Heart failure in the United States is a growing epidemic, with approximately 550,000 new cases per year.

An increasing number of patients are treated at home with drugs that require a working knowledge of both the syndrome and the various therapeutic agents in use. New understanding of the syndrome has led to a paradigm shift from treating signs and symptoms to increasing long-term survival. This article focuses on the syndrome as it relates to common agents prescribed for the patient in the home setting.

Oral Heart Failure Medications

A N U P D AT E F O R H O M E H E A LT H C L I N I C I A N S
Dennis J. Cheek, RN, PhD, FAHA, Melissa M. Sherrod, RN, PhD, Roger Graulty, BS, and Johnathon Hawkins, BSN

Oral Heart Failure Medications

Heart failure is a growing public health concern in the United States. Approximately 5 million Americans have heart failure, and more than 550,000 new diagnoses are determined each year. Heart failure is the primary reason for 12 to 15 million office visits and the leading cause of hospitalization among Medicare beneficiaries, with an annual cost exceeding 33 billion dollars. The aging population, improved care for those who already have a diagnosis of heart failure, and more rescues of those with acute myocardial infarction combine to foster the growing epidemic of heart failure (Bonow et al., 2005; Schocken, 2008. Heart failure is not a disease but a complex clinical syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. The chief symptoms are dyspnea and fatigue, which may limit exercise tolerance, increase fluid retention, and ultimately lead to pulmonary con-

gestion and peripheral edema. Both abnormalities can impair functional capacity and quality of life, but they may not be present at the same time. Some patients have exercise intolerance but little evidence of fluid retention, whereas others complain primarily of edema and report few symptoms of dyspnea or fatigue. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term heart failure is preferred over the older term congestive heart failure (Radford et al., 2005).

Heart Failure Defined

Diagnosis

Patients with signs and symptoms of heart failure should be evaluated with a complete physical examination and medical history. If heart failure is suspected, diagnostic tests such as an electrocardiogram (ECG), echocardiography, or multigated acquisition (MUGA) scanning may be ordered. Once the diagnosis is confirmed, the physician may classify the disease using the New

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staging classification includes the following: Stage A: Patients with coronary artery disease, hypertension, or diabetes mellitus who do not yet demonstrate impaired left ventricular (LV) function, hypertrophy, or geometric chamber distortion Stage B: Patients who are asymptomatic but demonstrate LV hypertrophy, impaired LV function, or both Stage C: Patients with current or previous symptoms of heart failure associated with underlying structural heart disease (the majority of patients with heart failure) Stage D: Patients with truly refractory heart failure who may be eligible for advanced treatment strategies such as mechanical circulatory support, procedures to increase fluid removal, cardiac transplantation, experimental surgical procedures, or end-of-life care such as hospice (Bonow et al., 2005; Hunt et al., 2005; Schocken, 2008). The ACC/AHA staging classification system is intended to complement but not replace the NYHA functional classification system. This staging system was created to identify patients reliably and objectively during the course of their developing disease and link them to treatments appropriate at each stage of illness. According to this approach, patients are expected to advance from one stage to the next unless progression of the disease is slowed or stopped by treatment. For example, although symptoms, as identified in the NYHA classification, may vary widely over

York Heart Association (NYHA) functional classification system, which places patients in 1 of 4 categories based on limitations in physical activity as follows: 1 (no symptoms and no limitations during ordinary physical activity), 2 (mild symptoms and slight limitation during ordinary activity), 3 (marked limitation in activity due to symptoms, even during less than ordinary activity, and comfortable feelings only at rest, 4 (severe limitations, symptoms even at rest) (Bonow et al., 2005; Hunt et al., 2005). A new staging classification system was developed in 2001 by the American College of Cardiology (ACC) and the American Heart Association (AHA). This system, updated in 2005, recognizes risk factors and prerequisites for heart failure and identifies therapeutic interventions that can be introduced even before symptoms appear. This system identifies 4 stages in the development of heart failure syndrome. Patients in stages A and B are at risk for development of the disease but do not have a diagnosis of heart failure. The ACC/AHA

