 Prime contributors to blood pressure are:
 Cardiac output
 Stroke volume
 Heart rate

 Peripheral vascular resistance


 Each of these factors can be manipulated by
drug therapy
Pathophysiology

 BP=TPR X CO (blood pressure is the product


of total peripheral resistance and cardiac output)
Autoregulation

BLOOD PRESSURE = CARDIAC OUTPUT X PERIPHERAL RESISTANCE


Hypertension = Increased CO and/or Increased PR

 Preload  Contractility Functional Structural


Constriction Hypertrophy

 Fluid Volume
Volume Redistribution

Renal Descreased Sympathetic Renin- Cell Hyperinsuli


Sodium filtration nervous angiotensin membrane nemia
retention surface overactivity excess alteration

Genetic Stress Genetic Obesity Endothelium


Excess
alteration alteration derived
sodium
factors
intake
capacitance preload

Cardiac output
veins
venules heart

Peripheral Sympathetic Blood


system volume
resistance

arterioles
Blood pressure
Angiotensin/ Renin release
aldosterone
Sympathetic Nervous System
 Sympathetic system activation produces
 vasoconstriction
 reflex tachycardia

 increased cardiac output

 In this way blood pressure is increased


 The actions of the sympathetic system are rapid
and account for second to second blood
pressure control
The renin-angiotensin-aldosterone system

 The RAAS is pivotal in long-term BP control


 The RAAS is responsible for:
 maintenance of sodium balance
 control of blood volume

 control of blood pressure


 The RAAS is stimulated by:
 fall in BP
 fall in circulating volume

 sodium depletion

 Any of the above stimulate renin release


from the juxtaglomerular apparatus
 Renin converts angiotensinogen to
angiotensin I
 Angiotensin I is converted to angiotensin II
by angiotensin converting enzyme (ACE)
 Angiotensin II is a potent
 vasoconstrictor
 anti-natriuretic peptide

 stimulator of aldosterone release from the


adrenal glands
 Aldosterone is also a potent antinatriuretic
and antidiuretic peptide
 Angiotensin II is also a potent hypertrophic
agent which stimulates myocyte and smooth
muscle hypertrophy in the arterioles
 Myocyte and smooth muscle hypertrophy:
 are both poor prognostic indicators in patients
with hypertension
 partially explain why hypertension and the risks
of hypertension persist in some patients despite
treatment

 Both the sympathetic and RAAS are key


targets in the treatment of hypertension
ANGIOTENSINOGEN Macula densa signal
Renin  Renal arteriolar pressure
 Renal nerve activity
ANGIOTENSIN I
Converting
enzyme
ANGIOTENSIN II ANGIOTENSIN III

ANGTIOTENSINASE A

Adrenal Kidney Intestine CNS Peripheral nervous Vascular Heart


cortex system smooth
muscle

Adrenergic
facilitation
Aldosterone Contractility
Sympathetic
discharge

Distal
nephron Sodium and water Thirst salt Vasopressin
Vasoconstriction
reabsorption reabsorption appetite release

Cardiac
Maintain or increase Total peripheral output
ECFV resistance
Angiotensinogen
Renin

Angiotensin I
ACE vasoconstriction

Angiotensin II Inc. PVR


aldosterone (inc. reabsorp of Na)

Inc. blood volume


Pre Established hypertension
hypertension 30-50 years
10-30 years
CO 

Complicated hypertension
40-60 years

(T. O. D)
HEREDITY - ENVIRONMENT
Age

PRE - HYPERTENSION 0 - 30

Normotension  EARLY HYPERTENSION 20 - 40

ESTABLISHED HYPERTENSION 30 - 50

UNCOMPLICATED COMPLICATED

Accelerated - CARDIAC LARGE CEREBRAL RENAL


malignant Hypertrophy VESSEL Ischemia Nephro-
course Failure Aneurysm Thrombosis sclerosis
Infarction Dissection Hemorrhage Failure
Causes of Hypertension
Essential or Primary
Underlying pathophysiologic alteration
of unknown cause;
95% of cases of HTN

