HYPERTENSION

Dr Akram SalehASS professor

Consultant Invasive CardiologistJordan 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

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

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 syndromePregnency: 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

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

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

http://www.familymedshop.com/prod_img/pc0007.jpg

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

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 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

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

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 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

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).

†‡

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

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

Logical Combinations

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a-          -*    

Thank you

Renal Angiogram

Angioplasty

Right Stent in-situ

Coronary Stents

Bilateral Stents In-Situ