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SYSTEMIC HYPERTENSION

This document outlines the classification and management of hypertension (HTN), including definitions, stages, and treatment protocols. It emphasizes the importance of accurate blood pressure assessment, risk stratification, and identifying secondary causes, while also detailing lifestyle modifications and medication options for treatment. The document serves as a comprehensive guide for healthcare professionals in managing patients with high blood pressure.

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By: Dr./ SAHAR H. MOSTAFA Consultant of internal medicine El-MatariaTeaching Hospital-Cairo- Egypt November,2016
Persistent elevation of BP above normal values ≥ (140 / 90), on three different occasions, under mental and physical rest
Question: Why above these values..? Answer:  Because this the value above which the benefits of treating hypertension(HTN), appear to outweigh the risks
 Normal BP: < (130 / 80)  Pre-Hypertension: 130 – 139 / 85 - 89  Hypertension: ≥(140/90) Normal BP: <(130 / 80) Pre- Hypertension: 130–139/85-89 Hypertension: ≥(140/90)
29 % of the world’s adult population will be projected to develop hypertension(HTN), by the year 2025
Stages of HTN Systolic BP Diastolic BP Stage I (mild) 140 – 159 90 – 99 Stage II (moderate) 160 – 179 100 – 109 Stage III (severe) ≥ 180 ≥ 110
 Question: when a person’s systolic and diastolic BP fall into different categories, which stage would be defined..?  Answer:The higher one
 Focusing on 3 Goals: • Accurate assessment of BPGoal 1 • Cardiovascular risk stratificationGoal 2 • Identification of 2ry causesGoal 3
 Goals would be achieved through:
 Personal History: • Age • Smoking • Alcohol • Job  Present History: • Co morbid disease(diabetes, gout, bronchial asthma, depression, migraine, ..) • Diet • Drugs • Lifestyle • Ask for 2ry causes • Search forTOD (target organ damage)  Past History: Record last BP and last treatment  Family History: • Hypertension • Renal disease • Premature stroke
 Asymptomatic: HTN may be termed the silent killer  Alerting symptoms: Headache, fatigue, blurring of vision, ..
 Face  Pulse  BMI  BP  Chest examination  Heart examination  Abdominal examination  Neurological examination
 Face: Cushingoid ?steroids, ?Cushing’s Lid edema Nephrotic syndrome Staring look Thyrotoxic Bloated Myxedema Acromegalic Acromegaly
 Pulse: ------> Radial • Equality • Volume • Special character • Femoral: radio-femoral delay in coarctation of aorta • Trousseau Sign: Carpopedal spasm when BP is increased above systolic for > 3 min. due to hypokalemia (Conn’s syndrome)
 BMI: Normally < 25 BMI = WEIGHT ( Kg) / HEIGHT (m2) NORMAL 18.5 – 25 OVERWEIGHT 25 – 30 OBESE 30 – 40 MORBID OBESITY > 40
 BP: • Supine: arm same level as heart • Sitting: back supported, feet on ground • Standing: after 5 min of standing; to elucidate autonomic insufficiency, as in: • Diabetes • Parkinsonism • Old age --------------------------------------------------------- N.B. : At 1st visit, document BP in both arms
 Home BP monitoring: • It engages the patient in his own heath care • Persistent nocturnal hypertension will increase the BP burden on cardiovascular system • The morning surge in BP is associated with increased incidence of stroke, myocardial infarction as well as sudden cardiac death • Elimination of over treatment(if the office readings are persistently elevated)  Ambulatory BP monitoring: • It measures the time integral BP burden on cardiovascular system • It also provides better correlation than office readings of BP, especially those withTOD(target organ damage) • Prevention of under treatment(if the office readings are less than the ambulatory ones, due to sympathetic overactivity in daily life)
Both Home and ambulatory BP monitoring are useful in: • Diagnosis of labile hypertension • Diagnosis of white coat hypertension • Diagnosis of intermittent hypertension(Fluctuations in pheochromocytoma)
 Chest examination: • For possible chronic airway obstruction
 Heart Examination: • Sustained apical impulse • Pulsation at 2nd aortic area(A2) • Accentuated S1 in left ventricular hypertrophy(LV H) • S3 gallop, at mitral area in LVH • S4 gallop, at mitral area in diastolic dysfunction • Ejection systolic click, at 1st aortic area in sclerotic valve • Soft Ejection systolic murmur of low intensity, at 1st aortic area(A1) in aortic valve ring dilatation • Accentuated aortic component of S2 with wide splitting, at 2nd aortic area(A2)
