Cheryl R. Dennison
Nancy Houston Miller
Susanna G. Cunningham
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Hypertension (HTN), also known as high blood pressure (BP), is the most common risk factor for cardiovascular disease (CVD) in developed and developing countries. The prevalence of HTN in America is 73 million and many more individuals have prehypertension, which indicates they are at high risk for developing HTN.1
Since the 1970s there has been a dramatic decrease in the mortality rate from hypertensive heart disease in Europe and the United States, primarily because of the development of effective antihypertensive drugs in conjunction with increased awareness, treatment, and control of HTN.2
Despite this progress, worldwide, an estimated 7.1 million premature deaths are caused each year by HTN.4
EVIDENCE FOR MANAGEMENT
BP has two components, which are continuous variables: systolic BP (SBP) and diastolic BP (DBP). Elevations in either SBP or DBP increase a person’s risk for a clinical event. Death from both ischemic heart disease and stroke increases progressively and linearly from levels as low as 115 mm Hg SBP and 75 mm Hg DBP upward among individuals whose ages range from 40 to 89 years.5
For every 20 mm Hg systolic and 10 mm Hg diastolic increase in BP, there is a doubling of mortality from ischemic heart disease and stroke.5
Conversely, it is generally true that the lower the pressures, the lower the risk of morbidity and mortality, except in the relatively uncommon situations of sympathetic nervous system dysfunction or hypovolemia.
The word “hypertension” can be confusing to patients, who might believe that they are neither “tense” nor “hyper” and therefore unlikely to have HTN. For this reason, “high blood pressure” may be a better term to use when communicating with the public. HTN can be considered as a sign, a risk factor, and a disease.
As new research has become available, many countries have established guidelines on the detection, evaluation, and treatment of HTN.6
Two widely promulgated guidelines defining normal and elevated BP levels were developed by The Joint National Committee of the National High Blood Pressure Education Program and the Guidelines subcommittee of the World Health Organization and the International Society of Hypertension.4
These guidelines define HTN as SBP of ≥140 mm Hg and/or DBP of ≥90 mm Hg. Both reports recommend considering BP together with other risk factors for atherosclerotic CVD when making decisions about when to initiate treatment.
To reflect the curvilinear nature of the relationship between SBP and DBP and risk, “normal” BP, prehypertension, and two stages of HTN have been delineated as shown in Table 35-1
Optimal or normal BP is <120/80 mm Hg. The term prehypertension (defined as BP 120-139/80-89 mm Hg) is intended to identify those individuals in whom early intervention by adoption of healthy lifestyles could reduce BP, decrease the rate of progression of BP to hypertensive levels with age, or prevent HTN entirely.7
HTN (defined as BP ≥ 140/90 mm Hg) is classified as either Stage 1 (SBP 140 to 159 mm Hg and/or DBP 90 to 99 mm Hg) or Stage 2 (SBP ≥ 160 mm Hg and/or DBP ≥ 100 mm Hg). Isolated systolic HTN is defined as the occurrence of SBP at or greater than 140 mm Hg with DBP less than 90 mm Hg. The incidence of isolated systolic HTN increases dramatically with age and thus is of particular concern among older adults.8
Types of HTN are classified as (1) systolic and diastolic HTN (either primary or secondary) and (2) isolated systolic HTN caused by increased cardiac output or increasing rigidity of the aorta.
Criteria used for categorizing BP in adults are not applicable to children. The level of BP, which is considered normal, increases gradually from infancy to adulthood.9
The definition of HTN in children and adolescents is based on the normative distribution of BP in healthy children.10
Normal BP is defined as SBP and DBP less than 90th percentile for gender, age, and height. HTN is defined as average SBP or DBP at or greater than 95th percentile for gender, age, and height on at least three separate occasions. Children and adolescents with BP ≥ 120/80 mm Hg but less than 95th percentile should be considered prehypertensive. Tables listing BP levels by age and height percentile for boys and girls can be found in the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents.10
Prevalence of HTN
Approximately 33.6%, or just over 73 million Americans have HTN.1
Based on data from the National Health and Nutrition Examination Survey (NHANES), conducted between 2003 and 2004, 75% of hypertensive individuals were aware of their condition, and 65% were being treated for HBP. Of those treated, only 56.6% had achieved BP control (BP < 140/90 mm Hg). Only 37.5% of individuals being treated for both HTN and diabetes mellitus had achieved the lower goal BP of <130/80.3
While the prevalence of HTN has increased, rates of HTN awareness, treatment, and control have also increased over the last decade.2
Age, Gender, and Weight
SBP and DBP levels correlate with age, height, and weight.9
Evidence suggests that HTN begins in childhood, perhaps even in utero,
although a meta-analysis of 55 studies of birth weight and BP later in life did not support this so-called fetal origins hypothesis.11
Because HTN in children is defined as a BP greater than the 95th percentile for a child of any given age and height, the initial incidence of HTN in children is automatically 5%. Normally, BP increases in children at a rate between 1 and 4 mm Hg per year for both SBP and DBP and then levels off after age 18 to 20 years. Children whose BP consistently falls above the 95th percentile for height, gender, and age are at risk for sustained HTN and should be evaluated and possibly treated.10
Table 35-1 ▪ CLASSIFICATION OF BLOOD PRESSURE FOR ADULTS
SBP (mm Hg)
DBP (mm Hg)
Stage 1 Hypertension
Stage 2 Hypertension
or ≥ 100
From Chobanian, A. V., Bakris, G. L., Black, H. R., et al. (2003). The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report. JAMA, 289(19), 2560-2572. (Erratum in JAMA, 2003, 290, 197.)
