Patients with atherosclerosis often have elevated lipids, including cholesterol and triglycerides. Total serum cholesterol levels should be below 200 mg/dL. Elevated cholesterol levels are confirmed by HDL and LDL measurements. Increased low-density lipoprotein cholesterol (LDL-C) (“bad” cholesterol) levels indicate that a person is at an increased risk for atherosclerosis. Low high-density lipoprotein cholesterol (“good” cholesterol) (HDL-C) levels also indicate an increased risk. A desirable LDL-C level is one below 100 mg/dL for healthy people and below 70 mg/dL for those diagnosed with CVD or who are diabetic. A desirable HDL-C level is 40 mg/dL or above (Pagana & Pagana, 2010).

Triglyceride level may also be elevated with atherosclerosis and is an emerging lipid risk factor by the classic Adult Treatment Panel Report No. 3 (ATP III) released by the National Heart, Lung, and Blood Institute (National Cholesterol Education Program, 2002). A level of 150 mg/dL or above indicates hypertriglyceridemia. Women should have a level below 135 mg/dL (Pagana & Pagana, 2010). Elevated triglycerides are considered a marker for other lipoproteins. They also suggest metabolic syndrome, which increases the risk for coronary heart disease (see Table 40-1 and discussion in Chapter 40).

People with multiple risk factors are grouped into high-risk patient categories termed “coronary heart disease equivalents.” These groups include:

Interventions for patients with atherosclerosis or those at high risk for the disease focus on lifestyle changes. Teach patients about the need to make daily changes by avoiding or minimizing modifiable risk factors. Modifiable risk factors are those that can be changed or controlled by the patient, such as smoking, weight management, and exercise. Nutrition is one of the most important parts of the risk-reduction plan. Chapter 40 describes how to manage modifiable risk factors in detail in the Health Promotion and Maintenance section, p. 831. If lipoprotein levels do not improve after lifestyle changes, the health care provider may prescribe drug therapy to lower cholesterol and/or triglycerides.

The Nutrition Committee of the American Heart Association (AHA) established dietary guidelines to promote healthy dietary habits as a strategy to reduce the risk for cardiovascular disease. The guidelines, revised in 2006, focus on the need to achieve and maintain a healthy weight and make appropriate food choices. Although most research focuses on individual nutrients or foods, the AHA guidelines aim to improve overall diet to ensure nutrient adequacy and energy balance (Lichtenstein et al., 2006). The AHA recommends that people consume a variety of nutritious foods including fruits, vegetables, whole grains, fat-free and low-fat dairy products, and lean meats. Specific AHA guidelines to decrease the risk for cardiovascular disease include minimizing fat and cholesterol intake. Chapter 63 describes the most recent U.S. government dietary guidelines, which include increasing daily vegetables and decreasing dairy food fats.

To decrease serum cholesterol level, a total fat intake of less than 30% of total calories should be consumed. Less than 10% of total caloric intake should be from saturated fat, up to 10% of total calories should be from polyunsaturated fat, and 10% to 15% should come from monounsaturated fat. Cholesterol intake should also be less than 300 mg daily.

In collaboration with the dietitian as needed, teach the patient about the types of fat content in food. Meats and eggs contain mostly saturated fats and are high in cholesterol. Recommend canola (rapeseed) oil (rich in monounsaturated fat) and safflower and sunflower oil (rich in polyunsaturated oils) over highly saturated oils such as palm or coconut oil.

The focus of cholesterol management is an aggressive approach to lowering LDL-C values and raising HDL-C levels. Having an LDL-C value of less than 100 mg/dL is optimal; values of 100 to 129 mg/dL are near or less than optimal. Patients with LDL-C values of 130 to 159 mg/dL (borderline high) are advised to follow a fat-modified diet and regular exercise regimen and increase omega-3 fatty acids in their diet or as a supplement. Increased fiber of 25 to 35 g in the daily diet is also recommended. In collaboration with the dietitian, teach patients with LDL-C values of 160 mg/dL or greater (high or very high) to follow a more structured nutritional plan aimed at decreasing saturated fat and cholesterol and, if appropriate, promoting weight loss.

For high-risk people, such as those with high cholesterol, diabetes, or CVD, the AHA recommends the NCEP Therapeutic Lifestyle Changes (TLC) diet, which outlines appropriate medical nutrition therapy. Recommendations include obtaining a patient’s baseline serum cholesterol level and then retesting 6 and 12 weeks after the initial nutritional intervention. If the cholesterol level has not significantly decreased, the patient may be referred to a dietitian for instruction on the NCEP–TLC diet, which limits saturated fat to less than 7% of total calories and cholesterol to less than 200 mg/day.

