Abstract
Hypertension is common and affects over 70 million adults in the United States. Hypertension is the major cause of cardiovascular morbidity and mortality related to stroke, heart disease, and chronic kidney disease. This chapter details the evaluation of hypertension and measurement of blood pressure in different settings, discusses the appropriate blood pressure goals in different populations, and elaborates on the treatment of hypertension with lifestyle and drug therapy in the general adult population and in specific subgroups.
Keywords
hypertension, blood pressure, elderly, chronic kidney disease, ambulatory blood pressure, home blood pressure, secondary hypertension, antihypertensive medication
Hypertension remains the leading cause of cardiovascular (CV) morbidity and mortality including stroke, heart disease, kidney disease, and other vascular disease. The relationship between blood pressure (BP) and CV risk is linear, continuous, and additive to other well-known risk factors including diabetes, dyslipidemia, obesity, and cigarette smoking. For individuals aged 40 to 69 years, each increment of either 20 mm Hg in systolic BP or 10 mm Hg in diastolic BP doubles the mortality risk related to stroke, ischemic heart disease, and other vascular causes across the entire BP range from 115/75 to 185/115 mm Hg.
Hypertension affects nearly a third of the US adult population, and the prevalence continues to increase steadily because of aging and increasing obesity in the US population. The lifetime risk of developing hypertension is about 90%. In 2003, the Joint National Committee (JNC 7) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure classified BP into four categories as listed in Table 65.1 ; this classification system remained unchanged in JNC 8, published in 2014. In JNC 7, a “prehypertension” category was created to reflect its association with higher CV risk compared with normal BP; prehypertension affects, on average, about a quarter of the US adult population.
| BP Classification | Systolic BP (mm Hg) | Diastolic BP (mm Hg) | |
|---|---|---|---|
| Normal | <120 | and | <80 |
| Prehypertension | 120–139 | or | 80–89 |
| Stage 1 hypertension | 140–159 | or | 90–99 |
| Stage 2 hypertension | ≥160 | or | ≥100 |
Correctly assessing BP status and overall CV risk is key to optimizing therapy to reduce CV morbidity and mortality. At first diagnosis, a comprehensive evaluation is usually undertaken in those with a consistent systolic BP greater than 140 mm Hg and/or diastolic BP greater than 90 mm Hg.
Evaluation of Hypertension
Three key questions are addressed when assessing each hypertensive patient. The first question is whether the BP increase is essential (primary) or represents a secondary form of hypertension. Most hypertensive patients have primary or essential hypertension and are likely to remain hypertensive for life. However, some patients have identifiable, or secondary, causes, for their elevated BP that may warrant specific therapy in addition to antihypertensive medications to address the underlying specific or dominant pathology and offer possible cure. The clinical clues suggesting the possible presence and cause of secondary hypertension are discussed later in this chapter.
The second question assesses the presence of other CV risk factors as summarized in Table 65.2 . Defining overall CV risk is important in the choice of antihypertensive medications, BP target, and management of other treatable factors such as dyslipidemia.
| Risk Factors | Level Considered Abnormal | Approximate Frequency (%) |
|---|---|---|
| Obesity | BMI >30 kg/m 2 | 40 |
| Increased total cholesterol | Total cholesterol >240 mg/dL | 40 |
| Reduced HDL | HDL cholesterol <35 mg/dL | 25 |
| Albuminuria a | ≥30 mg/g | 16 |
| Diabetes | Type 1 and type 2 diabetes mellitus; fasting glucose >126 mg/dL | 15 |
| Insulin resistance | Elevated fasting insulin and/or impaired glucose tolerance | 50 |
| LVH a | Defined by various ECG or echocardiogram criteria | ~30 b |
| Sedentary | Arbitrary | ~30 |
a Albuminuria and left ventricular hypertrophy are both risk factors and markers of target-organ damage.
The third question evaluates the presence of end-organ damage, defined as clinically evident cardiovascular diseases (CVDs) related to hypertension as summarized in Table 65.3 . The presence of end-organ damage redirects the goal of treating BP from primary prevention of target-organ integrity to the more challenging realm of secondary prevention.