In adults, BP tends to increase with age.2
The prevalence of HTN increases with advancing age to the point where more than half of the people aged 60 to 69 years and approximately three fourths of those aged 70 years and older are affected.14
The age-related rise in SBP, often manifesting as isolated systolic HTN, is primarily responsible for an increase in both incidence and prevalence of HTN with increasing age.8
Overall, women have a slightly higher prevalence of HTN (33.6%) than do men (33.2%).1
However, the age-adjusted percent for women is 28%, and for men, it is 30%.3
Although rates of HTN treatment are higher among women (58%) compared with men (52%), men achieved higher rates of HTN control (66%) than women (63%).3
Data from the Framingham and other epidemiologic studies have shown that as body weight increases, so do SBP and DBP in children and adults.3
In the Bogalusa Study, children and adolescents who were overweight (body mass index [BMI] > 85th percentile) were 2.4 times more likely to have HTN than those with BMI less than the 85th percentile.16
NHANES III data revealed that the prevalence of HTN in men and women with BMI < 25 kg/m2
was 15%, whereas in men and women with a BMI ≥ 30 kg/m2
prevalence was 42% and 38%, respectively.15
This relationship between weight and BP is thought to be one of the reasons that BP increases with age.
Family History and Genetic Factors
Family history of HTN has been used as an indicator of genetic influence on HTN. With the progress on the human genome project, it is possible that we may be able to predict risk with more precision; however, expense and issues of privacy must also be considered. Depending on how a positive family history of HTN is defined, a person with a positive history has a relative risk for HTN of between 2.4 and 5.0.18
The risks are greater when more family members have HTN and if these family members had HTN diagnosed before the age of 55 years. The risk associated with a positive family history is slightly greater for women than for men. The influence of family history is seen in children as well as adults.19
Recent genetic studies suggest that rather than a single genetic variant, alleles at many different loci contribute to HTN, with the combinations of causative alleles varying between individuals. Among the most studied genetic markers for the pathogenesis of HTN are the renin-angiotensin system, salt intake, CVD, obesity and insulin resistance, the sympathetic nervous system, and endothelial dysfunction.21
Ethnic and Geographic Differences
Geographic differences in the prevalence of HTN have been described for different regions within the United States as well as across the world. When comparing across non-Hispanic White, non-Hispanic Black, and Mexican American ethnic groups in the United States, the prevalence of HTN was highest among non-Hispanic Black women (46.6%) and men (42.6%) and lowest among Mexican American women (31.4%) and men (28.7%).1
Within the United States, HTN prevalence, associated stroke mortality, and all-cause mortality vary in geographic patterns and are higher in the Southeast than other regions of the United States. Ten of 11 states in the southeastern United States, the “Stroke Belt,” have stroke mortality rates >10% above the national mean. Contributors to this pattern include geographic variations in obesity, physical inactivity, and salt and nutritional intake but not in HTN treatment or control.2
A review of the global burden of HTN revealed that regions with the highest estimated prevalence of HTN had roughly twice the rate compared with regions with the lowest estimated prevalence.23
In men, the highest estimated prevalence was in the Latin America and Caribbean region, whereas for women the highest estimated prevalence was in the former socialist economies. The lowest estimated prevalence of HTN for both men and women was in the region “other Asian islands” (i.e., Korea, Thailand, and Taiwan).23
Existing data suggest that the prevalence of HTN has increased in economically developing countries during the past decade.23
Differences in HTN rates across regions may be caused by differences in BP measurement and treatment, genetics, lifestyle choices, or other confounding variables.
Income and Education
An inverse relationship between socioeconomic status, including educational level and income, and the prevalence of HTN has been documented.24
The Atherosclerosis Risk in Communities Study of 10,091 Black and White Americans has even found a relationship between the stretch capacity (elasticity) of the carotid arteries and socioeconomic status, with persons in the lowest socioeconomic stratum having the greatest impairment of carotid elasticity.28
The impact of socioeconomic status on BP and other cardiovascular risk factors is thought to be related to social, financial, and political barriers to health care and to adoption of low-risk lifestyles.29
Hemodynamics of HTN
BP is the product of the amount of blood pumped by the heart each minute (cardiac output) and the degree of dilation or constriction of the arterioles (systemic vascular resistance). Arterial BP is controlled over short time periods by the arterial baroreceptors that sense changes in pressure within major arteries and then through neurohumoral feedback mechanisms, which modulate heart rate, myocardial contractility, and vascular smooth muscle
contraction to maintain BP within normal limits. Over longer time periods (hours to days), neurohumoral and direct renal regulation of vascular volume also play an important role in maintaining normal BP. Baroreceptors in low-pressure components of the cardiovascular system such as the veins, atria, and pulmonary circulation have a role in neurohumoral regulation of vascular volume.
