Patients in Stage D have advanced structural heart disease and marked symptoms of HF at rest, despite treatment with maximal dosages of medications used in Stage C. Repeated and prolonged hospitalization is common. For eligible candidates, the best long-term solution is a heart transplant. An implantable LV mechanical assist device can be used as a “bridge” in patients awaiting a transplant and to prolong life in those who are not transplant eligible.
Management focuses largely on the control of fluid retention, which underlies most signs and symptoms. Intake and output should be monitored closely, and the patient should be weighed daily. Fluid retention can usually be treated with a loop diuretic, perhaps combined with a thiazide. If volume overload becomes severe, the patient should be hospitalized and given an IV diuretic. If needed, IV dopamine or IV dobutamine can be added to increase renal blood flow, thereby enhancing diuresis.
Patients should not be discharged until a stable and effective oral diuretic regimen has been established.
What about beta blockers and ACE inhibitors? These agents may be tried, but doses should be low and responses monitored with care. In Stage D, beta blockers pose a significant risk of making HF worse, and ACE inhibitors may induce profound hypotension or renal failure.
When severe symptoms persist despite application of all recommended therapies, options for end-of-life care should be discussed with the patient and family.
Device Therapy
Implanted Cardioverter-Defibrillators. Cardiac arrest and fatal ventricular dysrhythmias are relatively common complications of HF. Accordingly, implantable cardioverter- defibrillators are now recommended for primary or secondary prevention to reduce mortality in selected patients.
Cardiac Resynchronization. When the left and right ventricles fail to contract at the same time, cardiac output is further compromised. Synchronized contractions can be restored with a biventricular pacemaker. In clinical trials, cardiac resynchronization improved exercise tolerance and quality of life and reduced all-cause mortality.
Exercise Training
In the past, bed rest was recommended owing to concern that physical activity might accelerate progression of LV dysfunction.
However, we now know that inactivity is actually detrimental:
It reduces conditioning, worsens exercise intolerance, and contributes to HF symptoms. Conversely, studies have shown that exercise training can improve clinical status, increase exercise capacity, and improve quality of life. Accordingly, exercise training should be considered for all stable patients.
Evaluating Treatment
Evaluation is based on symptoms and physical findings. Reduc- tions in dyspnea on exertion, paroxysmal nocturnal dyspnea, and orthopnea (difficulty breathing, except in the upright position) indicate success. The physical examination should assess for reductions in jugular distention, edema, and crackles.
Success is also indicated by increased capacity for physical activity. Accordingly, patients should be interviewed to deter- mine improvements in the maximal activity they can perform without symptoms, the type of activity that regularly produces symptoms, and the maximal activity they can tolerate. (Activity is defined as walking, stair climbing, activities of daily living, or any other activity that is appropriate.) Successful treatment should also improve health-related quality of life in general.
Thus the interview should look for improvements in sleep, sexual function, outlook on life, cognitive function (alertness,
KEY POINTS
■ Heart failure with LV systolic dysfunction, referred to simply as heart failure (HF) in this chapter, is characterized by ventricular dysfunction, reduced cardiac output, signs of inadequate tissue perfusion (fatigue, shortness of breath, exercise intolerance), and signs of fluid overload (venous distention, peripheral edema, pulmonary edema).
■ The initial phase of HF consists of cardiac remodeling—a process in which the ventricles dilate (grow larger), hypertrophy (increase in wall thickness), and become more spherical—coupled with cardiac fibrosis and myocyte death.
As a result of these changes, cardiac output is reduced.
■ Reduced cardiac output leads to compensatory responses:
(1) activation of the SNS, (2) activation of the RAAS, and (3) retention of water and expansion of blood volume. As a result of volume expansion, cardiac dilation increases.
■ If the compensatory responses are not sufficient to maintain adequate production of urine, body water will continue to accumulate, eventually causing death (from complete cardiac failure secondary to excessive cardiac dilation and cardiac edema).
■ There are three major groups of drugs for heart failure:
diuretics, ACE inhibitors or ARBs, and beta blockers.