| Organ | History/Symptom(s) | Physical Examination | Laboratory |
|---|---|---|---|
| Retina | Blurry vision, headache, disorientation | Retinopathy | — |
| Brain | Stroke, TIA, confusion/disorientation | Signs of stroke, carotid bruits | MRI, CT, or ultrasound |
| Heart | Angina, MI, heart failure, cardiac arrest, atrial fibrillation | Cardiomegaly, S4, rales, irregular heartbeats | ECG may show LVH and/or prior MI |
| Kidney | Chronic kidney disease, polyuria, nocturia, anorexia, nausea, weight loss, peripheral edema | Palpable kidneys, epigastric bruits | Elevated creatinine, proteinuria, hematuria; ultrasound may show small kidneys with increased echogenicity |
| Circulation | Peripheral arterial disease, claudication, ischemic digits | Femoral bruits, diminished or absent pedal pulses | Ankle-brachial index <0.9 |
Measuring Blood Pressure
Measuring BP correctly is the key to proper BP classification. Fig. 65.1 lists steps recommended to obtain reliable BP readings, and Table 65.4 lists common mistakes leading to inaccurate BP measurements. During the initial visit, BP should be measured in both arms (and in the leg if aortic coarctation is suspected). For proper BP assessment, it is important to take the BP in the correct way at least twice on any occasion and on at least two, and preferably three, separate days for the initial diagnosis of hypertension. The 2015 US Preventive Services Task Force (USPSTF) guidelines on hypertension recommend that all individuals 18 years or older be screened for elevated BP.
| Failure to sit quietly for 5 min before a reading is taken Lack of arm and foot support Too small a cuff size relative to the arm (cuff bladder should encircle ≥80% of upper arm circumference) Too rapid cuff deflation (i.e., more than 2 mm Hg per second) On-going conversation Recent caffeine intake or cigarette smoking |
Pseudohypertension is a problem occasionally encountered in examining patients with very stiff and difficult to compress blood vessels due to arterial wall calcification. The pressure required to compress the stiff brachial artery and to stop the audible blood flow with a standard BP cuff can be much greater than the actual intraluminal BP obtained invasively. Osler’s maneuver can be used to identify this condition by inflating the BP cuff at least 30 mm Hg above the palpable systolic pressure and then trying to “roll” the brachial or radial artery underneath the fingertips. Pseudohypertension may be present when something resembling a stiff tube is felt underneath the skin because a normal artery should not be palpable when empty. It is important to identify pseudohypertension as it tends to occur in the elderly and chronically ill who are also more prone to orthostatic and postprandial hypotension, which can be aggravated by the unwarranted intensification of BP treatment.
Electronic devices are increasingly used to measure BP at home and in the office setting. Most of these devices work on oscillometric principles. The cuff is inflated until the disappearance of the brachial pulses is detected. Upon deflation, sensors detect the increasing amplitude in the brachial pulsation and measure the mean arterial pressure. The systolic and diastolic BP readings are then derived from the mean arterial BP. Typically, systolic BP is slightly lower and diastolic BP is slightly higher when measured with electronic devices when compared to invasively measured arterial pressure.
Also available are specialized electronic devices to perform automated office blood pressure monitoring (AOBP) in the office setting. With AOBP, multiple BP readings are recorded using a fully automated sphygmomanometer with the patient resting quietly and sitting alone. Proper timing, patient positioning, cuff size, and placement are still necessary to be certain that the readings are accurate. There are currently three validated devices available for performing AOBP, and each can be programmed to take multiple consecutive BP measurements in intervals of typically 1 to 2 minutes. The devices differ in the number of readings taken and the number of minutes before the first BP measurement is recorded. AOBP has the same cut-point as home BP and awake ambulatory BP (135/85 mm Hg) for defining hypertension, because systolic pressure readings are 5 to 10 mm Hg lower with AOBP than with auscultatory measurement. In 2011, the Canadian Hypertension Education Program recommended AOBP for the diagnosis of hypertension, and, in 2013, the European Society of Hypertension recommended using AOBP if feasible.
AOBP has some specific advantages, including that AOBP is not associated with the white-coat effect (the response in some patients in which BP readings taken by doctors and nurses tend to be higher because of increased patient anxiety), multiple readings are obtained, and readings more significantly correlate with awake ambulatory BP readings when compared with manual office readings as demonstrated in the Conventional Versus Automated Measurement of BP in the Office (CAMBO) study.
