Describe factors that regulate blood pressure.

  Describe how hypertension is classified.

  Discuss nonpharmacologic measures to control hypertension.

  Identify the prototype and describe the action, use, contraindications, adverse effects, and nursing implications of the angiotensin-converting enzyme inhibitors.

  Identify the prototype and describe the action, use, contraindications, adverse effects, and nursing implications of the angiotensin II receptor blockers.

  Describe the rationale for using combination drugs in the management of hypertension.

  Review the effects of alpha-adrenergic blockers, beta-adrenergic blockers, calcium channel blockers, and diuretics in the management of hypertension.

  Apply the nursing process in the care of patients with hypertension.

KEY TERMS

Angioedema: sudden swelling of the lips, tongue, throat, hands, or feet

Angiotensin-converting enzyme (ACE) inhibitor: drug that decreases activation of the renin–angiotensin–aldosterone system; specifically, the drug prevents inactive angiotensin I from being converted to angiotensin II

Angiotensin II receptor blocker: similar to ACE inhibitor, although the mechanism of action is blockade of the angiotensin II receptor site

Antiadrenergics: decrease or block the effects of sympathetic nerve stimulation

Autoregulation: ability of body tissues to regulate their own blood flow

Bradykinin: peptide that causes vasodilation and lowers blood pressure

Essential hypertension: high blood pressure for which no cause can be found

First-dose phenomenon: orthostatic hypotension with palpitations, dizziness, and perhaps syncope 1 to 3 hours after the first dose of a drug or an increased dose

Introduction

Antihypertensive drugs are used to treat hypertension, a common, chronic disorder affecting an estimated 50 to 60 million adults and an unknown number of children and adolescents in the United States. Hypertension increases risks of MI, heart failure, cerebral infarction and hemorrhage, and renal disease. To understand hypertension and antihypertensive drug therapy, it is necessary first to understand the physiologic mechanisms that normally control blood pressure, the characteristics of hypertension, and the characteristics of antihypertensive drugs.

Overview of Hypertension

Regulation of Blood Pressure

Arterial blood pressure reflects the force exerted on arterial walls by blood flow. Blood pressure normally remains constant because of homeostatic mechanisms that adjust blood flow to meet tissue needs. The two major determinants of arterial blood pressure are cardiac output (systolic pressure) and peripheral vascular resistance (diastolic pressure).

Cardiac output equals the product of the heart rate and stroke volume (CO = HR × SV). Stroke volume is the amount of blood ejected with each heartbeat (approximately 60–90 mL). Thus, cardiac output depends on the force of myocardial contraction, blood volume, and other factors. Peripheral vascular resistance is determined by local blood flow and the degree of constriction or dilation in arterioles and arteries (vascular tone).

Autoregulation of Blood Flow

Autoregulation is the ability of body tissues to regulate their own blood flow. This is a critical mechanism of major organs (e.g., heart, brain, kidneys) to preserve oxygenation and function. Local blood flow is regulated primarily by nutritional needs of the tissue, such as lack of oxygen or accumulation of products of cellular metabolism (e.g., carbon dioxide, lactic acid). Local tissues produce vasodilating and vasoconstricting substances to regulate local blood flow. Important tissue factors include histamine, bradykinin, serotonin, and prostaglandins.

Histamine is found mainly in mast cells surrounding blood vessels and is released when these tissues are injured. In some tissues, such as skeletal muscle, mast cell activity is mediated by the sympathetic nervous system (SNS), and histamine is released when SNS stimulation is blocked or withdrawn. In this case, vasodilation results from increased histamine release and the withdrawal of SNS vasoconstrictor activity. Bradykinin is released from a protein in body fluids. Kinins dilate arterioles, increase capillary permeability, and constrict venules. Serotonin is released from aggregating platelets during the blood clotting process. It causes vasoconstriction and plays a major role in control of bleeding. Prostaglandins are formed in response to tissue injury and include vasodilators (e.g., prostacyclin) and vasoconstrictors (e.g., thromboxane A₂).

