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 Sรฉnac 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-Sรฉquard, 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 T.R. 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 H.G. 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*:
- 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 American adults have essential hypertension, while secondary hypertension accounts for fewer than 5% of the cases.
Pathophysiology
Arterial blood pressure is a product of cardiac output and systemic vascular resistance. Therefore, determinants of blood pressure include factors that affect both cardiac output and arteriolar vascular physiology. There is potential relevance of blood viscosity, vascular wall sheer conditions (rate and stress), and blood flow velocity (mean and pulsatile components) on vascular and endothelial function regulating blood pressure in humans. 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.
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). For additional resource, please visit Angiotensin II Receptor Blockade.
Autoregulation of blood pressure occurs by way of intravascular volume contraction and expansion, as well as by transfer of transcapillary fluid. 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 hypotension. 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.
The early stage 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. In contrast, the chronic phase of essential hypertension characteristically has normal or reduced cardiac output and elevated systemic vascular resistance.
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
Click Here!Hypertension is likely to be related to multiple genes. Hypertension develops secondary to multiple environmental factors, as well as to several genes, whose inheritance appears to be complex. Very rare secondary causes are related to single genes.
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.
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 the 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 both 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.
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. 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. Recently, 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.
- The National High Blood Pressure Education Program (NHBPEP) has reported estimates of hypertension prevalence in United States. 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*
| Age Groups | All Races | White | Black |
|---|
| Men (%) | Women (%) | Total (%) | Men (%) | Women (%) | Total (%) | Men (%) | Women (%) | Total (%) |
| 18-24 | 2.6 | 4.6 | 0.7 | 2.5 | 4.6 | 0.5 | 2.6 | 4.1 | 1.4 |
| 25-34 | 5.4 | 8.4 | 2.4 | 4.9 | 8.1 | 1.6 | 8.2 | 10.6 | 6.2 |
| 35-44 | 13.0 | 16.0 | 10.2 | 11.3 | 14.3 | 8.5 | 25.9 | 29.5 | 22.9 |
| 45-54 | 27.6 | 30.0 | 25.2 | 25.8 | 29.1 | 22.6 | 46.9 | 44.3 | 48.8 |
| 55-64 | 43.7 | 44.2 | 43.2 | 42.1 | 43.0 | 41.4 | 60.0 | 58.0 | 63.0 |
| 65-74 | 59.6 | 55.8 | 62.7 | 58.6 | 54.9 | 61.7 | 71.0 | 65.2 | 75.6 |
| 75+ | 70.3 | 60.5 | 76.2 | 69.7 | 59.0 | 76.1 | 75.5 | 71.3 | 77.9 |
| Total | 23.4 | 23.5 | 23.3 | 23.2 | 23.4 | 23.1 | 28.1 | 27.9 | 28.2 |
*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. 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.
International
National health surveys in various countries have shown a high prevalence of poor control of hypertension. 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. 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.
- 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. 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.
- 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 rennin 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.
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.1
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 over-the-counter medication use, current and previous unsuccessful antihypertensive medication trials, and ethanol intake.
- 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 weakness suggests hyperaldosteronism. Abdominal bruit suggests the possibility of renal artery stenosis. Absence of femoral pulses suggests coarctation of aorta.
- Kidney stones raise the possibility of hyperparathyroidism. The presence of papilledema and other neurologic signs raises the possibility of increased intracranial pressure. A history of drug ingestion, including oral contraceptives, licorice, and sympathomimetics, should be obtained.
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.
- 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.