HTN occurs because there is an increase in cardiac output and/or systemic vascular resistance.31
It may be that either one or both are elevated. Because BP can be measured relatively easily and because it is not easy to measure cardiac output or systemic vascular resistance, we identify dysfunction of these variables as disorders of BP regulation. As discussion in several chapters of this book reveal, each of these variables, cardiac output and systemic vascular resistance, are themselves influenced by many factors. Given all the factors that can influence it, BP needs to be considered as an extremely complex variable.
The Causes of HTN
Despite decades of research, the main underlying cause of HTN is unknown. However, HTN has been linked to a family history and other factors, such as obesity, stress, excess sodium dysfunction, and sympathetic nervous dysfunction, which may all contribute to HTN. It is highly likely that in the future it will be the interaction of both genetic and environmental factors that play a role in the hypotheses of the causes of HTN.
Primary HTN is the term used to describe 90% to 95% of all cases of HTN for which the cause is unknown. Secondary HTN, which accounts for 5% to 10% of HTN cases, is linked to diseases of the kidney, endocrine system, vascular system, lungs, and central nervous system. These conditions are described below.
The cause of primary HTN remains in question. BP is a complex variable involving mechanisms that influence cardiac output, systemic vascular resistance, and blood volume. HTN is caused by one or several abnormalities in the function of these mechanisms or the failure of other factors to compensate for these malfunctioning mechanisms. Currently, the genetic basis for rare types of HTN has been identified, and there is hope that soon these discoveries will lead to understanding of the cause or causes of most HTN.
Genetic factors and the environmental issues of obesity, stress, and excess sodium as well as sympathetic nervous system dysfunction may all contribute to HTN. Several hypotheses are linked to understanding the cause of HTN and include the following:
Dysfunction of the autonomic nervous system imbalance may be a cause due to the inheritance of genes predisposing an individual to increased sympathetic nervous activity.
Variations in renal sodium absorption also suggest that genes involved in rare inherited forms of HTN may be related to mutations in several genes that increase one’s susceptibility to disorders of renal absorption of sodium, chloride, and water. To date, genes accounting for the vast majority of salt-sensitive HTN have not been identified.21
Dysfunction of the renin-angiotensin-aldosterone system results in an increase in renin-angiotensin-aldosterone activity resulting in extracellular fluid volume expansion and systemic vascular resistance. Angiotensin II has also been shown to act like a growth factor and a cytokine resulting in growth, differentiation, and apoptosis in vascular tissues. Studies have also identified gene coding for various components of the renin-angiotensin-aldosterone system and their roles in the development of HTN.21
Impaired vascular responsiveness, that is, impairments in vascular dilation and increased vascular contraction, due to the function of the endothelium, occurs in those individuals with HTN. Oxidative stress is also a critical factor in both HTN and atherogenesis.33
Insulin resistance may also play a role in the development of HTN. Insulin resistance may be the common factor that links HTN, diabetes, and other metabolic abnormalities. The metabolic syndrome of abdominal obesity, increased BP, dyslipidemia, and insulin resistance with or without impaired glucose tolerance plus prothrombotic and proinflammatory states may place individuals at high cardiovascular risk.
Secondary HTN affects between 5% and 10% of individuals with HTN, and a large number of children younger than 10 years have HTN due to a specific physiologic condition. In children younger than 10 years, the most common causes of persistent HTN are renal disease and vascular problems such as coarctation of the aorta. Common secondary causes of high BP in adults include chronic renal disease, renovascular disease, primary aldosteronism, and, increasingly, sleep apnea.7 Display 35-1
summarizes the major secondary causes of HTN in both children and adults. Aspects of diagnosis and management of some of the more common conditions are highlighted here.
Renal Parenchymal Disease.
Chronic renal disease causes HTN and, conversely, HTN contributes to the development of chronic renal disease. Three factors contribute to the development of HTN in those individuals with renal disease: loss of nephrons leading to retention of sodium, chloride, and water; decreased release of vasodilator substances such as nitric oxide; and activation of the renin-angiotensin system. NHANES III data indicates that 70% of all patients with chronic renal disease have HTN. Aggressive lowering of SBP may slow the progression of kidney disease, and clinicians must consider numerous options for treatment to reach goal BP.