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Because not all patients have volume overload at the time of initial or subsequent evaluation, the term heart failure is preferred over the older term congestive heart failure.
time in response to therapy or progression of disease, a patient who already has experienced the clinical syndrome of heart failure (stage C) can never return to stage B, and the therapies recommended for stage C are appropriate regardless of NYHA class (Hunt et al., 2005).
Management

effects outside the heart. Digoxin is a potentially dangerous drug that must be administered with care to avoid potential adverse effects. Mode of Action Digoxin binds to the enzyme sodium (Na+)-potassium (K+ )-adenosine triphosphatase (ATPase), inhibiting its pumping action and altering the ion distribution after passage of an action potential. With digoxin bound to Na+-K+-ATPase, sodium is retained within the cell, and potassium entry is prevented. The intracellular level of sodium increases with each successive action potential. The increased concentration of sodium in the cell suppresses the exchange of sodium for calcium, causing an increase in intracellular calcium. Digoxin also can slow the heart through its effects on cardiac electrical activity. It can directly inhibit the activity of the sinoatrial node and slow progression of electrical impulses from the sinoatrial node to the atrioventricular node. The drug decreases sympathetic outflow to the heart as a result of its action on the afferent fibers of the vagus nerve. Inhibition of Na+-K+-ATPase occurs, increasing cardiac baroreceptor sensitivity. As a result, these receptors fire more spontaneously, signaling the central nervous system (CNS) to reduce sympathetic outflow. Adverse Effects Digoxin toxicity may be recognized by any of the following: Gastrointestinal side effects such as anorexia, nausea, vomiting, diarrhea, or abdominal pain CNS effects such as headache and visual disturbances Cardiac symptoms such as bradycardia and arrhythmias Visual disturbances including yellow-green halos around objects, blurry vision, double vision, photophobia, and light flashes. Because gastrointestinal or visual disturbances are more frequently reported, they are among the earlier recognized signs of toxicity. Cardiac symptoms of digoxin toxicity generally occur later than gastrointestinal and CNS symptoms, with dysrhythmias among the most commonly reported (Aarnoudse, Dieleman, & Stricker, 2007).

Successful management of heart failure depends on a working relationship between the patient, the family, and the healthcare team. The 3 most important heart failure strategies include lifestyle modification, medication, and surgery. Patients who adopt changes related to diet, exercise, weight loss, and other lifestyle choices can alleviate symptoms, slow progression of the disease, and improve their quality of life. Such changes are difficult and often require support from family, home health clinicians, and physicians (Rosamond et al., 2008). The medication regimen has encountered a paradigm shift, from treatment of heart failure signs and symptoms to improvements in longterm survival. The first medications discussed relate to the signs and symptoms of heart failure. The second set of agents aid to improve longterm survival (Table 1).

Drugs That Have an Impact on Signs and Symptoms of Heart Failure

Positive Inotropic Drugs: Cardiac Glycosides

The cardiac glycoside digoxin is used to reduce the symptoms of heart failure. It resolves the symptoms and decreases hospitalizations but has little effect on prolonging life. Digoxin is extracted from purple foxglove (Digitalis purpurea) and Grecian foxglove (Digitalis lantana). These compounds increase cardiac contractility, change electrical conduction in the heart, and provide neurohormonal

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Home Health Clinician Considerations Patients should be monitored carefully for symptoms of toxicity. Potassium serum levels should be assessed before initiation of therapy because high or low serum potassium levels will alter the effects of the drug. Blood work should be done initially to evaluate therapeutic range. Dosing should be based on the patients ideal weight to avoid significant overdosing of overweight patients because serum levels are not affected by changes in weight due to fat accumulation (Aschenbrenner & Venable, 2009). Any dosing change during the course of therapy should be followed by an assessment of digoxin blood levels. Digoxin is excreted by the kidneys, thus promoting toxicity for patients with impaired renal function. Blood urea nitrogen (BUN) and creatinine levels should be checked periodically for assessment of renal function. Caution should be exercised when digoxin is administered to elderly patients, who are more likely to experience diminished renal function (Aarnoudse et al., 2007). Digoxin is the only oral inotropic drug that facilitates home administration. Patient education is critical because patients must understand the importance of taking the drug exactly as prescribed and also must know the signs and symptoms of digoxin toxicity development. Patients should be encouraged to eat consistently because their initial dosing was based on blood work reflecting their normal diet. Any dietary change, vomiting, or diarrhea should be noted because it may change the patients serum potassium level and alter the therapeutic effects of digoxin. The patients heart rate should be assessed before digoxin is taken. The patient should be taught to count the apical pulse for 1 full minute to allow accurate assessment of the heart rate. If the patients heart rate is below 55, the clinician should instruct the patient to notify the physician to determine whether digoxin should be given (Aschenbrenner & Venable, 2009).
Diuretics: Symptomatic Treatment of Fluid Overload