Secondary-Resulting from a specific cause


such as renal or endocrine disorders;
5% of cases
Primary Hypertension
 Is usually of gradual onset
 Usually develops between the ages of 30 and 50
 Tends to remain asymptomatic for 10 to 20
years
 Triggers include obesity, psychological stress,
high-sodium intake, and alcohol intake over 1
ounce per day
Aetiology of essential hypertension
 The aetiology of hypertension is
 polyfactorial
 polygenic
 Likely causes:
 Increased reactivity of resistance vessels and
resultant increase in peripheral resistance
 as a result of an hereditary defect of the smooth
muscle lining arterioles
 A sodium homeostatic effect
 In essential hypertension the kidneys are unable
to excrete appropriate amounts of sodium for
any given BP. As a result sodium and fluid are
retained and the BP increases
Other factors
 Age
 Genetics and family history
 Environment
 Weight
 Alcohol intake
 Race
 Age
 BP tends to rise with age, possibly as a result of
decreased arterial compliance.
 Hypertension in the elderly should be treated as
aggressively as in the young. They have more to
lose
 Studies such as EWPHE, Primary Care
Study,MRC Hypertension in the Older Adult,
SHEP, SYSTEUR and STOP-1 and 2 have
proven that treating both diastolic and systolic
hypertension in the elderly significantly reduces
stoke and MI.
 Genetics
 A history of hypertension tends to run in
families
 The closest correlation exists between sibs rather
parent and child
 It is also possible that environmental factors
common to members of the family also have a
role in the development of hypertension
 Environment
 Mental and physical stress both increase blood
pressure
 However removing stress does nor necessarily
return blood pressure to normal values
 True stress responders who have very high BP
when they attend their doctor but low normal
pressures otherwise tend to be highly resistant to
treatment
 Sodium Intake
 The SALT study and more recently the DASH
study have confirmed a strong relationship
between hypertension, stroke and salt intake
 Reducing salt intake in hypertensive individuals
does lower blood pressure
 However reducing salt intake in normotensives
appears to have no effect
 Reducing salt intake to 60-80mmol/day does
lower BP
 However there are real difficulties in achieving
this level of salt restriction (fast food)
 Alcohol
 The most common cause oh hypertension in the
young Scot
 Affects 1% of the population

 Small amounts of alcohol tend to decrease BP

 Large amounts of alcohol tend to increase BP

 If alcohol consumption is reduced BP will fall


over several days to weeks.
 Average fall is small 5/3 mmHg
 Weight
 Obese patients have a higher BP
 Up to 30% of hypertension is attributable in part
or wholly to obesity
 If a patient loses weight BP will fall

 In untreated patients a weight loss of 9Kg has


been reported to produce a fall in BP of 19/18
mmHg
 In treated patients a fall in BP of 30/21 mmHg
has been reported
 Weight reduction is the most important non-
pharmacological measure available
DYSLIPIDEMIA

Increased
Lipolysis Release of
Obesity + Androgen Abdominal
Fat Free Fatty
Acids

TYPE II
Peripheral Increased Decreased
DIABETES Insulin Pancreatic Hepatic Insulin
MELLITUS Resistance Insulin Secretion Extraction

Hyperinsulinemia

Sodium Vascular
Increased Retention
Sympathetic Hypertrophy
Nervous
Attenuated Activity
Vasodilatio
n
HYPERTENSION
 Race
 Caucasians have a lower BP than black
populations living in the same environment
 Black populations living in rural Africa have a
lower BP than those living in towns
 Reasons are not clear

 Possibly black populations are more susceptible


to stress when living in towns
 Respond in different ways to changes in diet

 Black populations are genetically selected to be


salt retainers and so are more sensitive to an
increase in dietary salt intake
Secondary Hypertension
 5-10% of all hypertension has an identifiable
cause
 Removal of the cause does not guarantee that
the hypertension or risk will return to normal
 Sustained hypertension produces end-organ
damage to blood vessels, heart and kidney
 This type of damage tends to increase BP
further and so a vicious self-propagating cycle
is established
Causes for Secondary Hypertension
 Renal disease
 20% of resistant hypertensive patients
 chronic pyelonephritis

 renal artery stenosis

 polycystic kidneys

 Drug Induced
 NSAIDs
 Oral contraceptive

 Corticosteroids
 Pregnancy
 pre-eclampsia
 Endocrine
 Conn’s Syndrome
 Cushings disease

