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HIPERTENSI

Dr, Suhaemi, SpPD,Finasim


DEFINISI
 Tekanan Darah (TD): refleksi kardiovaskular

 TD sistolik : dipengaruhi oleh curah jantung (CO),


dapat berubah dalam waktu singkat (aktifitas fisik ringan,
emosi)

 TD diastolik : refleksi dari resistensi perifer, bila


vasokonstriksi arteriol → TD diastolik ↑
sukar dipengaruhi faktor emosi dan aktifitas fisik ringan

 HIPERTENSI : kondisi abnormal hemodinamik (fungsi


pengaturan/kontrol)
→ batasan hipertensi dipakai kriteria TD sistolik
dan/atau TD diastolik
Who is at risk for HBP?
Individuals With Family History
Parents, brother, sister
Increasing age
Gender
Women - after menopause
Early middle age more common in men
Race
More common among blacks (Occurs earlier)
These factors are beyond our control.
Risk Factors
Factors Within our Control
 Excess weight
 Increases volume of blood
 Increases pressure/resistance that heart has to pump against---
enlarged heart muscle
 Inactivity
 Heart is not used to “work” = heart beats harder/faster = more force
on arteries = uses more oxygen per beat = higher heart rate at rest
 Tobacco use
 Can lead to damage of artery wall, increases heart rate, encourages
narrowing of arteries
 Stress
 Causes unpredictable blood pressure and pulse increases along with
potential inflammation in the vessel walls.
Risk Factors
More Factors Within Our Control
Sodium intake
Leads to more fluid/water in the vessels
= increased blood pressure
Low potassium intake
Potassium helps balance sodium in cells
and control heart rhythm
Excessive alcohol
Long term: damages liver and pressure
within our circulation and heart.
Primary vs. Secondary Hypertension
Most cases are called “primary”
No identifiable cause
Family history likely
~5-10% are secondary
Caused by underlying conditions:
Kidney abnormalities
Tumor of adrenal gland
Congenital heart failure defects
If we do not treat the hypertension

http://www.lifespan.org/adam/graphics/images/en/18166.jpg
Messerli, F. H. N Engl J Med 1995
Target Organ Damage
 Heart
• Left ventricular hypertrophy
• Angina or prior myocardial infarction
• Prior coronary revascularization
• Heart failure
 Brain
• Stroke or transient ischemic attack
 Chronic kidney disease
 Peripheral arterial disease
 Retinopathy
Diseases Attributable to
Hypertension
Stroke
Coronary heart disease
Heart failure
Cerebral hemorrhage
Myocardial infarction

Left ventricular
hypertrophy Hypertension Chronic kidney failure

Hypertensive
Aortic aneurysm encephalopathy
Retinopathy
Peripheral vascular disease All
Vascular
© Continuing Medical Implementation …...bridging the care gap
Adapted from: Arch Intern Med 1996; 156:1926-1935.
Mortality in Hypertension

• 50% from ischemic heart disease or


heart failure
• 33% from cerebrovascular disease
• 10 to 15% from renal failure

Harvard
Kaplan in Zipes, Libby, Bonow, and Braunwald. 2005 Medical
School
Consequences of Hypertension
Consequences of
Hypertension

http://www.massgeneral.org/vascularcenter/body/stroke.jpg
Hypertensive nephropathy

http://www.ndt-educational.org/images/Marcantonifig1.jpg
Retina Normal and Hypertensive
Retinopathy
A B

Normal Retina Hypertensive Retinopathy A: Hemorrhages


B: Exudates (Fatty Deposits)
C: Cotton Wool Spots (Micro
Strokes)
Peripheral Arterial Disease
(PAD)
 PAD is equivalent in risk to ischemic heart disease.

 Any class of drugs can be used in most PAD patients.

 Other risk factors should be managed aggressively.

 Aspirin should be used.


Dementia

 Dementia and cognitive impairment occur more commonly


in people with HTN.