- 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
- Primary or essential hypertension (90-95%)
- Secondary hypertension: A small percentage of patients (2-10%) have a secondary cause. The following is a list of secondary causes of hypertension:
- Renal (2.5-6%)
- Renal parenchymal disease
- Polycystic kidney disease
- Urinary tract obstruction
- Renin-producing tumor
- Liddle syndrome
- Renovascular hypertension (0.2-4%)
- Vascular
- Coarctation of aorta
- Vasculitis
- Collagen vascular disease
- Endocrine (1-2%) - Oral contraceptives
- Adrenal
- Primary aldosteronism
- Cushing syndrome
- Pheochromocytoma
- Congenital adrenal hyperplasia
- Hyperthyroidism and hypothyroidism
- Hypercalcemia
- Hyperparathyroidism
- Acromegaly
- Neurogenic
- Brain tumor
- Bulbar poliomyelitis
- Intracranial hypertension
- Pregnancy-induced hypertension
- Drugs and toxins
- Alcohol
- Cocaine
- Cyclosporin
- Erythropoietin
- Adrenergic medications
Adrenal Adenoma
Aortic Coarctation
Aortic Dissection
Apnea, Sleep
Atherosclerosis
Atherosclerotic Disease of the Carotid Artery
Cardiomyopathy, Cocaine
Cardiomyopathy, Hypertrophic
Hyperaldosteronism, Primary
Hypertension and Pregnancy
Hypertension, Malignant
Hypertensive Heart Disease
Hyperthyroidism
Obstructive Sleep Apnea-Hypopnea Syndrome
Pheochromocytoma
Renal Artery Stenosis
Lab Studies
- Unless a secondary cause for hypertension is suspected, only the following routine laboratory studies should be performed:
- CBC count, serum electrolytes, serum creatinine, serum glucose, uric acid, and urinalysis
- Lipid profile (total cholesterol, low-density lipoprotein [LDL] and high-density lipoprotein [HDL], and triglycerides)
- Additional tests described below are indicated when specific clinical situations warrant further investigation.
- Microalbuminuria is an early indication of hypertensive nephrosclerosis and is also a marker for a higher risk of cardiovascular morbidity and mortality. Present recommendations suggest that individuals with type I diabetes should be screened for microalbuminuria. Usefulness of this screening in hypertensive patients without diabetes has not been established.
- Plasma renin activity (PRA) is performed to detect evidence of primary hyperaldosteronism. Low renin values confirm the diagnosis of primary hyperaldosteronism; however, hypokalemia may be associated with a form of hypertension, but it is not often present.
- Determination of sensitive thyroid-stimulating hormone (TSH) level excludes hypothyroidism or hyperthyroidism as a cause of hypertension.
Imaging Studies
- Echocardiography: The limited echocardiography study, rather than the complete examination, may detect LVH more frequently than electrocardiography. The main indication for limited echocardiography is evaluation for end organ damage in a patient with borderline high blood pressure. Therefore, the presence of LVH despite normal or borderline high blood pressure measurements requires antihypertensive therapy.
- Imaging studies for renovascular stenosis: If the history suggests renal artery stenosis and if a corrective procedure is considered, further radiologic investigations are performed.
Other Tests
- Routine testing includes electrocardiograms.
- Ambulatory blood pressure monitoring: Indications for ambulatory blood pressure monitoring include labile blood pressure, a discrepancy between blood pressure measurement inside and outside the physician's office, and poor blood pressure control. Ambulatory monitoring also identifies patients who have the distinct syndrome called white coat hypertension.
Medical Care
Consider lifestyle modifications. As the cardiovascular disease risk factors are assessed in individuals with hypertension, pay attention to the lifestyles that favorably affect blood pressure level and reduce overall cardiovascular disease risk. A relatively small reduction in blood pressure may affect the incidence of cardiovascular disease on a population basis. A decrease in blood pressure of 2 mm Hg reduces the risk of stroke by 15% and the risk of coronary artery disease by 6% in a given population.
JNC VII recommendations to lower blood pressure and decrease cardiovascular disease risk include the following:
- Lose weight if overweight.
- Limit alcohol intake to no more than 1 oz (30 mL) of ethanol (ie, 24 oz [720 mL] of beer, 10 oz [300 mL] of wine, 2 oz [60 mL] of 100-proof whiskey) per day or 0.5 (15 mL) ethanol per day for women and people of lighter weight.