Assessing Cardiovascular Risk and End-Organ Damage
The evaluation of each hypertensive patient should include a detailed personal and family history, thorough physical examination, and selected tests focused on addressing the above three key questions. Key components of the history and physical examination are listed in Table 65.5 .
| Key Elements | Evaluation |
|---|---|
| History | |
| Age of onset, duration, and severity | Onset at younger age (<30 years) or older age (>55 years) suggests secondary causes; new onset of severe hypertension also suggests a secondary cause |
| Contributing factors | Dietary salt intake, physical inactivity, psychosocial stress, symptoms of sleep apnea |
| Concomitant medications | Common offenders include NSAIDs, oral contraceptives, corticosteroids, licorice, cough/cold/weight-loss sympathomimetic agents (pseudoephedrine, ma huang, ephedrine) |
| Risk factors for cardiovascular disease | Diabetes, smoking, family history of premature cardiovascular disease particularly in a first-degree relative (parent or sibling) |
| Symptoms suggestive of secondary causes | Palpitations or tachycardia, spontaneous sweating, migraine-like headaches in paroxysms (catecholamine excess); muscle weakness, polyuria (decreased potassium from aldosterone excess); personal or family history of kidney disease or findings (proteinuria, hematuria), or symptoms like ankle swelling (edema); thinning of skin and stigmata of cortical excess; snoring and daytime somnolence (sleep apnea); heat intolerance and weight loss (hyperthyroidism) |
| Target-organ damage | Chest pain or chest discomfort (possible coronary artery disease); neurologic symptoms consistent with stroke or transient ischemic attack; dyspnea and easy fatigue (possible heart failure); claudication (peripheral arterial disease) |
| Physical Examination | |
| General appearance, skin lesions, distribution of body fat | Patient may fit criteria for metabolic syndrome (increased cardiovascular risk); evidence of prior stroke from gain/station; rarely secondary forms as striae (Cushing syndrome) or mucosal fibromas (MEN II) |
| Fundoscopy | See text for lesion grades; retinal changes reflect severity of hypertension (target-organ damage to the eyes) and future cardiovascular risk |
| Neck | Diffuse multinodular goiter indicating Graves’ disease; presence of carotid bruits suggests potential stroke risk |
| Cardiopulmonary examination | Rales and cardiac gallops consistent with target-organ damage (heart enlargement or heart failure), interscapular murmur during auscultation of the back for aortic coarctation |
| Abdominal examination | Palpable kidneys suggest polycystic kidney disease; mid-epigastric bruits indicate renal artery disease |
| Neurologic examination | Signs of previous stroke (reduced grip, hyperreflexia, spasticity, Babinski sign, muscle atrophy, and gait disturbances) reflect target-organ damage |
| Pulse examination | Delayed or absent femoral pulses may reflect coarctation of the aorta or atherosclerosis |
A detailed personal history of hypertension includes its onset, duration, severity and related symptoms, presence of other CV risk factors, and target-organ complications. The medication history should include the prior and current use of any prescription and over-the-counter agents. Special attention should be paid to antihypertensive medications with their related clinical responses and adverse effects, as well as common offending agents, such as nonsteroidal antiinflammatory drugs (NSAIDs), oral contraceptives, and cold/cough remedies. NSAIDs can increase BP directly and can decrease the efficacy of antihypertensive medications by inhibiting the vasodilatory and natriuretic effects of prostaglandins and potentiating vasoconstrictive effects of angiotensin-II. Dietary salt intake, alcohol consumption, tobacco use, physical activity, and weight changes should be recorded. With the increasing prevalence of obesity, essential hypertension manifests at a younger age, often in the 30s. In addition, more elderly patients are expected to develop essential hypertension as systolic BP increases throughout life. Family history of hypertension, diabetes, and related CV complications should also be noted, as a positive family history further increases the individual’s CV risk. Excluding monogenic causes of hypertension, available data suggest that the heritability of essential hypertension ranges from 20% to 40%.
Physical examination should start with measurement of height, weight, and waist circumference. BP is usually measured in supine, sitting, and standing positions on the initial evaluation, and at least once in both arms (and at least one leg if aortic coarctation is suspected). Subsequent BP measurements are obtained in the seated position from the arm with the higher initial BP reading.
The optic fundi are the only place where blood vessels can be directly examined. The fundoscopic examination looks for arteriolar narrowing (grade 1), arteriovenous compression (grade 2), hemorrhages and/or exudates (grade 3), and papilledema (grade 4), which not only provide information on the degree of target-organ damage related to BP but also provide important prognostic information on overall CV outcomes.
Bruits in the neck, abdomen, and groin should be noted. Bruits may simply result from vascular tortuosity, particularly with high-flow vessels. However, they may be a sign of vascular stenosis and irregularity and be a clue to vascular damage leading to future loss of target-organ function. The radial artery is similarly distant from the heart as the femoral artery, and the pulse should arrive at approximately the same moment when palpating both sites simultaneously. In aortic coarctation, a palpable delay in the arrival of the femoral pulse compared with the radial pulse supports this diagnosis, as does an interscapular murmur heard during auscultation over the back of the patient. A systolic BP in the leg behind the knee (popliteal) lower than the brachial value suggests the presence of aortic or iliac obstruction, but it may also reflect more peripheral arterial disease in certain patients such as smokers and those with target-organ damage. Patients should be advised that measuring leg BP may be uncomfortable given the large cuff and the amount of pressure required to occlude the femoral artery.