An important component of regulating local blood flow is the production of several vasoactive substances by the endothelial cells that line blood vessels. Vasoconstricting substances, which increase vascular tone and blood pressure, include angiotensin II, endothelin-1, and thromboxane A₂. Vasodilating substances, which decrease vascular tone and blood pressure, include nitric oxide and prostacyclin. Excessive vasoconstrictors or deficient vasodilators may contribute to the development of atherosclerosis, hypertension, and other diseases. Injury to the endothelial lining of blood vessels by the sheer force of blood flow with hypertension or by rupture of atherosclerotic plaque leads to vasoconstriction, vasospasm, thrombus formation, and thickening of the blood vessel wall. All of these factors narrow the blood vessel lumen and increase peripheral vascular resistance.

Overall, regulation of blood pressure involves a complex, interacting, overlapping network of hormonal, neural, and vascular mechanisms, and any condition that affects heart rate, stroke volume, or peripheral vascular resistance affects arterial blood pressure. Many of these mechanisms are compensatory effects that attempt to restore balance when hypotension or hypertension occurs. Box 28.1 further describes these mechanisms.

Types of Hypertension

Hypertension is persistently high blood pressure that results from abnormalities in regulatory mechanisms. It is usually defined as a systolic pressure above 140 mm Hg or a diastolic pressure above 90 mm Hg on multiple blood pressure measurements. The Eighth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8) is long awaited and expected to be released in 2012. The recommendations have been the cornerstone in the detection, evaluation, and treatment of high blood pressure. The Seventh Report, published in 2004, classifies blood pressures in adults (in mm Hg) into four categories (Box 28.2). These guidelines also recommend a goal blood pressure of less than 130/80 mm Hg for people with diabetes or renal disease.

From U.S. Department of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute, National High Blood Pressure Education Program. The Seventh Report of the Joint National Committee on Prevention, Detection, Evolution, and Treatment of High Blood Pressure (JNC 7). NIH Publication No. 04–5230, August 2004.

A systolic pressure of 140 mm Hg or greater, with a diastolic pressure of less than 90 mm Hg, is called isolated systolic hypertension and is more common in the elderly. Systolic–diastolic hypertension, which may also occur in older adults, involves elevations of both systolic and diastolic pressures. Both types increase cardiovascular morbidity and mortality, especially heart failure and stroke, and warrant treatment.

A hypertensive emergency or crisis is a diastolic pressure of 120 mm Hg or higher and possible target organ damage. (A hypertensive urgency is an episode of marked elevation in blood pressure without target organ damage. The goal of management is to lower blood pressure within 24 hours.)

Etiology

Although it has frequently been indicated that the causes of primary hypertension, or essential hypertension, are not known, this is only partially true; genetic variations and inherited, behavioral, and environmental factors may increase blood pressure. These include obesity, high alcohol intake, insulin resistance, high salt intake in salt-sensitive people, aging, sedentary lifestyle, and stress. Furthermore, many of these factors are additive, such as obesity and alcohol intake. Primary hypertension makes up 90% to 95% of known cases. Appropriate therapy usually controls primary hypertension.

Secondary hypertension may result from renal, endocrine, or central nervous system disorders and from drugs that stimulate the SNS or cause retention of sodium and water, producing adverse effects. Secondary hypertension can sometimes be cured by managing the underlying condition or cause. Hypertensive emergencies often result from such conditions as cerebral hemorrhage, dissecting aortic aneurysm, renal disease, pheochromocytoma, or eclampsia.

Pathophysiology

Hypertension profoundly alters cardiovascular function by increasing the workload of the heart and causing thickening and sclerosis of arterial walls. The increased cardiac workload leads to myocardial hypertrophy as a compensatory mechanism, with eventual heart failure. As a result of endothelial dysfunction and arterial changes (vascular remodeling), the arterial lumen narrows, blood supply to tissues decreases, and the risk of thrombosis increases. In addition, necrotic areas may develop in arteries, and these may rupture with sustained high blood pressure. The areas of most serious damage are the heart, brain, kidneys, and eyes. These are often called target organs.