 Abdominal Examination: • Renal mass in polycystic kidney disease(PKD) • Audible bruits in: renal artery stenosis or abdominal aortic aneurysm
 Neurological Examination: • Speech • Gait • Reflexes • Sensory and Motor affections
 Routine blood tests: • Complete blood count(CBC) • Erythrocyte sedimentation rate(ESR) • Random blood sugar(RBS) ± Hb A1c • Blood Urea • Serum Creatinine • Serum uric acid • Liver enzymes(ALT / AST) • Serum albumin • Serum lipids(cholesterol and triglycerides)  Urine analysis (?proteinuria)  Resting 12- ECG leads ± Ecchocardiography  Fundus examination  Renal (ultrasonograhy ± isotope scanning)
MAJOR RISK FACTORS  Age (>55 in males and >65 in females)  Cigarette smoking  Obesity (BMI>30kg/m2)  Dyslipidemia  Chronic kidney disease: CKD, with urine protein: >150 mg/dl and GFR: <60 ml/min  Family history of premature stroke TARGET ORGAN DAMAGE(TOD)  Heart: • left ventricular hypertrophy: LVH/ or failure: LVF • Ischemic heart disease: IHD  Brain: • Stroke • Transient ischemic attacks: TIAs  Retinopathy: Grade I -to- IV  Peripheral vascular disease: PVD  Hypertensive nephrosclerosis
Low-risk Group { 2 % } Moderate-risk Group { 60 % } High-risk Group { 1/3 of cases } Clinical cardiovascular disease No No + TOD No No + Risk factors No 1 0r 2 (other than diabetes) 1 or more (including diabetes or CKD) Target BP Control < (140 / 90) < (135 / 85) < (125 / 75) Treatment Stage I HTN: Lifestyle modifications, for up to 12 months Stage II or III HTN: Add medications •Lifestyle modifications •Medications •Add low-dose aspirin •Add lipid-lowering agents •Lifestyle modifications •Medications •Add low-dose aspirin •Add lipid-lowering agents
1ry (Essential) HTN 2ry HTN Age (years) Young (35-55) <35 -or- >55 Apparent cause No + Family history + - Course Benign (slowly progressive, with long- term complications Malignant (rapidly progressive, with early complications)
 Theories of pathogenesis: • ↑activity of vasomotor center(VMC)  ↑sympathetic discharge • ↑activity of adrenals  ↑aldosterone secretion • ↑cardiac output(COP)  ↑peripheral resistance(PR) • ↑renin activity • Insulin resistance and obesity  metabolic syndrome • Alcohol • Excess salt intake  Na sensitivity • Impaired pressure natriuresis • Impaired baroreceptors  baroreceptor resetting • Genetic • Obstructive sleep apnea: OSA
Diet • Liquorice • Tyramine-rich food • Chewable tobacco Drugs • Corticosteroids / Oral contraceptive pills • NSAIDs • Erythropoeitin / Cyclosprine A • Cocaine / Amphetamine Renal • Glomerulonephritis / Interstitial nephritis • Diabetic nephropathy • PKD • Renal artery stenosis • Obstructive uropathy
Blood: polycythemia Cardiovascular: Coarctation of aorta Neurological: Increased ICT Endocrinal • Cushing’s and Conn’shypokalemic HTN • Acromegaly • Pheochromocytoma • Myxedema • Hyperparathyroidism • Hyperthyroidism isolated systolic HTN • Congenital adrenal hyperplasia
 Any hospitalization for urgent or emergent HTN  Recurrent “flash” pulmonary edema  Refractory HTN, especially if in a young or after age of 50  Precipitous worsening of renal function after treatment with ACE-Is  Unilateral small kidney by any radiographic study  Extensive peripheral atherosclerosis  Flank bruit
?The surgical/ pharmacological reversibility of the 2ry type of HTN..  RenalA. stenosis: • Renal angioplasty for fibromuscular dysplasia • Renal stenting for bilateral artery stenosis  Cushing’s: • Surgical removal of tumor • Metyrapone  Acromegaly: • Trans-sphenoidal hypophysectomy • Yttrium implantation  Pheochromocytoma: • Laparoscopic adrenalectomy  Coarctation of aorta: • Surgical repair
  When BP is often, but not always, in the hypertensive range.. It is usually border-line HTN
 Cushing’s disease  Conn’s syndrome  Renal artery stenosis  Glucocorticoid-remediable aldosteronism(GRA)  Liddle’s syndrome  Bartter’s syndrome  Gitelman’s syndrome  Congenital adrenal hyperplasia
Plasma aldosterone Plasma renin Liddle’s syndrome Decreased Decreased 2ry hyperaldosteronism (renal artery stenosis) Increased Increased Conn’s syndrome Increased Decreased GRA Increased Decreased
  Isolated rise in systolic BP(SBP) with normal diastolic BP (< 90 mmHg) also called: Isolated systolic hypertension (ISH)  Grades: • Grade I: SBP = 140 – 159 mmHg • Grade II: SBP = ≥ 160 mmHg  Causes: • Fever / anxiety • Atherosclerosis • Thyrotoxicosis • Aortic regurge(AR) • Coarctation of aorta • Patent ductus arteriosus(PDA) • Complete heart block(CHB)
  BP ≥ 200 / 120 mmHg  Classification: • Hypertensive urgency (accelerated HTN): o With noTOD o Gradual control of BP within 24-28 Hs • Hypertensive emergency: o In the form of: encephalopathy, LVF, aortic dissection, cerebrovascular stroke, or malignant HTN o Micro-angiopathic hemolytic anemia may be present o TOD is present o Rapid control of BP within 1-2 Hs, only by 25 % (target BP ~ 160/100)
