Health Articles

Patients whose diastolic pressure ranges between 90 and 109 mm Hy and whose blood pressure is not controlled by nonpharmacoiogic means may respond to a diuretic, ^-blocker, ACE inhibitor, calcium antagonist, ai-blqcker, or a/p-blocker in sub-maximal doses (see TABLE 35-5). The Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Rlood Pressure indicates that diuretics and β-hlockers are preferred he-cause placebo-controlled multicenter studies have demonstrated reduced total and cardiovascular morbidity and mortality wilh these drugs. Similarly controlled studies have not hcen conducted wilh Ihe other drugs.
The ai-blockers and a/p-blockers are particularly pertinent for men already taking an cu-blocker for benign prostatic hyperplasia. How ever, adding another α-blocker for hypertension may provoke postural hypotension—a potentially dangerous symptom in a patient who arises from bed frequently with nocturia.
If the initial dose of any of these drugs Tails to control blood pressure, the dose may be increased. This action is consistent with the currently advocated individualized stepped-care approach to treatment (see TABLE 3.5-6).
As an alternative to increasing the dose, a second drug may be added; this approach prevents side effects from maximum doses of the first drug. Thus, adding a β-blocker to hydrochlorothiazide 25 mg/day may prevent hypokalemia and hyperuricemia. In general, elderly patients respond to diuretics. Calcium antagonists and ACE inhibitors arc also effective with elderly patients, including blacks and those who have not responded to lower doses of β-blockers prescribed For coexisting angina pectoris.
Stages 3 and 4 hypertension: Inpatients with severe hypertension, any of the first-step drugs may be prescribed. If this does not control blood pressure adequately, however, a second or third drug may be necessary. These can be added sequentially, using lower doses first, ihcn increasing doses or adding different drugs.
Tailoring therapy by selecting drugs most appropriate to the pressor mechanisms of specific patients is possible. For example, the black or obese palient. who is more volume-dependent and has lower plasma renin activity, may respond well to a diuretic or calcium antagonist. The patient with renal arterial disease {unilateral but not in a solitary kidney) may be more responsive Io an ACE inhibitor.
Therapy with β-blockcrs may be appropriate for patients with a previous myocardial infarction, angina pectoris, migraine headaches, or glaucoma. An oral β-blockcr prescribed for hypertension usually does not adequately treat glaucoma as well. If the palient has not had side effects from prolonged therapy with a topical β-blocker. he probably will not have adverse effects from the addition of an oral agent.
The ACE inhibitors may be particularly valuable in hypertensive patients with heart failure. These drugs have been shown to improve left ventricular function, reduce hospital admissions for left ventricular dysfunction, prevent heart failure after a myocardial infarction, and prevent a second myocardial infarction. These findings have been demonstrated in the recent controlled, multicenter studies SOLVD (Studies of Left Ventricular Dysfunction) and SAVE (Study Against Ventricular Enlargemeni).
If the patient is already taking digitalis, a diuretic should be prescribed with care. Serum potassium levels should be closely monitored to prevent cardiac arrhythmias associated with hypokalemia. Impotence may result in patienls treated with diuretics, adrenergic inhibitors, and β-blockers; the ACE inhibitors antl calcium antagonists have been reported to produce fewer side effects.
Although elderly hypertensive patients have no more side effects from prolonged treatmenl than younger patients, they are more likely to have postural (orthostatic) hypotension from agents that inhibit adrenergic function. Also, centrally acting agents may be more likely to cause depression, forgetfulness, vivid dreams or hallucinations, and sleep problems.
Patients with chronic obstructive lung disease, asthma, or heart block greater than first degree should not be treated with β-blockers: calcium antagonists may be more appropriate. Patients with low heart rates may be good candidates for calcium antagonists that do not markedly reduce hearl rale.
All hypertensive patients should continue therapy after blood pressure is controlled because it is likely to rise if therapy is discontinued. Therapy can be “stepped down,” but this should be done slowly, one drug at a time. If blood pressure rises, Iherapy must be “stepped up” again.

The efficacy of reducing systolic arterial pressure in elderly patients with isolated systolic hypertension has been demonstrated in several clinical studies. These patients are at greater risk for stroke, myocardial infarction, and premature death than normolensivt; people; the elevated pressure and larger heart increase myocardial oxygen demand. The multicenter SHEP study strongly demonstrated that elevated systolic pressure can be controlled with diuretics (eg, hydrochlorothiazide or chlorthalidone, starting at 12.5 or 25 mg and increasing, if necessary, to 50 mg). Alternatively, β-blockers alone and in combination with a diuretic were also effective in the SHEP study. Also, angioiensin converting enzyme (ACE) inhibitors or calcium antagonists may be effective.

