What is the proper workup of a patient with hypertension?
ABSTRACTBecause hypertension is common and many tests are available, an uncritical approach to laboratory and radiologic evaluation leads to unnecessary expenses. However, in most patients, accurate blood pressure measurement, a focused history and physical examination, and a handful of basic tests are enough. In this review we address the key questions in the evaluation of the patient with an elevated pressure reading, ie, does the patient have sustained high blood pressure? And if so, is the hypertension primary or secondary, are other cardiovascular risk factors present, and is there evidence of target organ damage?
KEY POINTS
- To confirm the diagnosis of hypertension, multiple readings should be taken at various times.
- Proper technique is important in measuring blood pressure, including using the correct cuff size, having the patient sit quietly for 5 minutes before taking the pressure, and supporting the arm at the level of the heart.
- If white-coat hypertension is suspected, one can consider ambulatory or home blood pressure measurements to confirm that the hypertension is sustained.
PHYSICAL EXAMINATION
The physical examination starts with measurement of height, weight, waist circumference, and blood pressure—in both arms and the leg if coarctation of the aorta is suspected. Measurements with the patient supine, sitting, and standing are usually taken at the first visit, though such an approach is more suited to a hypertension specialty clinic than a primary care setting, in which time constraints usually limit the blood pressure readings to two or three seated values. Most prospective data on the benefits of hypertension treatment are based on a seated blood pressure, so we favor that measurement for follow-up.
Special attention in the physical examination is directed to:
The retina (to assess the vascular impact of the high blood pressure). Look for arteriolar narrowing (grade 1), arteriovenous compression (grade 2), hemorrhages or exudates (grade 3), and papilledema.2 Such findings not only relate to severity (higher grade = more severe blood pressure) but also predict future cardiovascular disease.14
The blood vessels. Bruits in the neck may indicate carotid stenosis, bruits in the abdomen may indicate renovascular disease, and femoral bruits are a sign of general atherosclerosis. Bruits also signal vascular stenosis and irregularity and may be a clue to vascular damage or future loss of target organ function. However, bruits may simply result from vascular tortuosity, particularly with significant flow in the vessel.
Also check the femoral pulses: poor or delayed femoral pulses are a sign of aortic coarctation. The radial artery is about as far away from the heart as the femoral artery; consequently, when palpating both sites simultaneously the pulse should arrive at about the same moment. In aortic coarctation, a palpable delay in the arrival of the femoral pulse may occur, and an interscapular murmur may be heard during auscultation of the back. In these instances, a low leg blood pressure (usually measured by placing a thigh-sized adult cuff on the patient’s thigh and listening over the popliteal area with the patient prone) may confirm the presence of aortic obstruction. When taking a leg blood pressure, the large cuff and the amount of pressure necessary to occlude the artery may be uncomfortable, and one should warn the patient about the discomfort before taking the measurement.
Poor or absent pedal pulses are a sign of peripheral arterial disease.
The heart (to detect gallops, enlargement, or both). Palpation may reveal a displaced apical impulse, which can indicate left ventricular enlargement. A sustained apical impulse may indicate left ventricular hypertrophy. Listen for a fourth heart sound (S4), one of the earliest physical findings of hypertension when physical findings are present. An S4 indicates that the left atrium is working hard to overcome the stiffness of the left ventricle. An S3 indicates an impairment in left ventricular function and is usually a harbinger of underlying heart disease. In some cases, lung rales can also be heard, though the combination of an S3 gallop and rales is an unusual office presentation in the early management of the hypertensive patient.
The lungs. Listen for rales (see above).
The lower extremities should be examined for peripheral arterial pulsations and edema. The loss of pedal pulses is a common finding, particularly in smokers, and is a clue to increased cardiovascular risk.
Strength, gait, and cognition. Perform a brief neurologic examination for evidence of remote stroke. We usually observe our patients’ gait as they enter or leave the examination room, test their bilateral grip strength, and assess their judgment, speech, and memory during the history and physical examination.
A great deal of research has linked high blood pressure to future loss of cognitive function,15 and it is useful to know that impairment is present before beginning treatment, since some patients will complain of memory loss after starting antihypertensive drug treatment.
LABORATORY EVALUATION
Routine tests
The routine evaluation of hypertensive patients should include, at a minimum:
- A hemoglobin or hematocrit measurement
- Urinalysis with microscopic examination
- Serum electrolyte concentrations
Serum creatinine concentrations- Serum glucose concentration
- A fasting lipid profile
- A 12-lead electrocardiogram (Table 5).
Nonroutine tests
In some cases, other studies may be appropriate, depending on the clinical situation, eg:
- Serum uric acid in those with a history of gout, since some antihypertensive drugs (eg, diuretics) may increase serum uric acid and predispose to further episodes of gout
- Serum calcium in those with a personal or family history of kidney stones, to detect subtle parathyroid excess
- Thyroid-stimulating hormone or other thyroid studies if the history suggests thyroid excess, or if a thyroid nodule is discovered
- Limited echocardiography, which is more sensitive than electrocardiography for detecting left ventricular hypertrophy.
We sometimes use echocardiography if the patient is overweight but seems motivated to lose weight. In these cases we might not start drug therapy right away, choosing rather to wait and see if the patient can lose some weight (which might lower the blood pressure and make drug therapy unnecessary)—but only if the echocardiogram shows that he or she does not have left ventricular hypertrophy.
We also use echocardiography in patients with white-coat hypertension (see below), in whom office pressures are consistently high but whom we have elected to either not treat or not alter treatment. In these cases the echocardiogram serves as a “second opinion” about the merits of not altering therapy and supports this decision when the left ventricular wall thicknesses are normal (and remain so during long-term follow-up). In cases of suspected white-coat hypertension, home or ambulatory blood pressure monitoring is valuable to establish or exclude this diagnosis.1
Urinary albumin excretion. Microalbuminuria is an early manifestation of diabetic nephropathy and hypertension. Although routine urine screening for microalbuminuria is typically done in the management of diabetes, it is still not considered a standard of care, though the growing literature on its role as a cardiovascular risk predictor16–18 and its value as a therapeutic target in diabetes19,20 make it an attractive aid in the overall assessment of patients with hypertension.
Plasma renin activity and serum aldosterone concentrations are useful in screening for aldosterone excess, but are usually reserved as follow-up tests in patients with either hypokalemia or failure to achieve blood pressure control on a three-drug regimen in which at least one drug is a diuretic.1,21
Of note, primary aldosteronism is not as rare as previously thought. In a study of patients referred to hypertension centers, 11% had primary aldosteronism according to prospective diagnostic criteria, almost 5% had curable aldosterone-producing adenomas, and 6% had idiopathic hyperaldosteronism.22