 Patient dialogue and patient education ▪Lifestyle modifications Medications
 Patient dialogue and Patient education: • HTN is not episodic and not symptomatic • Understanding medications cost • Trying for moderation of life stressful conditions (home/job) • Understanding that “almost” control isn’t good enough; hence the importance to achieve the “target” BP control • To < (140/90), in low-risk patients • To < (140/90), in moderate- and high-risk patients
 Lifestyle modifications: • Weight reduction:Target BMI <25 Kg/m2 • Aerobic exercises / RelaxationTechniques(± anxiolytics) • Avoid Alcohol • Avoid smoking: Major risk for coronary ischemia, nephrosclerosis • Moderate dietary Na intake: in processed food as well as salt shaker, reduce from 10 to 6 gm/d, will show full benefits in 5Wks • Advise balanced meals: • Encourage fresh vegetables/fruits(rich in K supplements) • Allow low-fat dairy milk products and low-fat diet(mainly of polyunsaturated fatty acids)
 Medications: Some Considerations: • Use long-acting preparations • Use combinations (synergism) • Avoid dose-dependent side effects
Drug categories used in HTN: • Diuretics • Angiotensin-converting-enzyme inhibitors(ACE- Is) • Angiotensin-receptor blocker(ARBs) • Calcium-channel Blockers(CCBs): Dihydropyridines( DHP), and Non-Dihydropyridines(Non-DHP) • Beta Blockers(BBs) • Alpha Blockers • Alpha and Beta Blockers • Central Sympatholytics • Vasodilators
 Diuretics: A. Loop Diuretics: • Frusemide(Lasix:20, 40mg) ( +Spironolactone= Lasilactone) • Bumetanide(Burinex:1mg) • Torsemide(Torseretic:5, 10mg) B. Thiazides: • Hydroclorothiazides: HCT(Hydrex:25mg) • Indapamide(Natrilix:2.5mg) • Chlorthalidone(Hygroton:50mg) C. K-sparing Diuretics: • Spironolactone(Aldactone:25, 100mg) ( +HCT= Aldactazide) • Amiloride( +HCT= Moduretic:5/50mg) • Tiamterene( +Xipamide= Epitens:30/10mg)
Site and mechanism of action Indications in HTN Unwanted Effects LOOP Block Na+/K+/Cl- transport in thick ascending limb of loop of Henle (Large filtered Na-load) •HTN with renal impairment •HTN with congestive heart failure •↓K+ (dose-dependent) •↓Na+ THIAZIDES Block Na+/Cl- Co-transport in distal convoluted tubule (Low-filtered Na load) •Isolated systolic HTN (ISH) •Long-Term treatment of HTN •Not if GFR<30 ml/min •↑blood glucose •↑plasma lipids •Precipitate gout •Erectile dysfunction K-SPARING Blocking ENac-receptors, in collecting duct: •Directly(Triamterene and amiloride •Via inhibiting aldosterone activity on receptors (Spironolactone) •Amiloride in Liddle’s Syndrome •Spironolactone in: oConn’s o2ry hyperaldosteronism , as heart failure or liver cirrhosis •↑K+ •C.I. in: oRenal failure oDiabetes with ↓↓(renin&aldosterone) •Sexual dysfunction(spironolactone) •Painful gynecomastia (spironolactone)
 ACE- Is: • Captopril(Capoten) • Enalapril(Ezapril) • Ramipril(Tritace:1.25, 2.5, 5, 10mg) • Lisinopril(Sinopril:5, 10mg) • Fosinopril(Monopril:10, 20mg) • Quinapril  ARBs: • Olmesartan(Erastapex:20, 40mg) • Valsartan(Tareg:80, 160mg) • Irbesartan(Approvel:150, 300mg) • Candesartan(Atacand:8, 16, 32mg) • Telmisartan(Micardis:40, 80mg)
Site and mechanism of action Indications in HTN Unwanted Effects ACE- Is •Block conversion of angiotensin III •Block metabolism of bradykinin •HTN with diabetic nephropathy(Type1) •HTN with renal impairement •HTN with congestive heart failure, or LV- dysfunction •HTN with hyperuricemia •After myocardial infarction •Dry cough(bradykinin- mediatedshift to use ARBs) •↑K+ •Acute renal failure, in bilateral renal artery stenosis and in hypovolemia •Angioedema(rare) •Teratogenic ARBs Block interaction of angiotensin II on AT1-receptors •HTN with diabetic nephropathy(Type2) •HTN with congestive heart failure, or LV- dysfunction •Acute renal failure, in bilateral renal artery stenosis and in hypovolemia •Angioedema(rare) •Teratogenic
 CCBs: A. DHPs: • Nifedipine(Epilat-Retard:20mg) • Amlodipine(Norvasc:5, 10mg) • Felodipine(Plendil:2.5, 5, 10mg) • Nimodipine(Nimotop) B. Non-DHPs: • Deltiazem(Altiazem:60, 90, 120mg) • Verapamil(Isoptin:80, 240mg)
Site and mechanism of action Indications in HTN Unwanted Effects CCBs: DHPs Non-DHPs •Block voltage-gated Ca+ channels, in: •Cardiac myocytes •Vascular smooth muscle cells •Prevention of Ca+influx V.D. •HTN with stroke •HTN with dementia •HTN in elderly, especially if diabetics •ISH •HTN with angina •DHPs: headache, flushing and ankle edema •Non-DHPs:C.I. in LV dysfunction and in heart block •Both can precipitate myocardial infarction; due to ↓BP but with ↑reflex sympathetic activity(RSA) •Both have –ve inotropic effect •Verapamil causes severe constipation