allows the left ventricle to contract more efficiently, improving cardiac output. Mode of Action Furosemide is known as a loop diuretic because it acts on the thick ascending portion of the loop of Henle, inhibiting the reabsorption of sodium and chloride. Water reabsorption is passively prevented by the increased solute concentration in the kidney tubule. Because a substantial amount of sodium and chloride are normally reabsorbed in this segment of the loop of Henle, blocking reabsorption will promote considerable diuresis. Furosemide is especially useful for patients with renal impairment because it is effective when glomerular filtration rates are low. The onset of orally administered furosemide is 20 to 60 minutes. Its action peaks in 1 to 2 hours and lasts for 6 to 8 hours. Intravenous furosemide acts more rapidly, with onset in about 5 minutes and a duration of about 2 hours (Wang & Gottlieb, 2008). Adverse Effects Most adverse effects are caused by an electrolyte imbalance. Furosemides diuretic effect can lead to hyponatremia, hypokalemia, hypochloremia, and dehydration. Hypokalemia can lead to dysrhythmias and toxicity when furosemide is given to patients receiving digoxin. Therefore, it may be necessary to supplement potassium or use a potassium-sparing diuretic. Because of its ability to reduce fluid volume, furosemide can decrease the volume of blood returning to the heart, which can significantly reduced cardiac output and may lead to orthostatic hypotension, dizziness, vertigo, and headache. A common and serious adverse effect of furosemide therapy is ototoxicity. Ototoxicity is more commonly seen in patients with renal dysfunction or when the drug is rapidly administered intravenously. Adverse effects can be enhanced if the patient is taking other ototoxic drugs such as aminoglycoside antibiotics. These effects can be temporary, lasting from 1 to 24 hours, or can result in permanent hearing loss. Symptoms of ototoxicity include tinnitus, feelings of fullness in the ears, and loss of hearing for medium- and high-frequency ranges. Patients should be instructed to report any hearing loss or other signs of ototoxicity immediately.

Furosemide is the most commonly prescribed diuretic. It normally is used in situations requiring rapid fluid mobilization such as pulmonary edema associated with heart failure. Furosemide reduces intravascular volume and venous return to the heart, which in turn reduces preload and

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Table 1. Heart Failure: Oral Medications

Indications
Heart failure to Digoxin toxicity: reduce the symptoms GI: anorexia, nausea, of the disease vomiting, diarrhea, Control of heart rate abdominal pain in atrial fibrillation or CNS: headache & visual atrial flutter disturbances (e.g., yellowgreen halos around objects, blurry vision, double vision, photophobia, light flashes) Cardiac: dysrhythmias (e.g., heart block) Note: Hypokalemia increases the incidence of digoxin toxicity

Drug

Class

Mechanism of Action & Effects Adverse Effects Nursing Considerations

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Assess serum K+ levels prior to and during digoxin therapy Obtain blood work when beginning therapy or any time dosing is changed to evaluate therapeutic drug levels Dosing should be based on ideal weight in order to avoid overdosing in patients with significant body fat Monitor for digoxin toxicity; caution use in elderly or patients with impaired renal function due to increased likelihood of toxicity (assess BUN & creatinine levels periodically) Assess apical pulse for 1 full minute prior to administration; hold if heart rate is less than 60 beats/min Patient Education: Dosing regimen Heart rate assessment Diet Signs/symptoms of toxicity Monitor for fluid and electrolyte imbalance; hold if signs of fluid/electrolyte imbalance present Patient Education: Will be increased urine volume & frequency; these symptoms will decrease 6-8 hours after taking each dose; to minimize, take in morning for once-daily dosing, or at 8:00 AM and 2:00 PM to avoid nocturia Take with food if GI upset occurs Monitor daily weights on same scale at same time of day Monitor BP; notify physician if there is a significant drop in BP Change positions slowly due to chance for orthostatic hypotension Minimize hypokalemia by eating a diet that includes potassium-rich foods (e.g., bananas, citrus fruits, and spinach) Wear protective clothing and sunscreen when exposed to direct sunlight due to potential for photosensitivity Situations requiring rapid fluid mobilization, such as pulmonary edema associated with heart failure Electrolyte and fluid imbalances: hyponatremia, hypokalemia, hypochloremia, and dehydration Hypokalemia can lead to dysrhythmias and toxicity when given to patients on digoxin (it may be necessary to supplement potassium or use a potassium-sparing diuretic) Orthostatic hypotension, dizziness, vertigo, headache Ototoxicity: more commonly seen in patients with renal dysfunction, increased incidence if given with other ototoxic drugs (e.g., aminglycosides) Drug of choice for edema associated with mild to moderate heart failure Electrolyte and fluid imbalances: hyponatremia, hypokalemia, hypochloremia, dehydration (less pronounced than furosemide) Patient Education: Take in the morning to avoid having to urinate during the night If a second dose is prescribed, this should be taken in the early afternoon

