Hypertension diagnosis and treatment updates

Causes ,diagnosis and treatment

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 Category Systolic 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

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 : R enal artery stenosis , G lomerulonephritis , P olycystic kidney disease Endocrine disease : P heochromocytoma , 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 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) 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 (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 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 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 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

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 Inhibitors Angiotensin -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 Antihypertensive Medications

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)