 Beta Blockers(BBs): A. Non-cardioselective: • Propranolol(Inderal:10, 40mg) • Sotalol(Betacor:80mg) B. Cardioselective: • Atenolol(Tenormin:50, 100mg) • Metoprolol(Betaloc:100mg) • Bisoprolol(Concor:5, 10mg) • Nebivolol(Nevilob:5mg)
Site and mechanism of action Indications in HTN Unwanted Effects BBs •-ve inotropic •-ve chronotropic •↓ COP •HTN with coronary ischemia •HTN with anxiety •After M.I. •HTN with CHF •HTN with tachyarrhythmia •Raynaud’s phenomenon •Bronchospasm •Hyperglycemia •Non-selective: oheart block oHeart failure oMask hypoglycemic symptoms oNight mares oDepression
 Alpha Blockers: • Prazosin(Minipress:1, 2mg) • Doxazocin(Dosin:1, 2mg) • Terazocin(Itrin) • Phenoxybenzamine  Alpha and Beta Blockers: • Carvedilol(Dilatrend or Carvid:6.25, 12.5, 25mg) • Labetalol
Site and mechanism of action Indications in HTN Unwanted Effects Alpha Blockers Combined Alpha and Beta Blockers •Alpha-1 blockade: Prazocin, Doxazosin •Alpha-1+Alpha-2 blockade: Phenoxybenzamine •Vasodilator effect •Dilatation of urethral smooth muscles •Prazocin and Doxazosin in: HTN with prostatism •Phenoxybenzamine in: Preoperative treatment of pheochromocytoma, followed by BBs •Carvedilol in: HTN with heart failure Orthostatic hypotension (Except: Carvedilol)
 Central Sympatholytics: • Alpha-methyl dopa(Aldomet:250, 500mg) • Reserpine(Brinerdin)  Vasodilators: • Hydralazine(Apresoline)
Site and mechanism of action Indications in HTN Unwanted Effects Central Sympatholytics Stimulation of Alpha-2 receptors in CNS  ↓Central sympathetic outflow Stimulation of Alpha-2 receptors, presynaptic  Inhibiting NE release ↓sympathetic drive to heart and peripheral circulation  o↓Heart rate o↓Cardiac Output o↓Peripheral resistance Alpha-methyl-dopa in: HTN with pregnancy •Autoimmune hemolytic anemia •SLE •Rebound HTN •Orthostatic hypotension •NOT with BBs; for fear of bradycardia •C.I. in depression Vasodilators Opening of ATP/K+ Channels V.D. Acute severe HTN with Pregnancy •Tachycardia •Peripheral edema •Hydralazine: oIV  ↓↓BP oOral  SLE
 Some Selected Combinations: • Captopril + HCT Capozide • Enalapril + HCT Ezapril-Co • Lisinopril + HCT Sinopril-Co • Ramipril + HCTTritace-Comb • Valsartan + HCT Co-Tareg • Irbesartan + HCT Co-Approvel • Candisartan + HCT Atacand-Plus • Bisoprolol + HCT Concor-Plus • Atenolol + ChlorthalidoneTenodone:50, 100mg • Atenolol + NifedipineTenolat • Amlodipine + BenazeprilAlkapress-Plus:5, 10mg • Amlodipine + PerindoprilCoviram:5/5mg
 Consider Some Precautions: • Initial treatment Low-dose combination therapy, then additional drug for every 10mmHg(SBP) above the target goal • Medications-induced sexual dysfunction, as:Thiazides,BBs • Ankle edema of CCBs (DHPs), can be treated by addition of venodilators as: ACE-Is or ARBs, not a diuretic • CCBs, better not to be combined with a diuretic in coronary ischemia • Grapefruit juice increase bioavailability of CCBs • BBs shouldn’t be combined with non-DHPs, for fear of bradycardia, especially in elderly • NSAIDs and ASA >325mgDecrease effect of ACE-Is based treatment • Consider HTN in Special Situations
YES NO ACE-Is (especially in type-1 DM) Thiazides; because: High dosesHyperglycemia ARBs (especially in type-2 DM) BBs; because: •Mask hypoglycemic symptoms •↑Hyperlipidemia Diuretic (Loop) CCBs (DHPs) &/OR BBs (cardioselective)
YES NO ACE-Is (with monitoring) Thiazides ARBs CCBs (DHPs) BBs &/OR Diuretic (Loop)
YES NO CCBs BBs; because: Alpha receptors ill b unopposed Severe V.C. Carvedilol Prazosin
YES NO ACE-Is Thiazides CCBs BBs Alpha-methyl dopa
YES NO BBs (cardioselective) CCBs (Except NifedipineRefl ex tachycardia ACE- Is
YES NO ACE- Is CCBs ( -ve inotropes) ARBs Diuretics BBs (Cardioselective: Nebivolol, metoprolol, bisoprolol) Alpha & Beta Blocker (Carvedilol)
YES NO BBs (Non-selective, which pass BBB) CCBs (Cinnarizine)
YES NO Alpha-methyl dopa ACE- Is (Teratogenic) Labetalol ARBs (Teratogenic) Atenolol Diuretics (↓placental blood flow) Hydralazine Propranolol (Fetal bradycardia) CCBs
YES NO Alpha-methyl dopa Diuretics BBs Labetalol
YES NO ACE- Is Thiazides CCBs BBs
YES NO CCBs (DHPs) ACE- Is ARBs BBs Diuretics Alpha & Beta Blockers
YES NO BBs
YES NO Prazocin Doxazocin Tetrazocin
YES NO Thiazides BBs ACE-Is
YES NO CCBs Thiazides ACE- Is ARBs
SYSTEMIC HYPERTENSION

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SYSTEMIC HYPERTENSION

  • 1.
