Overview and Definitions
Hypertension is defined as a systolic blood pressure (SBP) of 140 mm Hg or higher, a diastolic blood pressure (DBP) of 90 mm Hg or higher, or current use of antihypertensive medications. Hypertension persists as a major public health problem that affects 76.4 million U.S. adults—more than one third of the adult population. The aging of the population and, more importantly, an increase in the prevalence of obesity have contributed to the rising prevalence of hypertension, which is higher than the Healthy People 2020 goal of 26.9%. As a result of the age-related rise in blood pressure (BP), hypertension commonly occurs in middle-aged and older adults; adults aged 50 years and older have a lifetime risk for hypertension of 90%.
Hypertension is a major risk factor for coronary heart disease, stroke, renal failure, all-cause mortality, and shortened life expectancy. The positive association between SBP and DBP and cardiovascular outcomes is strong, continuous, graded, and etiologically significant. Hypertension is heterogeneous in its pathophysiology, and its effect on target organs is also a function of associated risk factors that include diabetes mellitus, dyslipidemia, and tobacco abuse. The current classification of BP in the adult population proposed by the Joint National Committee on Prevention, Evaluation, Diagnosis and Treatment of Hypertension (JNC 7) is provided in Table 28-1 . This classification is based on the average of two or more seated BP readings, properly measured with well-maintained equipment, at each of two or more visits to the office or clinic.
|CLASSIFICATION||SBP (MM HG)||DBP (MM HG)|
|Stage 1 hypertension||140-159||or||90-99|
|Stage 2 hypertension||≥160||or||≥100|
Most patients with hypertension can be evaluated and treated in the ambulatory care setting; however, a small minority require urgent or emergency treatment based on the clinical presentation of acute or accelerated hypertension-related target organ damage rather than BP values per se (see Chapter 32 ). Although adult hypertensive emergencies are usually associated with very high BP, often in excess of 220/110 mm Hg, patients with much lower BP also require emergency treatment in the presence of serious complications such as preeclampsia or eclampsia, hypertensive encephalopathy, or acute renal failure.
Evaluation of the Patient
The purpose of diagnosing and treating hypertension is to prevent the development of target organ damage, cardiovascular and cerebrovascular disease, and chronic kidney disease (CKD). To do this effectively, it is important to estimate the patient’s global cardiovascular risk and, in particular, to identify other modifiable risk factors such as dyslipidemia, smoking, and diabetes. Most contemporary guidelines for hypertension management stress the need to consider the likely impact of all risk factors before making clinical management decisions, and they recommend a system of evaluating combined risk factor effects. For example, the British National Institute for Health and Clinical Excellence guidelines recommend using a formal estimation of cardiovascular risk to discuss prognosis and health care options with hypertensive patients, both for increased BP and for other modifiable risk factors. Figure 28-1 and Boxes 28-1 and 28-2 show the pertinent elements of the history and physical assessment of the hypertensive patient.
Dietary intake of salt, processed foods, and fruits and vegetables
Alcohol consumption (specific amounts and type)
Caffeine intake (coffee, tea, cola beverages, pills)
Use of pressor agents (nasal sprays, cold remedies)
Licorice intake, with a focus on licorice of British, French, or Belgian origin; certain laxative abuse and chewing tobacco (rare causes)
Use or abuse of organic, herbal, and health food remedies
Use of nonsteroidal antiinflammatory drugs
Exercise type, frequency, and duration
Occupational history; note stress levels
Educational history if not defined by occupation
Chronic kidney disease
Coarctation of the aorta
Cushing syndrome and other glucocorticoid excess states, including long-term steroid therapy
Drug-induced or drug-related (includes nonsteroidal antiinflammatory drugs; illicit pressor agents such as cocaine; sympathomimetic agents, such as nasal decongestants and diet drugs, cyclosporine and tacrolimus, erythropoietin, and licorice; and alternative agents, such as ephedra [Ma haung] and bitter orange)
Primary aldosteronism and other mineralocorticoid excess states
The patient history should provide clues as to whether the patient truly has hypertension, whether it is primary or secondary, and whether it has resulted in target organ damage or cardiovascular disease outcomes. Patients should be queried about other modifiable risk factors—such as diabetes, smoking, or dyslipidemia—that would affect their prognosis and therefore possibly alter the treatment plan. A variety of cardiovascular risk estimation systems have been developed and adapted for the primary care setting. These vary in complexity and ease of use; current trends favor simpler systems of risk estimation and management, with minimal requirement for laboratory testing. Of these, the Framingham Risk Score has been assessed and validated in the broadest range of populations and has the most years of follow-up. A newer version of the Framingham Risk Score predicts 10-year risk of specific cardiovascular disease endpoints—coronary heart disease, stroke, heart failure, and peripheral vascular disease (PAD)—as well as global cardiovascular disease risk. An online and downloadable risk calculator is available at www.nhlbi.nih.gov/guidelines/cholesterol and www.framinghamheartstudy.org . Electronic risk estimation that can be automated and linked to the patient’s electronic medical record is gaining in popularity and facilitates the use of cardiovascular disease risk assessment in primary care.