 Phaeochromocytoma

 Hypo and hyperthyroidism

 Acromegaly

 Vascular
 Coarctation of the aorta
 Sleep Apnoea
The risks of hypertension
 A sustained increase in BP increases the load
on the heart and blood vessels
 This has two effects
 Myocardial hypertrophy
 Smooth muscle hypertrophy in the resistance
vessels
 Hypertrophy of this type increases the
strength of the heart and vasculature
 However it also reduces compliance
 The effects of reduced compliance are:
 A reduction in the ability of the heart to to
respond to increased or variable loads
 a decrease in the ability of the resistance vessels
to relax
 For the same level of BP and irrespective of
age the presence of left ventricular
hypertrophy increases 5 year mortality by
 33% in men
 21% in women
 Atheromatous disease
 Sustained hypertension is associated with
accelerated atheromatous disease of the blood
vessels
 Peripheral vascular disease

 Coronary artery disease

 Cerebrovascular disease

 Renal artery disease

 The Heart
 MI
 Heart failure

 Angina
 The kidney
 Hypertension produces an increase in renal vascular
resistance and a reduction in renal blood flow
 Renal disease

 RBF +  afferent glomerular arteriolar resistance

efferent glomerular arteriolar constriction

 glomerular hydrostatic pressure

glomerular hyperfiltration

Glomerusclerosis and impairtment of renal function


Clinical manifestations
 None in the early stages, other than high BP
reading, if taken
 eventually report symptoms, such as persistent
headaches, fatigue, dizziness, palpitations,
flushing, blurred vision or epitaxis
 may also see signs of target organ damage
 retinal changes, such as hemorrhages, exudates,
arteriolar narrowing, cotton wool spots (small
infarctions), and if severe, papilledema (swelling
of the optic disc)
 angina, MI

 LV Hypertrophy, heart failure

 BUN & Cr, nocturia

 stroke & TIA (cerebral infarcts) with such signs


as altered vision, speech, hemiplegia, etc.
Evaluation: Objectives
1. To identify known causes of high blood
pressure
2. To assess the presence or absence of target
organ damage and CV disease, and the
response to therapy
3. To identify other CV risk factors or
concomitant disorders that may define
prognosis and guide treatment
Evaluation: History
 Known duration and levels of elevated BP
 History or symptoms of CHD, heart failure,
cerebrovascular disease, PVD, renal disease, DM,
dyslipidemia, gout, sexual dysfunction, or other
comorbid conditions
 FH of HTN, premature CHD, stroke, DM,
dyslipidemia, or renal disease
 Symptoms suggesting causes of HTN
Evaluation: History cont.
 History of recent weight changes, physical
activity level, tobacco use
 Dietary assessment including intake of sodium,
alcohol, saturated fat, and caffeine
 History of all prescribed and meds, herbals, and
illicit drugs
 Results and adverse effects of previous
antihypertensive therapy
 Psychosocial and environmental factors
Evaluation:
Initial Physical Exam
 Two or more BP measurements 2 minutes apart
with pt either seated or supine and after standing
for at least 2 minutes
 Verification in the contralateral arm
 Measurement of height, weight, and waist
circumference
Evaluation:
Physical Exam cont.
 Funduscopic exam for hypertensive retinopathy
(arteriolar narrowing, arteriolar constrictions, AV
crossing changes, hemorrhages and exudates, disc
edema)
 Neck exam for bruits, distended veins, or enlarged
thyroid
 Heart exam for rate and rhythm, size, precordial heave,
clicks, murmurs, and extra heart sounds
Evaluation:
Physical Exam cont.
 Lung exam for rales and evidence of
bronchospasm
 Abdominal exam for bruits, enlarged kidneys,
masses, and aortic pulsation
 Extremity exam for decreased peripheral pulses
and edema
 Neurological exam
Evaluation:
Diagnostic Tests
 Used to determine the presence of target organ damage
and other risk factors
 UA: hematuria, proteinuria, and microalbuminuria looking for
signs of renal dysfunction
 evidence of DM or renal disease
 Lipid panel: as a screen for other risk factors for
atherosclerotic disease
 EKG: assess for LVH and evidence of prior ischemia
Overall Guide to Workup for Secondary
Causes of Hypertension
Diagnostic Procedure
Diagnosis Initial Additional

