eMedicine Specialties > Nephrology > Hypertension and the Kidney

Hypertension

Author: Albert W Dreisbach, MD, Associate Professor of Medicine, Divison of Nephrology, University of Mississippi Medical Center
Coauthor(s): Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital; Claude Kortas, MD, MEd, FRCP(C), Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada
Contributor Information and Disclosures

Updated: Feb 19, 2010

Introduction

Background

Hypertension is one of the most common worldwide diseases afflicting humans. Because of the associated morbidity and mortality and the cost to society, hypertension is an important public health challenge. Over the past several decades, extensive research, widespread patient education, and a concerted effort on the part of health care professionals have led to decreased mortality and morbidity rates from the multiple organ damage arising from years of untreated hypertension.

Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, health care professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population.

Historical perspectives

Blood pressure was measured for the first time by Stephen Hales in 1773. Hales also described the importance of blood volume in blood pressure regulation. The contribution of peripheral arterioles in maintaining blood pressure, described as "tone," was first described by Lower in 1669 and subsequently by Sénac in 1783. The role of vasomotor nerves in the regulation of blood pressure was observed by such eminent investigators as Claude Bernard, Charles E. Edouard, Charles Brown-Séquard, and Augustus Waller. William Dayliss advanced this concept in a monograph published in 1923. Cannon and Rosenblueth developed the concept of humoral control of blood pressure and investigated pharmacologic effects of epinephrine. Three contributors who advanced the knowledge of humoral mechanisms of blood pressure control are TR Elliott, Sir Henry Dale, and Otto Loew.

Richard Bright, a physician who practiced in the first half of the 19th century, observed the changes of hypertension on the cardiovascular system in patients with chronic renal disease. George Johnson in 1868 postulated that the cause of left ventricular hypertrophy (LVH) in Bright disease was the presence of muscular hypertrophy in the smaller arteries throughout the body. Further clinical pathologic studies by Sir William Gull and HG Sutton (1872) led to further description of the cardiovascular changes of hypertension. Frederick Mahomed was one of the first physicians to systematically incorporate blood pressure measurement as a part of a clinical evaluation.

The recognition of primary, or essential, hypertension is credited to the work of Huchard, Vonbasch, and Albutt. Observations of Janeway and Walhard led to the recognition of target organ damage, which branded hypertension as the "silent killer." The concepts of renin, angiotensin, and aldosterone were advanced by several investigators in the late 19th and early 20th centuries. The names of Irwine, Page, van Slyke, Goldblatt, Laragh, and Tuttle prominently appear throughout the hypertension literature, and their work enhances our understanding of the biochemical basis of essential hypertension. Cushman and Ondetti developed an orally acting converting enzyme inhibitor from snake venom peptides and are credited with the successful synthesis of the modern antihypertensive captopril.

Definition

Defining abnormally high blood pressure is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high blood pressure must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about aggressiveness of treatment or therapeutic interventions.

Based on recommendations of the Seventh Report of the Joint National Committee of Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII), the classification of blood pressure (expressed in mm Hg) for adults aged 18 years or older is as follows*:1

  • Normal† - Systolic lower than 120, diastolic lower than 80
  • Prehypertension - Systolic 120-139, diastolic 80-99
  • Stage 1 - Systolic 140-159, diastolic 90-99
  • Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100

*Based on the average of 2 or more readings taken at each of 2 or more visits after initial screening

†Normal blood pressure with respect to cardiovascular risk is less than 120/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.

Prehypertension, a new category designated in the JNC VII report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modifications are important preventive strategies.

Hypertension may be either essential or secondary. Essential hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 95% of the 50 million American adults with hypertension have essential hypertension, while secondary hypertension accounts for fewer than 5% of the cases. However secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension that requires 4 or more medications to control).