    By: Dr./ SAHARH. MOSTAFA Consultant of internal medicine El-MatariaTeaching Hospital-Cairo- Egypt November,2016
  • 2.
    Persistent elevation ofBP above normal values ≥ (140 / 90), on three different occasions, under mental and physical rest
  • 3.
    Question: Why abovethese values..? Answer:  Because this the value above which the benefits of treating hypertension(HTN), appear to outweigh the risks
  • 4.
     Normal BP:< (130 / 80)  Pre-Hypertension: 130 – 139 / 85 - 89  Hypertension: ≥(140/90) Normal BP: <(130 / 80) Pre- Hypertension: 130–139/85-89 Hypertension: ≥(140/90)
  • 5.
    29 % ofthe world’s adult population will be projected to develop hypertension(HTN), by the year 2025
  • 6.
    Stages of HTNSystolic BP Diastolic BP Stage I (mild) 140 – 159 90 – 99 Stage II (moderate) 160 – 179 100 – 109 Stage III (severe) ≥ 180 ≥ 110
  • 7.
     Question: whena person’s systolic and diastolic BP fall into different categories, which stage would be defined..?  Answer:The higher one
  • 8.
     Focusing on3 Goals: • Accurate assessment of BPGoal 1 • Cardiovascular risk stratificationGoal 2 • Identification of 2ry causesGoal 3
  • 9.
     Goals wouldbe achieved through:
  • 10.
     Personal History: •Age • Smoking • Alcohol • Job  Present History: • Co morbid disease(diabetes, gout, bronchial asthma, depression, migraine, ..) • Diet • Drugs • Lifestyle • Ask for 2ry causes • Search forTOD (target organ damage)  Past History: Record last BP and last treatment  Family History: • Hypertension • Renal disease • Premature stroke
  • 12.
     Asymptomatic: HTN maybe termed the silent killer  Alerting symptoms: Headache, fatigue, blurring of vision, ..
  • 14.
     Face  Pulse BMI  BP  Chest examination  Heart examination  Abdominal examination  Neurological examination
  • 16.
     Face: Cushingoid ?steroids,?Cushing’s Lid edema Nephrotic syndrome Staring look Thyrotoxic Bloated Myxedema Acromegalic Acromegaly
  • 17.
     Pulse: ------>Radial • Equality • Volume • Special character • Femoral: radio-femoral delay in coarctation of aorta • Trousseau Sign: Carpopedal spasm when BP is increased above systolic for > 3 min. due to hypokalemia (Conn’s syndrome)
  • 18.
     BMI: Normally< 25 BMI = WEIGHT ( Kg) / HEIGHT (m2) NORMAL 18.5 – 25 OVERWEIGHT 25 – 30 OBESE 30 – 40 MORBID OBESITY > 40
  • 19.
     BP: • Supine:arm same level as heart • Sitting: back supported, feet on ground • Standing: after 5 min of standing; to elucidate autonomic insufficiency, as in: • Diabetes • Parkinsonism • Old age --------------------------------------------------------- N.B. : At 1st visit, document BP in both arms
  • 20.
     Home BPmonitoring: • It engages the patient in his own heath care • Persistent nocturnal hypertension will increase the BP burden on cardiovascular system • The morning surge in BP is associated with increased incidence of stroke, myocardial infarction as well as sudden cardiac death • Elimination of over treatment(if the office readings are persistently elevated)  Ambulatory BP monitoring: • It measures the time integral BP burden on cardiovascular system • It also provides better correlation than office readings of BP, especially those withTOD(target organ damage) • Prevention of under treatment(if the office readings are less than the ambulatory ones, due to sympathetic overactivity in daily life)
  • 22.
    Both Home andambulatory BP monitoring are useful in: • Diagnosis of labile hypertension • Diagnosis of white coat hypertension • Diagnosis of intermittent hypertension(Fluctuations in pheochromocytoma)
  • 23.
     Chest examination: •For possible chronic airway obstruction
  • 24.
     Heart Examination: •Sustained apical impulse • Pulsation at 2nd aortic area(A2) • Accentuated S1 in left ventricular hypertrophy(LV H) • S3 gallop, at mitral area in LVH • S4 gallop, at mitral area in diastolic dysfunction • Ejection systolic click, at 1st aortic area in sclerotic valve • Soft Ejection systolic murmur of low intensity, at 1st aortic area(A1) in aortic valve ring dilatation • Accentuated aortic component of S2 with wide splitting, at 2nd aortic area(A2)
  • 26.
     Abdominal Examination: •Renal mass in polycystic kidney disease(PKD) • Audible bruits in: renal artery stenosis or abdominal aortic aneurysm
  • 28.
     Neurological Examination: •Speech • Gait • Reflexes • Sensory and Motor affections
  • 29.
     Routine bloodtests: • Complete blood count(CBC) • Erythrocyte sedimentation rate(ESR) • Random blood sugar(RBS) ± Hb A1c • Blood Urea • Serum Creatinine • Serum uric acid • Liver enzymes(ALT / AST) • Serum albumin • Serum lipids(cholesterol and triglycerides)  Urine analysis (?proteinuria)  Resting 12- ECG leads ± Ecchocardiography  Fundus examination  Renal (ultrasonograhy ± isotope scanning)
  • 33.