Digoxin, which had been used widely in the past, may be added as indicated.
■ Diuretics are first-line drugs for all patients with fluid overload. By reducing blood volume, these drugs can decrease venous pressure, arterial pressure, pulmonary edema, peripheral edema, and cardiac dilation.
■ Although diuretics can reduce symptoms of HF, they do not prolong survival.
Continued
■ Thiazide diuretics are ineffective when GFR is low, and cannot be used if cardiac output is greatly reduced.
■ Loop diuretics are effective even when GFR is low, and are preferred to thiazides for most patients.
■ Thiazide diuretics and loop diuretics can cause hypokalemia and can increase the risk of digoxin-induced dysrhythmias.
■ Potassium-sparing diuretics are used to counteract potassium loss caused by thiazide diuretics and loop diuretics.
■ Potassium-sparing diuretics can cause hyperkalemia. By doing so, they can increase the risk of hyperkalemia in patients taking ACE inhibitors or ARBs.
■ In patients with HF, ACE inhibitors improve functional status and reduce mortality. In the absence of specific contraindications, all patients should be prescribed one.
■ ACE inhibitors block formation of angiotensin II, promote accumulation of kinins, and reduce aldosterone release.
As a result, these drugs cause dilation of veins and arterioles, promote renal excretion of water, and favorably alter cardiac remodeling.
■ By dilating arterioles, ACE inhibitors (1) improve regional blood flow in the kidneys and other tissues and (2) reduce cardiac afterload, which causes stroke volume and cardiac output to rise.
■ By dilating veins, ACE inhibitors reduce venous pressure, which in turn reduces pulmonary congestion, peripheral edema, preload, and cardiac dilation.
■ By suppressing aldosterone release, ACE inhibitors increase excretion of sodium and water, and decrease excretion of potassium.
■ By increasing levels of kinins (and partly by decreasing levels of angiotensin II), ACE inhibitors can favorably alter cardiac remodeling.
■ Major side effects of ACE inhibitors are hypotension, hyperkalemia, cough, angioedema, and birth defects.
■ ARBs share the beneficial hemodynamic effects of ACE inhibitors, but not the beneficial effects on cardiac remodeling.
■ In patients with HF, ARBs should be reserved for patients intolerant of ACE inhibitors (usually owing to cough).
■ In patients with HF, aldosterone antagonists (e.g., spirono- lactone, eplerenone) reduce symptoms and prolong life.
Benefits derive from blocking aldosterone receptors in the heart and blood vessels.
■ Beta blockers can prolong survival in patients with HF, and are considered first-line therapy.
■ To avoid excessive cardiosuppression, beta-blocker dosage must be very low initially and then gradually increased.
■ Isosorbide dinitrate (which dilates veins) plus hydralazine (which dilates arterioles) can be used in place of an ACE inhibitor (or ARB) if an ACE inhibitor (or ARB) cannot be used.
■ BiDil, a fixed-dose combination of hydralazine and iso- sorbide dinitrate, is approved specifically for treating HF in African Americans.
■ Digoxin and other inotropic agents increase the force of myocardial contraction and thereby increase cardiac output.
■ Of the available inotropic agents, digoxin is the only one that is both effective and safe when used orally and the only one suitable for long-term use.
■ Digoxin increases contractility by inhibiting myocardial Na+/K+-ATPase, thereby (indirectly) increasing intracellular calcium, which in turn facilitates the interaction of actin and myosin.
■ Potassium competes with digoxin for binding to Na+/K+- ATPase. Therefore, if potassium levels are low, excessive inhibition of Na+/K+-ATPase can occur, resulting in toxicity.
Conversely, if potassium levels are high, insufficient inhibition can occur, resulting in therapeutic failure.
Accordingly, it is imperative to keep potassium levels in the normal physiologic range: 3.5 to 5 mEq/L.