Pathophysiology

Arterial blood pressure is a product of cardiac output and systemic vascular resistance. Therefore, determinants of blood pressure include factors that affect cardiac output and arteriolar vascular physiology. Blood viscosity, vascular wall sheer conditions (rate and stress), and blood flow velocity (mean and pulsatile components) have potential relevance with regard to the regulation of blood pressure in humans by vascular and endothelial function. Furthermore, changes in vascular wall thickness affect the amplification of peripheral vascular resistance in hypertensive patients and result in reflection of waves back to the aorta, increasing systolic blood pressure. Circulating blood volume is regulated by renal salt and water handling, a phenomenon that plays a particularly important role in salt-sensitive hypertension.

Regulation of blood pressure

Regulation of normal blood pressure is a complex process. Although a function of cardiac output and peripheral vascular resistance, both of these variables are influenced by multiple factors.

The factors affecting cardiac output include sodium intake, renal function, and mineralocorticoids; the inotropic effects occur via extracellular fluid volume augmentation and an increase in heart rate and contractility. Peripheral vascular resistance is dependent upon the sympathetic nervous system, humoral factors, and local autoregulation. The sympathetic nervous system produces its effects via the vasoconstrictor alpha effect or the vasodilator beta effect. The humoral actions on peripheral resistance are also mediated by other mediators such as vasoconstrictors (angiotensin and catecholamines) or vasodilators (prostaglandins and kinins).

Autoregulation of blood pressure occurs by way of intravascular volume contraction and expansion regulated by the kidney, as well as via transfer of transcapillary fluid. Through the mechanism of pressure natriuresis, salt and water balance is achieved at heightened systemic pressure, as proposed by Guyton. Interactions between cardiac output and peripheral resistance are autoregulated to maintain a set blood pressure in an individual. For example, constriction of the arterioles elevates arterial pressure by increasing total peripheral resistance, whereas venular constriction leads to redistribution of the peripheral intravascular volume to the central circulation, thereby increasing preload and cardiac output.

Pathogenesis of hypertension

The pathogenesis of essential hypertension is multifactorial and highly complex. Multiple factors modulate the blood pressure for adequate tissue perfusion and include humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. A possible pathogenesis of essential hypertension has been proposed in which multiple factors, including genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension. Although genetics appears to contribute to essential hypertension, the exact mechanism has not been established.

The natural history of essential hypertension evolves from occasional to established hypertension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension, in which target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system is evident. The progression begins with prehypertension in persons aged 10-30 years (by increased cardiac output) to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent) to established hypertension in persons aged 30-50 years, and, finally, to complicated hypertension in persons aged 40-60 years.

One mechanism of hypertension has been described as high-output hypertension. High-output hypertension results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis. A second mechanism manifests with normal or reduced cardiac output and elevated systemic vascular resistance due to increased vasoreactivity. Another (and overlapping) mechanism is increased salt and water reabsorption (salt sensitivity) by the kidney, which increases circulating blood volume.

The vasoreactivity of the vascular bed, an important phenomenon mediating changes of hypertension, is influenced by the activity of vasoactive factors, reactivity of the smooth muscle cells, and structural changes in the vessel wall and vessel caliber, expressed by a lumen-to-wall ratio. Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli. Alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function, are probably responsible for this abnormal behavior of vasculature. Furthermore, vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.

Genetic factors

 Hypertension develops secondary to environmental factors, as well as to multiple genes, whose inheritance appears to be complex.2,3 Very rare secondary causes are related to single genes and include Liddle syndrome, glucocorticoid remediable hyperaldosteronism, 11 beta-hydroxylase and 17 alpha-hydroxylase deficiencies, the syndrome of apparent mineralocorticoid excess, and pseudohypoaldosteronism type II.

Role of the vascular endothelium

The vascular endothelium is presently considered a vital organ, where synthesis of various vasodilating and constricting mediators occurs. The interaction of autocrine and paracrine factors takes place in the vascular endothelium, leading to growth and remodeling of the vessel wall and to the hemodynamic regulation of blood pressure.

