HYPERTENSION IN ELDERLY

INTRODUCTION
The elderly represent the most rapidly growing segment of the population globally and more than 50% of hypertensives are aged above 65 years. The high prevalence of hypertension in older persons suggest that the recognition and treatment of hypertension should be a priority . Both systolic blood pressure (SBP) and diastolic blood pressure (DBP) increase with advancing age . Systolic blood pressure continues to rise until the age of 70 or 80 years where as diastolic blood pressure rises upto the age of 50 or 60 years and then levels remain same or may even decrease slightly. The resultant widening of pulse pressure indicates stiffening of central aorta and there by causing more rapid return of reflected pulse waves from the periphery which causes an augmentation of systolic aortic pressure. Persons with the highest blood pressure at younger ages will have the greatest increase in blood pressure as they get older. Initially the rise in blood pressure is more in men than in women, but after menopause women show a greater rise and reach levels that are higher than in men. PHYSIOLOGICAL AND PATHOLOGICAL CHANGES WITH AGING Age related vascular and neurohormonal changes are important factors leading to development of hypertension in the elderly and the changes in systolic blood pressure and diastolic blood pressure with age in any individual are a consequence of relative change in arterial resistance and stiffness .Large vessels become less distensible, which increases pulse wave velocity causing increase in systolic blood pressure. Arterial compliance decreases because of structural and functional changes and increase in collagen, ground substance, elastin and extracellular protein matrix that occur with aging. This creates structural and mechanical alterations in vessel intima and media. The proliferation of connective tissue results in intimal thickening and fibrosis thus increasing stiffness of vessels with partial loss of contractility. Consequently, arterial compliance decreases and the so called windkessel function of the large arteries decreases. Pulse pressure

and pulse wave velocity increase with an earlier reflection of pressure waves from the periphery to a disproportionate increase in SBP. These vascular changes and their hemodynamic sequel may have several consequences that increase cardiovascular risk. Arterial stiffness increases afterload and myocardial oxygen demand, impairs ventricular relaxation and is strongly correlated with left ventricular hypertrophy HYPERTENSION AS A RISK FACTOR IN THE ELDERLY Elevation of both systolic blood pressure and diastolic blood pressure is well recognized as an important risk factor for cerebro vascular accidents (CVA),congestive heart failure(CHF),coronary artery disease (CAD), end stage renal disease (ESRD) and sudden death coronary perfusion pressure is reduced due to the decrease in diastolic blood pressure and prolongation of systole , this may cause ischemia regardless of the presence of epicardial coronary artery stenosis . Arterial stiffness also may have a primary role in atheroma development , due to the effects of increased pulsatile load and cyclic wall stress on endothelial function and atherogenesis .Elderly hypertensive patients are also at higher risk for arrhythmias. other condition for which hypertension is considered a risk factor include vascular dementia , aortic and peripheral arterial disease including abdominal aortic aneurysm ,thoracic aortic aneurysm, acute aortic dissection ophthalmologic disorders including hypertensive retinopathy, retinal artery stenosis, age related macular degeneration. INTERACTIONS BETWEEN AGING AND CARDIOVASCULAR RISK CONDITIONS ASSOCIATED WITH HYPERTENSION Because dyslipidemia and hypertension are common among the elderly, it is reasonable to be aggressive with lipid lowering in elderly hypertensive patients . Elderly patients with hypertension and diabetes mellitus have a higher mortality risk than similarly aged non diabetic controls. Albuminuria is a predictor of higher mortality risk among those with diabetes mellitus. Adipose tissue produces all components of renin- angiotensin- aldosterone system locally , leading to development of obesity related hypertension . Gout incidence rates are higher in hypertensive patients verses normotensive patients , thiazide diuretics may

increase serum uric acid levels and may provoke gout. Serum uric acid levels independently predicts cardiovascular events in older hypertensive patients , therefore monitoring serum uric acid levels during diuretic treatment is reasonable. CLINICAL ASSESSMENT AND DIAGNOSIS Blood pressure recordings should be obtained on at least 2 different occasions, each separated by 6 hrs apart before the diagnosis of hypertension is made. Patient should be seated comfortably with the back supported, feet on the floor, arm supported in the horizontal position and the BP cuff at heart level. White coat hypertension is more common among elderly . Pseudo hypertension is a falsely increased blood pressure that results from markedly sclerotic arteries that do not collapse during cuff inflation . this condition is suggested if the radial pulse remains palpable despite occlusion of brachial artery by the cuff-osler maneuver. identification of pseudo hypertension is necessary to avoid over treating falsely high blood pressure.

