1. Office Evaluation of Hypertension December 2, 2008

3. Prevalence

4. Why do we (physicians) get so excited about controlling hypertension? n Coronary artery disease n Stroke n End-stage renal disease n Congestive heart failure

6. Isolated systolic and systolic / diastolic hypertension in the elderly n Hypertension is the most common disease specific reason for Americans to visit a physician n Present in over 50% of all Americans over the age of 60 n Short-term benefit of treatment is greater than in young people because of overall greater cardiovascular risk

7. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md: National Institutes of Health, National Heart, Lung, and Blood Institute. 2003; NIH Publication 03-5231.

8. Classification of blood pressure n Normal BP: systolic < 120 and diastolic <80 n Pre-hypertension: systolic 120-139 or diastolic 80-89

9. Classification of blood pressure n Stage 1: systolic 140-159 or diastolic 90-99 n Stage 2: systolic > 160 or diastolic > 100

10. Lower Blood Pressure is Better n Not symptomatically hypotensive n Treated Blood Pressure must take into account the risk of medications n Low diastolic pressures are probably a marker for decreased arterial compliance in patients over age 65 years (Hardening of the arteries)

11. Initial evaluation n BP should be elevated on 2 separate occasions: office, home, ambulatory monitor n Rule out secondary causes (correctable) of hypertension n Evaluate for end-organ damage n Evaluate the patient’s overall cardiovascular risk status

13. Secondary Hypertension n Renovascular hypertension (secondary hyperaldosteronism) n Primary hyperaldosteronism n Primary hyperparathyroidism n Cushing’s disease n Pheochromocytoma

14. Secondary Hypertension n Primary renal disease n Hypothyroidism n Oral contraceptives n Sleep apnea n Coarctation of the aorta

15. Secondary Hypertension n Renovascular hypertension (secondary hyperaldosteronism)

16. Renovascular hypertension n Most common cause of secondary hypertension n Incidence 10-45% in severe or refractory hypertension n Clinical symptoms include ischemic loss of renal function and otherwise unexplained sudden onset pulmonary edema

17. n Atherosclerotic Disease n Fibromuscular dysplasia

19. Secondary Hypertension n Renovascular hypertension (secondary hyperaldosteronism) n Primary hyperaldosteronism n Primary hyperparathyroidism n Cushing’s disease n Pheochromocytoma

20. Hyperaldosteronism n Primary Hyperaldo-most common, prevalence around 1-2% n Aka Conn’s Syndrome (1955) n Hypertension, hypokalemia n Adrenal adenoma, bilateral adrenal hyperplasia

21. Cushing’s Syndrome n Excess glucocorticoid-either exogenous or endogenous n Hypertension results from the mineralocorticoid effect of the excess glucocorticoids

22. Pheochromocytoma n Very rare n Episodic headache, sweating and tachycardia n 50% have paroxysmal HTN, the rest apparently have “essential” HTN

23. History

24. Features of Essential Hypertension without End organ damage n None

25. Initial evaluation n BP should be elevated on 2 separate occasions: office, home, ambulatory monitor n Rule out secondary causes (correctable) of hypertension n Evaluate for end-organ damage n Evaluate the patient’s overall cardiovascular risk status

26. Cardiovascular risk factors n Smoking n Diabetes mellitus n Dyslipidemia n Physical inactivity n Chronic kidney disease

27. Symptoms of target organ damage n Headache n Transient weakness or blindness n Loss of visual acuity n Chest pain n Dyspnea n Claudication

28. Aggravating factors n Drugs: estrogens, adrenal steroids, sympathomimetics, and NSAIDS n Diet: salt, alcohol, caffeine, and weight n Family history n Race n Sleep apnea

29. Symptoms of secondary causes n Muscle weakness n Spells of tachycardia, sweating, and tremor n Thinning of the skin n Flank pain

30. Clues to the presence of Secondary Hypertension n Young age of onset n Sudden onset of HTN n Uncontrolled/Refractory HTN n Malignant HTN (End organ damage) n Features of a recognized underlying cause

