Chapter 9 / Clinical Evaluation 135 9 Clinical Evaluation of the Elderly Hypertensive

L. Michael Prisant, MD, FACC, FACP and Thomas W. Jackson, MD

CONTENTS MEASUREMENT OF AND CONFIRMATION EVALUATION CONSIDERATIONS HISTORY PHYSICAL EXAMINATION INTEGRATION OF INFORMATION REFERENCES

MEASUREMENT OF BLOOD PRESSURE AND CONFIRMATION When confronted with an elevation in blood pressure (BP) in an eld- erly patient, additional measurements are necessary because of increased variability in older persons possibly caused by impaired baroreceptor sensitivity (Fig. 1) (1). In addition to lability of BP, there should be consideration given to the presence of an auscultatory gap (2), orthos- tatic hypotension (3), and pseudohypertension (4). Orthostatic increases with aging and hypertension and is associated with impairment of baroceptor sensitivity (5). Among eld- erly persons with isolated systolic hypertension, a systolic decline of 20 mmHg or greater was observed in 17.3% of subjects at 1 or 3 minutes after standing (Fig. 2) (3). After a high-carbohydrate meal, supine BP

From: Clinical Hypertension and Vascular Diseases: Hypertension in the Elderly Edited by: L. M. Prisant © Humana Press Inc., Totowa, NJ 135 136 Hypertension in the Elderly

Fig. 1. Variability of blood pressure. Both the upper panel (women) and lower panel (men) show the increasing blood pressure with increasing standard devia- tion with aging. (Data from ref. 1.) declines, and heart rate increases without an increase in plasma nore- pinephrine levels (6). Standing postmeal ingestion magnifies the BP decline (7). In addition to the risk of falls and fractures, the risk of vascular death is increased (8). The quality of BP measurement is of prime importance for the initial diagnosis and the adjustment of medication (9). For the diagnosis of systemic hypertension, the initial set of sitting BP measurements should occur after 5 minutes of rest and the abstinence of both caffeine and tobacco for 30 minutes. BP should be measured in nontalking patients seated with their back supported and their legs uncrossed. Also, the arm should be bared and supported at heart level. The use of a mercury remains the gold standard for routine determina- tion of BP (10). Chapter 9 / Clinical Evaluation 137

Fig. 2. Prevalence of standing systolic blood pressure decline of 20 mmHg or greater. The prevalence of a decline in systolic blood pressure at 1 and 3 minutes increase with higher levels of systolic blood pressure. (Data from ref. 3.)

Palpation of the radial for the initial cuff inflation will help determine the level of systolic BP. This will avoid unnecessary cuff pressure that might cause pain and the potential underestimation of sys- tolic blood pressure (SBP) that could occur in the presence of an auscul- tatory gap. Not recognizing an auscultatory gap can result in an underestimation of SBP or an overestimation of diastolic blood pressure (DBP). An auscultatory gap is associated with older age, female gender, increased , and carotid atherosclerotic plaque (11). If the pulseless radial or brachial artery is palpable after ipsilateral occlusion by the cuff, then the patient is described as “Osler positive,” which was a sign of pseudohypertension caused by (12,13). Pseudohypertension is an elevation in cuff measurement with a normal intra-arterial measurement; thus, the implication of an Osler- positive patient is that the patient is receiving inappropriate treatment (13). However, despite a higher cuff pressure of +15.8/+16.4 mmHg in Osler-positive vs –3.0/+5.3 mmHg in Osler-negative patients, most subjects in this study had SBP measurements greater than 140 mmHg. Another study of geriatric patients identified a prevalence of 11% of Osler-positive patients of 205 screened (14). When Osler-positive and - negative patients were compared with intra-arterial measurements, there was no significant difference in BP. Furthermore, Osler’s maneuver did not predict the presence or absence of pseudohypertension (14). The failure to use a large cuff in an obese patient is another cause of pseudohypertension. should be performed with the bell of the stethoscope lightly applied over the brachial artery because are 138 Hypertension in the Elderly low pitched (9). BP measurements are recorded to the nearest 2 mmHg. A good procedure is to perform three measurements and take the average of the last two measurements as the value for that visit. Three visits with a total of six measurements are required to diagnose systemic hyperten- sion (15). Before the initiation of drug therapy, there should be a determination whether postural changes are present. Patients with symptoms of lightheadedness or dizziness; patients taking certain medications, includ- ing antipsychotic medications, antiparkinsonian drugs, α1-blockers, diuretics, and nitrates; and patients with Parkinson’s disease and dia- betes mellitus with autonomic insufficiency need their BP and heart rate measured in the supine position and standing after 1 and 3 minutes. Measurement of BP in the contralateral arm, which is lower, suggests subclavian stenosis.