For patients with elevated total and LDL-C levels that do not respond adequately to dietary intervention, the health care provider prescribes one or more lipid-lowering agents (Table 38-2). Drug choice depends on the serum lipid levels. Because most of these drugs can produce major side effects, they are generally given only when nonpharmacologic management has been unsuccessful.

Lovaza (omega-3 ethyl esters) is approved by the Food and Drug Administration (FDA) as an adjunct to diet to reduce TGs that are greater than 500 mg/dL. This drug also decreases plaque growth and inflammation and reduces clot formation (Harris et al., 2008).

Stabilizing mechanisms exist in the body to exert an overall regulation of systemic arterial pressure and to prevent circulatory collapse. Four control systems play a major role in maintaining blood pressure:

Arterial baroreceptors are found primarily in the carotid sinus, aorta, and wall of the left ventricle. They monitor the level of arterial pressure and counteract a rise in arterial pressure through vagally mediated cardiac slowing and vasodilation with decreased sympathetic tone. Therefore reflex control of circulation elevates the systemic arterial pressure when it falls and lowers it when it rises. Why baroceptor control fails in hypertension is not clear (McCance et al., 2010).

Changes in fluid volume also affect the systemic arterial pressure. For example, if there is an excess of sodium and/or water in a person’s body, the blood pressure rises through complex physiologic mechanisms that change the venous return to the heart, producing a rise in cardiac output. If the kidneys are functioning adequately, a rise in systemic arterial pressure produces diuresis (excessive voiding) and a fall in pressure. Pathologic conditions change the pressure threshold at which the kidneys excrete sodium and water, thereby altering the systemic arterial pressure.

The renin-angiotensin-aldosterone system also regulates blood pressure (see discussion in Chapter 13). The kidney produces renin, an enzyme that acts on angiotensinogen (a plasma protein substrate) to split off angiotensin I, which is converted by an enzyme in the lung to form angiotensin II. Angiotensin II has strong vasoconstrictor action on blood vessels and is the controlling mechanism for aldosterone release. Aldosterone then works on the collecting tubules in the kidneys to reabsorb sodium. Sodium retention inhibits fluid loss, thus increasing blood volume and subsequent blood pressure.

Inappropriate secretion of renin may cause increased peripheral vascular resistance in patients with hypertension. When the blood pressure is high, renin levels should decrease because the increased renal arteriolar pressure usually inhibits renin secretion. However, for most people with essential hypertension, renin levels remain normal.

The process of vascular autoregulation, which keeps perfusion of tissues in the body relatively constant, appears to be important in causing hypertension. However, the exact mechanism of how this system works is poorly understood.

In 2003 the JNC made significant changes in classifying blood pressure in adults. The classification for “normal” adult blood pressure is less than 120 mm Hg systolic and less than 80 mm Hg diastolic. Adults with a blood pressure (BP) of 120 to 139 mm Hg systolic or 80 to 89 mm Hg diastolic, considered “normal” under previous guidelines, are classified as prehypertensive. These patients need lifestyle changes to prevent cardiovascular complications (Table 38-3). The relationship between hypertension and cardiovascular events is direct and independent of other risk factors. The higher the patient’s blood pressure is, the greater the chance for coronary, cerebral, renal, and peripheral vascular disease.

Control of hypertension has resulted in major decreases in cardiovascular morbidity and mortality. The Healthy People 2020 campaign includes a number of objectives related to hypertension to decrease cardiovascular mortality (Table 38-4).

Hypertension can be essential (primary) or secondary (Table 38-5). Essential hypertension is the most common classification. Sustained BP elevation in patients with essential hypertension results in damage to vital organs by causing medial hyperplasia (thickening) of the arterioles. As the blood vessels thicken and perfusion decreases, body organs are damaged. These changes can result in myocardial infarctions, strokes, peripheral vascular disease (PVD), or renal failure.

Isolated systolic hypertension (ISH) is a major health threat, especially for older adults. It is defined as a systolic BP (SBP) reading at or above 140 with a diastolic BP (DBP) below 90. For years, emphasis was placed on the diastolic BP (DBP) reading and attempts were made to lower this number to under 80. However, as people age, the systolic BP (SBP) becomes more significant because it is a better indicator than DBP of risk for heart disease and stroke. Research has shown that DBP rises until age 55 years and then declines, whereas SBP continues to rise. New research demonstrates a significant association between isolated systolic hypertension and peripheral vascular disease (Safar et al., 2009). In older adults, isolated systolic hypertension is the most common form of hypertension.

