Hypertension

1. Hypertension

2. Introduction • Blood pressure is the force on the walls of the arteries as the bloodcirculates. • Blood pressure allows blood to flow and deliver nutrients to thebody. • We measure blood pressure with twonumbers. • The top number is the blood pressure whenyour heartbeats. • The bottom number is your blood pressurewhen your heart relaxes and refills withblood. • The higher your numbers and the longer they are high, the more damage is caused to your blood vessels.

3. Blood pressure increases with age. • High blood pressure is the leading riskfor death. • High blood pressure can cause strokes,heart attacks, and heart and kidneyfailure. • It is also related to dementia andsexual problems. • These problems can be prevented ifhigh blood pressure iscontrolled.

4. Definition • Hypertension is defined as the presence of a blood pressure(BP) elevation to a level that places patients at increased risk for target organ damage in several vascular beds including the retina, brain, heart, kidneysand large conduitarteries.

5. Hypertension : BP≥140/90mmHg • Isolated systolichypertension • sBP ≥ 140 and dBP<90 • associated with progressive reduction in vascularcompliance • usually begins in 5th decade; up to 11 % of 75 yrolds • Acceleratedhypertension • significant recent increase in BP over previous hypertensive levels associated with evidence of vascular damage on fundoscopy butwithout papilledema • Malignanthypertension • sufficient elevation in BP to cause papilledema and other manifestationsof vasculardamage • (retinal hemorrhages, bulging discs, mental status changes,increasing creatinine) • not defined by absolute level of BP, but often requires BP of>200/140 • - develops in about 1 % of hypertensivepatients • Hypertensive urgency: • - sBP >210 or dBP > 120 with minimal or no target-organdamage • Hypertensiveemergency • - high BP + acute target-organdamage

6. HypertensiveEmergencies • Malignant HTN withpapilledema • Cerebrovascular: • Hypertensiveencephalopathy • CVA with severehypertension • Intracerebralhemorrhage • -SAH • Cardiac: • Acute aorticdissection • Acute refractory LVfailure • Acute MI with persistentischemic • pain afterCABG

7. Renal: • Acuteglomerulonephritis • Renal crises from collagen vasculardiseases • Severe hypertension following renaltransplantation • Excessive circulatingcatecholamines: • Pheochromocytoma • Tyramine containing foods ordrug • - Sympathomimetic drug use (e.g.cocaine) • - Rebound HTN after cessation of antihypertensive drugs (e.g. clonidine) • Eclampsia • Surgical: • - Severe HTN prior to emergent surgery • - Severe post-opHTN • - Post-op bleeding from vascular suturelines • HTN following severeburns • Severeepistaxsis

8. Classification ofhypertension

9. World Health Organization2002

10. Epidemiology • 20-25% of adults have HTN (up to50% undiagnosed) • 16% have adequate BPcontrol • Approximately 50% of adult arehypertensive by age60 • 3rd leading risk factor associated withdeath • Risk factor for CAD, CHF, cerebrovascular disease, renal failure, peripheralvascular disease

11. RiskFactors • Age • Alcohol • CigaretteSmoking • Diabetesmellitus • Elevated serumlipids • Excess dietarysodium • Gender • Familyhistory • Obesity • Ethnicity – IS AN IMP. FACTOR IN OVERALLCARDIAC DISEASE • Sedentarylifestyle • Socioeconomicstatus • stress

12. Etiology: • Ofall90% have Essentialhypertension • The remainder have secondaryhypertension

13. Causes ofsecondary hypertension • Alcohol • Pregnancy • Renaldisease: • Renal arterystenosis, • Glomerulonephritis, • Polycystic kidneydisease • Endocrinedisease: • Pheochromocytoma, cushing’s disease, conn’ssyndrome, hyperparathyroidism, • acromegaly, primary hyperthyroidism,thyrotoxicosis, • congenital adrenalhyperplasia • Drugs: • OCPs, anabolic steroids,corticosteroids, • NSAIDs, sympathomimetics. • Co-arctation of aorta.

14. Pathophysiology • For HTN, there must be an increase in either CO or SVR. The hallmark of classic HTN is increasedSVR. • Heredity • Water/Sodiumretention • Altered renin-angiotensinmechanism • Stress and increased sympathetic NSactivity • Insulin resistance andhyperinsulinemia • High insulin concentration stimulates SNS activity and impairs nitric oxide-mediatedvasodilation • Pressor effects of insulin include vascular hypertrophy and increased renal sodiumreabsorption • Endothelial CellDysfunction • Enodthelin produces pronounced and prolongedvasoconstriction.