It is important to determine when the patient first became aware of having hypertension. Sudden or very recent onset or exacerbation of hypertension may increase the likelihood of a secondary cause. Ask about past physical examinations and determine what BP readings were obtained by other health care providers. Obtain a history of previous hypertension evaluation, with particular attention to data that may have already been collected and need not be duplicated. If the patient has been previously treated for hypertension, a detailed list of medications used, their effect or lack thereof, and any adverse effects is very useful. Importantly, patients who report multiple pharmacologically improbable and often bizarre “allergies” to medications may be having anxiety syndromes or panic attacks rather than true hypertension. Anxiety-induced hypertension may not respond to antihypertensive therapy. These patients require anxiolytic agents and care from a specialist in treating anxiety disorders.
Family history should be extended to both maternal and paternal grandparents, aunts and uncles, and siblings and children. Seek information on strokes, premature cardiac death, and kidney failure in addition to heart failure and hypertension.
Past Medical History
Medical records should be reviewed for BP readings taken at the time of hospitalizations or procedures, for imaging studies of the brain or kidneys, and for laboratory data that may reveal evidence of CKD or decreased serum potassium levels. Particular attention should be paid to pregnancy history in women because preeclampsia and other forms of pregnancy-related hypertension predict both sustained hypertension and increased cardiovascular disease risk later in life. Computed tomography (CT) or magnetic resonance imaging (MRI) scans taken because of headaches might provide evidence of hypertension-associated brain lesions.
Review of Systems
The review of systems should focus on clues to possible secondary causes of hypertension, target organ damage, and prior cardiovascular disease events. Details of prior hospitalizations should be queried. Recent weight gain may be associated with new-onset hypertension; if the patient is able to lose the weight, the loss offers the opportunity to control the BP without medication. Inadvertent weight loss may be a clue to hyperthyroidism or pheochromocytoma. A history of “spells” characterized by sweating, palpitations, and headache suggests the possibility of pheochromocytoma but may also be a manifestation of anxiety unrelated to hypertension or cardiovascular disease. A history of anxiety or depression is important because anxiolytic or antidepressant medications may adversely affect BP and response to antihypertensive medications, and patients with panic attacks and anxiety-induced BP elevations may not respond to conventional antihypertensive therapy. Furthermore, depression is associated with low adherence to antihypertensive medications and may be an important barrier to hypertension management.
Daytime sleepiness or a history of loud snoring, especially when associated with apneic spells, is strongly suggestive of obstructive sleep apnea, a condition known to be associated with treatment-resistant hypertension. The patient’s bed partner may be a good source of information on snoring, but a formal sleep study is needed to confirm the diagnosis and develop treatment strategies.
Detailed information about lifestyle that includes diet, physical activity, smoking, and alcohol consumption is needed to establish a basis for the lifestyle modification component of antihypertensive therapy (see Box 28-1 ). High intake of alcohol and caffeine-containing beverages—including coffee, tea, and soft drinks—can increase BP and make treatment more difficult. Patients should be queried about use of medications or dietary supplements that can elevate BP (see Box 28-1 ). Prominent among these are pain medications, particularly nonsteroidal antiinflammatory drugs (NSAIDs). Because many patients do not regard over-the-counter preparations as true “medicines,” it is important to ask specifically about pain and pain treatments, as well as herbal preparations, dietary supplements, and weight-loss preparations. Nasal decongestants and cold remedies have sympathomimetic effects that can elevate BP significantly. Immunosuppressive drugs and many agents used in cancer treatment also elevate BP.