Renovascular HTN, found in 1% to 5% of all hypertensives, occurs when one or both of the renal arteries are diseased, leading to decreased perfusion of the kidneys. The most common cause of renal artery stenosis is atherosclerosis, which leads to renal ischemia, release of renin from juxtaglomerular cells of the kidney, and a secondary increase in BP.35
Diagnosis of renal artery stenosis is made on the basis of difficult to control BP or deterioration in renal function or electrolyte imbalance and through identification of an abdominal bruit by physical examination. This is followed by the either magnetic resonance imaging or computed tomography and a renal angiogram with consideration of medical treatment, angioplasty, or surgery (which is the gold standard for severe renal artery stenosis).36
Primary aldosteronism is a disease characterized by excess secretion of aldosterone, caused by an adrenocortical adenoma, adrenal hyperplasia, adrenal carcinoma, or the cause may be unknown; in which case it is diagnosed as idiopathic hyperaldosteronism.37
A common form of primary aldosteronism is a benign aldosterone producing adenoma. With high levels of aldosterone there is retention of
sodium, chloride, and water resulting in an expanded extracellular fluid volume. This condition is now thought to be the cause of 5% to 13% of all cases of HTN.37
Primary hyperaldosteronism may be difficult to diagnose due to low serum potassium, the most common sign being found in only one third of the cases.37
The best screening test is now the plasma aldosterone to plasma renin activity ratio.38
Clinicians should look for this condition in those patients younger than 50 years who appear to have resistant HTN or HTN with hypokalemia. Surgical removal of an adenoma reduces BP and if no tumor is present, medical treatment with aldosterone antagonists such as spironolactone is indicated.38
Pheochromocytomas are largely benign neuroendocrine tumors of the adrenal medulla and present in up to 6% of those individuals with HTN. Because excessive amounts of catecholamine occurs with these tumors, individuals may experience chest discomfort, tachycardia and palpitations, panic attack, and headaches.35
A pheochromocytoma is normally diagnosed by undertaking measurement of urinary and plasma catecholamines, urinary metanephrine, and urinary vanillylmandelic acid. Nuclear imaging may also identify certain extra-adrenal tumors and once detected surgical intervention is needed.
Obstructive Sleep Apnea.
An association between sleep apnea and systemic HTN has been reported since the 1970s. Increasingly this condition has gained more widespread attention due to the growing rate of obesity. Obstructive sleep apnea affects 2% to 4% of the general population, and more than 50% of those affected by it have HTN.35
It is now a significant health problem causing disrupted sleep, memory loss, personality changes, decreased attention span, poor judgment, and frequent episodes of hypopnea (reduced chest movement with 4% or more decrease in oxyhemoglobin) and or apnea (cessation of airflow for 10 seconds or more).39
A good medical history about sleep patterns is warranted and referral to a sleep disorder clinic needed to confirm the diagnosis. Treatment involves not only the use of continuous positive airway pressure, the most common approach to this condition, but also weight loss and treatment of concomitant HTN with medicines as needed.39
Assessment of sleep patterns and snoring is also indicated for those individuals with resistant HTN.
Coarctation of the Aorta.
Coarctation or narrowing of the lumen of the aorta is rare in adults but relatively common in children, accounting for 7% of all congenital CVD.35
The most common narrowing occurs distal to the left subclavian artery.42
Those individuals with coarctation of the aorta normally have high upper extremity BPs with low pressures in the lower extremities including weak femoral pulses.43
If this condition is left untreated, it can cause left ventricular hypertrophy (LVH). Bruits may be present on physical findings, and screening tests, which include a transthoracic echocardiogram or contrast computed tomography/magnetic resonance imaging help to visualize this condition. Treatment includes surgical repair of the lesion or angioplasty. A comparison of the BP and left ventricular mass among patients who had surgical repair of a coarctation and controls found that these patients had significantly higher 24-hour ambulatory SBP and left ventricular mass compared with controls.44
Thus, follow-up remains important in these patients.
HTN occurs in 5.9% of all pregnancies and is classified as preeclampsia-eclampsia, preeclampsia superimposed on chronic HTN, chronic HTN, or gestational HTN.38
The cause of preeclampsia is not known but it includes proteinuria, renal insufficiency, impaired liver function, and abnormalities including thrombocytopenia, hemolysis, and fetal growth restriction.45
Early diagnosis is critical and close monitoring of BP essential with treatment being directed at medicines with proven safety for each condition.
As shown in Display 35-1
numerous other causes of secondary HTN are noted. A careful history and physical examination, which is discussed in more detail under the section on management, will help reveal many of these secondary causes.
Clinical Manifestations of HTN
Signs and Symptoms
Unfortunately, there are few signs and no symptoms of HTN until it becomes very severe and target organ damage (TOD) has occurred. The major sign, obviously, is the presence of elevated BP based on the criteria for the definition HTN (see Table 35-1
). Other signs and symptoms are described in the next section on complications of HTN.