15. Symptoms and signs ofHypertension • High blood pressure has no warning signs or symptoms – which is why it is often called a “silentkiller”. • Mostlyasymptomatic • Symptoms as a result of ↑arterialpressure: • headache(occipital, early morning for severalhours), • dizziness, • palpitation, • easYfatigability, • impotance. • Symptoms of hypertensive vasculardisease: • epistaxis, • hematuria, • blurring ofvision, • episodicweakness(TIA), • angina, • dyspnoea(HF), • chest pain(dissection ofaorta) • Symptoms of underlying disease (secondaryHTN)

16. Physical examination: • Cardiacmurmurs • neurologicdeficits • elevated jugularpressure • rales • retinopathy • unequalpulses • abdominalbruits

17. History: • Note the presence of medication (decongestants, OCP, NSAIDs, exogenous thyroid hormone, recent alcohol consumption,cocaine) • Secondary HTN should be considered: • Age <30 or>60 • Not controlled bytherapy • Occurrence of HTNcrisis • Sign & symptoms of scondary causes – HYPERKALEMIA , METABOLICACIDOSIS • FAMILYHISTORY

18. Complications Target OrganDiseases • Heart (hypertensive heartdisease) • Coronary artery disease (leading to MI andangina) • Left ventricular hypertrophy (from high cardiacworkload leading to heartfailure) • Heart failure (shortness of breath on exertion,nocturnal dyspnea, fatigue, enlargedheart) • Brain (cerebrovasculardisease) • Stroke/transischemicattacks • Hypertensive encephalopathy (cerebraledema)

19. Peripheral vasculature (peripheral vasculardisease) • Atherosclerosis in peripheral bloodvessels • Aortic aneurysm, aortic dissection, peripheralvascular disease • Intermittent claudication (pain with activity or lackof oxygen totissues)

20. Kidneys(nephrosclerosis) • End stage renal disease (ischemiafrom narrowed intrarenalvessels) • Urinalysis • Microalbuminuria • Proteinuria • Elevated blood urea nitrogen/elevated Serumcreatinine • » Usually ratio of 10:1 or15:1. • » BUN: 5-25mg/dl • » Creatinine: 0.5 – 1.5mg/dl • » Microscopichematuria • Earliest sign of renal damage isnocturia

21. Eyes (retinaldamage) • Eyes are only place vessels can bedirectly observed. • Retinal damage can indicate damage inother targetorgans. • Signs/Symptoms • Blurryvision • Retinalhemorrhage • Loss ofvision

22. Investigations • For all patients with hypertension(D) • - CBC, electrolytes, Cr, fasting glucose and lipid profile, 12- lead ECG,urinalysis. • For specific patient subgroups(D) • - DM OR renal disease: urinary proteinexcretion • Increasing Cr OR history of renal disease OR proteinuria OR HTN resistant to 3 meds OR presence of abdominal bruit: renal ultrasound, captopril renal scan, MRA/CTA(B) • If suspected endocrine cause: plasma aldosterone, plasma renin(D) • -If suspected pheochromocytoma: 24 h urine for metanephrines and catecholamines(C) • Echo cardiogram for left ventricular dysfunction assessment if indicated(C)

23. Keys to GradeofRecommendations for Hypertension Diagnosis and Treatment Grade • A = High levels of internal validity andstatistical precision • B/C = Lower levels of internal validityand statisticalprecision • D = Expertopinion

24. Monitoring • BP monitoring should be done under nonstressful circumstance ( rest,sitting,comfortable) • Should not be diagnosed on the basis of one measurement alone (unless > 210/120 mmofHg or with target organ damage. Two or morethan twoabnormalreading over a period of several weeks should be obtained beforeconsidering) • Pseudohypertention in elderly excluded due to stiffvessels

25. Approach toHypertension

27. Treatment • Behavioral • Nonpharmacologicaltherapy • Lifestyle modification ( exercise , cessation of smoking, reduction of body weight, judicious consumption of alcohol and adequate nutritional intake)

28. Diuretics • First line ofdefense • Thiazides (Hydrodiuril) • Inhibit sodium reabsorption in the distal convoluted tubule; increase excretion of sodium; decreases ECF; sustains a decrease inSVR • Lowers BP moderately in 2-4weeks • hydrochlorothiazide 12.5 -25 mg/day – S/E:fluid/electrolyte imbalances; CNS effects; GI effects; sexual impotence; • dermatologic effects(photosensitivity); decreased glucosetolerance • Monitor for orthostatic hypotension, hypokalemia andalkalosis. • Watch for digoxintoxicity. • AvoidNSAIDS. • Eat K+-richfoods

29. Loop Diuretics(furosemide/Lasix) • Inhibits NaCl reabsorption in ascending limb of loop of Henle; increases excretion of sodium andchloride. • Morepotentthanthiazides,butofshorterduration;less effective forHTN • S/E: fluid/electrolyte imbalances(hypokalemia);ototoxicity; metaboliceffects(hyperglycemia);increasedLDLand triglycerides with decreasedHDL –Monitorfororthostatichypotensionand electrolyte abnormalities.Loop diuretics remain effective despiterenal nsufficiency. Diuretic effect increases at higherdoses