Chronic renal disease Urinalysis, serum Isotopic renogram, renal biopsy


Creatinine, renal
Sonography
Renovascular disease Plasma renin before and 1 Aortagram, isotopic renogram 1 hour
after captopril
hour after captopril

Coarctation Blood pressure in legs Aortogram


Primary Aldosteronism Plasma potassium, plasma Urinary potassium, plasma or urinary
aldosterone after saline load; adrenal
renin and aldosterone (ratio) computed tomography (CT) and
scintiscans

Cushing’s syndrome Urinary cortisol after variable doses of


AM plasma cortisol after 1 dexamethasone; adrenal CT and
mg dexamethasone at scintiscans
bedtime Urinary catechols; plasma catechols,
basal and after 0.3 mg clonidine;
Pheochromocytoma Spot urine for metanephrine adrenal CT and scintiscans
Which Factors
Influence Prognosis? (1)
Decisions should not be made on BP
alone, but also on presence of other risk
factors, target organ damage, and
concomitant diseases, as well as on other
aspects of patients’ personal, medical,
social, economic, ethnic, and cultural
characteristics
1999 WHO-ISH HYPERTENSION PRACTICE GUIDELINES FOR PRIMARY CARE PHYSICIANS 26
Which Factors
Influence Prognosis? (2)
• Risk factors of CVD
I. Used for risk stratification
II.Other factors adversely influencing
prognosis

• Target organ damage (TOD)

• Associated clinical conditions (ACC)


Which Factors Influence Prognosis? (3)
Risk factors for CVD
I. Used for risk stratification
• Levels of systolic and diastolic blood
pressure (Grades 1-3)
• Men >55 years
• Women >65 years
• Smoking
• Total cholesterol >6.5 mmol/L (250
mg/dl)
• Diabetes
• Family history of premature
cardiovascular disease
Which Factors Influence Prognosis? (4)
Risk factors for CVD
II.Other factors adversely influencing
prognosis
• Reduced HDL cholesterol
• Raised LDL cholesterol
• Microalbuminuria in diabetes
• Impared glucose tolerance
• Obesity
• Sedentary lifestyle
• Raised fibrinogen
• High risk socioeconomic group
• High risk ethnic group
• High risk geographic region
Which Factors Influence Prognosis? (5)
Target organ damage (TOD)
• Left ventricular hypertrophy
(electrocardiogram, echocardiogram, or
radiogram)
• Proteinuria and/or slight elevation of plasma
creatinine concentration 106-177 mmol/L (1.2-
2.0 mg/dl)
• Ultrasound or radiological evidence of
atherosclerotic plaque (carotid, iliac, and
femoral arteries, aorta)
• Generalised or focal narrowing of the retinal
arteries
Which Factors Influence Prognosis? (6)
Associated clinical conditions (ACC)
Cerebrovascular disease
• Ischaemic stroke
• Cerebral haemorrhage
• Transient ischaemic attack (TIA)
Heart disease
• Myocardial infarction
• Angina pectoris
• Coronary revascularisation
• Congestive heart failure
Which Factors Influence Prognosis? (7)
Associated clinical conditions (ACC)
Renal disease
• Diabetic nephropathy
• Renal failure, plasma creatinine
concentration >177 mmol/L (>2.0 mg/dl)
Vascular disease
• Dissecting aneurysm
• Symptomatic arterial disease
Advanced hypertensive retinopathy
• Haemorrhages or exudates
• Papilloedema
Which Factors
Influence Prognosis? (8)
Typical 10 year risk of stroke
or myocardial infarction

