approach to the patient with hypertension

7/31/2019 Approach to the Patient With Hypertension

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APPROACH TO THE PATIENT WITH HYPERTENSION - Gordon H.

Williams

DEFINITION

Since there is no dividing line between normal and high blood pressure,

arbitrary levels have been established to define persons who have an increased

risk of developing a morbid cardiovascular event and/or will clearly benefit

from medical therapy. These definitions should take into account not only the

level of diastolic pressure but also systolic pressure, age, sex, and race. For

example, patients with a diastolic pressure greater than 90 mmHg have a

significant reduction in morbidity and mortality rate if they receive adequate

therapy. These, then, are patients who have hypertension and who should be

considered for treatment.

The level of systolic pressure is also important in assessing the influence of

arterial pressure on cardiovascular morbidity. Males with normal diastolic

pressures (<82 mmHg) but elevated systolic pressures (>158 mmHg) have a

cardiovascular mortality rate 2.5 times higher than individuals who have similar

diastolic pressures but whose systolic pressures clearly are normal (<130

mmHg). A reduction in mortality and morbidity with treatment, specifically in

the elderly, has been documented in these patients. This beneficial effect

results mainly from a reduction in strokes and occurs in women as well. Other

significant factors that modify the influence of blood pressure on thefrequency of morbid cardiovascular events are age, race, and sex, with young

black males being most adversely affected by hypertension.

When hypertension is suspected, blood pressure should be measured at least

twice during two separate examinations after the initial screening. In adults, a

diastolic pressure below 85 mmHg is considered to be normal; one between 85

and 89 mmHg is high normal; one of 90 to 104 mmHg represents mild

hypertension; one of 105 to 114 mmHg represents moderate hypertension; and

one of 115 mmHg or greater represents severe hypertension. When the

diastolic pressure is below 90 mmHg, a systolic pressure below 140 mmHgindicates normal blood pressure; one between 140 and 159 mmHg indicates

borderline isolated systolic hypertension; and one of 160 mmHg or higher

indicates isolated systolic hypertension. Increasing use of 12- or 24-h blood

pressure monitoring may provide additional useful information in patients who

are difficult to classify. However, normal values for this procedure and its

usefulness in relation to therapeutic outcomes are not currently known. A

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the course of a physical examination. When symptoms do bring the patient to

the physician, they fall into three categories. They are related to (1) the

elevated pressure itself, (2) the hypertensive vascular disease, and (3) the

underlying disease, in the case of secondary hypertension. Though popularly

considered a symptom of elevated arterial pressure, headache is characteristic

only of severe hypertension; most commonly such headaches are localized to the

occipital region and are present when the patient awakens in the morning but

subside spontaneously after several hours. Other complaints that may be

related to elevated blood pressure include dizziness, palpitations, easy

fatigability, and impotence. Complaints referable to vascular disease include

epistaxis, hematuria, blurring of vision owing to retinal changes, episodes of

weakness or dizziness due to transient cerebral ischemia, angina pectoris, and

dyspnea due to cardiac failure. Pain due to dissection of the aorta or to a

leaking aneurysm is an occasional presenting symptom.

Examples of symptoms related to the underlying disease in secondaryhypertension are polyuria, polydipsia, and muscle weakness secondary to

hypokalemia in patients with primary aldosteronism or weight gain, and

emotional lability in patients with Cushing's syndrome. The patient with a

pheochromocytoma may present with episodic headaches, palpitations,

diaphoresis, and postural dizziness.

History A strong family history of hypertension, along with the reported

finding of intermittent pressure elevation in the past, favors the diagnosis of

essential hypertension. Secondary hypertension often develops before the age

of 35 or after 55. A history of use of adrenal steroids or estrogens is of

obvious significance. A history of repeated urinary tract infections suggests

chronic pyelonephritis, although this condition may occur in the absence of

symptoms; nocturia and polydipsia suggest renal or endocrine disease, while

trauma to either flank or an episode of acute flank pain may be a clue to the

presence of renal injury. A history of weight gain is compatible with Cushing's

syndrome, and one of weight loss is compatible with pheochromocytoma. A

number of aspects of the history aid in determining whether vascular disease

has progressed to a dangerous stage. These include angina pectoris andsymptoms of cerebrovascular insufficiency, congestive heart failure, and/or

peripheral vascular insufficiency. Other risk factors that should be asked about

include cigarette smoking, diabetes mellitus, lipid disorders, and a family

history of early deaths due to cardiovascular disease. Finally, aspects of the

patient's lifestyle that could contribute to the hypertension or affect its

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treatment should be assessed, including diet, physical activity, family status,

work, and educational level.