EVALUATION CONSIDERATIONS The assessment of older patients is more complex than for younger patients. A lifetime history is likely to require more time. The reported details may not be as accurate, even if dementia is not present. In addi- tion, altered vision and hearing can present difficulties for the examiner. Believing a symptom is caused by aging, the patient if asked directly may not acknowledge the symptom. Also, the manifestations of a dis- ease may differ in older patients. An assessment of mental status to screen for dementia on initial examination can provide a baseline and provide important information regarding the ability of a patient to follow a medical regimen. The history of older patients should be verified with a family member. Discrepancies in the history often point to dementia. Failure to verify the history can impede the accuracy of diagnosis.

HISTORY The purpose of the history is to determine potential symptoms asso- ciated with or suggesting causes of hypertension, evaluate the presence of target organ damage, determine other cardiovascular risk factors, assess concomitant diseases that might interfere with the treatment of hypertension, seek clues suggestive of secondary hypertension, cata- logue all medications used (including over-the-counter medications and herbal remedies), assess resources, assess mental status, and determine general ability to implement the activities of daily living (4,15–17). Specific questions may provide important diagnostic clues (16). The duration and ease of hypertension control are important. For instance, a long history of hypertension that has been well controlled and is now Chapter 9 / Clinical Evaluation 139

Fig. 3. Prevalence of different secondary causes of hypertension in patients 18 years or older. There was an increased prevalence of renovascular hypertension, renal insufficiency, and hypothyroidism with increasing age. (Data from ref. 18.) uncontrolled suggests superimposed secondary hypertension, an inter- fering substance (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs], ethanol), or noncompliance (possibly because of finances or dementia). Essential hypertension accounts for most cases of hypertension in the elderly (18). The three most common secondary causes of hypertension are chronic renal insufficiency, hypothyroidism, and renovascular hyper- tension (Fig. 3). The abrupt onset of severe hypertension associated with declining renal function and recurrent pulmonary edema suggests reno- vascular hypertension (19–21). Generally, hypertension is asymptomatic. Symptoms caused by sec- ondary hypertension include (a) headaches, pallor, and diaphoresis (pheochromocytoma); (b) weight loss, tremor, anxiety, , fatigue, weakness (hyperthyroidism); (c) confusion, anorexia, weak- ness, myalgias, constipation, depression (hypothyroidism); (d) urinary frequency, nocturia, hematuria, fatigue (renal parenchymal disease); and (e) muscle cramps, muscle weakness, nocturia, hypokalemia (pri- mary aldosteronism). Symptoms secondary to diabetes and hypertensive target organ dam- age, ischemic heart disease, heart failure, cerebrovascular disease, aortic and peripheral , renal failure, and retinal disease must be determined to choose the most appropriate initial antihypertensive drug. 140 Hypertension in the Elderly