- Increase aerobic activity (30-45 min most days of the week).
- Reduce sodium intake to no more than 100 mmol/d (2.4 g sodium or 6 g sodium chloride).
- Maintain adequate intake of dietary potassium (approximately 90 mmol/d).
- Maintain adequate intake of dietary calcium and magnesium for general health.
- Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.
Clinical trials
Multiple clinical trials suggest that most antihypertensive drugs provide the same degree of cardiovascular protection for the same level of blood pressure control. Well-designed prospective randomized trials, such as the Swedish Trial in Old Patients with Hypertension (STOP-2), the Nordic Diltiazem (NORDIL) trial, and the Intervention as a Goal in Hypertension Treatment (INSIGHT) trial, have shown a similar outcome with older drugs (eg, diuretics, beta-blockers) compared to the newer antihypertensive agents (eg, ACE inhibitors, calcium channel blockers).
No consensus exists regarding optimal drug therapy for treatment of hypertension; most clinicians recommend initiating therapy with a single agent and advancing to the low-dose combination therapy. Any of the first-line medications decrease blood pressure in 40-60% of patients with mild-to-moderate hypertension. In unresponsive patients, switching to a second drug (rather than combining it with the first drug) or switching to a third drug if the second drug is not effective may allow a 70-80% response rate to monotherapy. Therefore, attempt to identify a particular class of drug to which the patient responds rather than adding multiple drugs (as in combination therapy).
The JNC VII report recommends either a thiazide diuretic or a beta-blocker as the initial therapy of uncomplicated hypertension. A low dose of thiazide diuretic (12.5-25 mg hydrochlorothiazide) is a low-cost therapy with fewer complications, and it provides equivalent cardiovascular protection. Patients unresponsive to low-dose thiazide therapy should try an ACE inhibitor, beta-blocker, or calcium channel blocker, sequentially. Patients unresponsive to a diuretic may not respond to a calcium channel blocker, and an ACE inhibitor or a beta-blocker should be tried as a second-line agent in these patients. Calcium channel blocking agents and diuretics may be more effective in hypertensive black patients.
Initial therapy based on the JNC VII report recommendations is as follows:
- Prehypertension (systolic 120-139, diastolic 80-89): No antihypertensive drug is indicated.
- Stage 1 hypertension (systolic 140-159, diastolic 90-99): Thiazide-type diuretics are recommended for most. ACE inhibitor, angiotensin II receptor blocker (ARB), beta-blocker, calcium channel blocker, or combination may be considered.
- Stage 2 hypertension (systolic more than 160, diastolic more than 100): Two-drug combination (usually thiazide-type diuretic and ACE inhibitor or ARB or beta-blocker or calcium channel blocker) is recommended for most.
- For the compelling indications, other antihypertensive drugs (eg, diuretics, ACE inhibitor, ARB, beta-blocker, calcium channel blocker) may be considered as needed.
Randomized trials
Two randomized controlled trials, the Hypertension Detection and Follow-up Program (HDFP) and the Medical Research Council (MRC) trials, randomized patients with elevated levels of diastolic blood pressure to either diuretic-based stepped-care treatment or usual care. The usual care group received some form of therapy from their own physicians, whereas the stepped-care group received systematic care. In both studies, stepped-care treatment reduced diastolic blood pressure by 5 mm more than that reduced in the control group. Both trials showed a benefit from stepped-care therapy compared to the control group. In the HDFP trial, stepped-care led to relative risk reduction of 17% for total mortality; 76 hypertensive patients needed to be treated with stepped-care therapy for 5 years to prevent one death.
A meta-analysis published in the Journal of the American Medical Association (JAMA) in 1997 included several randomized controlled clinical trials. The total number of participants randomized to active therapy was 24,294, and the number for the control therapy was 23,926. Active treatment reduced diastolic blood pressure by at least 5 mm Hg. The meta-analysis showed a risk reduction of coronary heart disease of 8-14% and the reduction in stroke incidence of 35-40%. Subsequent meta-analysis reported that benefits of active treatment are similar in men and women.