    MAJOR RISK FACTORS Age (>55 in males and >65 in females)  Cigarette smoking  Obesity (BMI>30kg/m2)  Dyslipidemia  Chronic kidney disease: CKD, with urine protein: >150 mg/dl and GFR: <60 ml/min  Family history of premature stroke TARGET ORGAN DAMAGE(TOD)  Heart: • left ventricular hypertrophy: LVH/ or failure: LVF • Ischemic heart disease: IHD  Brain: • Stroke • Transient ischemic attacks: TIAs  Retinopathy: Grade I -to- IV  Peripheral vascular disease: PVD  Hypertensive nephrosclerosis
  • 34.
    Low-risk Group { 2% } Moderate-risk Group { 60 % } High-risk Group { 1/3 of cases } Clinical cardiovascular disease No No + TOD No No + Risk factors No 1 0r 2 (other than diabetes) 1 or more (including diabetes or CKD) Target BP Control < (140 / 90) < (135 / 85) < (125 / 75) Treatment Stage I HTN: Lifestyle modifications, for up to 12 months Stage II or III HTN: Add medications •Lifestyle modifications •Medications •Add low-dose aspirin •Add lipid-lowering agents •Lifestyle modifications •Medications •Add low-dose aspirin •Add lipid-lowering agents
  • 35.
    1ry (Essential) HTN2ry HTN Age (years) Young (35-55) <35 -or- >55 Apparent cause No + Family history + - Course Benign (slowly progressive, with long- term complications Malignant (rapidly progressive, with early complications)
  • 36.
     Theories ofpathogenesis: • ↑activity of vasomotor center(VMC)  ↑sympathetic discharge • ↑activity of adrenals  ↑aldosterone secretion • ↑cardiac output(COP)  ↑peripheral resistance(PR) • ↑renin activity • Insulin resistance and obesity  metabolic syndrome • Alcohol • Excess salt intake  Na sensitivity • Impaired pressure natriuresis • Impaired baroreceptors  baroreceptor resetting • Genetic • Obstructive sleep apnea: OSA
  • 37.
    Diet • Liquorice • Tyramine-richfood • Chewable tobacco Drugs • Corticosteroids / Oral contraceptive pills • NSAIDs • Erythropoeitin / Cyclosprine A • Cocaine / Amphetamine Renal • Glomerulonephritis / Interstitial nephritis • Diabetic nephropathy • PKD • Renal artery stenosis • Obstructive uropathy
  • 38.
    Blood: polycythemia Cardiovascular: Coarctation of aorta Neurological: IncreasedICT Endocrinal • Cushing’s and Conn’shypokalemic HTN • Acromegaly • Pheochromocytoma • Myxedema • Hyperparathyroidism • Hyperthyroidism isolated systolic HTN • Congenital adrenal hyperplasia
  • 39.
     Any hospitalizationfor urgent or emergent HTN  Recurrent “flash” pulmonary edema  Refractory HTN, especially if in a young or after age of 50  Precipitous worsening of renal function after treatment with ACE-Is  Unilateral small kidney by any radiographic study  Extensive peripheral atherosclerosis  Flank bruit
  • 40.
    ?The surgical/ pharmacologicalreversibility of the 2ry type of HTN..  RenalA. stenosis: • Renal angioplasty for fibromuscular dysplasia • Renal stenting for bilateral artery stenosis  Cushing’s: • Surgical removal of tumor • Metyrapone  Acromegaly: • Trans-sphenoidal hypophysectomy • Yttrium implantation  Pheochromocytoma: • Laparoscopic adrenalectomy  Coarctation of aorta: • Surgical repair
  • 41.
      WhenBP is often, but not always, in the hypertensive range.. It is usually border-line HTN
  • 42.
     Cushing’s disease Conn’s syndrome  Renal artery stenosis  Glucocorticoid-remediable aldosteronism(GRA)  Liddle’s syndrome  Bartter’s syndrome  Gitelman’s syndrome  Congenital adrenal hyperplasia
  • 43.
    Plasma aldosterone Plasmarenin Liddle’s syndrome Decreased Decreased 2ry hyperaldosteronism (renal artery stenosis) Increased Increased Conn’s syndrome Increased Decreased GRA Increased Decreased
  • 44.
      Isolatedrise in systolic BP(SBP) with normal diastolic BP (< 90 mmHg) also called: Isolated systolic hypertension (ISH)  Grades: • Grade I: SBP = 140 – 159 mmHg • Grade II: SBP = ≥ 160 mmHg  Causes: • Fever / anxiety • Atherosclerosis • Thyrotoxicosis • Aortic regurge(AR) • Coarctation of aorta • Patent ductus arteriosus(PDA) • Complete heart block(CHB)
  • 45.
      BP≥ 200 / 120 mmHg  Classification: • Hypertensive urgency (accelerated HTN): o With noTOD o Gradual control of BP within 24-28 Hs • Hypertensive emergency: o In the form of: encephalopathy, LVF, aortic dissection, cerebrovascular stroke, or malignant HTN o Micro-angiopathic hemolytic anemia may be present o TOD is present o Rapid control of BP within 1-2 Hs, only by 25 % (target BP ~ 160/100)
  • 46.
     Patient dialogueand patient education ▪Lifestyle modifications Medications
  • 47.
     Patient dialogueand Patient education: • HTN is not episodic and not symptomatic • Understanding medications cost • Trying for moderation of life stressful conditions (home/job) • Understanding that “almost” control isn’t good enough; hence the importance to achieve the “target” BP control • To < (140/90), in low-risk patients • To < (140/90), in moderate- and high-risk patients
  • 48.
