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11.HTN

Diagnosis and treatment of hypertension

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11.HTN

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  1. Hypertension Professor Mohammed Bamashmoos

  2. Introduction • Blood pressure is the force on the walls of the arteries as the blood circulates. • Blood pressure allows blood to flow and deliver nutrients to the body. • We measure blood pressure with two numbers. • The top number is the blood pressure when your heart beats. • The bottom number is your blood pressure when your heart relaxes and refills with blood. • 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 risk for death. • High blood pressure can cause strokes, heart attacks, and heart and kidney failure. • It is also related to dementia and sexual problems. • These problems can be prevented if high blood pressure is controlled.

  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, kidneys and large conduit arteries.

  5. • Hypertension : BP≥140/90 mmHg • Isolated systolic hypertension - sBP ≥ 140 and dBP <90 - associated with progressive reduction in vascular compliance - usually begins in 5th decade; up to 11 % of 75 yr olds • Accelerated hypertension - significant recent increase in BP over previous hypertensive levels associated with evidence of vascular damage on fundoscopy but without papilledema • Malignant hypertension - sufficient elevation in BP to cause papilledema and other manifestations of vascular damage (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 hypertensive patients • Hypertensive urgency : - sBP >210 or dBP > 120 with minimal or no target-organ damage • Hypertensive emergency - high BP + acute target-organ damage

  6. Hypertensive Emergencies 1. Malignant HTN with papilledema 2. Cerebrovascular: - Hypertensive encephalopathy - CVA with severe hypertension - Intracerebral hemorrhage - SAH 3. Cardiac: - Acute aortic dissection - Acute refractory LV failure - Acute MI with persistent ischemic - pain after CABG

  7. 4. Renal: - Acute glomerulonephritis - Renal crises from collagen vascular diseases - Severe hypertension following renal transplantation 5. Excessive circulating catecholamines: - Pheochromocytoma - Tyramine containing foods or drug - Sympathomimetic drug use (e.g. cocaine) - Rebound HTN after cessation of antihypertensive drugs (e.g. clonidine) 6. Eclampsia 7. Surgical: - Severe HTN prior to emergent surgery - Severe post-op HTN - Post-op bleeding from vascular suture lines 8. HTN following severe burns 9. Severe epistaxsis

  8. Classification of hypertension

  9. World Health Organization 2002

  10. Epidemiology • 20-25% of adults have HTN (up to 50% undiagnosed) • 16% have adequate BP control • Approximately 50% of adult are hypertensive by age 60 • 3rd leading risk factor associated with death • Risk factor for CAD, CHF, cerebrovascular disease, renal failure, peripheral vascular disease

  11. Risk Factors • Age • Alcohol • Cigarette Smoking • Diabetes mellitus • Elevated serum lipids • Excess dietary sodium • Gender  • Family history • Obesity • Ethnicity – IS AN IMP. FACTOR IN OVERALL CARDIAC DISEASE • Sedentary lifestyle • Socioeconomic status • stress

  12. Etiology : • Of all 90% have Essential hypertension • The remainder have secondary hypertension

  13. Causes of secondary hypertension • Alcohol • Pregnancy • Renal disease: • Renal artery stenosis, • Glomerulonephritis, • Polycystic kidney disease • Endocrine disease: • Pheochromocytoma, cushing’s disease, conn’s syndrome, hyperparathyroidism, • acromegaly, primary hyperthyroidism, thyrotoxicosis, • congenital adrenal hyperplasia • 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 increased SVR. • Heredity • Water/Sodium retention • Altered renin-angiotensin mechanism • Stress and increased sympathetic NS activity • Insulin resistance and hyperinsulinemia • High insulin concentration stimulates SNS activity and impairs nitric oxide-mediated vasodilation • Pressor effects of insulin include vascular hypertrophy and increased renal sodium reabsorption • Endothelial Cell Dysfunction • Enodthelin produces pronounced and prolonged vasoconstriction.