The social history includes information about education, job status, marital history, and living situation, and it can provide valuable information about psychosocial stresses that can elevate BP and impair response to treatment. In extreme stress situations—such as the 2011 tsunami in Japan and the destructive tornadoes in the United States—hypertension and related cardiovascular disease events can appear de novo in epidemic fashion. Getting to know your patient’s social situation and expressing empathy are critical to developing trust and initiating a successful strategy for managing BP and cardiovascular risk over the long term.
To begin, the patient’s weight and height should be measured, and the body mass index (BMI) should be calculated. Measuring the waist circumference provides additional predictive information regarding metabolic syndrome and coronary heart disease risk. Examination of the skin for café-au-lait spots, neurofibromatomata, hair pattern changes, factitious lesions, and signs of domestic violence may reveal clues to diagnoses of secondary causes of hypertension. In addition, the optic fundi should be examined for retinal hemorrhages, exudates, papilledema, and arteriovenous crossing defects, all evidence of microvascular and macrovascular disease. This is particularly important for patients with very high BP and for those in whom hypertensive emergency is suspected. The eyes, facial features, and body habitus may also give clues to hyperthyroidism, hypothyroidism, and Cushing syndrome. Gingival hypertrophy should be looked for, because antecedent gingival hypertrophy is a relative contraindication to treatment with dihydropyridine calcium channel blockers.
Next, the carotid arteries should be examined by auscultation and palpation, looking for evidence of vascular disease. The thyroid should be palpated and the neck inspected for jugular venous distention indicative of volume overload and heart failure.
Moving to the trunk, the lungs should be examined for signs of heart failure, and the heart should be examined carefully for evidence of abnormalities of rate or rhythm, murmurs, and signs of heart failure. The abdominal examination should include careful auscultation for renal artery and abdominal aortic bruits and palpation for masses, enlarged kidneys indicative of polycystic kidney disease, and a distended urinary bladder indicative of urinary outflow obstruction. A distended bladder may cause increased sympathetic discharge and BP elevation.
The lower extremities should be palpated for edema and pulses; the radial and femoral arteries should be palpated simultaneously to detect a pulse delay suggestive of aortic coarctation. The femoral arteries should be examined by auscultation to look for evidence of vascular disease. Measurement of BP in the leg as well as in the arm can be used to calculate the ankle brachial index (ABI), an indirect measure of PAD and a predictor of all-cause mortality and cardiovascular disease mortality, and to detect aortic coarctation.
Neurologic examination should be performed as a baseline because stroke is a frequent complication of hypertension and also to document residual deficits in patients with previous stroke. Cognitive function should be assessed, particularly in elderly patients; cognitive decline and dementia are important complications of hypertension in the elderly.
Blood Pressure Measurement
The diagnosis and treatment of hypertension are critically dependent on accurate assessment of BP. JNC 7 and American Heart Association (AHA) guidelines for auscultatory measurement of office BP are outlined in Box 28-3 . The patient should be seated comfortably with feet on the floor and back supported. The patient should be at rest for at least 10 minutes and should not have consumed tobacco or caffeine in the previous 30 minutes. The possibility that the patient may have recently used illicit vasoactive drugs should be assessed. The bare arm should be fitted with a cuff of correct size and supported at heart level. The cuff should be inflated until either the radial or brachial pulse disappears from the palpating fingertip. The pressure should then be reduced by a few mm Hg per second, until the first Korotkoff sound is heard. Disappearance of the sound usually marks the diastolic pressure. BP should be measured in both arms and with the patient standing at the first office visit. The arm with the higher readings should be used for future examinations to minimize inconsistency in visit-to-visit measurements.
Regularly inspect and validate equipment.
Train and regularly retrain people who take blood pressure.
Properly prepare and position the patient. Patient should be:
Seated quietly in a chair with feet on floor for at least 5 minutes
Arm at heart level
No caffeine, exercise, or smoking for at least 30 minutes before
Use an appropriately sized cuff that encircles at least 80% of the arm.
Inflate the cuff to 20 to 30 mm Hg above the point at which palpated radial or brachial pulse disappears.
Deflate the cuff at about 2 mm Hg/second.
The first Korotkoff sound denotes systolic pressure; disappearance of the sounds denotes diastolic pressure.
On the first visit, take readings in both arms. Note and record the arm with the higher pressure, and use this arm for all subsequent readings. Note that the higher systolic and diastolic blood pressure may be found in different arms.
Take standing blood pressure, especially before titrating doses upward.