Cardiac examination by palpation may reveal a displaced apical impulse, indicative of left ventricular enlargement. A sustained apical impulse may suggest left ventricular hypertrophy (LVH). Auscultation should focus on listening for an S4 that is heard with left ventricular stiffness. An S3 indicates impairment in left ventricular function and usually underlying heart disease when rales are present on lung examination, although the presence of S3 and rales is uncommon on initial office evaluation of new hypertensive patients. The lower extremities should also be examined for peripheral arterial pulses and edema. The loss of pedal pulses is a sign of peripheral vascular disease (target-organ damage) and is associated with higher CV risk.
Finally, a brief neurologic examination for evidence of remote stroke should assess gait, bilateral grip strength, speech, memory, and mental acuity. Given the link between hypertension and future loss of cognitive function, it is useful to establish the cognitive function status before starting antihypertensive medications, as some patients may complain of memory loss after starting pharmacotherapy.
Several laboratory studies are recommended in the routine evaluation of the hypertensive patient. Testing should include hemoglobin or hematocrit, urinalysis with microscopic examination, serum potassium, bicarbonate, creatinine, fasting glucose, lipid profile, and 12-lead electrocardiogram (ECG). Assessing albuminuria is important as albuminuria has been associated with increased CV risk and may warrant more aggressive BP reduction. Assessing kidney function is also an important part of evaluation as chronic kidney disease (CDK) is not only a sign of target-organ damage but also a common cause of hypertension. Depending on the degree of glomerular filtration rate (GFR) loss, up to 90% of patients with advanced CKD or end-stage kidney disease have hypertension. Uric acid may be checked in those with a history of gout as diuretics can increase uric acid level and lead to gouty flares. In some cases, checking calcium, thyroid-stimulating hormone (TSH), or other thyroid studies may be reasonable when clinically indicated.
Plasma renin activity and serum aldosterone levels are useful in screening for aldosterone excess and salt sensitivity. However, these measurements are usually reserved for patients with hypokalemia, metabolic alkalosis, or those who fail to achieve BP control on a three-drug regimen (which includes a diuretic). A suppressed renin activity level with increased aldosterone-to-renin ratio supports a contribution of dietary sodium excess to hypertension; this scenario should respond well to dietary salt restriction and diuretics. It is worth noting that primary hyperaldosteronism is more common than previously thought. In patients referred to one hypertension center in Italy, 11% had primary hyperaldosteronism, with 5% having a potentially curable aldosterone-secreting adenoma and 6% having idiopathic hyperaldosteronism. In the same study, only 50% of patients with a confirmed aldosterone-producing adenoma had hypokalemia, underscoring the importance of considering this diagnosis in patients with normal levels of potassium.
Additional testing may be indicated in some patients depending on the clinical situation. Limited echocardiography is more sensitive than an ECG for detection of LVH. The presence of LVH, a sign of target-organ damage, can help establish or reinforce the need of antihypertensive therapy, especially in those who have borderline BP and/or are reluctant to start antihypertensive medications.
Ambulatory and Home BP Monitoring
Since BP can be influenced by an environment such as an office or hospital, ambulatory BP monitoring (ABPM) or self-monitored BP (SMBP) in the home is useful in establishing or excluding the diagnosis of hypertension in those with white-coat hypertension or masked hypertension ( Fig. 65.2 ). ABPM and SMBP are also useful in assessing the adequacy of BP control in outpatients and helping identify those with morning surges in BP (i.e., >55 mm Hg increase in systolic BP during the early waking hours compared with sleeping). The morning surge has been associated with increased risk of cerebrovascular diseases, including brain white matter lesions and stroke. In addition, ABPM is helpful in screening for nocturnal hypertension or nondipper status (i.e., <10% reduction in nighttime BP compared with daytime). Data from large ABPM cohorts suggests that nighttime BP provides the greatest information regarding CV risk. CV risks associated with elevated nighttime BP levels outweigh the risks associated with elevated routine office BP measurements and those of the cumulative daytime hours. In addition, the BP variability data from ABPM suggests that a greater degree of BP variability during the 24 hours of monitoring is associated with a greater risk of CV target-organ damage. ABPM is typically programmed to take BP measurements every 15 to 30 minutes during awake hours and every 30 to 60 minutes during sleep hours. It is important for patients to complete the diary correctly so that the hours of sleep (including naps) can be incorporated into the ABPM report.