31. Physical exam

32. Is there evidence for end- organ damage? n Retinopathy n Heart rhythm, extra sounds n Bruits (renal artery variety may suggest a secondary cause) n Pulses n Edema n Rales

34. Laboratory n Electrolytes (Na+, K+, Cl-, CO2-) n Creatinine n Urinalysis

35. Other tests n Lipid profile n EKG n Echocardiogram

36. Tests to pursue secondary causes of hypertension n Serum renin and aldosterone n 24 hour urine collection for metanephrines n Dexamethasone suppression test n Serum calcium n Renal angiogram

37. Treatment

38. Lifestyle modification n Weight loss for the overweight n Increased aerobic physical activity n Moderate sodium restriction n Moderate alcohol consumption n Minimize caffeine consumption

39. Pharmacologic treatment Low renin *older *thin *black - thiazide diuretics - calcium channel blockers - alpha blockers Essential HypertensionHigh renin *younger *overweight - beta blockers - angiotensin converting enzyme inhibitors - angiotensin II receptor antagonists

40. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Bethesda, Md: National Institutes of Health, National Heart, Lung, and Blood Institute. 2003; NIH Publication 03-5231.

41. Other agents n Alpha 2 central blockers n Direct vasodilators n Sympathetic blockers

42. Thiazide diuretics n Mechanism of action is unclear but probably is a combination of mild plasma volume decrease plus decreased intracellular calcium concentration leading to vasodilation n Cheap n Effective n Very low incidence of side effects at low doses

43. Thiazide diuretics provide cardioprotection in: n Left ventricular hypertrophy n Type 2 diabetes mellitus n Previous myocardial infarction n Previous stroke n Current cigarette smoking n Hyperlipidemia n Atherosclerotic cardiovascular disease

44. Angiotensin converting enzyme inhibitors: agents of choice in hypertension and …. n Congestive heart failure n ST elevation myocardial infarction n Non-ST elevation anterior myocardial infarction n Diabetes mellitus n Proteinuric chronic renal failure

45. Angiotensin converting enzyme inhibitors and angiotensin receptor blockers used together are indicated in: n Congestive heart failure n Proteinuric chronic renal failure

46. Angiotensin converting enzyme inhibitors act by... n Decreasing angiotensin II n Increasing kinin levels (block kininase activity) n Decrease aldosterone n Increase insulin sensitivity

47. Angiotensin II receptor antagonists n Impair binding of angiotensin II to AT1 receptors n No cough (no increased kinin levels) n No reduction in AT2 receptor activity (arterial hypertrophy, improved left ventricular activity after ischemia)

48. Angiotensin receptor antagonists n Production of angiotensin II in the heart may be through another enzyme (chymase), therefore AII receptor antagonists may be more effective than ACE inhibitors locally n No change in insulin sensitivity (kinin mediated) n Indications for and efficacy of ARB’s are not different from ACE inhibitors

49. Direct Renin Inhibitors n Aliskiren approved by the FDA in August 2007 n Inhibits renin production in the JG cells n Trade name Tekturna n Studies ongoing, not yet in widespread clinical use

50. Beta blockers (without intrinsic sympathomimetic activity) are indicated in: n Post myocardial infarction n Stable patients with congestive heart failure n Rate control in atrial fibrillation n Control of angina pectoris

51. Calcium channel blockers n Dihydropyridines n Verapamil n Diltiazem

52. Calcium channel blockers: no absolute indication in treatment of hypertension but are helpful in: n Rate control in atrial fibrillation n Control of angina pectoris n May be preferred in obstructive airway disease

53. Dihydropyridines: side effects n Headache n Dizziness n Flushing n Edema (due to a redistribution of fluid from vascular to interstitial space)

54. Pregnancy n Alpha Methyl Dopa n Labetalol n CCB n Diuretics +/- n No ACE-I or ARB