■ By increasing cardiac output, digoxin can reverse all of the overt manifestations of HF: cardiac output improves, heart rate decreases, heart size declines, constriction of arterioles and veins decreases, water retention reverses, blood volume declines, peripheral and pulmonary edema decrease, water weight is lost, and exercise tolerance improves. Unfortunately, although digoxin can improve symptoms, it does not prolong life.
■ In patients with HF, benefits of digoxin are not due solely to improved cardiac output; neurohormonal effects are important too.
■ Digoxin causes dysrhythmias by altering the electrical properties of the heart (secondary to inhibition of Na+/K+- ATPase).
■ The most common reason for digoxin-related dysrhythmias is diuretic-induced hypokalemia.
■ If a severe digoxin overdose is responsible for dysrhythmias, digoxin levels can be lowered using Fab antibody fragments [Digifab].
■ In addition to dysrhythmias, digoxin can cause GI effects (anorexia, nausea, vomiting) and CNS effects (fatigue, visual disturbances). Gastrointestinal and CNS effects often precede dysrhythmias and therefore can provide advance warning of serious toxicity.
■ Digoxin has a narrow therapeutic range.
■ Digoxin is eliminated by renal excretion.
■ Although routine monitoring of digoxin levels is generally unnecessary, monitoring can be helpful when dosage is changed, symptoms of HF intensify, kidney function declines, signs of toxicity appear, or drugs that affect digoxin levels are added to or deleted from the regimen.
■ Maintenance doses of digoxin are based primarily on observation of the patient: Doses should be large enough to minimize symptoms of HF but not so large as to cause adverse effects.
■ Maintenance doses of digoxin must be reduced if renal function declines.
■ Therapy of Stage C HF has four major goals: (1) relief of pulmonary and peripheral congestion, (2) improvement of functional status and quality of life, (3) delay of progression of cardiac remodeling and LV dysfunction, and (4) prolonga- tion of life.
■ For routine therapy, Stage C HF is treated with a diuretic, an ACE inhibitor or an ARB, and a beta blocker.
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DIGOXIN
Preadministration Assessment Therapeutic Goal
Digoxin is used to treat HF and dysrhythmias. Be sure to confirm which disorder the drug has been ordered for.
Baseline Data
Assess for signs and symptoms of HF, including fatigue, weakness, cough, breathing difficulty (orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea), jugular distention, and edema.
Determine baseline values for maximal activity without symptoms, activity that regularly causes symptoms, and maximal tolerated activity.
Laboratory tests should include an ECG, serum electrolytes, measurement of ejection fraction, and evaluation of kidney function.
Identifying High-Risk Patients
Digoxin is contraindicated for patients experiencing ventricu- lar fibrillation, ventricular tachycardia, or digoxin toxicity.
Exercise caution in the presence of conditions that can predispose the patient to serious adverse responses to digoxin, such as hypokalemia, partial AV block, advanced HF, or renal impairment.
Implementation: Administration Routes
Oral, slow IV injection.
Administration
Oral. Determine heart rate and rhythm before administra- tion. If heart rate is less than 60 beats/min or if a change in rhythm is detected, withhold digoxin and notify the prescriber.
Warn patients not to “double up” on doses in attempts to compensate for missed doses.
Intravenous. Monitor cardiac status closely for 1 to 2 hours following IV injection.
Promoting Adherence
Because digoxin has a narrow therapeutic range, rigid adher- ence to the prescribed dosage is essential. Inform patients that failure to take digoxin exactly as prescribed may lead to toxicity or therapeutic failure. If poor adherence is sus- pected, serum drug levels may help in assessing the extent of nonadherence.
Implementation: Measures to Enhance Therapeutic Effects
Advise patients to limit salt intake to 1500 mg/day and to avoid excessive fluids. Advise patients who drink alcohol to consume no more than one drink each day. Help patients establish an appropriate program of regular mild exercise (e.g., walking, cycling). Precipitating factors for HF (e.g., hypertension, valvular heart disease) should be corrected.