Numerous hormonal, humeral vasoactive, and growth and regulating peptides are produced in the vascular endothelium. These mediators include angiotensin II, bradykinin, endothelin, nitric oxide, and several other growth factors. Endothelin is a potent vasoconstrictor and growth factor that likely plays a major role in the pathogenesis of hypertension. Angiotensin II is a potent vasoconstrictor synthesized from angiotensin I with the help of an angiotensin-converting enzyme (ACE). Another vasoactive substance manufactured in the endothelium is nitric oxide. Nitric oxide is an extremely potent vasodilator that influences local autoregulation and other vital organ functions. Additionally, several growth factors are manufactured in the vascular endothelium; each of these plays an important role in atherogenesis and target organ damage. These factors include platelet-derived growth factor, fibroblast growth factor, insulin growth factor, and many others.

Pathophysiology of target organ damage

Hypertension and the cardiovascular system

Cardiac involvement in hypertension manifests as LVH, left atrial enlargement, aortic root dilatation, atrial and ventricular arrhythmias, systolic and diastolic heart failure, and ischemic heart disease. LVH is associated with an increased risk of premature death and morbidity. A higher frequency of cardiac atrial and ventricular dysrhythmias and sudden cardiac death may exist. Possibly, increased coronary arteriolar resistance leads to reduced blood flow to the hypertrophied myocardium, resulting in angina despite clean coronary arteries. Hypertension, along with reduced oxygen supply and other risk factors, accelerates the process of atherogenesis, thereby further reducing oxygen delivery to the myocardium.

Hypertension remains the most common cause of congestive heart failure. Antihypertensive therapy has been demonstrated to significantly reduce the risk of death from stroke and coronary heart disease. Two published meta-analyses have shown 14% and 26% reductions in cardiovascular mortality rates.

Left ventricular hypertrophy

The myocardium undergoes structural changes in response to increased afterload. Cardiac myocytes respond by hypertrophy, allowing the heart to pump more strongly against the elevated pressure. However, the contractile function of the left ventricle remains normal until later stages. Eventually, LVH lessens the chamber lumen, limiting diastolic filling and stroke volume. The left ventricular diastolic function is markedly compromised in long-standing hypertension.

The mechanisms of diastolic dysfunction have been elucidated only recently. An aberration in the passive relaxation of the left ventricle during diastole appears to exist. Over time, fibrosis may occur, further contributing to the poor compliance of the ventricle. As the left ventricle does not relax during early diastole, left ventricular end-diastolic pressure increases, further increasing left atrial pressure in late diastole. The exact determinants of left ventricular diastolic dysfunction have not been well studied; possibly, the abnormality is governed by abnormal calcium kinetics.

The central nervous system

Long-standing hypertension may manifest as hemorrhagic and atheroembolic stroke or encephalopathy. Both the high systolic and diastolic pressures are harmful; a diastolic pressure of more than 100 mm Hg and a systolic pressure of more than 160 mm Hg have led to a significant incidence of strokes. Other cerebrovascular manifestations of complicated hypertension include hypertensive hemorrhage, hypertensive encephalopathy, lacunar-type infarctions, and dementia.

Renal disease

Despite widespread treatment of hypertension in the United States, the incidence of end-stage renal disease continues to rise. The explanation for this rise may be concomitant diabetes mellitus, the progressive nature of hypertensive renal disease despite therapy, or a failure to reduce blood pressure to a protective level. A reduction in renal blood flow in conjunction with elevated afferent glomerular arteriolar resistance increases glomerular hydrostatic pressure secondary to efferent glomerular arteriolar constriction. The result is glomerular hyperfiltration, followed by development of glomerulosclerosis and further impairment of renal function.

Two studies have demonstrated that a reduction in blood pressure may result in improved renal function. Therefore, earlier detection of hypertensive nephrosclerosis using means to detect microalbuminuria and aggressive therapeutic interventions, particularly with ACE inhibitor drugs, may prevent progression to end-stage renal disease.4

Nephrosclerosis is one of the possible complications of long-standing hypertension. The risk of hypertension-induced end-stage renal disease is higher in black patients, even when blood pressure is under good control. Furthermore, patients with diabetic nephropathy who are hypertensive are also at high risk for developing end-stage renal disease.