Digoxin

Cardiac glycoside, positive inotropic agent

Inotropic Effects: Binds to Na+ K+-ATPase, inhibiting its pumping action of Na+ and K+ An increase in intracellular Na+ results in an increase in intracellular Ca+2 Ca+2 facilitates the interaction of actin

and myosin filaments, which increases cardiac contractility Cardiac Conduction Effects: Directly inhibits the activity of the SA node and slows conduction through the AV node Decreases sympathetic outflow from the CNS to the heart

Furosemide

Loop diuretic

Inhibits reabsorption of sodium and chloride in the thick, ascending portion of the loop of Henle, resulting in passive diuresis due to the increased solute concentration in the kidney tubule Reduces intravascular volume and venous return to the heart Reduces preload and may allow the left ventricle to contract more efficiently, improving cardiac output Especially useful in patients with renal impairment because it is effective when glomerular filtration rates are low Onset: 20 to 60 minutes Peak: 1-2 hours Duration: 6-8 hours

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Hydrochlorothiazide (HCTZ)

Thiazide diuretic

Acts on the distal segment of the nephron, inhibiting reabsorbtion of sodium and chloride resulting in passive diuresis due to the increased solute concentration in the kidney tubule

Hydrochlorothiazide (HCTZ) (continued)

HCTZ is dependent on kidney function in order to be effective (a reduced GFR decreases the effectiveness of these drugs)

Take with food if GI upset occurs Change positions slowly due to chance for orthostatic hypotension Wear protective clothing and sunscreen when exposed to direct sunlight due to potential for photosensitivity Headache (most common side effect) Orthostatic hypotension & tachycardia Syncope, dizziness, vertigo Weakness Anxiety NTG can be delivered via several delivery methods including: SL tablets, TD ointment or patches, oral capsules, transmucosal tablets, translingual sprays, IV infusion Continuously monitor vital signs while administering NTG; assess BP and pulse before giving Headaches are most common early in NTG therapy temporarily reducing the dosage may help alleviate headaches; however, they can be treated with aspirin or acetaminophen as needed Change positions slowly due to chance for orthostatic hypotension Gradually taper dose upon discontinuation avoid any reactions to its withdrawal (abrupt withdrawal can cause coronary artery spasm) Hydralazine is often administered with drugs that inhibit sympathetic activity and a diuretic

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Afterload reduction in heart failure Hypotension Tachycardia Fluid retention NYHA class II or III heart failure due to LV systolic dysfunction First-line agent to reduce long-term mortality in heart failure Hypotension, fluid retention, Monitor for therapeutic effectiveness: reduction in worsening heart failure (usu- the sign and symptoms of heart failure Monitor for dizziness, orthrostatic hypotension, and ally at initiation of therapy) decreased peripheral perfusion Bradycardia and heart block (rare at low doses) Persistent, dry, nonproductive cough (5-10% of patients; related to increased bradykinin levels) Hyperkalemia from aldosterone inhibition Angioedema (potentially lifethreatening edema of tongue, glottis, and pharynx) Monitor potassium level and white blood cell count Monitor for effectiveness of therapy For diabetics, monitor for proteinuria Contraindicated in pregnancy

Nitroglycerin (NTG)

Vasodilator

In vascular smooth muscles, NTG is con- Angina verted to nitric oxide, which activates an Preload/volume reduction in acute enzyme that catalyzes the formation of heart failure cyclic guanosine monophosphate (cGMP); elevation of cGMP in smooth vascular muscle cells promotes relaxation of smooth muscle NTG can rapidly decrease BP through relaxation of vascular smooth muscle resulting in dilation of venous and arterial vessels Effects are more pronounced in veins resulting in peripheral pooling of blood and decreased cardiac preload

Hydralazine

Vasodilator

Direct relaxation of smooth muscle in arteriole exact mechanism is unknown The sympathetic nervous system responds by increasing heart rate and stroke volume, which both increase cardiac output Increases activity of the reninangiotensin-aldosterone system which acts to increase water retention by the kidneys

Carvedilol

-adrenergic receptor antagonist

Diminishes effects of sympathetic nervous system through nonselective blockade of receptors; also possesses some a1 blocking actions

Home Healthcare Nurse

Enalapril

Angiotensin-converting enzyme (ACE) inhibitor

Inhibits ACE, blocking the conversion of angiotensin I to angiotensin II (a potent vasoconstrictor) By decreasing angiotensin II production, there is a decreased release of aldosterone (which normally minimizes Na+ loss) and a reduced degradation of bradykinin

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Table 1. Heart Failure: Oral Medications