Hypertension, when uncomplicated and nol associated with target organ involvement, is usually a silent disease. The medical literature suggests that hypertension is associated with headaches, epistaxis, and tinnitus, but these complaints are nonspecific. Young patients wilh borderline or mild essential hypertension and no target organ involvement may have symptoms of cardiac awareness (rapid heart rate, palpitations, or ectopic beats) associated with physiologic findings that confirm a hyperdynamic circulation. These changes may also occur in older patients and in those with severe hypertension.
Symptoms and signs occur more often in secondary hypertension. Pheochromocytoma may be associated with headache, flushing, blood pressure lability, and hypermetabolism. Occlusive renal arterial disease may produce a sudden onset or worsening of hypertension, headaches, and renal arterial bruits that are systolic and (more significantly) dia stolic in timing. Patients wilh renal parenchymal disease may experience recurrent urinary tract infeclion and urinary frequency, nocturia, impaired ability lo concentrale urine, microscopic or gross hematuria, and (with advanced disease) anemia. In younger patients, the coexistence of hypertension and anemia suggests renal parenchymal disease (if hemoglobinopathy is excluded): in the elderly, it may suggest a neoplasm.
Elderly patients with thyroid disease may not have the characteristic symptoms of hyperthyroidism or hypothyroidism; therefore, a recent onset of hypertension without renal arterial disease or other evident cause indicates the need to rule out thyroid disease (sec Ch. 79). Those wilh primary aldosteronism exhibit muscle weakness, nocturia, isosthenuria, altered carbohydrate metabolism, and hypokalemic alkalosis. Cushing’s disease is suggested by hypokalemic alkalosis and the typical facies, hirsutism, purplish abdominal striae, buffalo hump, and new appearance of acneiform lesions.
In patients with essential hyperlension. the presence of symptoms or signs suggests target organ involvement. Wilh cardiac involvement, the earliest complaints are easy fatigability, palpitations, and atrial or ventricular eclopy. Chest pain in patients without occlusive coronary artery disease reflects increased myocardial oxygen demand wilh persistently elevated arterial pressures and cardiomegaly (left ventricular hypertrophy). More advanced slagcs of cardiac involvement are marked by symptoms and signs of heart failure: exertional dyspnea, orthopnea, peripheral edema, and increased ventricular irritability. Edema without heart failure suggests secondary hypertension. A third heart sound (ventricular gallop rhythm) may develop, usually in association wilh a fourth heart sound (atrial gallop), which reflects the reduced distensi-bilily and compliance of the hyperIrophic left ventricle. A sudden onset of back pain and hypertension suggests aorlic dissection.
The earliest symplom of renal involvement is nocturia; later symptoms and signs result from functional renal impairment: frequency, proteinuria, anemia, and edema. Sensory or motor deficits signal brain involvement; subtle symptoms of transient ischemic attacks include transient speech impediments, numbness of fingers and extremities, and unusual weakness. Sudden onset of a severe vertical headache and hypertension suggests a subarachnoid hemorrhage.
All palients should be examined for hypcrlensive retinopathy. In elderly palients, this should not be confused with the sclerotic changes of increased arteriolar light slriping, arteriovenous nicking, and tortuosity. Arteriolar (and venul;ir)conslriclion and I he appearance of hemorrhages, exudates, and papilledema suggest advancing and more severe degrees of hypertensive vascular disease.
The physician should listen for renal, carolid, aorlic. brachial, and femoral arterial bruils. A carotid bruit wilh symptoms of a transient ischemic allack suggests embolic phenomena from thai vessel. Occlusive disease is tnore likely when a renal arterial bruit has a diastolic component limn when it has only a systolic component Laboratory Data
Laboratory studies in patients wilh hypertension should include a blood count (with hemoglobin, hematocrit, and while blood cell count): an ECG (to identify early evidence of left ventricular hypertrophy, left atrial abnormality, and arrhythmias); selected blood chemistries such as fasting blood glucose and serum levels of creatinine, uric acid, potassium, and lipids including high-density and low-density eholeslcrol fractions; and a urinalysis. A slightly elevated hemoglobin or hematocrit suggests hypertension-induced hemoeoncenlration, which may be confirmed by a proportionately higher plasma protein concentration. Hyperuricemia may indicate that the patient is taking a diuretic or is predisposed to gout; in an untreated hypertensive patient, hyperuricemia may indicate reduced renal blood flow.