The renin-angiotensin system activity influences the progression of renal disease. Angiotensin II acts at the afferent and the efferent arterioles, but more so on the efferent arteriole, which leads to an increase of the intraglomerular pressure. The excess glomerular pressure leads to microalbuminuria. Reducing intraglomerular pressure using an ACE inhibitor has been shown to be beneficial in patients with diabetic nephropathy, even in those who are not hypertensive. The beneficial effect of ACE inhibitors on the progression of renal insufficiency in patients who are nondiabetic is less clear. The benefit of ACE inhibitors is greater in patients with more pronounced proteinuria.

Hypertension in renal disease

Hypertension is commonly observed in patients with kidney disease. Volume expansion is the main cause of hypertension in patients with glomerular disease (nephrotic and nephritic syndrome). Hypertension in patients with vascular disease is the result of the activation of the renin-angiotensin system, which is often secondary to ischemia. Most patients with chronic renal failure are hypertensive (80-90%). The combination of volume expansion and the activation of the renin-angiotensin system is believed to be the main factor behind hypertension in patients with chronic renal failure.

Metabolic syndrome

The metabolic syndrome is an assemblage of metabolic risk factors that directly promote the development of atherosclerotic cardiovascular disease.5,6 Dyslipidemia, hypertension, and hyperglycemia are the most widely recognized metabolic risk factors. The combination of these risk factors leads to a prothrombotic, proinflammatory state in humans and identifies individuals who are at elevated risk for atherosclerotic cardiovascular disease.

The predominant underlying risk factors for the metabolic syndrome appear to be abdominal obesity and insulin resistance. Other associated conditions are physical inactivity, aging, hormonal imbalance, and atherogenic diet. Insulin resistance, an essential cause of the metabolic syndrome, predisposes to hyperglycemia and type 2 diabetes mellitus. Individuals who insulin resistant may not be clinically obese, but they commonly have an abnormal fat distribution that is characterized by predominant upper body fat. Upper body obesity can occur either intraperitoneally (visceral fat) or subcutaneously, both of which correlate strongly with insulin resistance and the metabolic syndrome.

The rising prevalence of the metabolic syndrome is secondary to the increasing burden of obesity in our society. The adipose tissue in people who are obese is insulin resistant, raises nonesterified fatty acid levels, alters hepatic metabolism, and produces several adipokines. These include increased production of inflammatory cytokines, plasminogen activator inhibitor-1, and other bioactive products, while the synthesis of potentially protective adipokine, adiponectin, is reduced. This syndrome has been noted to be associated with a state of chronic, low-grade inflammation. Although the metabolic syndrome unequivocally predisposes to type 2 diabetes mellitus, this syndrome is multidimensional risk factor for atherosclerotic cardiovascular disease.

Frequency

United States

Forty-three million people are estimated to have hypertension, defined by a systolic blood pressure of 140 mm Hg or greater and/or diastolic blood pressure of 90 mm Hg or greater or defined as those taking antihypertensive medications. The age-adjusted prevalence of hypertension varies from 18-32%, according to data from the National Health Examination Surveys. According to the National Center for Health Statistic Surveys, the awareness for hypertension increased from 53% in 1960-1962 to 89% in 1988-1991. The percentage of patients engaged in hypertension treatment increased from 35% to 79% during this period.7

  • The National High Blood Pressure Education Program (NHBPEP) has reported estimates of hypertension prevalence in United States.8 The hypertension survey was conducted from 1989-1994, and actual blood pressure and self-reported information was used. Hypertension was defined as systolic blood pressure equal to or more than 140 mm Hg, diastolic blood pressure equal or more than 90 mm Hg, or taking medication for hypertension. The data estimated 43.3 million adults with hypertension in November 1991. The prevalence according to age group, sex, and race is shown in Table 1.