Recommendations for management of hypertension
The JNC recommends certain situations for which a specific class of drug may be administered. An ACE inhibitor should be the initial treatment in situations in which hypertension is associated with congestive heart failure, diabetes mellitus with proteinuria, and postmyocardial infarction with systolic left ventricular dysfunction. In patients who develop persistent cough while on ACE inhibitor therapy, an angiotensin II receptor antagonist may be substituted, but these agents' efficacy in lowering cardiovascular mortality rates has not yet been proven. A beta-blocker should be prescribed following an acute myocardial infarction. A diuretic or a long-acting calcium channel blocker may be more effective in elderly patients with isolated systolic hypertension.
The 2004 Canadian Hypertension Society recommendations (similar to JNC VII guidelines) for the management of hypertension in specific patient groups are listed in Table 2 and Table 3, as follows:
Table 2. Synopsis of Considerations in the Use of Antihypertensive Drug Classes*
| Class of Medication | When to Use | When Not to Use |
|---|
| Diuretics | Loop diuretics | Renal insufficiency (additional therapy) | Gout |
| Potassium-sparing | Primary hyperaldosteronism (additional therapy in combination with thiazide diuretics) | Renal insufficiency |
| Thiazides | Uncomplicated hypertension (preferred therapy), systolic hypertension in elderly people (preferred therapy), for older diabetic patients without nephropathy | Gout, dyslipidemia (high-dose) |
| Beta-adrenergic antagonists | Post–myocardial infarction, uncomplicated hypertension (preferred therapy), diabetes (without nephropathy) | Asthma, peripheral vascular disease (severe) |
| ACE inhibitors | Diabetes, post–myocardial infarction, heart failure, renal disease, uncomplicated hypertension (preferred therapy) | Bilateral renovascular disease, pregnancy |
| Angiotensin II antagonists | Diabetes (alternative therapy), heart failure (alternative therapy), uncomplicated hypertension (preferred therapy) | Bilateral renovascular disease, pregnancy |
| Calcium channel blockers | Nondihydropyridines | Uncomplicated hypertension (alternative therapy) | Heart block, heart failure |
| Dihydropyridines | Systolic hypertension (preferred therapy), uncomplicated therapy (alternative therapy) | Heart block, heart failure |
| Alpha-adrenergic antagonists/central acting agents | Uncomplicated hypertension (alternative therapy) | Autonomic dysfunction |
*CMAJ 1999, 161:S1-S22
Table 3. Considerations in the Individualization of Antihypertensive Therapy*
| Risk Factor/Disease | Preferred Therapy | Alternative Therapy | Avoid Therapy |
|---|
| Uncomplicated hypertension (<60> | Low-dose thiazidelike diuretics, beta-blockers, ACE inhibitors, or long-acting dihydropyridine calcium channel blockers | Combinations of first-line drugs | … |
| Uncomplicated hypertension (³60 y) | Low-dose thiazidelike diuretics, ACE inhibitors, or long-acting dihydropyridine calcium channel blockers | Combinations of first-line drugs | … |
| Dyslipidemia | As for uncomplicated hypertension | … | … |
| Diabetes mellitus with nephropathy | ACE inhibitors | Angiotensin II receptor blockers | High-dose diuretics and centrally acting agents (in the setting of autonomic neuropathy) |
| Diabetes mellitus without nephropathy | ACE inhibitors or beta-blockers | … | … |
| Diabetes mellitus without nephropathy, with systolic hypertension | Low-dose thiazidelike diuretics or long-acting dihydropyridine calcium channel blockers | … | … |
| Angina | Beta-blockers (ACE inhibitors as add-on therapy) | Long-acting calcium channel blockers | … |
| Prior myocardial infarction | Beta-blockers, ACE inhibitors | … | … |
| Systolic dysfunction | ACE inhibitors (thiazide or loop diuretics, beta-blockers, spironolactone is additive therapy) | Angiotensin II receptor blockers, hydralazine/isosorbide dinitrate, amlodipine | Nondihydropyridine calcium channel blockers (diltiazem, verapamil) |
| Left ventricular hypertrophy | Most antihypertensives reduce LVH | … | Hydralazine, minoxidil |
| Peripheral arterial disease | As for uncomplicated hypertension | As for uncomplicated hypertension | Beta-blockers (with severe disease) |
| Renal disease | ACE inhibitors (diuretics as additive therapy) | Dihydropyridine calcium channel blockers | ACE inhibitors in cases of bilateral renal artery stenosis |
*Short-acting calcium channel blockers are not recommended in the treatment of hypertension
Several situations demand the addition of a second drug because 2 drugs may be used at lower doses to avoid adverse effects, which may occur with higher doses of an individual agent. Diuretics generally potentiate the effects of other antihypertensive drugs by minimizing volume expansion. Specifically, the use of the diuretic thiazide in conjunction with a beta-blocker or an ACE inhibitor has an additive effect, controlling blood pressure in up to 85% of patients.