Vascular symptoms of exertional fatigue, dyspnea, orthopnea, edema, , , claudication, transient ischemic attacks, and syn- cope need to be evaluated in terms of daily activities. Heart failure, either systolic or diastolic, and atrial fibrillation are common in the elderly (see Chapter 12). Some patients experience postprandial hypotension asso- ciated with either dizziness or fatigue. Patients should be asked about side effects of medications previously taken as well as allergies. It is wise to have the patient bring all medica- tions to the clinic, including over-the-counter medications and herbal remedies. NSAIDs precipitate heart failure and interfere with the treat- ment of hypertension. Venlafaxine raises BP also. Quantitation of alco- hol ingestion is important because excessive consumption increases BP. Long-standing tobacco use, vascular events (including myocardial inf- arction, strokes, and claudication), and renal insufficiency increase the likelihood of renovascular hypertension.

PHYSICAL EXAMINATION The physical examination is conducted in a methodical fashion (16). Routine vital signs of BP, heart rate, and weight are recorded at each visit. A funduscopic examination is performed as a part of the initial examination or at visits associated with very high BP measurements. The presence of retinal flame-shaped hemorrhages, retinal infarcts (“cot- ton wool” spots), and papilledema provides important information regard- ing the urgency of therapy and a clue to secondary hypertension. The neck is examined for jugular venous distention, the rate of rise of the carotid upstroke, the presence of carotid , and thyromegaly. Auscultation of the lungs is targeted for the presence of wheezes and rales. Inspection of the chest may localize the point of maximum impulse of the heart. Cardiac enlargement is suggested by its displacement past the midclavicular line. An enlarged and sustained apical impulse suggests left ventricular hypertrophy (LVH). A palpable S4 is occasionally present. An irregularly irregular rhythm suggests atrial fibrillation or frequent atrial or ventricular ectopy. A tambour S2 suggests aortic root dilatation. Systolic ejection murmurs are not uncommon with hyperten- sion; however, an increased SBP, a wide pressure, and a diastolic decrescendo murmur over the aortic area in the seated position support the diagnosis of . An S3 gallop associated with dys- pnea, rales, and tachycardia supports the diagnosis of heart failure. The abdominal examination should include liver size, assessment for enlarged kidneys (polycystic kidney disease), enlarged aorta, ascites, and the presence of bruits to suggest the presence of atherosclerosis. In Chapter 9 / Clinical Evaluation 141 asymptomatic patients, the sensitivity of physical examination as assessed by ultrasonography is a function of the diameter of the aneurysm: 29% for 3.0–3.9 cm, 50% for 4.0–4.9 cm, and 76% for 5 cm or greater (22). The positive predictive value is only 43%. However, if the waist circumfer- ence exceeds 40 inches, then the sensitivity is significantly reduced. Interobserver agreement between two examinations is 77% (23). A high pitch epigastric systolic–diastolic of long duration that lateralizes suggest renal artery stenosis (24). However, 4.9% of normal individuals above age 55 years will have a bruit. The absence of a bruit does not exclude a diagnosis of renovascular hypertension. Periumbilical bruits are frequently associated with abdominal aortic aneurysms (24). Femoral pulsations and bruits and pedal should be determined. The presence of peripheral edema may be caused by medications (NSAIDs, dihydropyridine calcium antagonist, or minoxidil), heart fail- ure, decreased albumin, chronic renal insufficiency, or venous insuffi- ciency. A careful neurological examination should define preexistent neurological deficits, including previous strokes, Parkinson’s disease, and dementia.