Table 1. Prevalence (%) of Hypertension in the United States, 1989-1994*

Open table in new window

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Table
Age GroupsAll RacesWhiteBlack
Men (%)Women (%)Total (%)Men (%)Women (%)Total (%)Men (%)Women (%)Total (%)
18-242.64.60.72.54.60.52.64.11.4
25-345.48.42.44.98.11.68.210.66.2
35-4413.016.010.211.314.38.525.929.522.9
45-5427.630.025.225.829.122.646.944.348.8
55-6443.744.243.242.143.041.460.058.063.0
65-7459.655.862.758.654.961.771.065.275.6
75+ 70.360.576.269.759.076.175.571.377.9
Total23.423.523.323.223.423.128.127.928.2
Age GroupsAll RacesWhiteBlack
Men (%)Women (%)Total (%)Men (%)Women (%)Total (%)Men (%)Women (%)Total (%)
18-242.64.60.72.54.60.52.64.11.4
25-345.48.42.44.98.11.68.210.66.2
35-4413.016.010.211.314.38.525.929.522.9
45-5427.630.025.225.829.122.646.944.348.8
55-6443.744.243.242.143.041.460.058.063.0
65-7459.655.862.758.654.961.771.065.275.6
75+ 70.360.576.269.759.076.175.571.377.9
Total23.423.523.323.223.423.128.127.928.2

*Includes racial/ethnic groups not shown separately because of small sample sizes

  • A 2005 survey in the United States found that in the population aged 20 years or older, an estimated 41.9 million men and 27.8 million women have prehypertension, 12.8 million men and 12.2 million women have stage 1 hypertension, and 4.1 million men and 6.9 million women have stage 2 hypertension.7 Age- and sex-adjusted rates of prehypertension and stage I hypertension increased among non-Hispanic white, African American, and Hispanic persons between 1988-1992 and 1999-2000. Age- and sex-adjusted rates of stage 2 hypertension decreased among non-Hispanic whites between 1988-1992 and 1999-2000, but they were unchanged for African American and Hispanic persons.9

International

National health surveys in various countries have shown a high prevalence of poor control of hypertension.10 These studies have reported that prevalence of hypertension is 22% in Canada, of which 16% is controlled; 26.3% in Egypt, of which 8% is controlled; and 13.6% in China, of which 3% is controlled. Hypertension is a worldwide epidemic; in many countries, 50% of the population older than 60 years has hypertension. Overall, approximately 20% of the world's adults are estimated to have hypertension. The 20% prevalence is for hypertension defined as blood pressure in excess of 140/90 mm Hg. The prevalence dramatically increases in patients older than 60 years.

Mortality/Morbidity

  • In the Framingham Heart Study, the age-adjusted risk of congestive heart failure was 2.3 times higher in men and 3 times higher in women when highest blood pressure was compared to the lowest.11 Multiple Risk Factor Intervention Trial (MRFIT) data showed that the relative risk for coronary heart disease mortality varied from 2.3-6.9 times higher for persons with mild to severe hypertension compared to persons with normal blood pressure.12
  • The relative risk for stroke ranged from 3.6-19.2. The population-attributable risk percentage for coronary artery disease varied from 2.3-25.6%, whereas the population-attributable risk for stroke ranged from 6.8-40%.

Race

Blacks have a higher prevalence and incidence of hypertension than whites.13 The prevalence of hypertension was increased by 50% in African Americans. In Mexican Americans, the prevalence and incidence of hypertension is similar to or lower than in whites. The National Health and Nutrition Examination Survey (NHANES) III reported an age-adjusted prevalence of hypertension at 20.6% in Mexican Americans and 23.3% in non-Hispanic whites.9

  • Are there ethnic differences in the pathogenesis of hypertension, and do these differences influence the choice of treatment? To understand ethnic influence, an understanding of the renin angiotensin system is essential. Renin secretion is suppressed when the kidney detects that the amount of sodium excretion is increased; thus, a clue to the excess sodium in the circulation. Black people tend to develop hypertension at an earlier age and have lower renin activity; target organ damage also differs in black people from that in white people.
  • Most studies in the United Kingdom and the United States report a higher prevalence and lower awareness of hypertension in black people than in white people. Mortality from hypertension in African-Caribbean–born people is 3.5 times the national rate; similar data have been published for African American citizens. Strokes are more common in black people, but coronary heart disease is more common in Asians. Both groups have a higher incidence of chronic renal failure than white people, but this is more due to hypertension in black people and diabetes in Asians.
  • Black people have a poorer response to treatment with ACE inhibitors compared to white people; the evidence for beta-blockers being less effective in black people is also clear. However, diuretics are more effective at a young age in black people.