Evaluation of hypertensive patients has three objectives: (1) to assess lifestyle and identify other cardiovascular risk factors or concomitant disorders that may affect prognosis and guide treatment (Display 35-2
); (2) to reveal identifiable causes of high BP (Display 35-1
); and (3) to assess the presence or absence of TOD and CVD (Display 35-2
Morbidity and mortality associated with HTN are predominately the consequence of damage to a selected set of organs, known as “TOD,” which include the blood vessels, heart, brain, kidneys, and eyes. Evidence of TOD is a serious prognostic indicator in a person with HTN. Mechanisms of TOD are described below.
Vascular Changes Associated With HTN
HTN can influence the endothelium, vascular smooth muscle, extracellular matrix, and connective tissue of the arteries. Alterations of vascular structure that occur during chronic HTN may be referred to as remodeling or hypertrophy.47
Eutrophic inward remodeling, or “remodeling,” refers to a decrease in lumen diameter without a change in the thickness of the arterial wall or the characteristic of the material within the vessel wall. In contrast, hypertrophic inward remodeling, or “hypertrophy,” is defined as a decrease in lumen diameter associated with an increase in wall thickness and vessel wall material. In either case, narrowing of the vessel lumen is associated with increased vascular resistance.48
Some of the factors that contribute to the hypertrophy and remodeling processes appear to be different. Mechanisms of hypertrophy may include increased arterial pulse pressure, sympathetic nerve activity, angiotensin II, genetic factors, endothelin-1, nitric oxide, and oxidative stress.47
Mechanisms of remodeling may include intravascular pressure, angiotensin II, genetic factors, endothelin-1, αβυ3 integrins.47
Changes in the Vascular Endothelium.
The vascular endothelium is the largest organ in the body.50
Vascular endothelial cells are extremely active and play a critical role in regulation of blood vessel tone and cellular activity in the vascular wall. Endothelial cells modulate blood vessel tone by secreting a variety of dilator and constrictor substances. In addition to their effect on vascular tone, these substances and other factors produced by the endothelium, may also modify platelet aggregation, thrombogenicity of the blood, vascular inflammation, and oxidative stress and, over the long term, influence cell migration and proliferation with subsequent development and progression of atherosclerosis and its complications.50
Impaired endothelial vasodilation has been identified in persons with HTN and even in the normotensive children of hypertensive parents.51
However, it is not yet clear whether endothelial dysfunction is a precursor of HTN or a sequel. Improved understanding of the molecular basis for endothelial dysfunction in HTN may provide a pathway to developing new therapies to reduce the impact of HTN. Other factors that cause endothelial dysfunction include aging, hyperlipidemia, insulin resistance/diabetes, tobacco use, physical inactivity, and hyperhomocysteinemia.50
Atherosclerosis is a complex degenerative condition that is characterized by endothelial dysfunction and lipid accumulation in the endothelium and media, followed by wall thickening and outward remodeling, and later by luminal encroachment, thrombosis, and occlusion.53
Atherosclerosis manifests as coronary heart disease, cerebrovascular, and peripheral arterial disease and is a major worldwide source of morbidity and mortality. Atherosclerotic plaque formation involves the interaction of genetic predisposition and environmental risk factors with diffuse vascular injury. Many of these factors are also involved in the pathogenesis of HTN. HTN promotes or accelerates all phases of the development of atherosclerotic lesions, from plaque formation to rupture.53
Parallel structural and functional changes in the large arteries (stiffness), cardiac mass (hypertrophy), and myocardial relaxation and filling (diastolic dysfunction) occur at an accelerated rate with chronic HTN. The pressure overload associated with HTN promotes left ventricular hypertrophy (LVH) that leads to left ventricular dysfunction and heart failure. HTN also promotes vascular endothelial and renal dysfunction that directly impacts the progression of heart failure, which in turn affects vascular endothelial and renal dysfunction.54
Hypertensive individuals have a two- to four-fold increased risk of coronary heart disease and heart failure and those individuals with prehypertension have a 1.6- to 2.5-fold increased risk of CVD, both compared with those who are normotensive.55
Aggressive HTN control can prevent the development of LVH and lead to regression of LVH. However, it remains controversial whether there are differential drug effects on reversing LVH related to HTN.
HTN is both a cause and consequence of chronic kidney disease (CKD). The incidence and prevalence of CKD and end-stage renal disease, presumed to be secondary to primary HTN, have increased considerably over the past two decades and are particularly high among African Americans. HTN causes renal damage through multiple mechanisms.57
One mechanism is ischemia with glomerular hypoperfusion causing glomerulosclerosis and subsequently tubulointerstitial fibrosis. Other mechanisms of injury, such as endothelial dysfunction, cholesterol oxidation, cigarette smoking, and proteinuria, act in concert with high systemic
and glomerular capillary pressures to accelerate nephrosclerosis. While the presence of macroalbuminuria (proteinuria > 300 mg/day), indicates presence of kidney disease, even lower level microalbuminuria (30 to 300 mg/day) is associated with increased cardiovascular risk.