LABORATORY ASSESSMENT A fasting complex metabolic profile, lipid profile, complete blood count, urinalysis with microscopic examination, and electrocardiogram are reasonable for an initial evaluation. Unprovoked hypokalemia sug- gests primary aldosteronism, but hypokalemia is also observed with Cushing’s syndrome and diuretic use. Hyperkalemia is associated with renal failure, potassium-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), type IV renal tubular acidosis, salt substitutes, and oral potassium supplements. A confirmed fasting glucose greater than 125 mg/dL is consistent with diabetes mellitus (25), but hyperglycemia is also seen with Cushing’s syndrome, acromegaly, and pheochromocytoma. Hypercalcemia may be caused by thiazide diuretics or hyperparathyroidism. Hyperuricemia is an early sign of renal disease, but is also associated with gout, diuretic use, chronic renal failure, polycythemia, hyperparathyroidism, hypothy- roidism, and polycystic kidney disease. Elevated cholesterol may be caused by a secondary lipid disorder, such as hypothyroidism, nephrotic syndrome, or hypercortisolism. A creatinine greater than 1.3 mg/dL should be viewed as abnormal because older patients have less muscle mass. In addition to primary renal disease, renovascular disease, ac- romegaly, ACE inhibitors, ARBs, NSAIDs, and over-diuresis may also elevate the serum creatinine. 142 Hypertension in the Elderly

The electrocardiogram is an economical adjunct to assess target organ damage in hypertensive patients (26,27). The rate, rhythm, PR and QT intervals, diagnostic Q waves, and voltage criteria of LVH provide information that can influence treatment. Although sick sinus syn- drome may be present, sinus should also suggest hypothy- roidism and would preclude the use of α2-stimulants, β-blockers, and nondihydropyridine calcium channel blockers. Alternatively, sinus tachy- cardia could be caused by heart failure, hyperthyroidism, pheochromocy- toma, or overdiuresis. Atrial fibrillation may be caused by underlying ischemic heart disease, hypertension, or thyroid disease. A prolonged PR interval raises concern about prescribing either verapamil or diltiazem. A short QT interval may be caused by the hypercalcemia associated with hyperparathyroidism. The gender-specific Cornell voltage criteria (for men, RaVL + SV3 > 35 mm; for women, RaVL + SV3 > 25 mm) have the best overall accuracy (28). One of the earliest electrocardiographic findings of hypertensive heart disease is the duration of the negative phase of the P wave in chest lead V1 > 0.04 seconds, a manifestation of left atrial enlargement or abnormality. There is no other classic cardiovascular risk factor more potent and dismal than LVH with “strain pattern” (29). The strain pattern is characterized by ST depression 1 mm in lead I, aVL, and V4–V6. The direction of the T wave is in the opposite direction of the upright QRS complex.

INTEGRATION OF INFORMATION Integrating information from the history, physical examination, and laboratory exam suggests additional evaluations to be performed (15). These include measurement of creatinine clearance, 24-hour urinary protein excretion, plasma renin activity, thyroid-stimulating hormone, glycosylated hemoglobin, and ambulatory BP and an echocardiogram (15). However, these tests do not need to be ordered routinely.

REFERENCES 1. Wiinberg N, Hoegholm A, Christensen HR, et al. Twenty-four-hour ambulatory blood pressure in 352 normal Danish subjects, related to age and gender. Am J Hypertens 1995;8(10 pt 1):978–986. 2. Askey JM. The auscultatory gap in sphygmomanometry. Ann Intern Med 1974;80:94–97. 3. Applegate WB, Davis BR, Black HR, Smith WM, Miller ST, Burlando AJ. Preva- lence of postural hypotension at baseline in the Systolic Hypertension in the Elderly Program (SHEP) cohort. J Am Geriatr Soc 1991;39:1057–1064. 4. Franklin SS. Geriatric hypertension. Med Clin North Am 1983;67:395–417. Chapter 9 / Clinical Evaluation 143