Physical Examination The physical examination starts with the patient's

general appearance. For instance, are the round face and truncal obesity of

Cushing's syndrome present? Is muscular development in the upper extremities

out of proportion to that in the lower extremities, suggesting coarctation of

the aorta? The next step is to compare the blood pressures and pulses in the

two upper extremities and in the supine and standing positions (for at least 2

min). A rise in diastolic pressure when the patient goes from the supine to the

standing position is most compatible with essential hypertension; a fall, in the

absence of antihypertensive medications, suggests secondary forms of

hypertension. The patient's height and weight should be recorded. Detailed

examination of the ocular fundi is mandatory, as funduscopic findings provide

one of the best indications of the duration of hypertension and of prognosis. Auseful guide is the Keith-Wagener-Barker classification of funduscopic changes(Table 35-2); the specific changes in each fundus should be recorded and a

grade assigned. Palpation and auscultation of the carotid arteries for evidence

of stenosis or occlusion are important; narrowing of a carotid artery may be a

manifestation of hypertensive vascular disease, and it also may be a clue to the

presence of a renal arterial lesion, since these two lesions may occur together.

In examination of the heart and lungs, evidence of left ventricular hypertrophy

and cardiac decompensation should be sought. Is there a left ventricular lift?

Are third and fourth heart sounds present? Are there pulmonary rales? A third

heart sound and pulmonary rales are unusual in uncomplicated hypertension.

Their presence suggests ventricular dysfunction. Chest examination also

includes a search for extracardiac murmurs and palpable collateral vessels that

may result from coarctation of the aorta.

The most important part of the abdominal examination is auscultation for bruits

originating in stenotic renal arteries. Bruits due to renal arterial narrowing

nearly always have a diastolic component or may be continuous and are best

heard just to the right or left of the midline above the umbilicus or in the

flanks; they are present in many patients with renal artery stenosis due tofibrous dysplasia and in 40 to 50 percent of those with functionally significant

stenosis due to arteriosclerosis. The abdomen also should be palpated for an

abdominal aneurysm and for the enlarged kidneys of polycystic renal disease.

The femoral pulses must be carefully felt, and, if they are decreased and/or

delayed in comparison with the radial pulse, the blood pressure in the lower

extremities must be measured. Even if the femoral pulse is normal to palpation,

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arterial pressure in the lower extremities should be recorded at least once in

patients in whom hypertension is discovered before the age of 30 years. Finally,

examination of the extremities for edema and a search for evidence of a

previous cerebrovascular accident and/or other intracranial pathology should be

performed.

Laboratory Investigation There is controversy as to what laboratory studies

should be performed in patients presenting with hypertension. In general, the

disagreement centers on how extensively the patient should be evaluated for

secondary forms of hypertension or subsets of essential hypertension. The

basic laboratory studies that should be performed in all patients with sustained

hypertension are described below (Table 35-3). The secondary studies that

should be added if (1) the initial evaluation indicates a form of secondary

hypertension and/or (2) arterial pressure is not controlled after initial therapy

as discussed in Chap. 246.

Renal status is evaluated by assessing the presence of protein, blood, and

glucose in the urine and measuring serum creatinine and/or blood urea nitrogen.

Microscopic examination of the urine is also helpful. The serum potassium level

should be measured both as a screen for mineralocorticoid-induced

hypertension and to provide a baseline before diuretic therapy is begun.

Other blood chemistry measurements also may be useful, particularly as they

often can be ordered as a battery of automated tests at minimal cost to the

patient. For example, a blood glucose determination is helpful both because

diabetes mellitus may be associated with accelerated arteriosclerosis, renal

vascular disease, and diabetic nephropathy in patients with hypertension and

because primary aldosteronism, Cushing's syndrome, and pheochromocytoma all

may be associated with hyperglycemia. Furthermore, since antihypertensive

therapy with diuretics, for example, can raise the blood glucose level, it is

important to establish a baseline. The possibility of hypercalcemia also may be

investigated. Serum uric acid determination is useful because of the increased

incidence of hyperuricemia in patients with renal and essential hypertension and

because, as with blood glucose, the level may be raised subsequently bytreatment with diuretics. Serum cholesterol, high density lipoprotein

cholesterol, and triglycerides may be measured to identify other factors that

predispose to the development of arteriosclerosis.

An electrocardiogram should be obtained in all cases to permit assessment of

cardiac status, particularly if left ventricular hypertrophy is present, and to

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provide a baseline. The echocardiogram is more sensitive than either the

electrocardiogram or physical examination in determining whether cardiac

hypertrophy is present. Thus, in some circumstances, this modality may be a

useful addition to the baseline evaluation of a hypertensive patient, particularly

as left ventricular hypertrophy is an independent cardiovascular risk factor and

its presence suggests the need for vigorous antihypertensive therapy.

Furthermore, while a substantial increase in arterial pressure usually correlates

with the presence of left ventricular hypertrophy, a mild increase may not.

Thus, one cannot use the blood pressure as a surrogate marker for the

presence or absence of left ventricular hypertrophy. On the other hand,

because of the cost of an echocardiogram and the uncertainty as to whether

the resultant information would modify therapy, it is unclear that routine

follow-up echocardiograms during therapy are justified. The chest

roentgenogram also may be helpful by providing the opportunity to identify

aortic dilation or elongation and the rib notching that occurs in coarctation ofthe aorta.

Certain clues from the history, physical examination, and basic laboratory

studies may suggest an unusual cause for the hypertension and dictate the need

for special studies are outlined in Chap 246.

TREATMENT

See Chap. 246.

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approach to the patient with hypertension

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