 Reduced progression of cognitive impairment occurs with


effective antihypertensive therapy.
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
The Arterial Pulse Wave

Systolic
pressure Dicrotic notch
125 (aortic valve closes)
Pressure (mm Hg)

Pulse Mean pressure = 1/3 SBP + 2/3 DBP


pressure

Diastolic decay
curve
75 Diastolic
pressure
Time
DEFINISI

• Tekanan nadi (pulse pressure) = TD sistolik – TD


diastolik

• Tekanan arteri rata-rata (mean arterial


pressure/MAP) = (TD sistolik + 2xTD diastolik)
3
BP = CO x SVR

SV x HR
 BP : blood pressure
 SVR: systemic vascular-resistance
 SV : stroke volume
 HR : heart rate
Hemodynamic Components of
BP
 MAP - STEADY COMPONENT (due to CO and SVR)

• PP – PULSATILE COMPONENT (due to LV ejection


and elastic artery stiffness)

• SBP – rises with increased resistance and stiffness

• DBP – rises with increased resistance and decreases


with increased stiffness

Elzinga G, Westerhof N. Circ Res 1973;32:178-186.


Yano, et al. Basic Res Cardiol 1997;92:115-122.
Berne RM, Levy MN. Cardiovascular Physiology 1992:135-151.
Patterns of Arterial Pressure Change With Aging
PP

SBP
%
Change
mm Hg
MAP

DBP

Age (yr)
Franklin SS et al. Circulation. 1997;96:308-315.
1976-98 Cumulative Incidence of HTN
in Women and Men Aged 65 Years
Risk of Hypertension %
100

80
Men
Women
60

40

20

0
0 2 4 6 8 10 12 14 16 18 20

Years of Follow-up

Vasan, et al. JAMA.2002;287:1003


BP is a risk marker for “The Metabolic Syndrome”
NCEP-ATP III Definition: ≥3 of the Following*
Abdominal obesity • Men: >102 cm (>40 in)
(waist circumference) • Women: >88 cm (>35 in)

Triglycerides • ≥150 mg/dL

• Men: <40 mg/dL


HDL-C
• Women: <50 mg/dL
Blood pressure • ≥130/≥85 mm Hg

Fasting glucose • ≥100 mg/dL

*Diagnosis is established when ≥3 of these risk factors are present.

Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults.
JAMA. 2001;285:2486-2497.
Blood Pressure
Determining Factors
Cardiac Output:
Peripheral
Stroke Volume Resistance **
Heart Rate
Vasodilators
Force of Contraction
ACE Inhibitors
Beta Blockers
Calcium Channel
BP
Blockers

Blood Volume **

Diuretics ACE Inhibitors


DEFINISI

• HIPERTENSI PRIMER (90 – 95%)


hipertensi yang tidak diketahui penyebabnya

• HIPERTENSI SEKUNDER (5 – 10%)


hipertensi yang diketahui penyebabnya
Causes of Secondary HTN
 Common  Uncommon
 Intrinsic renal disease  Pheochromocytoma
 Renovascular disease  Glucocorticoid excess
 Mineralocorticoid  Coarctation of Aorta
excess  Hyper/hypothyroidism
 Sleep Breathing
disorder
Hipertensi Sekunder
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

JNC 7 Express. JAMA. 2003 Sep 10; 290(10):1314


Patogenesis Hipertensi

MULTIFAKTORIAL
PATOGENESIS
Hipertensi primer : Penyakit multifaktorial

• Interaksi faktor-faktor risiko seperti : diet / asupan


garam, stres, ras, obesitas, merokok, genetis
• Sistim saraf simpatis : tonus simpatis dan variasi
diurnal
• Keseimbangan antara modulator vasodilatasi dan
vasokonstriksi pembuluh darah : endotel,
remodeling endotel, otot polos dan interstitium
• Pengaruh sistim otokrin setempat  sistem RAA
Renin - Angiotensin
Glomerulus and Bowman’s Capsule

Juxtaglomerular
Cells

Decreased BP
Renin Release

Formation of
Angiotensin

Increased Vasoconstriction
Increased Aldosterone
with Increased Na++ and
Fluid Retention
FAKTOR2 YANG BERPENGARUH PADA PENGENDALIAN TD
asupan Na jumlah stress perubahan obesitas faktor2 yg
berlebih nefron genetis berasal dari
Endotel

retensi permukaan Aktifitas Renin perubahan hiper-


Na ginjal filtrasi Berlebih Angiotensin membran sel insulinemia
Saraf simpatiis release

volume konstriksi vena


cairan

konstriksi hipertrofi
Preload kontraktilitas fungsional struktural

TEKANAN DARAH CURAH JANTUNG TAHANAN PERIFER


Hipertensi
= Peningkatan CJ
X Peningkatan TP
= dan/atau
autoregulation
Kaplan
• According to the National Institutes of
Health (NIH), if hypertension (HTN) is
left untreated
–1/2 of hypertensive clients will die of heart
disease
–1/3 of hypertensive clients will die of a
stroke
–Rest of clients will die of renal failure
Blood Pressure Classification
JNC VII
BP SBP DBP
Classification mmHg mmHg
Normal <120 and <80
Prehypertension 120–139 or 80–89
Stage 1 140–159 or 90–99
Hypertension
Stage 2 >160 or >100
Hypertension
JNC 7: Appropriate BP Targets