  15. Symptoms and signs of Hypertension High blood pressure has no warning signs or symptoms – which is why it is often called a “silent killer”.  • Mostly asymptomatic • Symptoms as a result of arterial pressure: • headache(occipital, early morning for several hours), • dizziness, • palpitation, • easY fatigability, • impotance. • Symptoms of hypertensive vascular disease: • epistaxis, • hematuria, • blurring of vision, • episodic weakness(TIA), • angina, • dyspnoea (HF), • chest pain(dissection of aorta) • Symptoms of underlying disease (secondary HTN)

  16. Physical examination : • Cardiac murmurs • neurologic deficits • elevated jugular pressure • rales • retinopathy • unequal pulses • abdominal bruits

  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 by therapy • Occurrence of HTN crisis • Sign & symptoms of scondary causes – HYPERKALEMIA , METABOLIC ACIDOSIS • FAMILY HISTORY

  18. Complications Target Organ Diseases • Heart (hypertensive heart disease) • Coronary artery disease (leading to MI and angina) • Left ventricular hypertrophy (from high cardiac workload leading to heart failure) • Heart failure (shortness of breath on exertion, nocturnal dyspnea, fatigue, enlarged heart) • Brain (cerebrovascular disease) • Stroke/transischemic attacks • Hypertensive encephalopathy (cerebral edema)

  19. Peripheral vasculature (peripheral vascular disease) • Atherosclerosis in peripheral blood vessels • Aortic aneurysm, aortic dissection, peripheral vascular disease • Intermittent claudication (pain with activity or lack of oxygen to tissues)

  20. Kidneys (nephrosclerosis) • End stage renal disease (ischemia from narrowed intrarenal vessels) • Urinalysis • Microalbuminuria • Proteinuria • Elevated blood urea nitrogen/elevated Serum creatinine • Usually ratio of 10:1 or 15:1. • BUN: 5-25 mg/dl • Creatinine: 0.5 – 1.5 mg/dl • Microscopic hematuria • Earliest sign of renal damage is nocturia

  21. Eyes (retinal damage) • Eyes are only place vessels can be directly observed. • Retinal damage can indicate damage in other target organs. • Signs/Symptoms • Blurry vision • Retinal hemorrhage • Loss of vision

  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 protein excretion - 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 Grade of Recommendationsfor Hypertension Diagnosis andTreatment Grade • A = High levels of internal validity and statistical precision • B/C = Lower levels of internal validity and statistical precision • D = Expert opinion

  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 more than two abnormal reading over a period of several weeks should be obtained before considering) • Pseudohypertention in elderly excluded due to stiff vessels

  25. Approach to Hypertension

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

  27. Diuretics • First line of defense • Thiazides (Hydrodiuril ) • Inhibit sodium reabsorption in the distal convoluted tubule; increase excretion of sodium; decreases ECF; sustains a decrease in SVR • Lowers BP moderately in 2-4 weeks • hydrochlorothiazide 12.5 -25 mg/ day • S/E: fluid/electrolyte imbalances; CNS effects; GI effects; sexual impotence; dermatologic effects(photosensitivity); decreased glucose tolerance • Monitor for orthostatic hypotension, hypokalemia and alkalosis.  • Watch for digoxin toxicity. •  Avoid NSAIDS. • Eat K+-rich foods

  28. Loop Diuretics (furosemide/Lasix) • Inhibits NaClreabsorption in ascending limb of loop of Henle; increases excretion of sodium and chloride. • More potent than thiazides, but of shorter duration; less effective for HTN • S/E: fluid/electrolyte imbalances(hypokalemia);ototoxicity; metabolic effects (hyperglycemia); increasedLDL and triglycerides with decreased HDL • Monitor for orthostatic hypotension and electrolyte abnormalities. Loop diuretics remain effective despiterenalnsufficiency. Diuretic effect increases at higher doses