 Low risk = <15 percent


 Medium risk = 15-20 percent
 High risk = 20-30 percent
 Very high risk = 30 percent or higher
Stratifying Risk - Quantifying Prognosis
Management
 The most essential element in reducing the
morbidity and mortality associated with
hypertension is long term
compliance/adherence
 achieved through life style modification alone or
in combination with pharmacologic therapy
(stepped care)
Lifestyle modification
 weight reduction
 sodium restriction

 dietary fat modification

 exercise

 alcohol restriction

 caffeine restriction

 relaxation techniques

 potassium supplementation
Lifestyle Modification to Manage
Hypertension
Approximate Systolic BP
Modification Recommendation Reduction, Range
Weight reduction Maintain normal body weight 5-20 mm Hg/10-Kg
(BMI, 18.5-24.9) weight loss
Adopt DASH eating Consume a diet rich in fruits, vegetables, and 8-14 mm Hg
Plan low-fat dairy products with a reduced
content of saturated and total fat
Dietary sodium Reduce dietary sodium intake to no more 2-8 mm Hg
reduction than 100 mEg/L (2.4 g sodium or 6 g
sodium chloride)
Physical activity Engage in regular aerobic physical activity 4-9 mm Hg
such as brisk walking (at least 30 minutes
per day, most days of the week)
Moderation of alcohol Limit consumption to no more than 2 drnks 2-4 mm Hg
consumption per day (1 oz or 30mL ethanol (eg. 24 oz
beer, 10 oz wine, or 3 oz 80-proof
whiskey) in most men and no more than
1 drink per day in women and
lighter-weight persons
Figure. Algorithm for Treatment of Hypertension
Lifestyle Modification

Not at Goal BP
(<140/90 mm Hg or <130/80 mm Hg for Those With Diabetes
Or Chronic Kidney Disease)

Initial Drug Choices

Hypertension Without Hypertension With


Compelling Indications Compelling Indications

Stage 1 Hypertension Stage 2 Hypertension Drug(s) for the


(systolic BP 140-159 mm Hg (systolic BP 160 mm Hg Compelling indication
Or Diastolic BP 90-99 mm Hg) Or Diastolic BP 100 mm Hg)
Other antihypertensive drugs
Thiazide type diuretics for most 2-Drug combination for most (diuretics, ACE inhibitor, ARB, -
blocker, CCB) as Needed
may consider ACE inhibitor, ARB, (usually thiazide - type diuretic
-blocker, CCB, or Combination and ACE inhibitor or ARB or
-blocker, CCB)

Not at Goal BP

Optimize Dosages or Add Additional Drugs Until Goal BP is Achieved


Consider Consultation With HypertensionSpecialist
Management Strategy (1)

 Is patient at:
Very High Risk

High Risk

Medium Risk

Low Risk
Management Strategy (2)

 Stratify Risk

Very High
High
Begin drug
treatment
Begin drug
treatment
Management Strategy (3)
 Stratify risk
Medium
Low
Monitor BP & other
risk factors for 3-6 months
Monitor BP & other
risk factors for 6-12 months
SBP >140 SBP <140
or DBP >90 or DBP <90
SBP >150 SBP <150
Begin drug Continue to or DBP >95 or DBP <95
treatment monitor
Begin drug Continue
treatment to monitor
Principles of Drug Treatment (1)
 Use a low dose of one drug to initiate
therapy
 If good response and tolerability but
inadequate control increase the dose of
the first drug
 If little response or poor tolerability
change to another drug class
Principles of Drug Treatment (2)

 Itis often preferrable to add a small


dose of a second drug rather than
increase the dose of the first drug
 Use long-acting drugs providing 24-
hour efficacy on a once daily basis.
Improves adherence to therapy and
minimizes BP variability.
Principles of Drug Treatment (3)
• More evidence of beneficial CVD
effects with older drugs (e.g.,
diuretics and beta-blockers)

• Evidence of benefit with newer


drugs (e.g., ACE inhibitors and
calcium antagonists) is
accumulating.
Principles of Drug Treatment (4)
There are six main drug classes used
worldwide :
diuretics
beta-blockers
ACE inhibitors
calcium antagonists
alpha blockers
angiotensin II antagonists
Principles of Drug Treatment (5)
All6 classes are suitable for the initiation and
maintenance of BP lowering therapy, but the
choice of drugs will be influenced by cost and
by many factors for special groups of patients.