• For both CVD and kidney disease, systolic BP is far


more important than diastolic BP

• Systolic BP should be <140 mm Hg in all patients, and


ideally between 120-130 mm Hg in patients with
complications (diabetes, heart failure, kidney disease)

• Only a small fraction of hypertensives are achieving


appropriate BP control

• Multiple antihypertensive agents are needed for most


patients

• Those with SBP 120–139 mmHg or DBP 80–89 mmHg


should be considered pre-hypertensive who require health-
promoting lifestyle modifications to prevent CVD.
JNC 7: Considerations for special
populations with hypertension

• Treatment generally similar for all


demographic groups
• Socioeconomic factors and lifestyle
important
barriers to BP control
• Prevalence, severity of hypertension
increased
in blacks
JNC 7. JAMA. 2003;289:2560-2672.
- very important is the circadian rhythm of blood
pressure!
- physiological profound nocturnal decline, mostly
around 4 a.m. ("dipping"), acts as a protection
against pathological lesions of blood vessels, resp.
reduces them
- also hypertensive patients with significant nightime
BP decrease have a more favorable prognosis ,as
patients whose blood pressure at night compared to
daytime values d​ oesn´t decrease (worse prognosis)
- → according to it are patients diveded to „dippers“
versus „non-dippers“
- ≅ improvement of diagnosis ← broader application of
24-hour blood pressure monitoring
Mengapa Tekanan Darah
Harus Diturunkan ?
FRAMINGHAM STUDY
CV Mortality Risk Doubles with
Each 20/10 mm Hg BP Increment*
8
7
6

CV 5
mortality 4
risk
3
2
1
0
115/75 135/85 155/95 175/105
SBP/DBP (mm Hg)

*Individuals aged 40-70 years, starting at BP 115/75 mm Hg.


CV, cardiovascular; SBP, systolic blood pressure; DBP, diastolic blood pressure
Lewington S, et al. Lancet. 2002; 60:1903-1913.
JNC 7. JAMA. 2003;289:2560-2572.
HIPERTENSI :
The Disease Continuum
Early Paradigm
Natural History of CVD Progression
Elevated BP Target Organ Damage
More Recent Paradigm

Vascular Dysfunction Elevated BP Target Organ Damage

A Proposed Future Paradigm

Endothelial Vascular Elevated BP Target Organ


Dysfunction Damage
? Dysfunction LVH
Angina
Pectoris
Renal MI Stroke
Damage
Hypertension Syndrome
It’s More Than Just Blood Pressure

Decreased
Arterial
Obesity Compliance Endothelial
Dysfunction

Abnormal
Abnormal Lipid
Glucose
Metabolism
Metabolism

Accelerated HYPERTENSION Neurohormonal


Atherogenesis Dysfunction

LV Hypertrophy Renal-Function
and Dysfunction Changes
Abnormal Blood-Clotting
Insulin Mechanism
Metabolism Changes

Kannel WB. JAMA. 1996;275:1571-1576. Weber MA et al. J Hum Hypertens. 1991;5:417-423. Dzau
VJ et al. J Cardiovasc Pharmacol. 1993;21(suppl 1):S1-S5.
Routine steps for accurate measurement
of blood pressure
• Rest the patient (seated) for at least 5 mins in a quiet
confortable room
. Use a calibrated sphygmomanometer (a validated and recently
calibrated electronic device may may also be used)
. Choose cuff with appropriate width of bladder
. Record with cuff at heart level
. Deflate cuff at 2 mmHg/sec
. First sound = systolic reading, disappearance = diastolic
reading
. Repeat measurement at least x2 (first visit: x3) & take average
value
. Take BP in both arms at least once; record which arm is used;
patient position ( seated, supine, standing) & pulse rate.
. Measure BP at + 1 & 5 mins after standing ( especially in older
patients and those with diabetes).
BP Measurement Techniques