CKD mandates more aggressive treatment and lower target BP: <130/80 mm Hg in patients with diabetes or CKD and <120/75 mm Hg in patients with proteinuria >1 g/day.7
Antihypertensive drugs classes differ in ability to lower proteinuria and slow the progression of CKD. Drugs that block the rennin-angiotensin system, that is, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), are the most potent antiproteinuric agents and also have been shown to be highly effective in slowing the progression of renal insufficiency.58
HTN has profound effects on the structure and function of the eye. Hypertensive retinopathy refers to a spectrum of microvascular signs in the retina related to HTN.59
HTN initially causes retinal circulation vasospasm and increased vasomotor tone, which are reflected as the sign of generalized arteriolar narrowing. Persistent HTN leads to arteriosclerotic changes, including intimal thickening, media wall hyperplasia, and hyaline degeneration. This is seen as increasingly severe generalized arteriolar narrowing, arteriolar wall opacification, and focal narrowing. Thickening of the retinal arteriolar wall by these arteriosclerotic processes may compress the venules, resulting in the sign of AV nicking. In the presence of more acute elevations in BP, an exudative stage may occur, manifesting as microaneurysms, hemorrhages, hard exudates, and cotton wool spots. Optic disk swelling and macular edema may occur with severely elevated BP. These processes may not occur in the sequence described above. Numerous studies have confirmed the strong association between the presence of signs of hypertensive retinopathy and elevated BP.59
The strongest evidence of the usefulness of the evaluation of hypertensive retinopathy for risk stratification is based on its association with stroke as the retinal circulation shares anatomical, physiological, and embryologic features with the cerebral circulation. A simplified classification of hypertensive retinopathy—none, mild, moderate, and malignant —according to the severity of the retinal signs is presented in Table 35-2
HTN has adverse consequences in the brain, including ischemia and hemorrhagic stoke, cognitive impairment/dementia, and encephalopathy. HTN contributes to the development of atherosclerotic plaques in the extracerebral and intracranial vessels as well as the process of microatheroma and hypertensive hyalinosis. Despite the brain’s adaptive mechanisms to maintain cerebral blood flow, loss or reduction of blood flow results in stroke producing pathologic changes related to the duration and degree of ischemia. Research has documented the positive relationships between stroke and HTN as well as the reduction in stroke with HTN control.5
Cognitive impairment spans the spectrum from mild cognitive impairment to dementia. Cerebrovascular damage leading to cognitive impairment can occur not only from atherothrombosis but also through cerebral hemorrhage, hypoperfusion, and other arteriopathies. Longitudinal studies strongly suggest an adverse effect of elevated BP in middle age on cognitive functioning.64
There is also an adverse effect of low BP in the older adults for development of dementia; however, studies suggest no deterioration in cognitive performance with antihypertensive therapy in older adults hypertensive individuals who are well. Hypertensive encephalopathy is a consequence of accelerated or malignant HTN. Encephalopathy occurs when the BP levels exceed the upper limit of autoregulation so that the cerebral arteries become dilated, disrupting the blood-brain barrier and leading to the formation of cerebral edema; local changes in ion and cytokine concentrations; and/or alteration in neural function.65
Table 35-2 ▪ CLASSIFICATION OF HYPERTENSIVE RETINOPATHY
No detectable signs
One or more of the following signs: Generalized arteriolar narrowing, focal arteriolar narrowing, arteriovenous nicking, opacity (“copper wiring”)
Modest association with risk of clinical stroke, subclinical stroke, coronary heart disease, and death
Hemorrhage (blot, dot, or flame-shaped), microaneurysm, cotton-wool spot, hard exudate, or a combination of these signs
Strong association with risk of clinical stroke, subclinical stroke, cognitive decline, and death from cardiovascular causes
Signs of moderate retinopathy plus swelling of the optic disk†
Strong association with death
* A modest association is defined as an odds ratio of greater than 1 but less than 2. A strong association is defined as an odds ratio of 2 or greater.
† Anterior ischemic optic neuropathy, characterized by unilateral swelling of the optic disk, visual loss, and sectorial visual field loss, should be ruled out.
From Wong, T. Y., & Mitchell, P. (2004). Hypertensive retinopathy. New England Journal of Medicine, 351, 2310-2317.