Indications
Fetal harm Renal failure in patients with bilateral renal stenosis (angiotensin II maintains efferent arterial tone in the glomerulus, which maintains GFR) Commonly used as second-line drug for heart failure when ACE inhibitors are not tolerated Side effects similar to ACE inhibitors, except no cough (bradykinin levels not affected with ARBs) Angioedema Fetal harm Renal failure in patients with bilateral renal stenosis (angiotensin II maintains efferent arterial tone in the glomerulus, which maintains GFR) Monitor for effectiveness of therapy For diabetics, monitor for proteinuria Contraindicated in pregnancy

Drug

Class

Mechanism of Action & Effects Adverse Effects Nursing Considerations

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Onset of 1-2 days Give with meals to enhance absorption Monitor weight, electrolyte levels, and BP Avoid foods high in potassium like bananas, citrus fruits and apricots Treatment of heart failure in AfricanAmerican patients Headache Dizziness, lightheadedness Weakness Palpitations Postural hypotension Assess BP and pulse before administration Monitor the patient for orthostatic hypotension; change positions slowly

All of these effects reduce preload and afterload and increase cardiac output

Losartan

Angiotensin II receptor antagonist (ARB)

Bind preferentially to AT1 receptor subtype (in vascular, myocardial, kidney, adrenal glomerulosa cells) of the AT II receptor with more complete inhibition of angiotensin II effects Effects similar to ACE inhibitors

Spironolactone

Aldosterone antagonist; potassiumsparing diuretic

Antagonizes aldosterone receptors in the In conjunction with May cause dehydration, HCTZ and furosemide hyponatremia, and hyperdistal nephron, thereby decreasing the to reduce potassium synthesis of cell membrane proteins kalemia loss needed for the transport of sodium and Dysrhythmias may occur potassium in and out of the cell secondary to hyperkalemia Weak diuretic; seldom used alone for Impotence, menstruation diuresis irregularities, and gynecomastia CNS effects: drowsiness, lethargy, confusion, ataxia

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Isosorbide dinatrate + hydralazine

Combination vasodilator agent

Combined vasodilatory effects of isosorbide dinatrate (nitrate vasodilator) and hydralazine (non-nitrate vasodilator)

Furosemide also can cause photosensitivity. Because of the potential for photosensitivity, patients taking furosemide should wear protective clothing and sunscreen when exposed to direct sunlight (Wang & Gottlieb, 2008). Home Health Clinician Considerations Patients should be taught that although treatment will increase urine volume and voiding frequency, these symptoms will decrease in 6 to 8 hours. This is important because many patients find increased voiding frequency annoying and are less compliant as a result. Patients should be instructed to take furosemide in the morning for once-daily dosing or at 8:00 a.m. and 2:00 p.m. for twice-daily administration to avoid nocturia. If patients experience gastrointestinal upset, they should be instructed to take furosemide with food. Daily weights should be obtained on the same scale and at the same time, preferably before breakfast. Patients should be instructed to use a weight record and report any excessive weight gain or loss. Patients also should be instructed to report signs of dehydration and electrolyte imbalance. Signs of dehydration include dry mouth, unusual thirst, decreased urine output, dark urine or anuria, irritability, and weakness. Electrolyte imbalance may cause muscle pain or cramps, muscle fatigue, and tetany in rare instances. Hypokalemia can be minimized by a diet that includes potassium-rich foods such as bananas, citrus fruits, and spinach. Some patients experience hypotension while taking furosemide. They should be instructed to monitor their blood pressure and to notify their physician or home health clinician if it drops significantly. Patients should be warned about the possibility of postural hypotension and informed about how to avoid injury when standing or ambulating.
Hydrochlorothiazide

of the nephron. It inhibits the reabsorption of sodium and chloride, resulting in retention of these solutes and water in the distal convoluted tubule and causing an increase in urine production. Because the amount of sodium and chloride normally reabsorbed in the distal tubule is low (~10%), the maximum increase in urine flow is relatively less than with the use of loop diuretics. To be effective, HCTZ is dependent on kidney function. With a reduced glomerular filtration rate, these diuretics lose their effectiveness. For this reason, HCTZ cannot be prescribed for patients with renal impairment. Adverse Effects The adverse effects of HCTZ are similar to those seen with furosemide except for ototoxicity. The effects of HCTZ are less pronounced because of its weaker diuretic effect, but dehydration, hyponatremia, hypokalemia, and hypochloremia are possible (Wang & Gottlieb, 2008). Home Health Clinician Considerations Medication instructions and education for HCTZ are the same as for furosemide, with the exception of ototoxicity.
Vasodilators: Nitroglycerin and Hydralazine