  29. 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 of aldosterone. • S/E: hyperkalemia, N/V, diarrhea, headache,leg cramps, dizziness, maybe gynecomastia, impotence,decreased libido, menstrual irregularis

  30. Angiotensin InhibitorsAngiotensin-Converting Enzyme Inhibitors (ACE-Inhibitors) (“-pril”) • First line of defense for diabetics • Inhibit angiotensin-converting enzyme; reduce conversion of angiotensin I to angiotensin II; prevent angiotensin II mediated vasoconstriction.  • Inhibits angiotensin-converting enzyme when oral agents are not appropriate. • Enalapril 20 mg , ramipril 5-10 mg • S/E: Hypotension, loss of taste, cough, hyperkalemia, acute renal failure, skin rash angioneurotic edema. • ASA/NSAIDS may reduce drug effectiveness.  • Diuretic enhances drug effect.  • Do not use with K+-sparing diuretics. Fetal morbidity or mortality

  31. Antiotensin II Receptor Blockers (ARBs) (“-sartan”) • Prevents action of angiotensin II and produces vasodilation and increased salt and water excretion. • S/E: Hyperkalemia, decreased renal function. • Full effect on BP takes 3 to 6 weeks.

  32. Calcium Channel Blockers(“-dipine”) • Blocks movement of extracellular calcium into cells, causing vasodilation and decreased SVR. • Effective and well tolerated particularly in the elderly - Verapamil 240mg , Diltazem, amlodipine 2.5-10mg • S/E: Nausea, headache, dizziness, peripheral edema. Reflex tachycardia (with dihydropyridines). Reflex decreased heart rate; constipation. • Use with caution in patients with heart failure.  • Contraindicated in patients with second- or third-degree heart block. IV use available for HTN crisis.

  33. Beta Blockers (“-olol”) • Reduces BP by antagonizing beta adrenergic effects.  • Decreases CO and reduces sympathetic vasoconstrictor tone.  • Decreases renin secretion by kidneys. • Also used as first line therapy • Metoprolol 100-200mg, atenolol 50-100 mg • S/E:Bronchospasm, a/v conduction block; impaired peripheral circulation; nightmares; depression; weakness; reduced exercise capacity; may exacerbate heart failure; Sudden withdrawal may cause rebound hypertension and cause ischemic heart disease. • Monitor pulse regularly; use with caution in diabetics because drug may mask signs of hypoglycemia

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

  35. Alpha-1 Adrenergic Blocker (“-azosin”) • Blocks alpha-1 effects producing peripheral vasodilation (decreases SVR and BP) • Prazosin 0.5 – 20mg ; doxazosin 1-16mg • 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 peptic ulcer. • Reduced resistance to the outflow of urine in benign prostatic hyperplasia. Take drugs at bedtime(orthostatic hypotension); beneficial effects on lipid profile.

  36. How to Combine AntihypertensiveMedications

  37. Common side effects • Orthostatic hypotension • Sexual dysfunction (ask provider about changing med/dose or getting Viagra) • Dry mouth (chew sugarless gum or hard candy) • Frequent voiding (take diuretics earlier in the day to avoid nocturia) • Sedation (take med in the evening) • BP is lowest during the night and highest after awakening…take med with 24-hour duration as early in the morning aspossible.

  38. Follow-Up • Assess and encourage adherence to pharmacological and non-pharmacological therapy at every visit . • lifestyle modification - 3-6months • Pharmacological - 1 -2months until BP under target for 2 consecutive visits - more often for symptomatic HTN, severe HTN,antihypertensive drug intolerance, target organ damage - 3-6months once at target BP • Referral is indicated for cases of refractory hypertension, suspected secondary cause or worsening renal failure • Hospitalization is indicated for malignant hypertension

  39. Pharmacologic Treatment of Hypertension in Patients with Unique Conditions

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

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