Response to Hypotension

When hypotension (and decreased tissue perfusion) occurs, the SNS is stimulated, the hormones epinephrine and norepinephrine are secreted by the adrenal medulla, angiotensin II and aldosterone are formed, and the kidneys retain fluid. These compensatory mechanisms raise the blood pressure. Specific effects include the following:

Chapter 27 contains an additional discussion of the effects and management of hypotension.

Response to Hypertension

•  When arterial blood pressure is elevated, the following sequence of events occurs:

•  Kidneys excrete more fluid (increase urine output).

•  Fluid loss reduces both extracellular fluid volume and blood volume.

•  Decreased blood volume reduces venous blood flow to the heart and therefore decreases cardiac output.

•  Decreased cardiac output reduces arterial blood pressure.

•  The vascular endothelium produces vasodilating substances (e.g., nitric oxide, prostacyclin), which reduce blood pressure.

Clinical Manifestations

Initially, and perhaps for years, primary hypertension may produce no symptoms. If symptoms occur, they are usually vague and nonspecific. Hypertension may go undetected, or it may be incidentally discovered when blood pressure measurements are taken as part of a routine physical examination, screening test, or assessment of other disorders. Eventually, symptoms reflect target organ damage. Hypertension is often discovered after a person experiences angina pectoris, MI, heart failure, stroke, or renal disease.

Symptoms include severe headache, nausea, vomiting, visual disturbances, neurologic disturbances, disorientation, and decreased level of consciousness (drowsiness, stupor, coma). Hypertensive emergencies require immediate blood pressure reduction with parenteral antihypertensive drugs to limit damage to target organs.

Therapy

Goals of Treatment

After the diagnosis of hypertension is established, it is essential that a therapeutic regimen be designed and implemented. The goal of management for most patients is to achieve and maintain blood pressure well below 140/90 mm Hg. The target blood pressure for people with diabetes is 130/80 mm Hg. If the goal is impossible to achieve, lowering blood pressure to any extent is still considered beneficial in decreasing the incidence of coronary artery disease (CAD) and stroke. In most instances, it is better to lower blood pressure gradually and to avoid wide fluctuations in blood pressure.

Nonpharmacologic Treatment

The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) recommends management guidelines in which initial interventions include lifestyle modifications (i.e., reduction of weight and sodium intake, regular physical activity, moderate alcohol intake, and no smoking) to maintain normal blood pressure. If these modifications do not produce the target blood pressure or substantial progress toward the target blood pressure, it is important to initiate antihypertensive drug therapy and continue lifestyle modifications.

Dietary Management

Key behavioral determinants of blood pressure are related to dietary consumption of calories and salt; the prevalence of hypertension rises proportionally to average body mass index. The Dietary Approaches to Stop Hypertension (DASH) study demonstrated that people with prehypertension or stage 1 hypertension can reduce their blood pressures by adhering to a diet abundant in fresh fruits and vegetables and low-fat dairy products even without restricting calorie or sodium intake. The effects of the DASH diet demonstrate blood pressure–lowering effects that parallel the degree of benefit from drug monotherapy and may include dietary sodium restriction. Effects are evident in all ethnic groups, particularly African Americans.

Severe restrictions of sodium intake usually are not acceptable to people; however, moderate restrictions (4–6 g of salt a day) are beneficial and more easily implemented. Avoiding heavily salted foods (e.g., cured meats, sandwich meats, pretzels, potato chips) and not adding salt to food at the table can achieve this. Research and clinical observations indicate the following:

Lifestyle Management

Considerable evidence demonstrates that regular aerobic exercise by itself effectively reduces blood pressure. However, the direct benefits of exercise on blood pressure control are often difficult to isolate from those of the changes that often accompany exercise, such as improved diet, weight loss, decreased alcohol consumption, and decreased cigarette smoking. The JNC 7 recommendations include increasing exercise to at least 30 minutes per day at least 4 days per week, achieving a weight loss goal of at least 10 pounds, limiting alcohol consumption to two drinks or less per day for men and one drink or less per day for women, and ceasing smoking.