Sex

The age-adjusted prevalence of hypertension was 34%, 25.4%, and 23.2% for men and 31%, 21%, and 21.6% for women among African Americans, whites, and Mexican Americans, respectively. In the NHANES III study, the prevalence of hypertension was 12% for white men and 5% for white women aged 18-49 years. However, the age-related blood pressure rise for women exceeds that of men. The prevalence of hypertension was reported at 50% for white men and 55% for white women aged 70 years or older.9

Age

A progressive rise in blood pressure with increasing age is observed. The third NHANES survey reported that the prevalence of hypertension grows significantly with increasing age in all sex and race groups. The age-specific prevalence was 3.3% in white men (aged 18-29 y); this increased to 13.2% in the group aged 30-39 years. The prevalence further increased to 22% in the group aged 40-49 years, to 37.5% in the group aged 50-59 years, and to 51% in the group aged 60-74 years. In another study, the incidence of hypertension appeared to increase approximately 5% for each 10-year interval of age. Age-related hypertension appears to be predominantly systolic rather than diastolic. The systolic blood pressure rises into the eighth or ninth decade, while the diastolic blood pressure remains constant or declines after age 40 years.9

Clinical

History

  • Following the documentation of hypertension, which is confirmed after an elevated blood pressure, properly measured, has been documented on at least 3 separate occasions (based on the average of 2 or more readings taken at each of 2 or more visits after initial screening), a detailed history should extract the following information:
    • Extent of target organ damage
    • Assessment of patients' cardiovascular risk status
    • Exclusion of secondary causes of hypertension
  • Patients may have undiagnosed hypertension for years without having had their blood pressure checked. Therefore, a careful history of end organ damage should be obtained.
  • A history of cardiovascular risk factors includes hypercholesterolemia, diabetes mellitus, and tobacco use (including chewing tobacco).
  • Obtain a history of the patient's use of over-the-counter medications and herbal medicines, such as herbal tea containing licorice, ephedrine, current and previous unsuccessful antihypertensive medication trials, oral contraceptives, ethanol, and illicit drugs, such as cocaine.
  • The historical and physical findings that suggest the possibility of secondary hypertension are a history of known renal disease, abdominal masses, anemia, and urochrome pigmentation.
  • A history of sweating, labile hypertension, and palpitations suggests the diagnosis of pheochromocytoma.
  • A history of cold or heat tolerance, sweating, lack of energy, and bradycardia or tachycardia may indicate hypothyroidism or hyperthyroidism.
  • A history of obstructive sleep apnea
  • A history of weakness suggests hyperaldosteronism.
  • Kidney stones raise the possibility of hyperparathyroidism.

Physical

An accurate measurement of blood pressure is the key to diagnosis. Several determinations should be made over a period of several weeks.

At any given visit, an average of 3 blood pressure readings taken 2 minutes apart using a mercury manometer is preferable. Blood pressure should be measured in both the supine and sitting positions, auscultating with the bell of the stethoscope. On the first visit, blood pressure should be checked in both arms and in one leg to avoid missing the diagnosis of coarctation of aorta or subclavian artery stenosis.

As the improper cuff size may influence blood pressure measurement, a wider cuff is preferable, particularly if the patient's arm circumference exceeds 30 cm.

The patient should rest quietly for at least 5 minutes before the measurement.

Although somewhat controversial, the common practice is to document phase V (a disappearance of all sounds) of Korotkoff sounds as the diastolic pressure.

Ambulatory blood pressure monitoring provides a more accurate prediction of cardiovascular risk than does office blood pressure.14

"Non-dipping" is the loss of the usual physiologic nocturnal drop in blood pressure and is associated with an increased cardiovascular risk.

Home blood pressure predicts cardiovascular events much better than do office readings and can be a useful clinical tool.