Nitroglycerin (NTG) is most commonly associated with angina. It can be delivered via sublingual tablet, transdermal ointment, patches, oral capsules, transmucosal tablets, translingual sprays, and intravenous infusion. The delivery method affects onset and duration as well as whether the drug is subjected to first-pass effects by the liver. Mode of Action Nitroglycerin relaxes vascular smooth muscle, resulting in dilation of venous and arterial vessels. Because it is converted to nitric oxide, NTG activates an enzyme that catalyzes the formation of cyclic guanosine monophosphate (cGMP). Elevation of cGMP in smooth vascular muscle cells dephosphorylates myosin, rendering it unable to react with actin and causing relaxation of the muscle as well as a rapid decrease in blood pressure (Klinger, 2007). Adverse Effects Headache, the most common side effect of NTG, can be severe. Other symptoms related to the

Hydrochlorothiazide (HCTZ) is used to manage edema associated with heart failure. It is not as potent as furosemide because the site of action in the kidney is different, and dependence on kidney function for efficacy is greater. Thiazides are the drugs of choice for mobilizing edema resulting from mild to moderate heart failure (Wang & Gottlieb, 2008). Mode of Action Hydrochlorothiazide acts on the distal segment

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drugs vasodilatory actions include orthostatic hypotension, tachycardia, and syncope. The drug may cause CNS symptoms including dizziness, vertigo, weakness, and anxiety. Home Health Clinician Nursing Considerations For the common side effect of headaches, temporary reduction of the dosage may help. However, the headaches can be treated with aspirin or acetaminophen as needed. Patients should be informed that tolerance of NTG may develop and that the incidence of headaches should decline. The patient should be educated regarding orthostatic hypotension and the need to use caution during ambulation. When discontinuing NTG therapy, the clinician should be aware of the need to taper the dose gradually because abrupt withdrawal can cause spasm of the coronary arteries.
Hydralazine

systolic dysfunction unless they are intolerant or have a contraindication (Hunt et al., 2005). Adverse Effects The major adverse effects of carvedilol include hypotension, fluid retention, and worsening condition, usually at initiation of therapy. Bradycardia and heart block are rare with low doses, but occur in 5% to 10% of cases as the dose is increased. Other adverse effects are similar to those with other beta-blockers, although some adverse effects are minimized due to alpha-blocking activity (Hunt et al., 2005). Home Health Clinician Nursing Considerations The clinician should monitor for therapeutic effectiveness, which is demonstrated by a reduction in the signs and symptoms of heart failure. The patient should be taught to assess for dizziness, which could indicate a risk for orthostatic hypotension. Peripheral perfusion should be checked and patients educated to observe and report poor skin perfusion; skin that is clammy, pale, or mottled; and prolonged capillary refill times (Lehne, 2007).
ACE Inhibitors: Enalapril

Hydralazine is given to patients with heart failure to reduce afterload. The exact mode of action is unknown, but the drug is thought to modify cellular calcium metabolism, resulting in relaxation of vascular smooth muscle. This results in peripheral vasodilation and a decrease in blood pressure. The sympathetic nervous system responds to this drop in blood pressure by increasing heart rate and stroke volume, which increases cardiac output. Hydralazine also increases activity of the renin-angiotensin-aldosterone system, which acts to increase water retention by the kidneys. Because of these 2 effects, hydralazine often is administered with a diuretic and drugs that inhibit sympathetic activity (Taylor, 2005).

Drugs That Increase Long-Term Survival

Beta-Blockers: Carvedilol

The preferred initial therapy in most heart failure cases, ACE inhibitors are among the few classes of drugs shown to improve long-term survival. They block the conversion of angiotensin I to angiotensin II , a potent vasoconstrictor. Decreasing the angiotensin II-directed release of aldosterone, which normally minimizes Na+ loss, and reducing the degradation of bradykinin result in preload and afterload reduction, thus increasing cardiac output. (Kazi & Deswal, 2008). Nearly all patients with LV systolic dysfunction should receive an ACE inhibitor unless they are intolerant or have a contraindication. Adverse Effects Usually, ACE inhibitors are well tolerated. The most common adverse effect is a persistent, dry, irritating, nonproductive cough. This cough occurs in 5% to 10% of the patients started on an ACE inhibitor and is the main reason for discontinuing therapy. Hyperkalemia, another adverse effect, also is relatively common and should be monitored as well. The most serious and life-threatening reaction is angioedema, which results in swelling of

The results from clinical trials have shown a reduction in hospitalizations and mortality with the use of carvedilol and other beta-blockers. The beneficial effects were also seen in patients taking angiotensin-converting enzyme (ACE) inhibitors, suggesting that combination therapy may have additive effects. Carvedilol acts to reduce the effects of the sympathetic nervous system through a nonselective blockade of beta receptors. The beta-blockade is indicated for patients with NYHA class 2 or 3 disease due to LV

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The results from clinical trials have shown a reduction in hospitalizations and mortality with the use of carvedilol and other beta-blockers.

riousness of these conditions, patient education is of great significance. Home Health Clinician Considerations As with ACE inhibitors, clinicians should evaluate for the effectiveness of the ARB therapy, for hypertension based on the targeted blood pressure, and for changes in signs and symptoms. Patients with diabetes also should be monitored for proteinuria.