Method Brief Description


In-office Two readings, 5 minutes apart, sitting
in chair. Confirm elevated reading in
contralateral arm.
Ambulatory BP Indicated for evaluation of “white-coat”
monitoring HTN. Absence of 10–20% BP decrease
during sleep may indicate increased
CVD risk.
Self-measurement Provides information on response to
therapy. May help improve adherence
to therapy and evaluate “white-coat”
HTN.
JNC 7 2003
How to measure blood pressure
accurately

 ……… sphygmomanometer
 Patient should be seated and relaxed, preferably for several minutes
prior to to the measurement and in a quiet room.
 Appropriate cuff size.
 Average the readings. If the first two readings differ by more than 10 mmHg
systolic or 6 mmHg diastolic or if the initial readings are high, take several
readings after five minutes of quiet rest, until consecutive readings do not
vary by greater than these amounts.
 Ideally, patients should not take caffeine-containing beverages or
smoke for at least two hours before blood pressure is measured,
…………………..
Australia, 2004
CV Mortality Risk Doubles with
Each 20/10 mm Hg BP Increment*
8
7
6

CV 5
mortality 4
risk
3
2
1
0
115/75 135/85 155/95 175/105
SBP/DBP (mm Hg)

*Individuals aged 40-70 years, starting at BP 115/75 mm Hg.


CV, cardiovascular; SBP, systolic blood pressure; DBP, diastolic blood pressure
Lewington S, et al. Lancet. 2002; 60:1903-1913.
JNC 7. JAMA. 2003;289:2560-2572.
Clinical Trials in Hypertension
Should we
What is the Should we treat What is the treat ISH in Can we
Should we treat goal of DBP in older best way to older prevent
diastolic HBP? treatment? persons? treat HBP? persons? hypertension?

1960s 1970s 1980s 1990-1995 1996-1999 2000 2001-2003 2004-2008

HDFP HOT
UKPDS SCOPE
CONVINCE VALUE
VA EWPHE ALLHAT ASCOT
Cooperative MRC-1 Syst-Eur
ANBP2 ACCOMPLISH
Studies ANHBP-1 SHEP Syst-China LIFE TROPHY
MRC-2 INSIGHT
CAPPP
STOP-1 STOP-2 NORDIL
HAPPHY
MAPHY
TOMHS
VA MONORx
HR Black, 2003.
Preparation for measurement
• Patient should
abstain from eating,
drinking, smoking
and taking drugs
that affect the blood
pressure one hour
before
measurement.
Preparation for measurement

• Because a full
bladder affects the
blood pressure it
should have been
emptied.
Preparation for measurement

• BP take in quiet
room and
comfortable
temperature, must
record room
temperature and
time of day.
BLOOD PRESSURE: MEASUREMENT
Ascultatory method of
blood pressure measurement Nokolai Korotkoff, 1905
Blood Pressure Assessment:
Patient preparation and posture
Standardized Preparation:

Patient
√ 1. No acute anxiety, stress or pain.
2. No caffeine, smoking or nicotine in the
preceding 30 minutes.
3. No use of substances containing adrenergic
stimulants such as phenylephrine or
pseudoephedrine (may be present in nasal
decongestants or ophthalmic drops).
√ 4. Bladder and bowel comfortable.
5. No tight clothing on arm or forearm.
6. Quiet room with comfortable temperature
7. Rest for at least 5 minutes before
measurement
√ 8. Patient should stay silent prior and during the
procedure.
Measuring Blood Pressure

Slide 9-59
Complications of Hypertension:

Hypertension
is a risk factor
TIA, stroke LVH, CHD,
HF
Renal
Peripheral vascular failure
disease
TIA = transient ischemic attack; LVH = left ventricular hypertrophy; CHD = coronary heart disease
HF = heart failure.
Cushman WC. J Clin Hypertens. 2003;5(Suppl):14-22.
Benefits of Lowering BP

Average Percent Reduction


Stroke incidence 35–40%

Myocardial infarction 20–25%

Heart failure 50%


Framingham Heart Study (1983)