30. Potassium-Sparing(spironolactone/Aldactone) • Reduce K+ and Na+ exchange in the distal tubules; Reduces excretion of K+, H+, Ca++ and Mg++; Inhibitthe Na+ retaining and K+ excreting effects ofaldosterone. • S/E: hyperkalemia, N/V, diarrhea, headache,leg cramps, dizziness, maybe gynecomastia, impotence,decreased libido, menstrualirregularis

31. AngiotensinInhibitors Angiotensin-Converting Enzyme Inhibitors (ACE-Inhibitors)(“-pril”) • First line of defense fordiabetics • Inhibit angiotensin-converting enzyme; reduce conversion ofangiotensin I to angiotensin II; prevent angiotensin II mediatedvasoconstriction. • Inhibits angiotensin-converting enzyme when oral agents arenot appropriate. • Enalapril 20 mg , ramipril 5-10mg • S/E: Hypotension, loss of taste, cough, hyperkalemia, acute renalfailure, skin rash angioneuroticedema. • ASA/NSAIDS may reduce drugeffectiveness. • Diuretic enhances drugeffect. • Do not use with K+-sparing diuretics. Fetal morbidity ormortality

32. Antiotensin II Receptor Blockers (ARBs)(“-sartan”) • Prevents action of angiotensin II and produces vasodilation and increased saltand waterexcretion. • S/E: Hyperkalemia, decreased renalfunction. • Full effect on BP takes 3 to 6weeks.

33. Calcium ChannelBlockers(“-dipine”) • Blocks movement of extracellular calcium into cells, causingvasodilation and decreasedSVR. • Effective and well tolerated particularly in theelderly • - Verapamil 240mg , Diltazem, amlodipine2.5-10mg • S/E: Nausea, headache, dizziness, peripheral edema. Reflextachycardia (with dihydropyridines). Reflex decreased heart rate;constipation. • Use with caution in patients with heartfailure. • Contraindicated in patients with second- or third-degree heart block.IV use available for HTNcrisis.

34. Beta Blockers(“-olol”) • Reduces BP by antagonizing beta adrenergiceffects. • Decreases CO and reduces sympathetic vasoconstrictortone. • Decreases renin secretion bykidneys. • Also used as first linetherapy • Metoprolol 100-200mg, atenolol 50-100mg • S/E:Bronchospasm, a/v conduction block; impaired peripheralcirculation; nightmares; depression; weakness; reduced exercise capacity; may exacerbate heart failure; Sudden withdrawal may cause rebound hypertension and cause ischemic heartdisease. • Monitor pulse regularly; use with caution in diabetics because drugmay mask signs ofhypoglycemia

35. Combined Alpha/Beta Blockers(labetalol/Normodyne) • Produces peripheral vasodilatation anddecreased heartrate. • S/E: dizziness, fatigue, N/V, dyspepsia, paresthesia, nasal stuffiness, impotence, edema. HEPATIC TOXICITY • Keep patient supine during IVadministration. • Assess pt tolerance of upright position(severe postural hypotension) before allowing upright activities

36. Alpha-1 Adrenergic Blocker(“-azosin”) • Blocks alpha-1 effects producing peripheralvasodilation (decreases SVR andBP) • Prazosin 0.5 – 20mg ; doxazosin1-16mg • S/E: Hypotension dependent on volume. May produce syncope within 90 minutes of initial dose; retention of sodium and water; cardiac arrhythmias, tachycardia, weakness, flushing; abdominal pain; N/V and exacerbation of pepticulcer. • Reduced resistance to the outflow of urine in benignprostatic hyperplasia. Take drugs at bedtime(orthostatic hypotension); beneficial effects on lipidprofile.

37. How to CombineAntihypertensive Medications

38. Common sideeffects • Orthostatichypotension • Sexual dysfunction (ask provider about changing med/dose or gettingViagra) • Dry mouth (chew sugarless gum or hardcandy) • Frequent voiding (take diuretics earlier in the day to avoid nocturia) • Sedation (take med in theevening) • BP is lowest during the night and highest after awakening…take med with 24-hour duration as early in the morningaspossible.

39. Follow-Up • Assess and encourage adherence to pharmacologicaland non-pharmacological therapy at every visit. • lifestylemodification - 3-6months • Pharmacological • - 1 -2months until BP under target for 2 consecutivevisits • - more often for symptomatic HTN, severe HTN, antihypertensive drug intolerance, target organdamage • - 3-6months once at targetBP • Referral is indicated for cases of refractory hypertension, suspected secondary cause or worsening renalfailure • Hospitalization is indicated for malignanthypertension

40. Pharmacologic Treatment of Hypertensionin Patients with UniqueConditions

42. Pharmacologic Treatment of Hypertension in Patients with Unique Conditions(continued)