Most drug combinations using agents that act by different mechanisms have an additive effect. The combination of a calcium channel blocker with either an ACE inhibitor or a dihydropyridine calcium channel blocker and a beta-blocker has additive effects. An ACE inhibitor may be combined with an angiotensin II receptor antagonist because the blocking of angiotensin I receptors may lead to increased plasma angiotensin II concentration, which may compete with a drug for the receptor. Some combinations may not be additive, including a beta-blocker and ACE inhibitor, a beta-blocker and an alpha1-blocker and an alpha2 stimulant, and, more controversially, a diuretic and a calcium channel blocker. Some combinations may have additive adverse effects; these include a beta-blocker combined with verapamil or diltiazem, which leads to cardiac depression, bradycardia, or heart block.
Clinical trials have shown that the effective control of blood pressure reduces the risk of cardiovascular events in high-risk patients. In the patients who achieved optimal blood pressure control compared with those with uncontrolled hypertension, significant reductions in the incidence of cardiac events, stroke, and all-cause mortality occurred (according to the Valsartan Antihypertensive Long-term Use Evaluation [VALUE] Trial). The lack of significant difference in cardiovascular mortality and morbidity among patients receiving diuretics, calcium channel blockers, or ACE inhibitors in the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) possibly occurred due to confounding because of differences in the blood pressure reductions achieved with the 3 treatments.
Recent studies have consistently shown that newer antihypertensive agents, such as ACE inhibitors and calcium channel blockers, reduce cardiovascular events to a similar, or possibly greater, extent as older therapies, such as diuretics and beta-blockers. ACE inhibitors specifically offer additional benefits beyond blood pressure reduction, which include reduction of cardiovascular events and renal protection. Similarly, ARBs have demonstrated beneficial effects in heart failure, stroke, and renal protection.
- Key messages of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) are as follows:
- In those older than 50 years, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease risk factor than diastolic BP.
- Beginning at 115/75 mm Hg, the cardiovascular disease risk doubles for each increment of 20/10 mm Hg.
- Individuals who are normotensive at 55 years will have a 90% lifetime risk of developing hypertension.
- Prehypertension (systolic 120-139, diastolic 80-89) requires health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and cardiovascular disease.
- In uncomplicated hypertension, a thiazide diuretic, either alone or combined with drugs from other classes, should be used for the drug treatment of most.
- In specific high-risk conditions, there are compelling indications for the use of other antihypertensive drug classes (eg, ACE inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers).
- Two or more antihypertensive medications will be required to achieve goal BP (<140/90>
- For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using 2 agents, one of which usually will be a thiazide diuretic, should be considered.
- Regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan.
- Resistant hypertension: Some patients may have persistent diastolic blood pressures above 100 mm Hg despite the use of 3 or more antihypertensive medications. These patients may be experiencing of the following factors as the cause of resistant hypertension:
- Inadequate treatment was described as the most common cause of resistant hypertension in several published series. Patients may not be on an effective drug, or concomitant volume expansion may occur as a side effect of the drug.
- Extracellular volume expansion: Volume expansion may contribute to the inability to lower systemic blood pressure. The volume expansion may occur because of renal insufficiency, sodium retention due to treatment with vasodilators, high-salt diet, or insufficient dosing of diuretic. This situation can be treated with more aggressive diuretic therapy until clinical signs of extracellular volume depletion (eg, orthostatic hypotension) develop.
- Poor compliance: Noncompliance with medical therapy or dietary modifications (eg, salt restriction) may play a role in causing resistant hypertension. Address noncompliance with extensive patient education, simplification of the drug regimen, and use of drugs with the fewest adverse effects.
- Secondary hypertension: Whenever confronted with resistant hypertension, try to exclude any secondary causes of hypertension. A reevaluation of the patient's history, physical examination, and laboratory results may provide clues to secondary hypertension (eg, renal artery stenosis, primary hyperaldosteronism).
- White coat hypertension: Blood pressure rise secondary to anxiety may be observed in 20-30% of patients. This may be avoided by having patients rest prior to measurement, having a nurse check the blood pressure, or arranging to have the blood pressure monitored at home. Development of hypotensive symptoms on medications is an indication of white coat hypertension. White coat hypertension can also be evaluated by the use of a 24-hour ambulatory monitor.
- Pseudohypertension may be observed in elderly individuals who have thickened, calcified arteries. Much higher cuff pressure may be required to occlude a thickened brachial artery, and diastolic pressure may also be overestimated. Consider pseudohypertension in situations in which no organ damage occurs despite marked hypertension, when patients develop hypotensive systems on medications, and when calcification of the brachial artery is observed on radiologic examination. Direct measurement of intra-arterial pressure may be required in this setting.
- Vasoactive substances: Resistant hypertension may be encountered in patients who are ingesting vasoactive substances despite taking antihypertensive drugs regularly. Use of salt and alcohol are the common examples; others include use of cocaine, amphetamines, anabolic steroids, oral contraceptives, cyclosporine, antidepressants, and nonsteroidal anti-inflammatory drugs.
- Hypertension in special populations
- Age
- The systolic pressure continues to progressively rise throughout life, reaching the highest levels in later stages of life. Isolated systolic hypertension may be present in 10% of the population aged 70 years and in 24% of those aged 80 years. Furthermore, severe arteriosclerosis may lead to pseudohypertension. Isolated hypertension results in low cardiac output because of the decreased stroke volume and high peripheral resistance. This may reduce glomerular filtration further, which is why low activity of renal angiotensin aldosterone cascade is encountered in elderly individuals who are hypertensive.
- Despite low PRA, blood pressure responds well to ACE inhibitor and angiotensin receptor inhibitor therapy. Low doses of diuretics may also be effective. Calcium antagonists are quite useful because of their strong antihypertensive effects. Often, combining 2 drugs at a lower dose may be preferable to using a single drug at a high dose that has the potential for adverse effects.
- Sex: The prevalence of hypertension is similar between men and women, but women are protected from coronary heart disease prior to menopause. Premenopausal women have a higher resting heart rate, a higher cardiac index, and a lower peripheral resistance than men. These changes are not encountered in postmenopausal females. Therefore, in premenopausal situations, a medication such as beta-blocker may be effective. However, postmenopausal hypertension is treated similarly to that in men.
- Race
- Blacks have a higher prevalence of hypertension and a much higher frequency of end organ damage, such as occurs in end-stage renal disease, strokes, and heart failure. Black patients also develop more severe LVH than white patients. Renal function in hypertensive black patients continues to deteriorate over time despite aggressive management of the blood pressures.
- Black patients respond less well to beta-blockers, ACE inhibitors, and angiotensin receptor blockers than white patients. At times, this relative lack of efficacy may be overcome by increasing the dosage of the medications. Blacks may respond well to treatment with calcium antagonists, diuretics, and postsynaptic alpha-blockers.
- Obesity
- Hypertensive patients who are obese have a higher cardiac output and a lower peripheral vascular resistance than hypertensive patients who are not obese. The increase in cardiac output manifests secondary to increased preload. The end-diastolic volume and pressure are elevated, leading to left ventricular dilatation. Left ventricular wall thickening also occurs secondary to increased afterload, which increases the risk of congestive heart failure. The concomitant diabetes often present in patients who are obese produces a devastating effect on kidneys and leads to a much higher incidence of renal failure.
- No class of drugs seems to be of particular advantage in hypertensive patients who are obese, but thiazide diuretics may be helpful, unless the patient also has coexisting diabetes. In patients who are diabetic and who may have microalbuminuria, ACE inhibitors or calcium antagonists are recommended because they may slow declining renal function. Because of the high preload and afterload, drugs that have negative inotropic effects, such as beta-blockers, should be avoided.
- The management of secondary hypertension may result in cure by the surgical correction of the underlying problem, such as removal of a pheochromocytoma. Surgery may not be feasible in a substantial number of patients for whom medical therapy is instituted to control hypertension.
- Renovascular hypertension
- The goals of therapy are maintenance of normal blood pressure and prevention of end-stage renal disease. The therapeutic options include medical therapy, percutaneous transluminal renal angioplasty, and surgical revascularization. These options must be individualized because no randomized studies document the superiority of one option over the other. The indications for surgery or angioplasty include an inability to control blood pressure while on a medical regimen, the need to preserve renal function, and intolerable effects of medical therapy.
- Aortal renal bypass using saphenus vein or hypogastric artery is a common revascularization technique. A synthetic graft has also been used. Percutaneous transluminal renal angioplasty (PTRA) can be effective treatment for both hypertension and preservation of renal function. PTRA may be the initial choice in younger patients with fibromuscular lesions amenable to balloon angioplasty. Renal artery stenting of osteal lesions has been associated with improved long-term patency. PTRA may also be used for arthrosclerotic renal artery stenosis; the outcome may be comparable to surgical revascularization. Medical therapy is required in the preoperative phase of interventional therapy. Medical therapy is also indicated for high-risk individuals and for older patients who have easily controlled hypertension.
- ACE inhibitors are quite effective in patients with unilateral renal artery stenosis; however, avoid ACE inhibitors in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. A diuretic can be combined with an ACE inhibitor. Because of their glomerular vasodilatory effect, calcium antagonists are effective in renal artery stenosis and do not compromise renal function.
- Pheochromocytoma
- Following suspicion of pheochromocytoma, the presence of a tumor should be confirmed biochemically by measuring urine and plasma concentrations of catecholamine or their metabolites. In most situations, a CT scan or an MRI may be used to localize the tumor in the abdomen. In the absence of abdominal imaging, nuclear scan with metaiodobenzylguanidine (MIBG) may further help with the localization.
- Surgical resection is the treatment of choice because hypertension is cured by tumor resection. In the preoperative phase, combined alpha- and beta-adrenergic blockade is recommended for hypertension control. Alpha-adrenergic blockade is initiated with phenoxybenzamine or prazosin, and, following adequate alpha-adrenergic blockade, beta-adrenergic blockade is initiated. These patients are often volume contracted and require saline or sodium tablets. Catecholamines can be reduced further by metyrosine. For adrenal pheochromocytoma, laparoscopic adrenalectomy is becoming the procedure of choice in suitable patients. Follow-up 24-hour urinary excretion studies of catecholamines should be performed 2 weeks following surgery (and periodically thereafter) to detect recurrence, metastases, or development of second primary lesion.
- Primary hyperaldosteronism
- Hyperkalemia is an important clue to the presence of primary aldosteronism. However, in a subset of patients, the serum potassium concentration may be within the reference range. Measurement of PRA has been used as a screening test. A suppressed PRA value that fails to rise above 2 mg/mL/h after salt and water depletion is considered a positive test result. The best initial test is the determination of the aldosterone excretion rate during prolonged salt loading.