Ongoing Evaluation and Interventions Evaluating Therapeutic Effects
Evaluation is based on symptoms and physical findings. Assess for reductions in orthopnea, dyspnea on exertion, paroxysmal nocturnal dyspnea, neck vein distention, edema, and crackles, and for increased capacity for physical activity. In addition,
assess for improvements in sleep, sexual function, outlook on life, cognitive function, and ability to participate in social, recreational, and work activities.
Plasma BNP levels reflect cardiac status: The lower the level, the better the odds for long-term survival.
Measurement of plasma drug levels can help determine the cause of therapeutic failure. The optimal range for digoxin is 0.5 to 0.8 ng/mL.
Minimizing Adverse Effects
Cardiotoxicity. Dysrhythmias are the most serious adverse effect of digoxin. Monitor hospitalized patients for alterations in heart rate or rhythm, and withhold digoxin if significant changes develop.
Inform outpatients about the danger of dysrhythmias.
Teach them to monitor their pulses for rate and rhythm, and instruct them to notify the prescriber if significant changes occur. Provide the patient with an ECG rhythm strip; this can be used by providers unfamiliar with the patient (e.g., when the patient is traveling) to verify suspected changes in rhythm.
Hypokalemia, usually diuretic induced, is the most frequent underlying cause of dysrhythmias. Monitor serum potassium concentrations. If hypokalemia develops, potassium levels can be raised with potassium supplements, a potassium-sparing diuretic, or both. Teach patients to recognize early signs of hypokalemia (e.g., muscle weakness), and instruct them to notify the prescriber if these develop. Severe vomiting and diarrhea can increase potassium loss; exercise caution if these events occur.
To treat digoxin-induced dysrhythmias: (1) withdraw digoxin and diuretics (make sure that a written order for digoxin withdrawal is made); (2) administer potassium (unless potassium levels are above normal or AV block is present); (3) administer an antidysrhythmic drug (phenytoin or lidocaine, but not quinidine) if indicated; (4) manage bradycardia with atropine or electrical pacing; and (5) treat with Fab fragments if toxicity is life threatening.
Noncardiac Effects. Nausea, vomiting, anorexia, fatigue, and visual disturbances (blurred or yellow vision) frequently foreshadow more serious toxicity (dysrhythmias) and should be reported immediately. Inform patients about these early indications of toxicity, and instruct them to notify the pre- scriber if they develop.
Minimizing Adverse Interactions
Diuretics. Thiazide diuretics and loop diuretics increase the risk of dysrhythmias by promoting potassium loss. Monitor potassium levels. If hypokalemia develops, it should be corrected with potassium supplements, a potassium-sparing diuretic, or both.
ACE Inhibitors and ARBs. These drugs can elevate potas- sium levels and decrease therapeutic responses to digoxin.
Exercise caution if an ACE inhibitor or ARB is combined with potassium supplements or a potassium-sparing diuretic.
Sympathomimetic Agents. Sympathomimetic drugs (e.g., dopamine, dobutamine) stimulate the heart, thereby increasing the risk of tachydysrhythmias and ectopic pace- maker activity. When sympathomimetics are combined with digoxin, monitor closely for dysrhythmias.
Quinidine. Quinidine can elevate plasma levels of digoxin.
If quinidine is employed concurrently with digoxin, digoxin dosage must be reduced. Do not use quinidine to treat digoxin- induced dysrhythmias.
49 Antidysrhythmic Drugs
INTRODUCTION TO CARDIAC ELECTROPHYSIOLOGY, DYSRHYTHMIAS, AND THE ANTIDYSRHYTHMIC DRUGS, p. 546
Electrical Properties of the Heart, p. 547
Impulse Conduction: Pathways and Timing, p. 547 Cardiac Action Potentials, p. 547
The Electrocardiogram, p. 549 Generation of Dysrhythmias, p. 549
Disturbances of Automaticity, p. 549 Disturbances of Conduction, p. 550
Classification of Antidysrhythmic Drugs, p. 550 Class I: Sodium Channel Blockers, p. 550 Class II: Beta Blockers, p. 550
Class III: Potassium Channel Blockers (Drugs That