hypertension dr akram saleh ass professor consultant invasive cardiologist jordan university...
TRANSCRIPT
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HYPERTENSION
Dr Akram SalehASS professor
Consultant Invasive CardiologistJordan University Hospital
22-NOV-2010
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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.
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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:
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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
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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
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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
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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)
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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
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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
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PathophysiologyMechanism
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
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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
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Aetiology of Hypertension Primary
– 90-95% of cases – also termed “essential” or “idiopathic”
Secondary – about 5% -10% of cases
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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
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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 syndromePregnency: pre-eclampsia, eclampsia
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SECONDARY HYPERTENSION
Drug-induced or related causes • NSAIDs • oral contraceptives, steroids • Cocaine, amphetamines, other illicit drugs• Sympathomimetics • Cyclosporine and tacrolimus• Erythropoietin
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CLASSIFICATION
Category Systolic BP Diastolic BP
• Normal <120 and <80• PREHTN 120-139 or 80-
90• Hypertension
-Stage 1 140-159 or 90-99 -Stage 2 >160 or >100
JNCVII
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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,..
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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.
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Evaluation
History
Examination
Investigation
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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
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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
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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
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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)
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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
http://www.familymedshop.com/prod_img/pc0007.jpg
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Xanthelesma, arcus, fundoscopy
Carotid pulse, bruit, goiter
Abex beat, A2, S4,syst bruite
Radial pulse, R-F delayxanthoma, A-V fistula
Renal bruite, polycysticKidney, aortic aneurysm
Prox muscle weaknessDist sens loss( DM, Alcohol)
Pulses: dorsalis ped, post tibialedema
Upper body hypertrophy
General appearance,Azotemia,cushinoid
acromegaly
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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
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Retinopathy
Grade 1: Narrowing and tortousity
Grade2 : 1+ A/V Nipping
Grade 3: 2+ flame shaped HG and soft exudate
Grade 4: 3+ papilloedema
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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
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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
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Treatment Treatment
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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.
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Benefits of Lowering BP
Average Percent Reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%
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GOALS OF THERAPY
Goal BP:• HTN: <140/90• Diabetics: <130/85• Renal failure:
<130/85• Proteinuria (>1
gm/24 hrs): <125/75
• Goal BP:– HTN:
<140/90– Diabetics:
<130/80– Renal
failure: <130/80
JNCVI JNCVII
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GOALS OF THERAPY
Base medication decisions on: • compelling indications• comorbid conditions• side effect profile• drug interactions• cost
Always favor the long-acting formulations
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Lifestyle Modification
Modification Approximate SBP reduction(range)
Weight reduction 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
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Classification and Management of BP for adults
BP classification
SBP* mmHg
DBP* mmHg
Lifestyle modification
Initial drug therapy
Without compelling indication
With compelling indications
Normal <120 and <80 Encourage
Prehypertension 120–139 or 80–89 Yes No antihypertensive drug indicated.
Drug(s) for compelling indications. ‡
Stage 1 Hypertension
140–159 or 90–99 Yes Thiazide-type diuretics for most. May consider ACEI, ARB, BB, CCB, or combination.
Drug(s) for the compelling indications.‡
Other antihypertensive drugs (diuretics, ACEI, ARB, BB, CCB) as needed.
Stage 2 Hypertension
>160 or >100 Yes Two-drug combination for most† (usually thiazide-type diuretic and ACEI or ARB or BB or CCB).
†‡
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ANTIHYPERTENSIVE MEDICATIONS
Compelling Indications
• Diabetes mellitus (type 1) with proteinuria
• Heart failure
• High coronary disease risk
(stable angina/silent ischemia)
JNCVII
ACE-I, ARB, CCB
Diuretic, -blocker,
Diuretic, -blocker, ACE-I, ARB, and aldo antagonist
-blocker, ACE-I, CCB , Diuretic
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ANTIHYPERTENSIVE MEDICATIONS
Compelling Indications
• Post Myocardial infarction
• Chronic kidney disease
• Recurrent stroke prevention
JNCVII
-blockers, ACE-I, aldo antagonist (w/ HF)
ACE-I, ARB
Diuretic, ACE-I
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Logical Combinations
b-
a-
- -
b- - -
- -
a- -*
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Thank you
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Renal Angiogram
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Angioplasty
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Right Stent in-situ
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Coronary Stents
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Bilateral Stents In-Situ