In some parts of the world, reserpine and


methyldopa are also used frequently.
Indications

Compelling Possible
Diuretics
Heart failure Diabetes
Elderly patients
Systolic hypertension

Contraindications
Compelling Possible
Gout Dyslipidaemia
Sexually active
males
Indications
Beta-Blockers Compelling Possible
Angina Heart failure
After myocardial infarct Pregnancy
Tachyarrhythmias Diabetes

Compelling
Contraindications
Possible
Asthma and Dyslipidaemia
Chronic obstructive Athletes and
Pulmonary disease Physically active
Heart block (AV 2,3) Patients
Peripheral
vascular disease
Indications

Antagonists Compelling Possible


Angina Peripheral
Calcium

Elderly patients Vascular disease


Systolic hypertension

Contraindications
Compelling Possible
Heart block (AV 2,3) Heart failure*
* verapimil or diltiazem
Indications
ACE Inhibitors Compelling Possible
Heart failure
Left ventricular dysfunct
After myocardial infarct
Diabetic nephropathy

Contraindications
Compelling Possible
Pregnancy
Bilateral renal
artery stenosis
Hyperkalaemia
Indications
Alpha-Blockers
Compelling Possible
Prostatic Hypertrophy Glucose intolerance
Dyslipidaemia

Contraindications
Compelling Possible
Orthostatic
hypotension
Indications
Angiotensin II
Compelling Possible
Antagonists ACE-I cough Heart failure

Contraindications
Compelling Possible
Pregnancy
Bilateral renal
artery stenosis
Hyperkalaemia
Combination Therapy (1)
In most patients, appropriate combination
therapy produces BP reductions that are
twice as great as those obtained with
monotherapy,
for example, 12-22 mm Hg systolic BP and
7-14 mm Hg diastolic BP for patients with
initial BP of >160/95 mm Hg
Combination Therapy (2)
Effective drug combinations to treat
hypertension are:
• diuretic and beta-blocker
• diuretic and ACE inhibitor (or
Angiotensin II antagonist)
• calcium antagonist
(dihydropyridine) and beta-blocker
• calcium antagonist and ACE
Causes of Resistant Hypertension

Improper blood pressure measurement


Volume overload and pseudotolerance
Excess sodium intake
Volume retention from kidney disease
Inadequate diuretic therapy
Drug-induced or other causes
Nonadherence
Inadequate doses
Inappropriate combinations
Nonsteroidal anti-inflammatory drugs; cyclooxygenase 2 inhibitors
Cocaine, amphetamines, other illicitdrugs
Sympathomimetics (decongestants, anorectics)
Oral contraceptives
Adrenal steroids
Cyclosporine and taerolimus
Erythropoictin
Licorice (including some chewing tobbaco)
Selected over-the-counter dictary supplement and medicines (eg. Ephedra, ma haung,
bitter orange)
Associated conditions
Obesity
Excess alcohol intake
Identifiable causes of hypertension
Causes of inadequate responsiveness to therapy

Pseudoresistance Nonadherence to therapy


 White-coat Volume overload
hypertension” or office  Excess salt intake
elevations  Progressive renal
 Pseudohypertension in damage
older patient (nephrosclerosis)
 Use of regular cuff on  Fluid retention from
very obese arm reduction of blood
pressure
 Inadequate diuretic
therapy
Causes of inadequate responsiveness to
therapy
 Drug-related causes
 Doses too low
 Wrong type of diuretic
 Inappropriate combinations
 Rapid inactivation (e.g. hydralazine)
 Drug actions and interactions
 Sympathomimetics - Adrenal steroids
 Nasal decongestants - Oral contraceptives
 Appetite suppressants - Cyclosporine, tacrolimus
 Caffeine - Erythropoietin
 Licorice (as may be found in chewing tobacco)
 Cocaine and other illicit drugs
 Antidepressants
 Nonsteroidal anti - inflammatory drugs
Causes of inadequate responsiveness to therapy
 Associated conditions
 Smoking
 Increasing obesity
 Sleep apnea
 Insulin resistance/hyperinsulinemia
 Ethanol intake of more than 1 oz (30 mL) per day
 Anxiety-induced hyperventilation or panic attacks
 Chronic pain
 Intense vasocondtriction (arteritis)
 Organic brain syndrome (e.g. memory deficit)

 Identifiable causes of hypertension

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