     Lifestyle modifications: •Weight reduction:Target BMI <25 Kg/m2 • Aerobic exercises / RelaxationTechniques(± anxiolytics) • Avoid Alcohol • Avoid smoking: Major risk for coronary ischemia, nephrosclerosis • Moderate dietary Na intake: in processed food as well as salt shaker, reduce from 10 to 6 gm/d, will show full benefits in 5Wks • Advise balanced meals: • Encourage fresh vegetables/fruits(rich in K supplements) • Allow low-fat dairy milk products and low-fat diet(mainly of polyunsaturated fatty acids)
  • 50.
     Medications: Some Considerations: •Use long-acting preparations • Use combinations (synergism) • Avoid dose-dependent side effects
  • 51.
    Drug categories usedin HTN: • Diuretics • Angiotensin-converting-enzyme inhibitors(ACE- Is) • Angiotensin-receptor blocker(ARBs) • Calcium-channel Blockers(CCBs): Dihydropyridines( DHP), and Non-Dihydropyridines(Non-DHP) • Beta Blockers(BBs) • Alpha Blockers • Alpha and Beta Blockers • Central Sympatholytics • Vasodilators
  • 52.
     Diuretics: A. LoopDiuretics: • Frusemide(Lasix:20, 40mg) ( +Spironolactone= Lasilactone) • Bumetanide(Burinex:1mg) • Torsemide(Torseretic:5, 10mg) B. Thiazides: • Hydroclorothiazides: HCT(Hydrex:25mg) • Indapamide(Natrilix:2.5mg) • Chlorthalidone(Hygroton:50mg) C. K-sparing Diuretics: • Spironolactone(Aldactone:25, 100mg) ( +HCT= Aldactazide) • Amiloride( +HCT= Moduretic:5/50mg) • Tiamterene( +Xipamide= Epitens:30/10mg)
  • 53.
    Site and mechanismof action Indications in HTN Unwanted Effects LOOP Block Na+/K+/Cl- transport in thick ascending limb of loop of Henle (Large filtered Na-load) •HTN with renal impairment •HTN with congestive heart failure •↓K+ (dose-dependent) •↓Na+ THIAZIDES Block Na+/Cl- Co-transport in distal convoluted tubule (Low-filtered Na load) •Isolated systolic HTN (ISH) •Long-Term treatment of HTN •Not if GFR<30 ml/min •↑blood glucose •↑plasma lipids •Precipitate gout •Erectile dysfunction K-SPARING Blocking ENac-receptors, in collecting duct: •Directly(Triamterene and amiloride •Via inhibiting aldosterone activity on receptors (Spironolactone) •Amiloride in Liddle’s Syndrome •Spironolactone in: oConn’s o2ry hyperaldosteronism , as heart failure or liver cirrhosis •↑K+ •C.I. in: oRenal failure oDiabetes with ↓↓(renin&aldosterone) •Sexual dysfunction(spironolactone) •Painful gynecomastia (spironolactone)
  • 54.
     ACE- Is: •Captopril(Capoten) • Enalapril(Ezapril) • Ramipril(Tritace:1.25, 2.5, 5, 10mg) • Lisinopril(Sinopril:5, 10mg) • Fosinopril(Monopril:10, 20mg) • Quinapril  ARBs: • Olmesartan(Erastapex:20, 40mg) • Valsartan(Tareg:80, 160mg) • Irbesartan(Approvel:150, 300mg) • Candesartan(Atacand:8, 16, 32mg) • Telmisartan(Micardis:40, 80mg)
  • 55.
    Site and mechanismof action Indications in HTN Unwanted Effects ACE- Is •Block conversion of angiotensin III •Block metabolism of bradykinin •HTN with diabetic nephropathy(Type1) •HTN with renal impairement •HTN with congestive heart failure, or LV- dysfunction •HTN with hyperuricemia •After myocardial infarction •Dry cough(bradykinin- mediatedshift to use ARBs) •↑K+ •Acute renal failure, in bilateral renal artery stenosis and in hypovolemia •Angioedema(rare) •Teratogenic ARBs Block interaction of angiotensin II on AT1-receptors •HTN with diabetic nephropathy(Type2) •HTN with congestive heart failure, or LV- dysfunction •Acute renal failure, in bilateral renal artery stenosis and in hypovolemia •Angioedema(rare) •Teratogenic
  • 56.
     CCBs: A. DHPs: •Nifedipine(Epilat-Retard:20mg) • Amlodipine(Norvasc:5, 10mg) • Felodipine(Plendil:2.5, 5, 10mg) • Nimodipine(Nimotop) B. Non-DHPs: • Deltiazem(Altiazem:60, 90, 120mg) • Verapamil(Isoptin:80, 240mg)
  • 57.
    Site and mechanismof action Indications in HTN Unwanted Effects CCBs: DHPs Non-DHPs •Block voltage-gated Ca+ channels, in: •Cardiac myocytes •Vascular smooth muscle cells •Prevention of Ca+influx V.D. •HTN with stroke •HTN with dementia •HTN in elderly, especially if diabetics •ISH •HTN with angina •DHPs: headache, flushing and ankle edema •Non-DHPs:C.I. in LV dysfunction and in heart block •Both can precipitate myocardial infarction; due to ↓BP but with ↑reflex sympathetic activity(RSA) •Both have –ve inotropic effect •Verapamil causes severe constipation
  • 58.