5. Ooi WL, Barrett S, Hossain M, Kelley-Gagnon M, Lipsitz LA. Patterns of orthos- tatic blood pressure change and their clinical correlates in a frail, elderly population. JAMA 1997;277:1299–1304. 6. Haigh RA, Harper GD, Burton R, Macdonald IA, Potter JF. Possible impairment of the sympathetic nervous system response to postprandial hypotension in elderly hypertensive patients. J Hum Hypertens 1991;5:83–99. 7. Maurer MS, Karmally W, Rivadeneira H, Parides MK, Bloomfield DM. Upright posture and postprandial hypotension in elderly persons. Ann Intern Med 2000;133:533–536. 8. Luukinen H, Koski K, Laippala P, Kivela SL. Prognosis of diastolic and systolic orthostatic hypotension in older persons. Arch Intern Med 1999;159:273–280. 9. Perloff D, Grim C, Flack J, et al. Human blood pressure determination by sphygmo- manometry. Circulation 1993;88(5 pt 1):2460–2470. 10. Jones DW, Frohlich ED, Grim CM, Grim CE, Taubert KA. Mercury sphygmoma- nometers should not be abandoned: an advisory statement from the Council for High Blood Pressure Research, American Heart Association. Hypertension 2001;37:185–186. 11. Cavallini MC, Roman MJ, Blank SG, Pini R, Pickering TG, Devereux RB. Asso- ciation of the auscultatory gap with vascular disease in hypertensive patients. Ann Intern Med 1996;124:877–883. 12. Messerli FH, Ventura HO, Amodeo C. Osler’s maneuver and pseudohypertension. N Engl J Med 1985;312:1548–1551. 13. Messerli FH. Osler’s maneuver, pseudohypertension, and true hypertension in the elderly. Am J Med 1986;80:906–910. 14. Belmin J, Visintin JM, Salvatore R, Sebban C, Moulias R. Osler’s maneuver: absence of usefulness for the detection of pseudohypertension in an elderly population. Am J Med 1995;98:42–49. 15. Chobanian AV, Bakris GL, Black HR, et al. The Seventh Report of the Joint Na- tional Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560–2572. 16. Prisant LM, Carr AA. Initial evaluation of the hypertensive patient. Postgrad Med 1988;84:197–202, 215–217. 17. Prisant LM, Carr AA. Over-the-counter drugs that may increase blood pressure. Postgrad Med 1989;86:205–208. 18. Anderson GH Jr, Blakeman N, Streeten DH. The effect of age on prevalence of secondary forms of hypertension in 4429 consecutively referred patients. J Hypertens 1994;12:609–615. 19. Pickering TG, Herman L, Devereux RB, et al. Recurrent pulmonary oedema in hypertension due to bilateral renal artery stenosis: treatment by angioplasty or sur- gical revascularisation. Lancet 1988;2:551–552. 20. Olin JW, Vidt DG, Gifford RW Jr, Novick AC. Renovascular disease in the elderly: an analysis of 50 patients. J Am Coll Cardiol 1985;5:1232–1238. 21. Novick AC, Ziegelbaum M, Vidt DG, Gifford RW Jr, Pohl MA, Goormastic M. Trends in surgical revascularization for renal artery disease. Ten years’ experience. JAMA 1987;257:498–501. 22. Lederle FA, Simel DL. The rational clinical examination. Does this patient have abdominal ? JAMA 1999;281:77–82. 23. Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas MA. The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med 2000;160:833–836. 144 Hypertension in the Elderly

24. Turnbull JM. Is listening for abdominal bruits useful in the evaluation of hyperten- sion? JAMA 1995;274:1299–1301. 25. Diagnosis and classification of diabetes mellitus. Diabetes Care 2004;27(suppl 1):S5–S10. 26. Prisant LM, Carr AA. Beyond diagnosis of left ventricular hypertrophy in patients with essential hypertension. Am J Hypertens 1992;5(12 pt 1):927–929. 27. Prisant LM. Hypertension images: electrocardiographic left ventricular hypertro- phy. J Clin Hypertens (Greenwich) 2001;3:389–391, 398. 28. Casale PN, Devereux RB, Alonso DR, Campo E, Kligfield P. Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings. Circulation 1987;75:565–572. 29. Kannel WB. Left ventricular hypertrophy as a risk factor: the Framingham experi- ence. J Hypertens Suppl 1991;9:S3–S8; discussion S8–S9.