CV Risk Profile
703
700
8 Year Probability Per 1,000

600
500 459
400
326
300
210
200
100 46

Systolic BP: 105 >>> 185 105 >>> 185 105 >>> 185 105 >>> 185 105 >>> 185
Cholesterol: 185 335 335 335 335
Glucose Intol.:0 0 + + +
Cigaretes: 0 0 0 + +
ECG-LVH: 0 0 0 0 +

Kannel, 1983
CXR:
Cardiomegaly
pleural effusions
interstitial edema
Pulmonary venous redistribution
Echocardiography

“Confirm” diagnosis with transthoracic echocardiography


– LV dimensions and ejection fraction
– Systolic versus diastolic function
– Valvular disease
– Pulmonary hypertension

All patients, Class 1C


National Heart, Lung, and Blood
Institute
National High Blood Pressure
U.S. Department of
Health and Human
Education Program
Services
The Seventh Report of
the
National Institutes
Joint National
of Health
Committee on
Prevention, Detection,
National Heart, Lung,
Evaluation, and
and Blood Institute
Treatment of High Blood
Lifestyle Interventions for Prevention or
Treatment of Hypertension

Intervention Blood Pressure Effect

Exercise 5-10 mm Hg (>30 min >3x/wk)

Weight reduction 1-2 mm Hg/Kg

Alcohol intake reduction 1 mm Hg/drink/d

Sodium intake reduction 1-3 mm Hg/40 mmol/d

DASH diet 3-10 mm Hg 

Adapted from Cushman et al. Endocrine Practice 1997;3:106 & Sacks, et al. NEJM 2001;334:3
DASH Fact Sheet
JNC 7 Algorithm for Treatment of Hypertension

Lifestyle Modifications

Not at Goal Blood Pressure (<140/90 mm Hg)


(<130/80 mm Hg for those with diabetes or chronic kidney disease)

Initial Drug Choices

Without Compelling With Compelling


Indications Indications

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


(SBP 140-159 or DBP 90-99 mm Hg) (SBP >160 or DBP >100 mm Hg) indications
Thiazide-type diuretics for most 2-drug combination for most (usually Other antihypertensive drugs
May consider ACEI, ARB, BB, CCB, thiazide-type diuretic and (diuretics, ACEI, ARB, BB, CCB)
or combination ACEI, or ARB, or BB, or CCB) as needed

Not at Goal
Blood Pressure

Optimize dosages or add additional drugs


until goal blood pressure is achieved
Consider consultation with hypertension specialist

Chobanian et al. JAMA. 2003;289:2560-2572.


Complications of hypertension

Brain  Strokes
TIA (transient ischemic attack)

Heart  Left ventricular hypertrophy


 Coronary artery disease
 Myocardial infarction
 Heart Failure
 Arrhythmia

Kidney  Renal failure

Retinopathy

Aneurysm (rupture) of the aorta

Peripheral artery disease

72
Laboratory Tests
 Routine Tests
• Electrocardiogram
• Urinalysis
• Blood glucose, and hematocrit
• Serum potassium, creatinine, or the corresponding estimated GFR, and calcium
• Lipid profile, after 9- to 12-hour fast, that includes high-density and low-density
lipoprotein cholesterol, and triglycerides
 Optional tests
• Measurement of urinary albumin excretion or albumin/creatinine ratio
 More extensive testing for identifiable causes is not generally indicated unless BP control is not
achieved
Classes of
Antihypertensive Drugs

• ACE inhibitors
• Adrenergic inhibitors
• Angiotensin II receptor blockers
• Calcium antagonists
• Direct vasodilators
• Diuretics
Combination Therapies

• -adrenergic blockers and diuretics


• ACE inhibitors and diuretics
• Angiotensin II receptor antagonists and
diuretics
• Calcium antagonists and ACE inhibitors
• Other combinations
Followup

• Followup within 1 to 2 months after initiating


therapy.
• Recognize that high-risk patients often require
high dose or combination therapies and
shorter intervals between changes in
medications.
• Consider reasons for lack of responsiveness if
blood pressure is uncontrolled after reaching
full dose.
• Consider reducing dose and number of agents
after 1 year at or below goal.
Pregnant Women

• Chronic hypertension is high blood pressure


present before pregnancy or diagnosed before
the 20th week of gestation.
• Preeclampsia is increased blood pressure that
occurs in pregnancy (generally after the 20th
week) and is accompanied by edema,
proteinuria, or both.
• ACE inhibitors and angiotensin II receptor
blockers are contraindicated for pregnant
women.
• Methyldopa is recommended for women
Antihypertensive Drugs
Used in Pregnancy

These agents* may be used with chronic hypertension


(DBP > 100 mm Hg) or acute hypertension (DBP > 105 mm Hg).