The chest x-ray is less sensitive than the ECG for detecting cardiac enlargement. Electrocardiographic evidence of left atrial enlargement provides an early clue to left venlricular hypertrophy before it can be detected by the usual criteria of increased voltage, delayed inlrinsicoid deflection of the ORS complex, or left ventricular hypertrophy and strain pattern. The enlarged left atrium does not indicate atrial disease per sc. Rather, it indicates reduced left ventricular distensibility associated with the development of left venlricular hypertrophy.
Even more sensitive than the ECG, the echocardiogram clearly demonstrates venlricular hypertrophy in a patienl whose ECG shows only a left atrial abnormality. Moreover, before systolic functional changes are apparent, diastolic functional changes are revealed by echocardio-graphic or radionuclide studies showing a reduced left atrial filling rate. Echocardiography evidence o\’ left ventricular hypertrophy usually precedes early evidence of renal functional impairment, which includes renal blood flow slightly reduced in proportion to the height o\’ serum urit acid concentration. Later evidence of renal impairment includes rising serum creatinine orBUN concentrations, as well as reduced creatinine clearance (glomerular filtration rate) and ability to concentrate urine.
Hypercalcemia is frequently associated with hypertension. When hypercalcemia occurs in younger patients, the clinician should first rule out hyperparathyroidism; in older patients, the clinician should first rule out metastatic bone disease. Because hypercalcemia is frequently associated with diuretic therapy, Ihis possibility should be explored when taking the patient’s history.
Proteinuria occurs infrequently in patients with uncomplicated essential hypertension. When daily urinary protein excretion exceeds 400 mg, nephrosclerosis (associated with essential hypertension or aging) is not likely to be the cause; the entire differential diagnosis of renal parenchymal disease should be considered. A fresh urine sample wiih an alkaline pH suggests hypokalemia or primary aldosteronism.
Diagnosis
The diagnosis of hypertension depends on finding elevated arterial pressure as defined in TABLE 35-1. The elevated pressure should be documented on at least three separate occasions with at least two separate blood pressure measurements on each occasion.
Proper measurement technique is especially important in the elderly patient. Blood pressure should be measured in both arms during the initial examination and periodically thereafter. Frequently, occlusive atherosclerotic disease of the subclavian or brachial artery reduces systolic pressure in one arm, producing an abrupt, unexplained decline. Measurements should be obtained while the patient is supine or sitting and immediately after the patient stands because postural (orthostatic) hypotension is common in elderly patients, particularly after meals.
If pressures are persistently and strikingly elevated but chest x-ray and ECG indicate that cardiac size is normal, the physician should suspect pseudohypertension. This finding occurs when the sphygmomanometer cuff cannot compress a sclerotic brachial artery. A direct arterial pressure measurement may be needed to verify this phenomenon. Once true hypertension has been diagnosed, the physician must determine whether it is primary or secondary.
Treatment
Nonpharmacologic measures include maintaining an ideal body weight, moderating alcohol intake i≤ I oz of cthanol equivalent per day), controlling dietary sodium i≤ 100 mEq/day). exercising regularly, and avoiding smoking. (Smokers who take certain antihypertensive drugs such as propranolol have more hypertensive complications, eg, stroke, and myocardial infarction, than smokers who take other drugs such as thiazide diuretics.) These measures may not control arterial pressure completely, but they may control it adequately in some patients and reduce the number and doses of antihypertensive drugs needed in others.

The hemodynamic characteristics of elderly hypertensive patients are similar to those of younger hypertensive patients. However, in the elderly, calculated total peripheral resistance may be higher and compliance of the large arteries may be lower. Arterial pressure is the product of two hemodynamic variables: cardiac output and vascular resistance to blood flow through systemic circulation (total peripheral resistance). Cardiac output, in turn, is the product of two variables: heart rate and stroke volume. Enhanced myocardial contractility or venous return may increase stroke volume. Vascular resistance may be increased^ by adrenergic stimulation, increased renopressor activity, and many circulating hormonal or humoral substances. The many factors that can increase arteriolar smooth muscle tone and total peripheral resistance are presented in TABLE 35-3. All these factors act inter-dependently in normal and hypertensive persons.