Aldosterone Antagonists
Spironolactone

the tongue, glottis, and pharynx, requiring immediate attention. Patients should be instructed to notify emergency personnel immediately if signs and symptoms occur (Kazi & Deswal, 2008). Home Health Clinician Considerations When assessing drug effectiveness and patient toxicity, clinicians should give special consideration to lab work, specifically the potassium level and white blood count. The patient should be evaluated for hypertension based on the targeted blood pressure. Diabetic patients should be assessed for proteinuria.
Angiotensin II Receptor Antagonists: Losartan

Spironolactone is used to treat edema associated with heart failure. However, the drug has a limited diuretic effect and seldom is used alone for this reason. Spironolactone is a potassium-sparing diuretic that increases urine production and actually increases the reabsorption of potassium. It often is used in conjunction with HCTZ and furosemide (Pitt, 2008). Mode of Action Spironolactone antagonizes aldosterone in the distal nephron. It stimulates transport protein synthesis in distal nephron cells. These proteins are required for sodium and potassium transport. By blocking aldosterone at the distal nephron receptor sites, new protein production is halted. Spironolactone has an onset of 1 to 2 days because previously produced proteins will continue to transport ions until the supply is exhausted. The drug antagonizes all aldosterone receptors such as mineralcorticoid, glucocorticoids, androgen, and progesterone receptors, which leads to some of its adverse effects. Adverse Effects The diuretic effects of spironolactone can cause dehydration and hyponatremia. Unlike HCTZ and furosemide, spironolactone can cause hyperkalemia, which can lead to potentially fatal dysrhythmias. It also may cause impotence, menstrual irregularities, and gynecomastia. Its CNS effects include drowsiness, lethargy, confusion, and ataxia (Pitt, 2008). Home Health Clinician Considerations Patients should be instructed to take spironolactone in the morning to avoid nocturia. Taking the medication with meals enhances absorption. Patients should be monitored for weight changes,

Angiotensin II receptor antagonists (ARBs) are relatively new drugs, with the prototypical Losartan approved in 1995. These drugs are indicated when ACE inhibitors are not tolerated. Angiotensin II receptor antagonists bind preferentially to the AT1 subtype (in vascular and myocardial tissue, kidney, and adrenal glomerulosa cells) of the AT II receptor, with more complete inhibition of angiotensin II effects. The effects and side effects are similar to those for ACE inhibitors, although early data suggest that maximum blood pressure reduction is not as great as with ACE inhibitors (Boehm, 2007). Adverse Effects Unlike ACE inhibitors, ARBs usually do not cause clinically significant hyperkalemia. The cough and angioedema have not yet been observed. However, ARBs do have the potential to cause angioedema, fetal harm, and renal failure for patients with bilateral renal stenosis. Due to the se-

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Our understanding of heart failure continues to evolve as advances in research and pharmacotherapeutics shed new light on the problem.

Headaches are common and can be treated with aspirin or acetaminophen as needed. As with other oral agents, patients should be advised that they will generally develop tolerance for BiDil and that the incidence of headaches should decline as tolerance develops. If they continue to have adverse effects, temporary reduction of the dosage may be helpful.

Conclusion
Our understanding of heart failure continues to evolve as advances in research and pharmacotherapeutics shed new light on the problem. Heart failure is not a disease but a complex clinical syndrome. Because patients do not have consistent signs and symptoms, the term heart failure is preferred over the older term congestive heart failure. To provide better aid for the clinician, the ACC/AHA staging classification system was developed to complement the NYHA functional classification system. The ACC/AHA staging system reliably and objectively identifies patients during the course of their developing disease and links their treatments to each stage of illness. The current neurohormonal hypothesis of heart failure has generated a paradigm shift in the pharmacologic treatment currently and for the future. No longer do clinicians focus merely on treating the signs and symptoms of the disease. Instead, they focus currently on improving quality of life and long-term survival. Dennis J. Cheek, RN, PhD, FAHA, is Abell-Hanger Professor of Gerontological Nursing at Texas Christian University, Harris College of Nursing and Health Sciences & School of Nurse Anesthesia, TCU Box 298620, Fort Worth, Texas 76129 (e-mail: d.cheek@tcu.edu). Melissa M. Sherrod, RN, PhD, is Assistant Professor at Texas Christian University, Harris College of Nursing & Health Sciences, TCU Box 298620,Fort Worth, Texas 76129 (e-mail: m.sherrod@tcu.edu). Roger Graulty, BS, is Senior Accelerated Track Nursing Student at Texas Christian University, Harris College of Nursing and Health Sciences, TCU Box 298620, Fort Worth, Texas 76129 (e-mail: r.gaultry@tcu.edu). Johnathon Hawkins, BSN, is Nurse Anesthesia Student at Texas Christian University, Harris College of Nursing and Health Sciences, TCU Box 298620, Fort Worth, Texas 76129 (email: j.hawkins@tcu.edu).