Central -agonists Methyldopa is the drug of choice.

-blockers and Atenolol, metoprolol, and labetalol appear safe


--blockers and effective in late pregnancy.

Calcium antagonists Potential synergism with magnesium sulfate may lead


to precipitous hypotension.

*Limited or no controlled trials in pregnant women.


Antihypertensive Drugs
Used in Pregnancy (continued)

These agents* may be used with chronic hypertension


(DBP > 100 mm Hg) or acute hypertension (DBP > 105).

Diuretics Diuretics are recommended for chronic


hypertension if prescribed before gestation,
but they are not recommended for
preeclampsia.
Direct Hydralazine is the parenteral drug of choice
vasodilators based on its long history of safety and
efficacy.
*Limited or no controlled trials in pregnant women.

ACE inhibitors and angiotensin II receptor blockers are contraindicated.


Mechanism of Action of
Angiotensin II Receptor Antagonists
Angiotensinogen
Alternate
Bradykinin Angiotensin I pathways
ACE
inhibitors
Angiotensin II
Inactive
peptides AIIRAs
?
AT1 receptor

Vasodilation
? Attenuate growth and
disease progression
Long-Term Antihypertensive Therapy
Significantly Reduces CV Events
Myocardial
Stroke infarction Heart failure
0

–10

–20
Average
reduction –30 20%-25%
in events
(%) –40
35%-40%
–50
>50%
–60

Blood Pressure Lowering Treatment Trialists’ Collaboration. Lancet. 2000;355:1955-1964.


Treated hypertensive subjects with BP <140/90 mmHg
34% 22% 6%
9% 3%

USA Canada UK
India China

<140/90 mmHg

140/90 mmHg

24% 27% 25%


2% 10%

France Italy Belgium


Zaire Egypt
Modifikasi Gaya Hidup untuk
Pengendalian Hipertensi
Modifikasi Rekomendasi Penurunan Tekanan
Darah Sistolik
kurang lebih
Menurunkan berat badan Pelihara berat badan 5-20 mm Hg utk
normal (BMI 18.5-24.9)
setiap penurunan
10 kg BB
Menjalankan menu DASH Konsumsi makanan kaya 8-14 mm Hg
buah, sayur, susu rendah
lemak dan rendah lemak
jenuh
Mengurangi asupan Kurangi natrium sampai 2-8 mm Hg
tidak lebih dari 2.4 g/hari
garam/sodium
atau NaCl 6 g/hari
Meningkatkan aktifitas Berolah raga erobik teratur 4-9 mm Hg
seperti berjalan kaki
fisik
(30 men/hari, 4-5 hari
seminggu)
Source: The Seventh Report of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure JNCVII. JAMA. 2003;289:2560-2572.
Management Strategy Assessed The
Patient Risk Profile
Blood Pressure (mm Hg)
Grade I (mild) Grade II Grade III
Risk Factors & Disease (moderate) (severe)
History SBP:140-159 160-179 > 180
DBP:90-99 100-109 > 110
I. No Other Risk Factors LOW RISK MED RISK HIGH RISK

II. 1-2 Risk Factors MED RISK MED RISK V. HIGH RISK

III. 1-2 Risk Factors or TOD HIGH RISK HIGH V. HIGH RISK
or Diabetes
IV. Associated Clinical V. HIGH RISK V. HIGH V. HIGH RISK
Condition RISK

WHO – ISH, 1999


84
Goal Hypertension Therapy

To achieve the maximum reduction in the


total risk of cardiovascular/ target vital organ
morbidity and mortality

Target:
BP: SBP < 130 – 140 mm Hg
DBP < 90 mm Hg

JNC. VII, 03, WHO – ISH, 1999


85
ESH-ESC 2007
Pharmacotherapy based on : Efficacy, Safety, + Costly (WHO-
ISH, 1999)
Class of Compelling Possible Compelling C.I Possible C.I
drug indication indications
Diuretics •Heart Failure Diabetes Out
•ELDERLY
•Systalic hypertension
ß-Blockers • Angina Heart Failure •Asthma & CoPD •Phslipidemia
• After M.I Pregnancy •Heart Block •Athletes, physically active
• Tachyarrhythmia Diabetes (gr 2/3 AV) patients
•Peripheral vascular disease
Calcium •Angina Peripheral Heart block Congestive heart failure
antagonists •ELDERLY vascular disease
•Systolic hypertension
ACE •Heart Failure •Pregnancy
inhibitors •LU Dysfunction •Hyperkalaemia
•After myocardial infarct •Renalartery stenosis
(bilateral)
 - Blocker Prostatic hypertrophy •Glucose Orthostatic hypotension
intolerance
•dyslipidemia
Angiotensin II Ace – inhibitor cough Heart failure •Pregnancy
Receptor •Hyperkalaemia
antagonist •Renalartery stenosis 87
(bilateral)
Choice of initial drugs

 Diuretics
 β - blockers
 Calcium channel blocker
 ACE inhibitor
 AIIRA / ARB

88
Choice of the initial drugs

 Should tailored to the patients, for example


in gout do not administered thiazide

 In asthmatic patients do not give beta


blocker.

 In “blacks people” ACE inhibitor or


beta-blockers are not very effective

89
Thiazide Diuretics
mechanism of action

lower plasma volume

monotherapy for mild to


moderate hypertension
Hydrochlorothiazide
ALLHAT: reduction of CVD
superior to other agents

adjunct agent

most effective in patients with


normal kidney function
Drugs interacting with Renin-Angiotensin system

ACE inhibitors: inhibit Angiotensin II formation

Angiotension receptor antagonists: block Angiotensin


receptor activation
Systemic Effects of ACE inhibitors
Reduction in
total peripheral resistance
systolic and diastolic pressure
mean arterial pressure
aldosterone secretion
cardiac remodeling
Increase in
regional blood flow in vascular beds
large artery compliance
Types of ACE inhibitors
Active Molecules
Captopril (Capoten)
Lisinopril (Prinivil)
Enalaprilat
Prodrugs: Enalaprilat

must be biotransformed for


activity by esterases
•Enalapril (Vasotec)
•Fosinopril (Monopril)
•Quinapril (Accupril)
•Ramipril (Altace) Enalapril
Side Effects
hypotension
cough
hyperkalemia
angioedema
renal insufficiency
teratogenic
skin rash
neutropenia
proteinuria (protein in urine)
ageusia (loss of taste)
Types of AT1 receptor antagonists

Losartan (Cozaar)
competitive antagonist
Valsartan (Diovan)
non-competitive
Candesartan (Atacand)
non-competitive
Losartan
Irbesartan (Aprovel)
non-competitive
Therapeutic Uses
same uses as ACE inhibitors

excellent for inhibiting cell growth

no bradykinin effects

no cough

useful for hypertension secondary to CHF

used for prevention of re-stenosis after angioplasty


Adrenergic receptor antagonists
β-adrenergic receptor antagonists
“β-blockers”
Non-selective: Propranolol, Nadolol, Timolol,
Pindolol, Labetolol
Cardioselective: Metoprolol, Atenolol, Esmolol,
Betaxolol
α1-adrenergic receptor antagonists
“α-blockers”
Non-selective: Phentolamine, Phenoxybenzamine,
Dibenamine
Selective: Prazosin, Doxazosin, Terazosin
-blockers: Side Effects
Bradycardia
Bronchospasm
Coldness of extremities
Heart failure
Contraindicated in insulin-dependent diabetes
CNS effects
Increased plasma triglyceride concentration
Decreased plasma HDL concentration
Do not use in conjunction with Ca2+ channel
lockers, conduction effects in heart
NSAID’s blunt β-blocker effects
Ca2+ channel antagonists
an initial choice for monotherapy of mild to moderate
hypertension
all antagonists are equally effective for Stage 1
hypertension
Verapamil and Diltiazem do not cause reflex tachycardia
directly inhibit cardiac chronotropy
Effective in low-renin hypertension
African-americans
Elderly
Do not cause fluid retention
Hypertension in Women

 Oral contraceptives may increase BP, and BP should be


checked regularly. In contrast, HRT does not raise BP.

 Development of HTN—consider other forms of contraception.

 Pregnant women with HTN should be followed carefully.


