S.Moradmand MD. SYSTEMIC HYPERTENSION

DEFINITION: A level of blood pressure that is associated With increased morbidity & mortality At some future time when compared With the whole population

BP Range mm Hg Category DBP <85 Normal BP 85 – 89 High normal BP 90 – 104 Mild hypertension 105 – 114 Moderate hypertension >115 Severe hypertension SBP when DBP <90mm Hg < 140 Normal BP 140 – 159 Borderline isolated systolic hypertension >160 Isolated systolic hypertension

CLASSIFICATION of BLOOD PRESSURE Normal <130 <85 High Normal Hypertension Stage 1(Mild) Stage 2(Moderate) Stage3(Severe) Stage4(Very severe) >210 >120 Category Systolic Diastolic

5 Guidelines The Seventh Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) uses the following guidelines to define HTN in adults: (Brashers, 2006, p.1) CategorySystolicDiastolic Normal <120and<80 Pre-hypertension or85-89 Stage 1 hypertension or90-99 Stage 2 hypertension >160or>100

Pulse Pressure: Systolic minus Diastolic Presurre Mean BP = DP + 1/3 Pulse Pressure ( A good indicator of tissue perfusion)

Angiotensinosion Angiotensin 1 Angiotensin 2 Angiotensin3 ReninRenin Release B-blocker Coverting Enzyme ACEI Receptor Antagonist Angiotensinases

Persistently raised Clinic BP Target organ damage Home BP Ambulatory BP Continue to monitor Clinic & home BP Start Treatment yes high

Systolic Pressure 1.Stroke volume 2.The velocity of ejection 3.The elastic properties of aorta

Diastolic Pressure 1.Competency of aortic valve 2.The condition of arteries & their ability to stretch & store energy 3.Resistance of arterioles

Blood Pressure Cardiac output X Peripheral resistance cardiac HR contractility Renal Fluid volume humoral sympathethic local Dilator (beta) Constictor ( Alpha) Vasodilator Prostaglandins Vasoconstrictors Angiotensin-endothelin n

classification 1.Essential HTN 2.Renal HTN 92-94% Paranchymal Renovascular 3.Endocrine HTN Primary Hyperaldostronism Cushing’s syndrome Pheochromocytoma OCP

Essential HTN Hereditery Enviromental Salt sensitivity High renine Low renine Nonmodulating Cell membrane defect Insulin resistance

Renin Release control 1.Blood volume, Renal perfusion 2.Na filtrated to Macula Densa 3.Sympathetic nervous system 4.Dietary Potassium

Low renin HTN 1. 20% of patients 2. Increased extracellular volme 3. On high sodium diet mild degree of hyperaldostronism 4. Increased sensitivity of adrenal cortex to angiotensin II

Nonmodulating Essential HTN 1. Adrenal defect apposite to low renin % of patients 3. Normal or high renin 4. Na intake dosen’t modulate adrenal or renal response 5. Corrected with ACEI

Cell Membrane Defect Abnormality in Na transport Calcium accumulation in Vascular smooth muscle cells Increased vascular reactivity to Vasoconstrictor agents

Calcium in HTN 1.Low ca++ intake increase BP 2.Ca++ blockers are effective antihypertensives 3.Salt loading increase NF 4.Digital sensitive Na-K ATPase lead to intracellular calcium accumulation

Insulin Resistanse 1. Increased sympathetic activity 2. Vascular smooth muscle hypertrophy 4. Increase cytosolic calcium

Natural hx of HTN 1.Progressive & lethal if untreated 2.Shortening of life years 3.If untreated in 7-10 years develope 30 % athersclerosis, 50% CHF, Cardiomegaly,CVA, Renal insufficeincy & retinopathy. 4.Morbid Cardiovascular events by as much as 20 fold

Hx., Ph.E., Lab. Tests 1.Uncovering secondary HTN 2.Establishing a pretreatment baseline 3.The factors that may influence therapy 4.Determining if target organ damage? 5.Determining if other CAD risk factors?

Renal Paranchymal HTN 1. Volume expansion 2. Renin-Angiotensin system 3. Unidentified pressure agent 4.Fail to produce vasodilator substance 5. Fail to inactivate vasopressores

Endocrine HTN 1.Aldostronism 2.Cushing Sndrome 3.Adrenogenital Syndrome 4.Pheochromocytoma 5.Acromegaly 6.Hypercalcemia 7.Oral contraceptives

Oral Contraceptives 1.Estogen stimulate hepatic angiotensinogen 2.5% increase BP 3.Familial Factors 4.Age over 35 5.Obesity

Symptoms & Signs 1.Elevated pressure itself headache,dizziness,palpitation, easy fatigability 2.Hypertension vascular disease: epistaxis,hematuria,TIA,angina,dyspnea 3.Underlying disease in secondary HTN: polyuria & polydipsia,… 4.Most patients are asymptomatic

Factors indicating adverse prognosis 1.Black race 2.Youth age 3.Male 4.Persistent diastolic pressure >115 mmhg 5.Smoking 6.Diabetes Mellitus 7.Hypercholesterolemia 8.Obesity 9.Excess alcohol intake 10.Evidence of End Organ Damage

Manifestation of Target Organ Disease 1.Cardiac :CAD LVH Cardiac Failure 2.Cerebrovascular:TIA / CVA 3.Peripheral Vascular 4.Renal 5.Retinopathy Infarction Hemorrhage Encephalopathy

Medical Therapy 1.DIURETICS 2.ACEI 3.BETA-BLOCKERS 4.CALCIUM BLOCKERS

Drugs used in Emergency HTN 1.Hydralazine 2.Minoxidil 3.Diazoxide 4.Nitroprusside

Basis of Treatment Salt restriction Na intake <100mm Relaxation Reduce sympathetic Weight loss Diet /Exercise Exercise Aerobic

Basic Tests for Evaluation Urinalysis CBC(Hct) Na-K Creatinine/BUN EKG FBS-Cholestrol(LDL-HDL)-TG Ca++-Phosphate-Uric Acid Chest-X-Ray / Echocardiogram

Coarctation of Aorta Diminished or delayed Femoral Pulses Rib notching on chest-X-Ray

Pheochromocytoma Unusual lability of BP Symptomatic Paroxysm of HTN Spell of Pallor Palpitation Perspiration Headache Hypertensive reaction to G/A or antihypertensive drugs

Renovascular HTN 1.Age under 30 2.DBP > 120 mmHg 3.Continuous bruit in epigasrium or flanks 4.Accelerated HTN 5.Hx. Of flank pain,hematuria or renal truma 6.palpable kidney 7.HTN resistant to treatment

Conn’s Syndrome 1.Serum potassium less than Urinary Potassium more than 30/24h in the absence of diuretic therapy

Isolated Systolic HTN A.Decreased aortic compliance as in arteriosclerosis B.Increased stroke volume 1-AI 2-Thyrotoxicosis 3-Hyperkinetic heart syndrome 4-Fever 5-AVF 6-PDA