Malignant hypertension is a severe type of elevated blood pressure that rapidly progresses. A person with this health problem usually has symptoms such as morning headaches, blurred vision, and dyspnea and/or symptoms of uremia (accumulation in the blood of substances ordinarily eliminated in the urine). Patients are often in their 30s, 40s, or 50s with their systolic blood pressure greater than 200 mm Hg. The diastolic blood pressure is greater than 150 mm Hg or greater than 130 mm Hg when there are pre-existing complications. Unless intervention occurs promptly, a patient with malignant hypertension may experience renal failure, left ventricular failure, or stroke.

Essential hypertension can develop when a patient has any one or more of the risk factors listed in Table 38-5.

Renal disease is one of the most common causes of secondary hypertension. Hypertension can develop when there is any sudden damage to the kidneys. Renovascular hypertension is associated with narrowing of one or more of the main arteries carrying blood directly to the kidneys, known as renal artery stenosis (RAS). Many patients have been able to reduce the use of their antihypertensive drugs when the narrowed arteries are dilated through angioplasty with stent placement. All patients requiring three or four categories of antihypertensive drugs at high doses should be screened for RAS.

Dysfunction of the adrenal medulla or the adrenal cortex can also cause secondary hypertension. Adrenal-mediated hypertension is due to primary excesses of aldosterone, cortisol, and catecholamines. In primary aldosteronism, excessive aldosterone causes hypertension and hypokalemia (low potassium levels). It usually arises from benign adenomas of the adrenal cortex. Pheochromocytomas originate most commonly in the adrenal medulla and result in excessive secretion of catecholamines, resulting in life-threatening high blood pressure. In Cushing’s syndrome, excessive glucocorticoids are excreted from the adrenal cortex. The most common cause of Cushing’s syndrome is either adrenocortical hyperplasia or adrenocortical adenoma.

Drugs that can cause secondary hypertension include estrogen, glucocorticoids, mineralocorticoids, sympathomimetics, cyclosporine, and erythropoietin. The use of estrogen-containing oral contraceptives is likely the most common cause of secondary hypertension in women. Drugs that cause hypertension are discontinued to reverse this problem.

One in every three American adults has high blood pressure or is being treated for hypertension (AHA, 2010). The disease shortens life expectancy. A higher percentage of men than women have hypertension until age 45 years. From 45 to 54 years, women have a slightly higher percentage of hypertension than men. After age 54 years, women have a much higher percentage of the disease (AHA, 2010). The causes for these differences are not known.

When a diagnosis of hypertension is made, most people have no symptoms. However, patients may experience headaches, facial flushing (redness), dizziness, or fainting as a result of the elevated blood pressure. Obtain blood pressure readings in both arms. Two or more readings may be taken at each visit (Fig. 38-2). Some patients have high blood pressure due to anxiety associated with visiting a health care provider. Be sure to take an accurate blood pressure by using an appropriate-size cuff. Anderson et al. (2010) found that forearm blood pressure measurements are as accurate as upper arm blood pressures, especially in patients who are obese. In ambulatory care settings, such as clinics and office practices, wrist blood pressure measurements can be used.

Although no laboratory tests are diagnostic of essential hypertension, several laboratory tests can assess possible causes of secondary hypertension. Kidney disease can be diagnosed by the presence of protein, red blood cells, pus cells, and casts in the urine; elevated levels of blood urea nitrogen (BUN); and elevated serum creatinine levels. The creatinine clearance test directly indicates the glomerular filtration ability of the kidneys. The normal value is 107 to 139 mL/min for men and 87 to 107 mL/min for women (Pagana & Pagana, 2010). Decreased levels indicate kidney disease.

Urinary test results are positive for the presence of catecholamines in patients with a pheochromocytoma (tumor of the adrenal medulla). An elevation in levels of serum corticoids and 17-ketosteroids in the urine is diagnostic of Cushing’s disease.

No specific x-ray studies can diagnose hypertension. Routine chest radiography may help recognize cardiomegaly (heart enlargement).

An electrocardiogram (ECG) determines the degree of cardiac involvement. Left atrial and ventricular hypertrophy is the first ECG sign of heart disease resulting from hypertension. Left ventricular remodeling can be detected on the 12-lead ECG (see Chapter 40 for discussion of remodeling).

The priority problems for patients with hypertension are: