utero, although a meta-analysis of 55 studies of birth weight and BP later in life did not support this so-called fetal origins hypothesis.11, 12, 13 Because HTN in children is defined as a BP greater than the 95th percentile for a child of any given age and height, the initial incidence of HTN in children is automatically 5%. Normally, BP increases in children at a rate between 1 and 4 mm Hg per year for both SBP and DBP and then levels off after age 18 to 20 years. Children whose BP consistently falls above the 95th percentile for height, gender, and age are at risk for sustained HTN and should be evaluated and possibly treated.10
Table 35-1 ▪ CLASSIFICATION OF BLOOD PRESSURE FOR ADULTS | ||||||||||||||||||
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contraction to maintain BP within normal limits. Over longer time periods (hours to days), neurohumoral and direct renal regulation of vascular volume also play an important role in maintaining normal BP. Baroreceptors in low-pressure components of the cardiovascular system such as the veins, atria, and pulmonary circulation have a role in neurohumoral regulation of vascular volume.
Dysfunction of the autonomic nervous system imbalance may be a cause due to the inheritance of genes predisposing an individual to increased sympathetic nervous activity.
Variations in renal sodium absorption also suggest that genes involved in rare inherited forms of HTN may be related to mutations in several genes that increase one’s susceptibility to disorders of renal absorption of sodium, chloride, and water. To date, genes accounting for the vast majority of salt-sensitive HTN have not been identified.21
Dysfunction of the renin-angiotensin-aldosterone system results in an increase in renin-angiotensin-aldosterone activity resulting in extracellular fluid volume expansion and systemic vascular resistance. Angiotensin II has also been shown to act like a growth factor and a cytokine resulting in growth, differentiation, and apoptosis in vascular tissues. Studies have also identified gene coding for various components of the renin-angiotensin-aldosterone system and their roles in the development of HTN.21
Impaired vascular responsiveness, that is, impairments in vascular dilation and increased vascular contraction, due to the function of the endothelium, occurs in those individuals with HTN. Oxidative stress is also a critical factor in both HTN and atherogenesis.33,34
Insulin resistance may also play a role in the development of HTN. Insulin resistance may be the common factor that links HTN, diabetes, and other metabolic abnormalities. The metabolic syndrome of abdominal obesity, increased BP, dyslipidemia, and insulin resistance with or without impaired glucose tolerance plus prothrombotic and proinflammatory states may place individuals at high cardiovascular risk.
sodium, chloride, and water resulting in an expanded extracellular fluid volume. This condition is now thought to be the cause of 5% to 13% of all cases of HTN.37 Primary hyperaldosteronism may be difficult to diagnose due to low serum potassium, the most common sign being found in only one third of the cases.37 The best screening test is now the plasma aldosterone to plasma renin activity ratio.38 Clinicians should look for this condition in those patients younger than 50 years who appear to have resistant HTN or HTN with hypokalemia. Surgical removal of an adenoma reduces BP and if no tumor is present, medical treatment with aldosterone antagonists such as spironolactone is indicated.38
Acromegaly
Hypothyroidism
Hyperthyroidism
Hyperparathyroidism
Adrenal cortical
Cushing syndrome
Primary aldosteronism
Apparent mineralocorticoid excess
Adrenal medulla
Pheochromocytoma
Carcinoid syndrome
Left ventricular hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
Stroke or transient ischemic attack
Chronic kidney disease
and glomerular capillary pressures to accelerate nephrosclerosis. While the presence of macroalbuminuria (proteinuria > 300 mg/day), indicates presence of kidney disease, even lower level microalbuminuria (30 to 300 mg/day) is associated with increased cardiovascular risk.
Table 35-2 ▪ CLASSIFICATION OF HYPERTENSIVE RETINOPATHY | |||||||||||||||||||||
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to morbid events is the average level, although there is also accumulating evidence that suggests that hypertensive patients whose BP remains high at night (nondippers) are at greater risk for cardiovascular morbidity than dippers.67 Less data are available to define the clinical significance of BP variability, although it has been suggested that it is a risk factor for cardiovascular morbidity.
Table 35-3 ▪ TRENDS IN AWARENESS, TREATMENT, AND CONTROL AMONG PARTICIPANTS WITH HYPERTENSION IN THE U.S. POPULATION, 1999 TO 2004 | ||||||||||||||||||||||||||||
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prevent the onset of HTN are as follows: weight loss, sodium restriction, reduction in alcohol intake, increased exercise, potassium supplementation, and a diet high in fruits and vegetables.74, 75, 76, 77, 78, 79, 80 Efforts to begin the lifestyle habits that prevent the development of HTN should begin during childhood.76
Urinalysis | |
Hematocrit | |
Blood chemistries | |
Potassium, calcium, creatinine or estimated glomerular filtration rate, fasting glucose, fasting lipid profile | |
12-lead electrocardiogram |
energy intake with energy expenditure through a suitable dietary plan and physical activity is effective and an important component of weight loss and weight management. The JNC 7 recommendations for these lifestyle modifications are listed in Table 35-4.7 In addition, persons with HTN are encouraged to modify their other risk factors for CVD such as dyslipidemia and smoking because of their additive impact on the rate of development and progression of atherosclerosis.
Table 35-4 ▪ LIFESTYLE MODIFICATIONS TO MANAGE HYPERTENSION*,† | ||||||||||||||||||||||||
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(defined as an increased waist-to-hip ratio of more than 0.85 in women and 0.95 in men) and the development of HTN, diabetes, dyslipidemia, and increased CHD mortality.83, 84, 85, 86, 87 Studies in Framingham, Massachusetts and Evans County, Georgia revealed that overweight people have from two to three times the risk for HTN compared with persons who are not overweight.17,88 The exact mechanism by which obesity contributes to HTN is unclear. However, the influence of weight may be related to alterations in cardiovascular, endocrine, and metabolic factors caused by obesity. These alterations include increased cardiac output, increased blood volume, and sodium retention. Research now suggests that adipose tissue acts as a major endocrine organ, secreting bioactive substances which may induce metabolic disorders, such as hyperinsulinemia, insulin resistance, decreased carbohydrate tolerance, and decreased insulin sensitivity.89, 90, 91 Alterations in endothelial function have also been demonstrated in persons who are overweight.90,92