Semiautomated devices that use an oscillometric method of BP determination are increasingly being used in hypertension studies and in office practice. If the instrument has been validated and the correct procedures for patient positioning have been followed, these devices eliminate observer error and free staff time. Check www.dableducational.org to determine whether your instrument has been validated.
Although office BP measurement remains the gold standard for assessing treatment responses in randomized, controlled trials, home BP measurements taken by the patient or a friend or family member are increasingly being used for monitoring treatment. Engaging hypertensive patients in self-monitoring of BP has the advantage of involving them in their own care and is cost effective. Ambulatory BP monitoring (ABPM), in which BP is measured and recorded at frequent intervals throughout the day (usually every 15 or 30 minutes), has been shown to provide important prognostic information in untreated patients and is now required by some guidelines to make a diagnosis of hypertension. ABPM is indicated for the diagnosis of “white coat hypertension,” in which BP is elevated in the office but is normal or controlled in the out-of-office setting, and masked hypertension, in which BP is normal or controlled in the office but elevated in other settings. ABPM is useful in diagnosing episodic hypertension and treatment resistance. The disadvantages of ABPM include high cost and inconvenience to the patient.
In the absence of specific clues to secondary hypertension from the history and physical examination, the basic initial laboratory evaluation should be simple ( Box 28-4 ). A baseline electrocardiogram (ECG) should be part of the initial evaluation of every hypertensive patient to assess target organ damage. If left ventricular hypertrophy is evident, it should be confirmed by echocardiogram. Urinalysis, measurement of serum creatinine, and calculation of estimated glomerular filtration rate (eGFR) using the four-part Modification of Diet in Renal Disease equation are useful for assessing damage to the kidney as a target organ. These measures are particularly important in older patients with long-standing hypertension, among whom CKD is a growing problem that may require modification of antihypertensive treatment regimens, such as administration of more potent diuretics. Measurement of albuminuria and calculation of the albumin/creatinine ratio in morning-voided spot-urine samples has predictive value for both renal and cardiovascular disease, particularly in patients with diabetes.
Urinalysis (check for microalbuminuria in patients with diabetes)
Blood glucose level
Serum potassium level
Serum creatinine level and estimated glomerular filtration rate
Urinary albumin level
Serum potassium measurement may provide important clues to secondary hypertension such as that seen with hyperaldosteronism. Elevated serum glucose should lead to further testing given the important interaction between hypertension and diabetes. Although not specifically part of the hypertensive workup, an assessment of the lipoprotein profile should be made because of risk factor clustering. Assays of plasma renin activity and plasma and urinary aldosterone levels are not recommended for the initial evaluation of the hypertensive patient; however, these assays may play a role in the diagnosis of secondary or resistant hypertension, as discussed in Chapter 31 .
Overview of Treatment of the Hypertensive Patient
Once the initial evaluation of the patient has been completed, decisions on the choice of therapy must be made. The JNC 7 algorithm ( Figure 28-2 ) is a useful guide for most hypertensive patients. Lifestyle modifications discussed in the remainder of this chapter should be initiated and maintained in all hypertensive patients. For those who require pharmacologic treatment, compelling indications such as heart failure, recent MI, high coronary disease risk, diabetes, CKD, and recurrent stroke prevention should first be identified because a compelling indication may drive the selection of antihypertensive medication. If there is no such indication, treatment is based on the stage of hypertension. Once treatment has begun, regular follow-up should be scheduled, and the frequency of follow-up visits depends on the level of BP control and on the presence of other cardiovascular risk factors or target organ damage.
If the patient fails to achieve goal BP despite treatment with full doses of three or more antihypertensive agents of different classes, one of which is a diuretic, the diagnosis is resistant hypertension. Although the cause of resistant hypertension is almost always multifactorial, common factors include lifestyle characteristics such as obesity, high alcohol intake, and excess sodium intake; drug-related causes, such as with sympathomimetic agents or NSAIDs; and secondary causes of hypertension that may include primary aldosteronism, CKD, renal artery stenosis, and obstructive sleep apnea (see Boxes 28-2 and 28-5 ). The most frequent cause of resistant hypertension is volume overload. A recent National Health and Nutrition Examination Survey (NHANES) reported that in treated hypertensive U.S. adults, apparent treatment-resistant hypertension has increased in prevalence from 15.9% (1998 through 2004) to 28.0% (2005 through 2008). In this nationwide survey, four or more health care visits per year, obesity, CKD, and a Framingham 10-year coronary risk score above 20% were associated with apparent treatment-resistant hypertension.