  • A funduscopic evaluation of the eyes should be performed to detect any evidence of hypertensive retinopathy. These are flame-shaped hemorrhages and cotton wool exudates.
  • Palpation of all peripheral pulses should be performed. Absence of femoral pulses suggests coarctation of the aorta or severe peripheral vascular disease.
  • Look for renal artery bruit over the upper abdomen; the presence of a unilateral bruit with both a systolic and diastolic component suggests renal artery stenosis.
  • A careful cardiac examination is performed to evaluate signs of LVH. These include displacement of apex, a sustained and enlarged apical impulse, and the presence of an S4. Occasionally, a tambour S2 is heard with aortic root dilatation.

Causes

More on Hypertension

Overview: Hypertension
Differential Diagnoses & Workup: Hypertension
Treatment & Medication: Hypertension
Follow-up: Hypertension
References
Further Reading
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References

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Further Reading

Clinical guidelines:
ACR Appropriateness Criteria® renovascular hypertension. American College of Radiology - Medical Specialty Society. 1995 (revised 2007). 9 pages. NGC:006003

American Association of Clinical Endocrinologists medical guidelines for clinical practice for the diagnosis and treatment of hypertension. American Association of Clinical Endocrinologists - Medical Specialty Society. 2006 Mar-Apr. 30 pages. NGC:005007

Diagnosis and classification. In: Diagnosis, evaluation and management of the hypertensive disorders of pregnancy. Society of Obstetricians and Gynaecologists of Canada - Medical Specialty Society. 2008 Mar. 7 pages. NGC:006792

Pulmonary hypertension/Eisenmenger physiology. In: ACC/AHA 2008 guidelines for the management of adults with congenital heart disease. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). American College of Cardiology Foundation - Medical Specialty Society
American Heart Association - Professional Association. 2008. 23 pages. NGC:007067

The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. National Heart, Lung, and Blood Institute (U.S.) - Federal Government Agency [U.S.]. 2004 Aug. 22 pages. NGC:003761

Treatment of the hypertensive disorders of pregnancy. In: Diagnosis, evaluation and management of the hypertensive disorders of pregnancy. Society of Obstetricians and Gynaecologists of Canada - Medical Specialty Society. 2008 Mar. 13 pages. NGC:006812

Clinical trials:
Early, Simple and Reliable Detection of Pulmonary Arterial Hypertension (PAH) in Systemic Sclerosis (SSc) (DETECT)

Effect of High Blood Pressure and Antihypertensive Treatment on Brain Functioning in Children

High Blood Pressure Strategy (HBPS)

Pharmacogenomics in Pulmonary Arterial Hypertension

SPHERE Hypertension Intervention Study

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Keywords

hypertension, high blood pressure, HBP, angiotensin, left ventricular hypertrophy, LVH, peripheral vascular disease, angiotensin II, hypercholesterolemia, essential hypertension, angiotensin I, intracranial hypertension, hypertensive hemorrhage, hypertensive encephalopathy, hypertensive nephrosclerosis, subclavian artery stenosis, hypertensive retinopathy, renal artery stenosis

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Contributor Information and Disclosures

Author

Albert W Dreisbach, MD, Associate Professor of Medicine, Divison of Nephrology, University of Mississippi Medical Center
Disclosure: Nothing to disclose.

Coauthor(s)

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Claude Kortas, MD, MEd, FRCP(C), Program Director, Associate Professor, Department of Medicine, University of Western Ontario, Canada
Claude Kortas, MD, MEd, FRCP(C) is a member of the following medical societies: American Society of Nephrology, College of Physicians and Surgeons of Ontario, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada
Disclosure: Nothing to disclose.

Medical Editor

L Michael Prisant, MD, FACC, Director of Hypertension and Clinical Pharmacology Unit, Professor of Medicine, Department of Medicine, Medical College of Georgia
L Michael Prisant, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Clinical Pharmacology, American College of Forensic Examiners, American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Abbott Grant/research funds Investigator; Boehringer-Ingelheim Grant/research funds Other; Eli Lilly None Investigator; Novartis None Investigator; Abbott, Boehringer-Ingelheim, Forest, Gilead, Merck, Merck/Schering-Plough, Novartis, Oscient, Sciele, SunTech Medical Consulting fee Consulting; Abbott, Boehringer-Ingelheim, Merck, Merck/Schering-Plough, Novartis, Oscient Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

George R Aronoff, MD, Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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