1. Medications for Treating Hypertension Jeannie Collins Beaudin, RPh Keswick Pharmacy 1

2. WIDESPREAD PROBLEM... CANADIAN STATISTICS: More than 1 in 5 adults have hypertension (22%) 46% of Canadians age 55-65 42% - No diagnosis Only 16% are controlled 9% of those with diabetes (more stringent targets) 2

3. IMPORTANCE OF NURSES’ ROLE Nurses have: Frequent patient contact Patient trust Favourable financial model Educational role 3

4. ...PART OF THE PICTURE METABOLIC SYNDROME: Hypertension Insulin resistance Hypercholesterolemia Abdominal weight gain Prothrombic state Pro-Inflammatory state All are risk factors for cardiovascular disease #1 cause of death 4

5. CAUSES OF METABOLIC SYNDROME Obesity Inactivity Poor diet Unknown genetic factors Stress? Cortisol Increases BP, heart rate, lipids, blood glucose Weight gain around waist 5

6. KEY CHEP MESSAGES... Need to assess overall CVD risk Combination of drug therapy and lifestyle changes are most effective Monitor regularly when above target Regular screening for all adults Focus on adherence 6

7. ADHERENCE Assess regularly Encourage patients to bring bottles Check date filled and amount remaining Fit to daily schedule Strive for once daily dosing Long-acting formulas Fixed-dose combinations Fewer pills per day Often more expensive, not covered Use unit-of-dose packaging Improve patient education Encourage patient involvement in monitoring 7

8. TYPES OF HYPERTENSION MEDICATIONS Those that affect hormone systems Beta-blockers ACE Inhibitors (angiotensin converting enzyme inhibitors) ARBs (angiotensin receptor blockers Those that affect electrolytes Fluid balance Diuretics Vasodilation Calcium channel blockers 8

9. ABCs OF HYPERTENSION MEDS A. Angiotensin Converting Enzyme Inhibitors (ACE-I), Angiotensin Receptor Blockers (ARB) B. Beta-Blockers C. Calcium channel blockers (CCBs) D. Diuretics E. “Everything else”... Alpha-Blockers 9

10. ACE-Inhibitors End with “-pril” Block the enzyme that converts Angiotensin I to Angiotensin II Also reduce morbidity/mortality of HF, angina, stroke, DM neuropathy Generally well tolerated 25% can develop dry cough ACE enzyme also block breakdown of bradykinin (xs causes cough) Teratogenic – caution in pre-menopausal women 10

11. ANGIOTENSIN RECEPTOR BLOCKERS (ARBs) End with “-sartan” Block the effect of Angiotensin II instead of blocking production Actions similar to ACE-I But does not affect bradykinin No cough side effect Better tolerated More expensive Also teratogenic 11

12. BETA-BLOCKERS End with “-olol” “Beta adrenergic receptor blockade” Block beta receptors for adrenalin Beta-1, Beta-2 receptors Beta-1 - heart, blood vessels Beta-1 selective BB’s (e.g. Atenolol, Metoprolol) Beta-2 - lungs, brain Non-selective BB’s (e.g. Propranolol, Nadolol) 12

13. BETA-BLOCKERS BETA-2: Lungs Bronchodilation Site of action of Salbutamol (beta-agonist) Brain Dreaming Migraine Beta-blockers can decrease frequency 13

14. BETA-BLOCKERS Block action of adrenalin and beta(adrenalin) agonists on lungs: Can worsen bronchospasm, asthma Block action of inhaled Salbutamol Can be useful for blocking essential tremor 14

15. BETA-BLOCKERS Disadvantages: Slow heart rate, lower blood pressure (fatigue) Reduce blood flow to extremities (cold hands, feet, impotence) Less heart-selective can increase dreaming Increase risk of diabetes (especially with diuretics) Not recommended over 65 years Advantages: Reduce mortality post-MI Also useful for HF, angina Non-cardio selective can prevent migraine Inexpensive 15

16. CALCIUM CHANNEL BLOCKERS Calcium is necessary for smooth muscle contraction Calcium enters cells via tiny channels Blocking calcium channel inhibit muscle contraction Vasodilation Reduced force of heart muscle contraction Affect heart, blood vessels – not skeletal muscle 16

17. CALCIUM CHANNEL BLOCKERS Three types: Dihydropyridines (DRPs) - end with “-dipine” Amlodipine, Felodipine, Nifedipine Phenylalkylamines Verapamil Benzothiazepines Diltiazem Last 2 have similar characteristics Often referred to as “non-dihydropyridines” (non-DRPs) Essentially 2 classes now: DRPs and non-DRPs 17

18. CALCIUM CHANNEL BLOCKERS DIFFERENT SITES OF ACTION: DRPs (-dipines) act mainly on blood vessels “vasodilating” Excess relaxation -> peripheral edema Adversely affect renal function in diabetes Non-DRPs (verapamil, diltiazem) also act on heart “modulating” Verapamil has the strongest effect on heart Diltiazem is “middle of the road” Both slow conduction of impulse through AV node Caution with 2 nd and 3 rd degree heart block Avoid in heart failure Renal protective Preferable if risk of diabetes or kidney damage 18

19. CALCIUM CHANNEL BLOCKERS No effect on: Insulin secretion or action Blood glucose Plasma protein levels Potassium balance Magnesium balance Grapefruit interaction Amlodipine, felodipine 19

20. CALCIUM CHANNEL BLOCKERS Short-acting nifedipine Spike in norepinephrine, transient rise in plasma renin Reflex tachycardia, BP rise No longer used for emergency hypertension 20

21. DIURETICS End with “-ide” Hydrochlorothiazide, indapamide, furosemide Act on kidney to increase fluid excretion Reduced blood volume -> reduced pressure Thiazides – act on tubules Furosemide - “Loop” diuretic, more potent Most cause loss of potassium Increased risk of electrolyte imbalances Exceptions “potassium sparing”: Spironolactone (Aldactone) Amiloride (in Moduret, Apo-Amilzide), Triamterene (in Dyazide, Apo-Triazide, Nov0-Triamzide ) 21

22. DIURETICS Many side effects: Lethargy, reduced exercise tolerance, polyuria Hypokalemia Skeletal muscle weakness, GI hypomotility (ileus, constipation) Leg cramps, arrhythmia Can precipitate gouty arthritis (increased uric acid) Adverse effect on glucose and lipids (especially with B- Blockers) Poorer compliance noted than with other classes Very inexpensive, effective 22

23. “EVERYTHING ELSE” ALPHA BLOCKERS End with “-azosin” Prazosin, terazosin Also used for enlarged prostate Block alpha adrenalin receptors Strong rapid blood pressure reduction Dose must be started low and raised slowly Side effect: Postural hypotension (may be severe) 23

24. CONCLUSION... HTN is most important cause of stroke, angina and renal and heart failure Most important key for successful treatment is patient education Important to focus on multiple CV risk factors: 10%  in BP + 10%  in TC = 45%  in CVD! 24

25. QUESTIONS? THANK YOU! THANK YOU! 25