MANAGEMENT GENERAL CONSIDERATIONS Evaluation of the elderly patient with known or suspected hypertension starts with accurate measurement of blood pressure and if elevated: 1) Identify reversible and/ or treatable causes 2) Evaluate for organ damage 3) Assess for other cardiovascular risk factors which affect prognosis INVESTIGATIONS THAT SHOULD BE CONSIDERED ARE: 1) Urine analysis for evidence of microalbuminuria/ albuminuria

2) Serum electrolytes( sodium & potassium levels) 3) Fasting blood sugar, post lunch blood sugar& HbA1c 4) Lipid profile- total cholesterol, low density lipoprotein, high density lipoprotein & triglycerides. 5) electrocardiogram(ECG) GOALS OF TREATMENT According to JNC-8 guidelines the recommended BP goal in hypertensives aged 60 yrs is 150/90 mm hg and in those age < 60 yrs goal is 140 /90 mm hg. in diabetics and CKD patients , the goal is 149/90 mm hg irrespective of age. NON PHARMACOLOGICAL TREATMENT Smoking cessation , reduction in excess body weight and mental stress, reduction of excessive sodium and alcohol intake , and increased physical activity are recommended. PHARMACOLOGICAL TREATMENT The initial antihypertensive drug should be started at the lowest dose and gradually increased depending on the response to the maximum tolerated dose. If the response to the initial drug is inadequate even after reaching full dose, a second drug from another class should be added . If the person is having no therapeutic response or significant adverse effects, a drug from another class should be substituted. If a diuretic is not the initial drug, it is usually indicated as the second drug. If the antihypertensive response is inadequate after reaching the full dose of 2 classes of drugs, a third drug from another class should be added. Before adding new antihypertensive drugs, reasons for inadequate BP response should be evaluated. These include noncompliance, drug interactions and associated conditions such as obesity, smoking, excessive alcohol intake, insulin resistance, and pseudoresistance. Pseudoresistance is an inadequate response to antihypertensive therapy because the Blood pressure recordings in the physicians office are falsely high compared with those measured at home or by 24-hour ambulatory BP monitoring. Causes of secondary hypertension should be

identified and treated. Associated comorbid conditions should be kept in mind while prescribing antihypertensive drug therapy . SPECIFIC DRUG CLASSES Thiazides. Thiazide diuretics, such as Hydrochorthiazide chlorthalidone, are recommended for initiating drug therapy in elderly. Chlorthalidone differs from HCTZ by its longer duration of action and greater potency, and for this reason, may be associated with a higher risk of metabolic adverse effects. Diuretics can cause hypomagnesemia, hypokalemia and hyponatremia. hypomagnesemia and Hypokalemia can develop within the first few days of treatment. However, after that, the body can achieve a new homeostatic balance, and loss of these ions is lessened. These agents are not advised in patients with baseline electrolyte abnormalities. serum electrolytes levels should be monitored in patients taking diuretics .

Angiotensin-Converting Enzyme Inhibitors. ACEIs block conversion of angiotensinI to angiotensin-II. The latter lowers total peripheral vascular resistance, and BP is reduced without reflex stimulation of heart rate and cardiac output. Benefits of ACEI are reduction in morbidity and mortality in patients with MI, reduced systolic function heart failure , diabetic nephropathy. The main adverse effects of ACEIs include hypotension, chronic dry cough, and, rarely, angioedema or rash. Hyperkalemia can occur in patients with renal insufficiency or those taking potassium supplements or potassium-sparing diuretics Angiotensin Receptor Blockers. ARBs selectively block the AT1-receptor subtype that mediates all known physiological effects of angiotensin-II believed relevant to cardiovascular and cardiorenal homeostasis. ARBs protect the kidney in type 2 diabetes mellitus both in established diabetic nephropathy with proteinuria and in patients with microalbuminuria. ARBs also reduce mortality and morbidity in patients with heart failure . In elderly patients with hypertension with diabetes mellitus, ARBs are considered first-line treatment and as an alternative to ACEI in patients with hypertension and heart failure who cannot tolerate ACEI Calcium channel blockers. Calcium channel blockers include a heterogeneous group of drugs with widely variable effects on heart muscle, sinus node function,

atrioventricular conduction, peripheral arteries, and coronary circulation. Chemically, they can be divided into phenylalkylamines (verapamil); benzothiazepines (diltiazem); and dihydropyridines (nifedipine, nicardipine, nimodipine, amlodipine etc).They block influx of calcium ions into the cells of vascular smooth muscle and myocardial tissue, and are significantly more effective inhibiting contraction in coronary and peripheral arterial smooth muscle than in cardiac and skeletal muscle. Vascular smooth muscle is more dependent on external calcium entry for contraction, whereas cardiac and skeletal muscle rely on a recirculating internal pool of calcium. Because Calcium channel blockers are membrane active, they reduce calcium entry into cells and therefore exert a much greater effect on vascular tissue. This preferential effect allows Calcium channel blockers to dilate coronary and peripheral arteries in doses that do not severely affect myocardial contractility or skeletal muscle. Calcium channel blockers appear well suited for elderly patients whose hypertensive profile is based on increasing arterial stiffness and diastolic dysfunction secondary to decreased atrial and ventricular compliance. Because they have multiple clinical applications, including treatment of angina and supraventricular arrhythmias, Calcium channel blockers hold promise for treatment of elderly patients with hypertension and comorbid Cardio vascular conditions. In general, calcium channel blockers are well tolerated by the elderly. Most adverse effects of the dihydropyridines relate to vasodilation (ankle edema, headache, and postural hypotension). Peripheral edema also may be confused with heart failure. Verapamil, which may be useful for LV diastolic dysfunction, may increase constipation. Verapamil and diltiazem may precipitate heart block in elderly patients with underlying conduction defects.