MANAGEMENT OF HTN
Assessment and Diagnosis
HTN is relatively easy to diagnose. However, in part due to the lack of symptoms, an individual may not seek evaluation or treatment of HTN. In fact, more than 30% of the hypertensive population in the United States are unaware of their condition.3
The awareness, treatment, and control rates for HTN in the United States between 1999 and 2004 are shown in Table 35-3
. While the 37% HTN control rate in 2004 demonstrates continued improvement, it also clearly indicates a need for increased efforts on the part of health care professionals to better manage the treatment of HTN.3
Accurate BP measurement is essential to classify individuals, to ascertain BP-related risk, and to guide HTN management.66
Proper training of observers, positioning of the patient, and selection of cuff size are all essential. Because an individual’s BP can vary markedly, diagnosis of HTN requires documentation of elevated BP (average of two or more BPs) on at least three separate occasions. Three measures of BP potentially could contribute to the adverse effects of HTN. The first is the average level, the second is the diurnal variation, and the third is the short-term variability. The measure of BP that is most clearly related
to morbid events is the average level, although there is also accumulating evidence that suggests that hypertensive patients whose BP remains high at night (nondippers) are at greater risk for cardiovascular morbidity than dippers.67
Less data are available to define the clinical significance of BP variability, although it has been suggested that it is a risk factor for cardiovascular morbidity.
Table 35-3 ▪ TRENDS IN AWARENESS, TREATMENT, AND CONTROL AMONG PARTICIPANTS WITH HYPERTENSION IN THE U.S. POPULATION, 1999 TO 2004
National Health and Nutrition Examination Survey (%)
† Among all with hypertension
From Ong, K. L., Cheung, B., Man, Y. B., et al. (2007). Prevalence, awareness, treatment, and control of hypertension among United States adults 1999-2004. Hypertension, 49, 69-75.
The recognition of these limitations of the traditional clinic readings has led to two parallel developments: first, increasing use of measurements made out of the clinic, which avoids the unrepresentative nature of the clinic setting and also allows for increased numbers of readings to be taken; and second, the increased use of automated devices, which are being used both in and out of the office setting.66
It is increasingly recognized that office measurements correlate poorly with BP measured in other settings and that they can be supplemented by self-measured readings taken with validated devices at home. There is increasing evidence that home readings predict cardiovascular events and are particularly useful for monitoring the effects of treatment.
Home BP Monitoring.
Home BP monitoring overcomes many of the limitations of traditional office BP measurement and is both cheaper and easier to perform than ambulatory BP monitoring. Monitors using the oscillometric method are currently available and are accurate, reliable, easy to use, and relatively inexpensive. An increasing number of individuals are using them regularly to check their BP at home. Home BP monitoring has been endorsed by national and international guidelines and the American Heart Association recently provided detailed recommendations for their use.68
Home BP monitoring has the potential to improve the quality of care while reducing costs.
White Coat HTN.
Approximately 15% to 20% of people with stage 1 HTN have persistently elevated BP in the presence of a health care worker, particularly a physician. However, when BP is measured elsewhere, including at work, BP is not elevated. When this phenomenon is detected in patients not taking medications, it is referred to as white coat HTN. The commonly used definition is a persistently elevated average office BP of ≥140/90 mm Hg and an average awake ambulatory reading of <135/85 mm Hg.66
Although it can occur at any age, it is more common in older men and women. The phenomenon responsible for white coat HTN is commonly referred to as the white coat effect and is defined as the difference between the office and daytime ambulatory BP; it is present in the majority of hypertensive patients. Its magnitude can be reduced (but not eliminated) by the use of stationary oscillometric devices that automatically determine and analyze a series of BPs over 15 to 20 minutes with the patient in a quiet environment in the office or clinic.
Masked HTN or Isolated Ambulatory HTN.
The converse condition of normal BP in the office and elevated BPs elsewhere, such as at work or at home is somewhat less frequent than white coat HTN but more problematic to detect.66
Lifestyle can contribute to this, for example, alcohol, tobacco, and caffeine consumption and physical activity away from the clinic or office.
The objectives of the medical assessment for HTN are to determine (1) diagnosis and stage of HTN, (2) secondary causes of HTN, (3) presence of TOD, (4) level of global CVD risk, and (5) the plan for individualized monitoring and therapy. The assessment should include a thorough history and physical examination, including orthostatic BP change. Display 35-3
lists many of the important variables to assess during the history and physical examination.69
It is also important to ask the patient about any nontraditional remedies they may be using including herbs, vitamins, and other supplements. Display 35-4
lists the basic and optional laboratory tests recommended by the Joint National Committee on Prevention, Detection and Treatment of Hypertension (JNC 7) for the assessment of TOD.