     Beta Blockers(BBs): A.Non-cardioselective: • Propranolol(Inderal:10, 40mg) • Sotalol(Betacor:80mg) B. Cardioselective: • Atenolol(Tenormin:50, 100mg) • Metoprolol(Betaloc:100mg) • Bisoprolol(Concor:5, 10mg) • Nebivolol(Nevilob:5mg)
  • 59.
    Site and mechanismof action Indications in HTN Unwanted Effects BBs •-ve inotropic •-ve chronotropic •↓ COP •HTN with coronary ischemia •HTN with anxiety •After M.I. •HTN with CHF •HTN with tachyarrhythmia •Raynaud’s phenomenon •Bronchospasm •Hyperglycemia •Non-selective: oheart block oHeart failure oMask hypoglycemic symptoms oNight mares oDepression
  • 60.
     Alpha Blockers: •Prazosin(Minipress:1, 2mg) • Doxazocin(Dosin:1, 2mg) • Terazocin(Itrin) • Phenoxybenzamine  Alpha and Beta Blockers: • Carvedilol(Dilatrend or Carvid:6.25, 12.5, 25mg) • Labetalol
  • 61.
    Site and mechanismof action Indications in HTN Unwanted Effects Alpha Blockers Combined Alpha and Beta Blockers •Alpha-1 blockade: Prazocin, Doxazosin •Alpha-1+Alpha-2 blockade: Phenoxybenzamine •Vasodilator effect •Dilatation of urethral smooth muscles •Prazocin and Doxazosin in: HTN with prostatism •Phenoxybenzamine in: Preoperative treatment of pheochromocytoma, followed by BBs •Carvedilol in: HTN with heart failure Orthostatic hypotension (Except: Carvedilol)
  • 62.
     Central Sympatholytics: •Alpha-methyl dopa(Aldomet:250, 500mg) • Reserpine(Brinerdin)  Vasodilators: • Hydralazine(Apresoline)
  • 63.
    Site and mechanismof action Indications in HTN Unwanted Effects Central Sympatholytics Stimulation of Alpha-2 receptors in CNS  ↓Central sympathetic outflow Stimulation of Alpha-2 receptors, presynaptic  Inhibiting NE release ↓sympathetic drive to heart and peripheral circulation  o↓Heart rate o↓Cardiac Output o↓Peripheral resistance Alpha-methyl-dopa in: HTN with pregnancy •Autoimmune hemolytic anemia •SLE •Rebound HTN •Orthostatic hypotension •NOT with BBs; for fear of bradycardia •C.I. in depression Vasodilators Opening of ATP/K+ Channels V.D. Acute severe HTN with Pregnancy •Tachycardia •Peripheral edema •Hydralazine: oIV  ↓↓BP oOral  SLE
  • 64.
     Some SelectedCombinations: • Captopril + HCT Capozide • Enalapril + HCT Ezapril-Co • Lisinopril + HCT Sinopril-Co • Ramipril + HCTTritace-Comb • Valsartan + HCT Co-Tareg • Irbesartan + HCT Co-Approvel • Candisartan + HCT Atacand-Plus • Bisoprolol + HCT Concor-Plus • Atenolol + ChlorthalidoneTenodone:50, 100mg • Atenolol + NifedipineTenolat • Amlodipine + BenazeprilAlkapress-Plus:5, 10mg • Amlodipine + PerindoprilCoviram:5/5mg
  • 65.
     Consider SomePrecautions: • Initial treatment Low-dose combination therapy, then additional drug for every 10mmHg(SBP) above the target goal • Medications-induced sexual dysfunction, as:Thiazides,BBs • Ankle edema of CCBs (DHPs), can be treated by addition of venodilators as: ACE-Is or ARBs, not a diuretic • CCBs, better not to be combined with a diuretic in coronary ischemia • Grapefruit juice increase bioavailability of CCBs • BBs shouldn’t be combined with non-DHPs, for fear of bradycardia, especially in elderly • NSAIDs and ASA >325mgDecrease effect of ACE-Is based treatment • Consider HTN in Special Situations
  • 66.
    YES NO ACE-Is (especially intype-1 DM) Thiazides; because: High dosesHyperglycemia ARBs (especially in type-2 DM) BBs; because: •Mask hypoglycemic symptoms •↑Hyperlipidemia Diuretic (Loop) CCBs (DHPs) &/OR BBs (cardioselective)
  • 67.
  • 68.
    YES NO CCBs BBs;because: Alpha receptors ill b unopposed Severe V.C. Carvedilol Prazosin
  • 69.
    YES NO ACE-Is Thiazides CCBsBBs Alpha-methyl dopa
  • 70.
  • 71.
    YES NO ACE- IsCCBs ( -ve inotropes) ARBs Diuretics BBs (Cardioselective: Nebivolol, metoprolol, bisoprolol) Alpha & Beta Blocker (Carvedilol)
  • 72.
  • 73.
    YES NO Alpha-methyl dopaACE- Is (Teratogenic) Labetalol ARBs (Teratogenic) Atenolol Diuretics (↓placental blood flow) Hydralazine Propranolol (Fetal bradycardia) CCBs
  • 74.
  • 75.
    YES NO ACE- IsThiazides CCBs BBs
  • 76.
    YES NO CCBs (DHPs)ACE- Is ARBs BBs Diuretics Alpha & Beta Blockers
  • 77.
  • 78.
  • 79.
  • 80.