Drug Treatment

Drugs used in the management of primary hypertension belong to several different groups, including angiotensin-converting enzyme (ACE) inhibitors; angiotensin II receptor blockers (ARBs), also called angiotensin II receptor antagonists; antiadrenergics; calcium channel blockers; diuretics; and direct vasodilators. In general, these drugs act to decrease blood pressure by decreasing cardiac output or peripheral vascular resistance. This chapter focuses on ACE inhibitors and ARBs. Various chapters describe other drugs discussed in this chapter—for example, chapters related to heart failure (see Chap. 24), dysrhythmias (see Chap. 25), and angina (see Chap. 26).

Table 28.1 outlines the antihypertensive drugs, and Table 28.2 lists antihypertensive–diuretic combination products. Product labeling and JNC 7 recommendations are the basis for adult dosages. Product labeling and recommendations from the National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents (2004) are the basis for pediatric dosages.

TABLE 28.2

DRUGS AT A GLANCE: Oral Antihypertensive Combination Products*

*Note that one trade-name product may be available in multiple formulations, with variable amounts of antihypertensive, diuretic, or both components.

HCTZ, hydrochlorothiazide.

The JNC 7 guidelines suggest thiazide diuretics be used as first-line therapy, either alone (monotherapy) or with a beta blocker, ACE inhibitor, ARB, or calcium channel blocker. If the initial drug (and dose) does not produce the desired blood pressure, options for further management include increasing the dose, substituting another drug, or adding a second drug from a different group. If the response is still inadequate, addition of a second or third drug, including a diuretic if not previously prescribed, is a possibility. When current management is ineffective, it is necessary to reassess the patient’s adherence to lifestyle modifications and drug therapy. In addition, it is also important to review other factors that may decrease the therapeutic response, such as the use of over-the-counter appetite suppressants, dietary or herbal supplements, or nasal decongestants, which raise blood pressure.

The guidelines of the World Health Organization and the International Society of Hypertension for management of hypertension include considering age, ethnicity, and concomitant cardiovascular disorders when choosing an antihypertensive drug; starting with a single drug, in the lowest available dose; changing to a drug from a different group, rather than increasing dosage of the first drug or adding a second drug, if the initial drug is ineffective or not well tolerated; and using long-acting drugs (i.e., a single dose effective for 24 hours). The guidelines also note that many patients require two or more drugs to achieve adequate blood pressure control. When this is the case, fixed-dose combinations or long-acting agents may be preferred, because they decrease the number of drugs and doses that are required and may increase compliance.

Variation exists in the response to drug therapy for hypertension in ethnic populations. Experts credit nearly 70% of the familial considerations related to blood pressure to shared genes rather than to shared environment. For most antihypertensive drugs, few research studies have compared effects among different genetic or ethnic groups. However, several studies indicate that beta blockers have greater effects in people of Asian heritage compared with those of Caucasian background. For hypertension, Asians in general need much smaller doses because they metabolize and excrete beta blockers slowly. Other populations known to metabolize beta blockers slowly include Arab and Egyptian Americans and possibly German Americans. In African Americans, diuretics are effective and recommended as initial drug therapy. Calcium channel blockers, alpha₁ receptor blockers, and the alpha–beta blocker labetalol are reportedly equally effective in African Americans and Caucasians. ACE inhibitors, some ARBs (e.g., losartan and telmisartan), and beta blockers are less effective as monotherapy in African Americans. When beta blockers are used, they are usually one component of a multidrug regimen, and higher doses may be necessary. Overall, African Americans are more likely to have severe hypertension and require multiple drugs as a result of having low circulating renin, increased salt sensitivity, and a higher incidence of obesity.

Angiotensin-Converting Enzyme Inhibitors

Authorities recommend captopril (Capoten), the prototype angiotensin-converting enzyme (ACE) inhibitor, and other drugs in this class as first-line agents for treating hypertension in people with diabetes, particularly those with type 1 diabetes and/or diabetic nephropathy. These drugs reduce proteinuria and slow progression of renal impairment in people with this disease. (However, they may cause or aggravate proteinuria and renal damage in people who do not have diabetes.) ACE inhibitors may be used alone or in combination with other antihypertensive agents, such as thiazide diuretics.

Stay updated, free articles. Join our Telegram channel

Join