Methyldopa, BBs, and vasodilators, preferred for the safety of
the fetus. ACEI and ARBs contraindicated in pregnancy.
Women

• Clinical trials have not demonstrated


significant differences between men and
women in treatment response and
outcomes.
• Some women using oral contraceptives
may have significant increases in blood
pressure.
• High blood pressure is not a
contraindication to hormone replacement
Pregnant Women

• Chronic hypertension is high blood pressure


present before pregnancy or diagnosed before
the 20th week of gestation.
• Preeclampsia is increased blood pressure that
occurs in pregnancy (generally after the 20th
week) and is accompanied by edema,
proteinuria, or both.
• ACE inhibitors and angiotensin II receptor
blockers are contraindicated for pregnant
women.
• Methyldopa is recommended for women
Antihypertensive Drugs
Used in Pregnancy

These agents* may be used with chronic hypertension


(DBP > 100 mm Hg) or acute hypertension (DBP > 105 mm Hg).

Central -agonists Methyldopa is the drug of choice.

-blockers and Atenolol, metoprolol, and labetalol appear safe


--blockers and effective in late pregnancy.

Calcium antagonists Potential synergism with magnesium sulfate may lead


to precipitous hypotension.

*Limited or no controlled trials in pregnant women.


Important Aspects of the Physical
Examination in the Hypertensive Patient

• Accurate measurement of blood pressure


• General appearance: distribution of body fat, skin lesions,
muscle strength, alertness
• Fundoscopy
• Neck: palpation and auscultation of carotids, thyroid
• Heart: size, rhythm, sounds
• Lungs: rhonchi, rales
• Abdomen: renal masses, bruits over aorta or renal
arteries, femoral pulses
• Extremities: peripheral pulses, edema
• Neurologic assessment
© Continuing Medical Implementation …...bridging the care gap
CHS Recommendations
Routine Laboratory Investigations

Routine laboratory tests for the investigation of all


patients with hypertension:
1. Urinalysis
2. Complete blood cell count
3. Blood chemistry (potassium, sodium and
creatinine)
4. Fasting glucose
5. Fasting total cholesterol, high-density lipoprotein
(HDL) cholesterol, low-density lipoprotein
(LDL) cholesterol, triglycerides
6. Standard 12 ECG

© Continuing Medical Implementation …...bridging the care gap


Barriers to Controlling Hypertension

Patients Providers

Healthcare
System
Self-Measurement of BP

 Provides information useful for:


1. assessing response to antihypertensive Rx
2. improving adherence with therapy
3. evaluating white-coat HTN
 Home BP is more strongly related to target
organ damage and has better prognostic
accuracy than office BP.
Understanding hypertensive CV Risk

• Epidemiology Summary:
– Increasing prevalence; world wide problem
– Blood pressure as a moving target
– ↑ PVR in the young, ↑ stiffness in the elderly
– Predominantly isolated systolic hypertension
– Consider special populations at increased risk
– Hypertension as a part of absolute global CV
risk
– Population vs. high risk approaches for
prevention
- very important is the circadian rhythm of blood pressure!
- physiological profound nocturnal decline, mostly around 4
a.m. ("dipping"), acts as a protection against pathological
lesions of blood vessels, resp. reduces them
- also hypertensive patients with significant nightime BP
decrease have a more favorable prognosis ,as patients
whose blood pressure at night compared to daytime values
doesn´t decrease (worse prognosis)
- → according to it are patients diveded to „dippers“ versus
„non-dippers“
- ≅ improvement of diagnosis ← broader application of 24-
hour blood pressure monitoring
Strategies for Prevention of High Blood Pressure

General Population Strategy


Following Before
Intervention Intervention
Attempt to shift (downwards) the
distribution of BP in entire population

Targeted Intensive Strategy

More intensive efforts to reduce BP


in individuals/groups at highest
risk of hypertension Estimated Effect of 2 mm Hg Reduction in
Average Diastolic BP in General Population
35-64 year old White Residents of United States

 High normal BP  17% reduction in prevalence of


hypertension
 Family history of hypertension
 14% reduction in average
 High risk groups annual incidence of stroke

 Environmental exposures that  6% reduction in average annual


increase probability of hypertension incidence of CHD
 High weight
 High salt intake
 Alcohol consumption Cook N R et al., Arch Intern M ed 1996
 Physical inactivity

Whelton, PK, He J, Appel LA et al., JAMA 2002;288:1882-1888

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