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11.HTN.pptx
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- 2. Introduction • Blood pressureis 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 pressureincreases 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 isdefined 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. MalignantHTN 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: - Acuteglomerulonephritis - 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 CategorySystolic BP mm Hg Diastolic BP mmHg Normal <120 <80 Prehyprtension 120-139 80-89 Stage I hypertension 140-159 90-99 Stage II hypertension 160-199 100-109
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- 10. Epidemiology • 20-25% ofadults 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 secondaryhypertension •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 signsof Hypertension • Mostly asymptomatic • Symptoms as a result of ď‚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) High blood pressure has no warning signs or symptoms – which is why it is often called a “silent killer”.
- 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 (retinaldamage) – 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 allpatients 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 Gradeof Recommendations for Hypertension Diagnosis and Treatment 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 – BPmonitoring 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
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- 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 lineof 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
- 29. • Loop Diuretics(furosemide/Lasix) – Inhibits NaCl reabsorption 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 despiterenal nsufficiency. Diuretic effect increases at higher doses
- 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 of aldosterone. – S/E: hyperkalemia, N/V, diarrhea, headache,leg cramps, dizziness, maybe gynecomastia, impotence,decreased libido, menstrual irregularis
- 31. Angiotensin Inhibitors Angiotensin-Converting EnzymeInhibitors (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
- 32. Antiotensin II ReceptorBlockers (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.
- 33. 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.
- 34. 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
- 35. 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
- 36. 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.
- 37. How to CombineAntihypertensive Medications
- 38. 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.
- 39. Follow-Up • Assess andencourage 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
- 40. Pharmacologic Treatment ofHypertension in Patients with Unique Conditions
- 42. Pharmacologic Treatment of Hypertensionin Patients with Unique Conditions (continued)