electrolyte levels, and blood pressure. Male patients should be warned of the potential for breast enlargement and tenderness. To help minimize hyperkalemia, patients should avoid eating foods high in potassium such as bananas, citrus fruits, and apricots. If potassium serum levels exceed 5 mEq/L or if the patient experiences abnormal heart rhythms, the physician should be notified because the drug may be discontinued and potassium intake minimized until serum levels normalize. Insulin can be administered to reduce serum potassium levels. To avoid potential injury, patients should be instructed not to operate machinery or perform hazardous tasks if they experience CNS effects while taking spironolactone.
Isosorbide Dinitrate and Hydralazine

The combination of isosorbide dinitrate and hydralazine has demonstrated a strong efficacy in the treatment of heart failure, especially in the African American patient. The AfHrt study demonstrated a 43% reduction in mortality among African Americans treated with the combination known as BiDil for heart failure (Taylor, 2005). Adverse Effects The adverse effects observed with isosorbide dinitrate and hydralazine include headache, dizziness, weakness, light-headedness, palpitations, and postural hypotension. Home Health Clinician Considerations The patient should monitor blood pressure and pulse before taking the combination agent. Patient education related to orthostatic hypotension and the use of caution during ambulation are strongly encouraged.

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Address correspondence to: Dennis J. Cheek, RN, PhD, FAHA, Abell-Hanger Professor of Gerontological Nursing, Texas Christian University, Harris College of Nursing and Health Sciences, TCU Box 298620, Fort Worth, Texas 76129 (e-mail: d.cheek@tcu.edu). The authors of this article have no ties, financial or otherwise, to any company that might have an interest in the publication of this educational activity.
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pathway in pulmonary hypertension. Clinics in Chest Medicine, 28, 143-167. Lehne, R. A. (2007). Pharmacology for nursing care (6th ed.). St. Louis: Saunders Elsevier. Pitt, B. (2008). Aldosterone blockade in patients with chronic heart failure. Cardiology Clinics, 26(1), 15-21. Radford, M.J., Arnold, J.M., Bennett, S.J., Cinquegrani, M.P., Cleland, J.G., Havranek, E.P., et al. (2005). American College of Cardiology; American Heart Association Task Force on Clinical Data Standards; American College of Chest Physicians; International Society for Heart and Lung Transplantation; Heart Failure Society of America. ACC/AHA key data elements and definitions for measuring the clinical management and outcomes of patients with chronic heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (Writing Committee to Develop Heart Failure Clinical Data Standards): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Failure Society of America. Circulation, 112(12),1888-1916. Rosamond, W., Flegal, K., Furie, K., Go, A., Greenlund, K., Haase, N., et al. (2008). American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation, 117(4), e25-146. Epub 2007 Dec 17. Schocken, D.D., Benjamin, E.J., Fonarow, G.C., Krumholz, H.M., Levy, D., Mensah, G.A., et al. (2008). American Heart Association Council on Epidemiology and Prevention; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Nursing; American Heart Association Council on High Blood Pressure Research; Quality of Care and Outcomes Research Interdisciplinary Working Group; Functional Genomics and Translational Biology Interdisciplinary Working Group. Prevention of heart failure: a scientific statement from the American Heart Association Councils on Epidemiology and Prevention, Clinical Cardiology, Cardiovascular Nursing, and High Blood Pressure Research; Quality of Care and Outcomes Research Interdisciplinary Working Group; and Functional Genomics and Translational Biology Interdisciplinary Working Group. Circulation, 117(19), 2544-2565. Taylor, A. L. (2005). The African American heart failure trial: A clinical trial update. American Journal of Cardiology, 96(Suppl), 441i-448i. Wang, D. J., & Gottlieb, S. S. (2008). Diuretic: Still the mainstay of treatment. Critical Care Medicine, 36(1), S89-94.

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