- The appropriate therapy depends on the cause of excessive aldosterone production. A CT scan may help localize an adrenal mass, indicating adrenal adenoma. If the results of the CT scan are inconclusive, adrenal venous sampling for aldosterone and cortisol levels should be performed. Medical therapy is indicated in patients with adrenal hyperplasia, patients with adenoma who are poor surgical risks, and patients with bilateral adenomas. These patients are best treated with sustained salt and water depletion. Hydrochlorothiazide or furosemide in combination with either spironolactone or amiloride corrects hypokalemia and normalizes the blood pressure. Some patients may require the addition of a vasodilator or a beta-blocker for better control of hypertension.
- Adrenal adenomas may be resected via a laparoscopic procedure. Surgical resection often leads to the control of blood pressure and the reversal of biochemical abnormalities. These patients may develop hypoaldosteronism during the postoperative follow-up period and require supplementation with fludrocortisone.
Surgical Care
Aortorenal bypass using saphenus vein graft or hypogastric artery is a common revascularization technique for renovascular hypertension. Surgical resection is the treatment of choice for pheochromocytoma because hypertension is cured by tumor resection. In patients with fibromuscular renal disease, angioplasty has a 60-80% success rate for cure or improvement of hypertension. Surgical correction of renal artery stenosis has resulted in cure of hypertension in approximately 61% of patients and amelioration in 27% of patients with fibromuscular lesions. With respect to renal artery stenosis secondary to atherosclerotic lesions, surgical correction has resulted in cure of hypertension in 38% of patients and amelioration in about 41% of patients. See Medical Care for more details.
Consultations
Consultations with a nutritionist and exercise specialist are often helpful in changing lifestyle and initiating weight loss. Consultations with an appropriate consultant are indicated for management of secondary hypertension attributable to a specific cause.
Diet
A number of studies have documented an association between sodium chloride intake and blood pressure. The effect of sodium chloride is particularly important in individuals who are middle-aged to elderly with a family history of hypertension. A moderate reduction in sodium chloride intake can lead to a small reduction in blood pressure. The American Heart Association recommends that the average daily consumption of sodium chloride not exceed 6 g, this may lower blood pressure by 2-8 mm Hg.
- The Dietary Approaches to Stop Hypertension (DASH) eating plan encompasses a diet rich in fruits, vegetables, and low-fat dairy products and may lower blood pressure by 8-14 mm Hg.2
- Dietary potassium, calcium, and magnesium consumption have an inverse association with blood pressures. Lower intake of these elements potentiates the affect of sodium on blood pressure. Oral potassium supplementation may lower both systolic and diastolic pressure. Calcium and magnesium supplementation have elicited small reductions in blood pressures.
- In population studies, low levels of alcohol consumption have shown a favorable effect on blood pressure, with reductions of 2-4 mm Hg. However, the consumption of 3 or more drinks per day is associated with elevation of blood pressure. Alcohol intake should be restricted to less than 1 oz of ethanol in men and 0.5 oz in women.
- Weight reduction may lower blood pressure by 5-20 mm Hg per 10 kg of weight loss in a patient who weighs more than 10% of ideal body weight.
Activity
Up to 60% of all individuals with hypertension are more than 20% overweight. The centripetal fat distribution is associated with insulin resistance and hypertension. Even modest weight loss (5%) can lead to reduction in blood pressure and improved insulin sensitivity. Regular aerobic physical activity can facilitate weight loss, decrease blood pressure, and reduce the overall risk of cardiovascular disease. Blood pressure may be lowered by 4-9 mm Hg with moderately intense physical activity. These activities include brisk walking for 30 minutes a day, 5 days per week. More intense workouts for 20-30 minutes, 3-4 times a week may also lower blood pressure and have additional health benefits.
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