Recent studies strongly indicate a local renin-angiotensin system within the vascular myocyte and suggest that this system may also contribute to the tone of vascular smooth muscle. This may explain the effectiveness of the angiotensin converting enzyme (ACE) inhibitors in patients with low plasma renin activity, including the elderly.
Atherosclerotic disease, so common in the elderly, reduces large artery distensibility, resulting in elevaled systolic pressure as the left ventricle ejects its stroke volume into a more rigid and less compliant aorta. This reduced distensibility of the aorta and other large arteries is a major factor in the pathophysiology of isolated systolic hypertension and augments left ventricular impedance. Other pathologic conditions that can contribute to systolic hypertension in the elderly are hyperthyroidism, aortic insufficiency, malnutrition (with clinical or subclinical beriberi), diseases with arteriovenous fistulas, and fever.
As vascular resistance increases, so do systolic and diastolic pressures. The heart adapts to this progressively increasing afterload by a process of concentric hypertrophy (see TABLE 35-4). Because of the frequent coexistence of myocardial ischemia, blood supply to the myocardium may be insufficient—even if arterial pressure is not dramatically elevated. These changes are compounded by cardiac enlargement; reduced β-adrenergic responsiveness; and possible deposition of collagen, amyloid, and other substances in the aging myocardium, even if hypertension is nol present.
Racli of the above factors may cause reduced myocardial contractility oi the left ventricle that may eventually predispose it to heart failure. This process may be aggravated further by exogenous obesity. Obesity is associated with expanded intravascular volume, increased venous return to the heart, and elevated cardiac output. This volume overload provides an eccentric component to the left ventricular hypertrophy and may explain the facilitated heart failure observed in obesity-associated hypertension.
In contrast to the plasma volume expansion that occurs with obesity. intravascular volume contracts as arterial pressure and total peripheral resistance rise in most patients with essential hypertension. Because renopressor system activity seems to be reduced and less sensitive in elderly patients with primary hypertension, an attenuated relationship
between intravascular volume and the renopressor system results. This may explain the enhanced responsiveness to diuretics and calcium antagonists in some elderly hypertensive patients (particularly those with isolated systolic hypertension). The superiority of calcium antagonists over other agents, however, has not yet been proved.
Laplace’s law is another important hemodynamic consideration in elderly hypertensive patients. Myocardial oxygen demand is directly related to left ventricular wall tension, which in turn is directly related to the product of the left ventricular diameter and the systolic pressure generated within this chamber during contraction.
In hypertensive patients (and even in elderly normolensive people), left ventricular and systolic vascular pressures are increased. Both of these tension-dependent factors further increase left ventricular demand for oxygen, which explains the development of coronary artery insufficiency and angina pectoris and provides a rationale for reducing arterial pressure in patients who have only mild diastolic hypertension or isolated systolic hypertension.
Hypertension may also impair brain and kidney function. Transient ischemic attacks and strokes may impair brain funclion, which results in reduced sensory, motor, and intellectual function. Hypertension diminishes renal parenchymal function in a manner similar to the aging process. Histologic evidence of nephrosclerosis in hypertensive and aging patients demonstrates the altered structure associaleil with impaired parenchymal function. Thus, renal blood flow decreases in proportion to cardiac output reduction. Consequently, intrarenal vascular resistance increases, and the glomerular filtration rate and the ability to concentrate urine decrease. Hypertension and aging syneryistically exacerbate these changes. In patients wilh untreated essential hypertension, the lower the renal blood flow, the higher the serum uric acid concentration, explaining the high incidence of hyperuricemia in these patients.

A persistent elevation of systolic and/or diastolic arterial pressure of primary or secondary origin that may impair heart, brain, or kidney function.
In industrialized societies, both systolic and diastolic blood pressure tend to rise until about age 60. After that, systolic pressure may continue to rise, but diastolic pressure tends !o stabilize or decline. More than 50% of Americans s 65 yr have abnormally elevated systolic or diastolic pressures. In some primitive societies, however, neilher systolic nor diastolic pressure increases with aye, and hypertension is practically nonexistent. This difference is attributed (o less dietary sodium (< 60 mEq/day) in these populations.