Secondary HTN, a potentially curable condition, occurs in an estimated 5% to 10% of HTN cases; therefore, clinicians should evaluate for secondary causes (see Display 35-1
Additional evaluation is recommended in patients whose age, severity of HTN, medical history, physical examination, or laboratory findings are suggestive of secondary HTN. Poor response to antihypertensive drug therapy or an accelerated phase of previously well-controlled HTN also indicates a need for further investigation.7
In the vast majority of cases, HTN cannot be cured. The relationship between BP and risk of CVD events is continuous, consistent, and independent of other risk factors.7
For individuals aged 40 to 70 years, each increment of 20 mm Hg in SBP or 10 mm Hg in DBP doubles the risk of CVD across the entire BP range from 115/75 to 185/115 mm Hg.5
The effectiveness of lifestyle and pharmacologic treatment in reducing BP has been demonstrated and substantial evidence indicates that controlling BP in hypertensive patients significantly lowers risk of CV morbidity and mortality.5
A small reduction in BP could markedly reduce the risk of heart failure, stroke, and myocardial infarction.7
The recent improvements in HTN control rates and decreased mean BPs, especially among the older adults, may help to decrease the incidence of strokes and heart attacks, which is highly encouraging.3
The prevention of HTN is a major public health challenge. Many cases of HTN, cardiovascular and renal disease, and stroke might be prevented if the rise in BP with age could be prevented or diminished.7
The six interventions that have been shown to delay or
prevent the onset of HTN are as follows: weight loss, sodium restriction, reduction in alcohol intake, increased exercise, potassium supplementation, and a diet high in fruits and vegetables.74
Efforts to begin the lifestyle habits that prevent the development of HTN should begin during childhood.76
The goal of therapy for patients with HTN is the prevention of morbidity and mortality related to the elevated BP, specifically the prevention of TOD and progression of atherosclerotic cardiovascular and renal disease.7
Factors to consider in making treatment choices are any comorbid conditions, cost of treatment, patient preference, and potential impacts on the individual’s quality of life. Figure 35-1
provides an algorithm for treatment of HTN in adults.7
Treatment options, which will be described in greater detail below, include nonpharmacologic, or lifestyle modifications, and pharmacologic options. Treatment to achieve a goal BP, <140/90 or <130/80 mm Hg among those patients with diabetes mellitus or renal disease, is associated with reductions in CVD morbidity and mortality.
Nonpharmacologic Management of HTN
Adoption of a healthy lifestyle is recommended for all persons for the prevention of HTN and is an indispensable part of the management of those with HTN.7
Well-established lifestyle modifications that lower BP include weight loss, increased physical activity, and dietary modifications including sodium restriction, a diet high in fruits and vegetables and potassium and reduction in alcohol intake.79
A combined approach that aims to balance
energy intake with energy expenditure through a suitable dietary plan and physical activity is effective and an important component of weight loss and weight management. The JNC 7 recommendations for these lifestyle modifications are listed in Table 35-4
In addition, persons with HTN are encouraged to modify their other risk factors for CVD such as dyslipidemia and smoking because of their additive impact on the rate of development and progression of atherosclerosis.
▪ Figure 35-1 Algorithm for treatment of hypertension in adults. ACEI, angiotensin-converting enzyme inhibitor; BB, β-blocker; CCB, calcium channel blocker. (Chobanian, A. V., Bakris G. L., Black, H. R., et al. . The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report. JAMA, 289, 2560-2572. [Erratum in JAMA, 290(2), 197].)
▪ LIFESTYLE MODIFICATIONS TO MANAGE HYPERTENSION*,†
Approximate SBP Reduction (Range)
Maintain normal body weight (body mass index 18.5-24.9 kg/m2).
5-20 mm Hg/10 kg weight loss
Adopt DASH diet plan
Consume a diet rich in fruits, vegetables, and low fat dairy products with a reduced content of saturated and total fat.
8-14 mm Hg
Dietary sodium reduction
Reduce dietary sodium intake to no more than 100 mmol/day (2.4 g sodium or 6 g sodium chloride).
2-8 mm Hg
Engage in regular aerobic physical activity such as brisk walking (at least 30 min/day, most days of the week).
4-9 mm Hg
Moderation of alcohol consumption
Limit consumption to no more than two drinks (1 oz or 30 mL ethanol; e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day in most men and to no more than one drink per day in women and lighter weight persons.
2-4 mm Hg
*For overall cardiovascular risk reduction, stop smoking.
†The effects of implementing these modifications are dose- and time dependent and could be greater for some individuals.
From Chobanian, A. V., Bakris, G. L., Black, H. R., et al. (2003). The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report. JAMA, 289(19), 2560-2572. (Erratum in JAMA, 2003, 290, 197.)
The results of many studies indicate a direct relationship between HTN and obesity.17
There is also a correlation between the presence of excess abdominal adiposity
(defined as an increased waist-to-hip ratio of more than 0.85 in women and 0.95 in men) and the development of HTN, diabetes, dyslipidemia, and increased CHD mortality.83
Studies in Framingham, Massachusetts and Evans County, Georgia revealed that overweight people have from two to three times the risk for HTN compared with persons who are not overweight.17
The exact mechanism by which obesity contributes to HTN is unclear. However, the influence of weight may be related to alterations in cardiovascular, endocrine, and metabolic factors caused by obesity. These alterations include increased cardiac output, increased blood volume, and sodium retention. Research now suggests that adipose tissue acts as a major endocrine organ, secreting bioactive substances which may induce metabolic disorders, such as hyperinsulinemia, insulin resistance, decreased carbohydrate tolerance, and decreased insulin sensitivity.89
Alterations in endothelial function have also been demonstrated in persons who are overweight.90
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