Download Goal BP

HYPERTENSION
Dr Akram Saleh
ASS professor
Consultant Invasive Cardiologist
Jordan University Hospital
22-NOV-2010
HYPERTENSION
 HTN prevalence ~ age > 18 years 25-30%
age > 65 years 50%
 Only 30-35% of hypertensive patients are well control
 The BP relationship to risk of CVD is continuous, consistent, and
independent of other risk factors.
 Blood pressure is a continuous variable which
fluctuates widely during the day
• physical stress
• mental stress
• High during the day ( early morning)
• Low during sleep
 The definition of hypertension has been arbitrarily
set as: abnormal elevation of blood pressure:
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
 BP= C.O.P× Peripheral Resistant
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
Pathophysiology
Mechanism
 Neurogenic: sympathetic activation– high
catecholamin– high arteriolar tone– high resistent
 Abnormal Na balance:
Na excretion----Salt and
Water retention----increase volume----increase COP---Increase tone
 At cellular level----Inhibition of Na pump –Increase
Na intracellular---Activate Na-Ca pump ---increase
intracellular Ca --Vasoconstriction
Pathophysiology
 Multifactorial in origin and caused by a
breakdown of the control mechanisms which
regulates:
 Cardiac Out Put
 Blood volume
 Na balance
 Systemic vascular resistant
Aetiology of Hypertension
 Primary
– 90-95% of cases – also termed “essential” or
“idiopathic”
 Secondary
– about 5% -10% of cases
Essential HTN
 Usually occurs in the fourth or fifth decade
 Risk factors
• Obesity
• Excessive salt intake
• Excessive alcohol intake
• Lack of exercise
• Stress
• Family history of essential HTN
• Others: fetal weight, humoral factors, metabolic
syndrome X
 Caffeine and smoking increase the BP acutely but are not
risk factors for the development of chronic essential HTN
Secondary – about 5% -10% of cases
• Renal : 1- Paranchymal: GN, Pylonephritis, Polycystic
kidney,…
•
2- Renal artery stenosis: atherosclerosis, fibromuscular dysplasia
• Endocrine disease
•
•
•
•
Phaeochomocytoma
Cusings syndrome
Conn’s syndrome
Acromegaly and hypothyroidism, hyperparathyroidism
• Iatrogenic
• Hormonal / oral contraceptive
• NSAIDs
• Steroid, sympathomimetic, carbenoxolone,
• Coarctation of the aorta
• Sleep apnea syndrome
Pregnency: pre-eclampsia, eclampsia
SECONDARY HYPERTENSION
 Drug-induced or related causes
• NSAIDs
• oral contraceptives, steroids
• Cocaine, amphetamines, other illicit drugs
• Sympathomimetics
• Cyclosporine and tacrolimus
• Erythropoietin
CLASSIFICATION
JNCVII
Category
•
•
•
Normal
PREHTN
Hypertension
-Stage 1
-Stage 2
Systolic BP
Diastolic BP
<120
120-139
and
or
<80
80-90
140-159
>160
or
or
90-99
>100
Clinical manifestation
 Asymptomatic
 Non-specific symptoms: headache, epistaxis,
nocturia,..
 Target organ damage: CVS, CNS, Kidney, Eye,
Periphral vascular disease
 Symptoms of secondary causes: Muscle weakness,
palpitation, sweating, tremors, flank pain,
hematuria,..
Patient Evaluation
Evaluation of patients with documented HTN has three
objectives:
1. Assess lifestyle and identify other CV risk factors or
concomitant disorders that affects prognosis and
guides treatment.
2. Reveal identifiable causes of high BP.
3. Assess the presence or absence of target organ
damage.
Evaluation
 History
 Examination
 Investigation
Evaluation- History