According to the Fifth Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, systolic pressure elevation is defined as ^ 140 mm Hg and diastolic pressure elevation as £ 90 mm Hg (see TABLE 35-1). Isolated systolic hypertension is defined as a systolic pressure of £ 140 mm Hg and a diastolic pressure of < 90 mm Hg. Formerly, it was defined as a systolic pressure of s 160 mm Hg; this revision reflects the importance of systolic pressure as a risk factor for cardiovascular disease.
The prevalence of elevated arterial pressure in the USA has led many to believe that a rising arterial pressure associated with aging is normal and innocuous. To the contrary, several multicenler prospective studies have shown that the higher the systolic or diastolic pressure, the greater the cardiovascular and tolal morbidity and mortality rates. Moreover, Ihese studies have shown that an elevated systolic pressure is a better predictor of cardiovascular complications than an elevated diastolic pressure. In fact, isolated systolic hypertension increases the risk of cardiovascular death by 2 to 5 limes and the risk of stroke by 2.5 times; it also increases overall mortality by 51% compared with age-, race-, and sex-matched normotensive people.
In general, hypertension predisposes a person to heart failure, stroke, renal failure, coronary heart disease, and peripheral vascular disease. Anlihypertensive therapy reduces the risk of developing many of these catastrophic complications. For example, treating hypertension has helped reduce the incidence of fatal stroke in the USA by almost 60% and fatal myocardial infarction by almost 50%. Similar treatment benefits have been reported by researchers in Europe; for instance, the European Working Party on Hypertension in the Elderly demonstrated a 60% reduction in fatal myocardial infarction. The Sys tolie Hypertension in the KIderly Program (SHEP) in the USA also demonstrated a reduction in fatal and nonfatal stroke and nonfatal myocardial infarction.
Etiology
The causes of arterial hypertension are no different in elderly p;t-licnls than in younger patients (see TABLE 35-2). Primary (essential) hypertension, afflicting at least 9(1% of Ihe 50 million hypertensive Americans, may develop from changes in any or all of the pressor and depressor mechanisms responsible for maintaining normal arterial pressure levels.
Many different mechanisms may underlie hypertension. Among the more important pressor mechanisms are increased participation of (he adrenergic nervous system and/or catecholamines: increased activity of the renopressor (renin-angiotensin) system (systemically or in autocrine systems of arteries, heart, brain, or other organs): reduced distensibilily of the great vessels (eg, from atherosclerosis) with augmented left ventricular impedance: excessive production of pressor hormones; occlusive diseases of the renal arteries or aortic coarctation: and altered regulation of fluid and electrolyte balance. The last mechanism may be associated with either subclinical renal parenchymal disease or Ihc hormonal and humoral factors that directly affect fluid and electrolyte balance. Underactivity of various depressor systems including the kallikrein-kinin system, the prostaglandins, atrial natriuretic peptide, and others may also play a role.
Bach of these pressor and depressor mechanisms helps control arterial pressure in normotensive and hypertensive people of all ages. Catecholamine (particularly norepinephrine) levels increase with age, which suggests reduced β-adienergic receptor responsiveness (down regulation). However, α-adrenergic receptor responsiveness seems to be unchanged. Plasma renin activity and angiotensin II levels are suppressed in elderly people with hypertension, but this has not been associated with intravascular volume expansion. Thus, participation of the pressor and depressor mechanisms seems to be as variable and unresolved in elderly hypertensive patients as it is in younger patients.
because atherosclerosis is common in the elderly, the presence of an atherosclerotic renal arterial lesion is a major secondary eliologic consideration. Such a lesion may elevate arterial pressure tie novo or aggravate essential hypertension. Underlying endocrine disorders (eg. thyroid diseases, hypercalcemic diseases, release of humoral agents from malignant tumors, primary aldosteronism, and pheochromo-cytoina) also may account for a recent onset of hypertension in the elderly.
Because elderly patients frequently have many diseases, medications (including over-the-counter drugs) should be considered when identifying the cause of recent onset, aggravation, or complication of hypertension. Some medications and diseases may predispose hypertensive patients to complications. For example, use of digitalis and a diuretic may cause hypokalemia-relaled cardiac arrhythmias: chronic diarrhea and laxative abuse may also predispose a patienl to hypokalemia; corticosteroids may produce a hypokalemic form of hypertension; cyelospor-ine. tricyclic antidepressants, monoamine oxidase (MAO) inhibitors, and phenylpropanolamine and other vasoconstrictors in over-the-counter cold preparations may also elevate arterial pressure.