Duration, Coarse, Treatment
Dietary: Salt, Fat, Alcohol
Family history
Symptoms of secondary causes: muscle weakness,
palpitation, anxiety, sweating, tremors, flank pain,..
Symptoms of target organ damage: CVS, CNS,..
Other risk factors: DM, Smoking, Hyperlipidemias,..
Drug history
Features of sleep apnea syndrome
Examination
 Detection and Confirmation of hypertension:
Patient position
Cuff size, inflation, deflation
Stethoscope position
phase 1 and phase IV
SIGNS OF SECONDARY CAUSES
SIGNS OF ORGAN DAMAGE
BP MEASUREMENT
 Measurement of BP should be obtained:
• In all adults (age >18) at each visit
• > 30 minutes after use of nicotine or caffeine
• After 5 minutes of rest with arm supported at
heart level
• With appropriate sized cuff
• bladder should encircle 80% of the arm
BP MEASUREMENT
 Measurement of BP should be obtained:
• Twice, at least two minutes apart
• repeat if >5 mm pressure difference
• With patient seated with feet flat on floor, back and
arm supported, and arm at heart level
• Use manual mercury sphygmomanometer or
recently calibrated aneroid manometer or validated
automated device (JNCVI and VII)
BP MEASUREMENT
 Self measurement of BP
• An avg BP more than
135/85 mmHg measured
at home is generally
considered to be
hypertensive
• Wrist and finger
manometers are not
recommended
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General appearance,
Azotemia,cushinoid
acromegaly
Xanthelesma, arcus,
fundoscopy
Abex beat, A2, S4,
syst bruite
Carotid pulse, bruit,
goiter
Upper body hypertrophy
Renal bruite, polycystic
Kidney, aortic aneurysm
Radial pulse, R-F delay
xanthoma, A-V fistula
Prox muscle weakness
Dist sens loss( DM, Alcohol)
Pulses: dorsalis ped, post tibia
edema
Target Organ Damage
 Heart: Increase 3 folds of cardiac death
• Left ventricular hypertrophy
• Coronary Atherosclerosis: Angina or prior myocardial infarction
•Heart failure
 Brain: Increase 6 folds of stroke
• Stroke or transient ischemic attack
•Subarachnoid HG, Intracerebral HG
 Chronic kidney disease: Nephropathy, Renal failure
 Peripheral arterial disease: atherosclerosis, aneurysm,
dissection
 Retinopathy
Retinopathy
 Grade 1: Narrowing and tortousity
 Grade2 : 1+ A/V Nipping
 Grade 3: 2+ flame shaped HG and soft exudate
 Grade 4: 3+ papilloedema
Laboratory Tests
 Routine Tests
• Electrocardiogram
• Urinalysis
• Blood glucose, and hematocrit
• Serum potassium, creatinin, 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
•Echocardiography
•CXR (no more routine)
 More extensive testing for identifiable causes is not generally indicated unless BP control
is not achieved
Secondary HTN – who to evaluate
 Young patients 20<Age > 50 with no family history
 Createnin >1.2 mg/dl
 Patients resistant to treatment
• Uncontrolled HTN on adequate doses of three medicines one of which is a
diuretic
 Patients who have
• Physical findings (abdominal bruits) sensitivity 40%, specificity 90%
• Biochemical abnormalities (unprovoked hypokalemia)




An acute rise in BP over previously stable baseline
Flash pulmonary edema
Unexplained raise in createnin after ACE inhibitor
Moderate-sever hypertension in patient with diffuse atherosclerosis
Treatment
Goals of Therapy
 Reduce morbidity and mortality
 Treat to BP <140/90 mmHg or BP <130/80 mmHg in
patients with diabetes or chronic kidney disease.
Benefits of Lowering BP
Average Percent Reduction
Stroke incidence
35–40%
Myocardial infarction
20–25%
Heart failure
50%
GOALS OF THERAPY
JNCVI
 Goal BP:
• HTN: <140/90
• Diabetics: <130/85
• Renal failure:
<130/85
• Proteinuria (>1
gm/24 hrs):
<125/75
JNCVII
• Goal BP:
– HTN: <140/90
– Diabetics:
<130/80
– Renal failure:
<130/80
GOALS OF THERAPY
 Base medication decisions on:
• compelling indications
• comorbid conditions
• side effect profile
• drug interactions
• cost
 Always favor the long-acting formulations
Lifestyle Modification
Modification
Weight reduction
Approximate SBP reduction
(range)
5–20 mmHg/10 kg weight loss
Adopt DASH eating plan
8–14 mmHg
Dietary sodium reduction
2–8 mmHg
Physical activity
4–9 mmHg
Moderation of alcohol
consumption
2–4 mmHg
Classification and Management
of BP for adults
BP
classification
Normal
SBP*
mmHg
DBP*
mmHg
Lifestyle
modification
<120
and <80
Encourage
Initial drug therapy
Without compelling
indication
Prehypertension 120–139 or 80–89
Yes
No antihypertensive drug
indicated.
Stage 1
Hypertension
Yes
Thiazide-type diuretics for
most. May consider ACEI,
ARB, BB, CCB, or
combination.
Yes
Two-drug combination for
most† (usually thiazide-type
diuretic and ACEI or ARB or
BB or CCB).
Stage 2
Hypertension
140–159 or 90–99
>160
or >100
*Treatment determined by highest BP category.
Initial combined therapy should be used cautiously in those at risk for orthostatic
hypotension.
Treat patients with chronic kidney disease or diabetes to BP goal of <130/80 mmHg.
With compelling
indications
Drug(s) for compelling
indications. ‡
Drug(s) for the
compelling
indications.‡
Other antihypertensive
drugs (diuretics, ACEI,
ARB, BB, CCB) as
needed.
ANTIHYPERTENSIVE
MEDICATIONS
JNCVII
Compelling Indications
• Diabetes mellitus (type 1)
with proteinuria
ACE-I, ARB, CCB
• Heart failure
Diuretic, -blocker, ACE-I,
ARB, and aldo antagonist
• High coronary disease risk
(stable angina/silent
ischemia)
Diuretic,
-blocker,
-blocker, ACE-I, CCB ,
Diuretic
ANTIHYPERTENSIVE
MEDICATIONS
JNCVII
Compelling Indications
• Post Myocardial infarction
-blockers, ACE-I, aldo
antagonist (w/ HF)
• Chronic kidney disease
ACE-I, ARB
• Recurrent stroke
prevention
Diuretic, ACE-I
Logical Combinations
Diuretic
bDiureti
c
blocker

-
ACE
inhibitor

CCB
ablocker

b-blocker

-
*
-

CCB
-
*
-


ACE



inhibitor




a-blocker
* Verapamil + beta-blocker = absolute contra-indication
Thank you
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