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Acute Heart Failure: An Evidence-Based Approach
The author explores diagnostic issues and recaps the latest thinking on a wide range of therapeutic choices, from diuretics, nitrates, morphine, and inotropes to ACE inhibitors, beta blockers, angiotensin receptor blockers, digoxin, aldosterone antagonists, nitrate-hydralazine combinations, nonpharmacologic measures, and device therapy.
By Jeremy Golding, MD, FAAFP
Approximately 5 million people in the United States have heart failure, and some 550,000 new diagnoses are made yearly. The condition affects 6% to 10% of those over age 65; due to our aging population and perhaps also because of success in treating acute coronary syndromes, the incidence has doubled in the past 10 years. About 50,000 people die each year as a direct consequence of heart failure.
Heart failure already represents the single most common Medicare hospital diagnosis-related group. More Medicare dollars are spent on the diagnosis and treatment of heart failure than any other diagnosis, accounting for some $28 billion in direct and indirect costs.
Heart failure has been the subject of extensive research. Evidence-based heart failure guidelines were published in 2005 by the American Heart Association/American College of Cardiology (AHA/ACC) and are available online (see Suggested Reading), as are guidelines from the Institute for Clinical Systems Improvement.
WHAT IS HEART FAILURE?
Heart failure is a clinical syndrome that may result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with and eject blood. Heart failure models continue to evolve. The precise pathology varies somewhat with the underlying etiology of the patient’s disease, but potentially it includes more recently described immunologic (cytokine) and neurohumoral mechanisms, as well as more traditional hemodynamic mechanisms.
Two conditions are the underlying cause of approximately 80% of all cases of heart failure in the United States—namely, ischemic heart disease and chronic hypertension. Other conditions that can cause heart failure include idiopathic and other cardiomyopathies and valvular heart disease.
Heart failure may be further subdivided into systolic dysfunction, which is generally defined as an ejection fraction (EF) below 35% to 40%, and diastolic dysfunction. Approximately half of all cases of heart failure in the United States are due to diastolic dysfunction, with the prevalence of this condition increasing with age. The prognosis for this condition may be slightly better than for systolic dysfunction heart failure, but this is uncertain. Regardless of the underlying cause or the type of heart failure, cardiac myocyte injury leads to systemic neurohumoral activation and left ventricular remodeling, which in turn alters left ventricular chamber geometry and function.
establishing an accurate diagnosis
Acutely decompensated heart failure (ADHF) typically presents with acute or subacute dyspnea, pulmonary or peripheral edema, and either hyper- or hypotension. Some patients may present with only a decrease in exercise tolerance, cough, or nocturnal dyspnea. Establishing an accurate diagnosis of heart failure is critical to initiating proper therapy and to treating the underlying cause. Although many cases of heart failure presenting in the emergency department are clinically obvious, many others are less clear. Differential considerations often include exacerbation of chronic obstructive pulmonary disease, pneumonia, myocardial ischemia, and occasionally pulmonary embolism, asthma exacerbation, and other less common entities. Further complicating the workup, multiple diagnoses may be present at the same time, especially in the elderly population.
Initial evaluation begins with a focused history and physical examination. Behaviors that may contribute to heart failure, like high salt intake, should be identified. Early assessment of the patient’s volume status is critical to guiding subsequent therapy. Is edema present? Rales, jugular venous distension, hepatomegaly, and hepatojugular reflux are all signs of heart failure. The patient should be asked about changes in body weight. Checking orthostatic vital signs may be appropriate.
Laboratory tests are usually helpful. Routine determination of serum electrolytes, creatinine, and glucose is recommended. Depending on the clinical scenario, the physician may also want to order a glycosylated hemoglobin measurement, a lipid panel, liver function tests, and thyroid function testing. A chest x-ray may detect interstitial or alveolar pulmonary edema, vessel cephalization, pleural effusions, and cardiomegaly. A 12-lead ECG may reveal patterns of ischemia or infarction, left ventricular hypertrophy, and arrhythmias.
BNP TESTING
The development of bedside or stat brain-type natriuretic peptide (BNP) testing has revolutionized heart failure diagnosis. Because BNP is a natriuretic hormone derived from the ventricle, its level will rise and fall within minutes to an hour of changes in left ventricular stress and function. Most dyspneic patients with heart failure have a BNP level above 400 pg/ml. (Almost all individuals without heart failure or another condition that can cause a false-positive BNP measurement will have a level below 50 pg/ml.) A BNP above 100 has an approximate sensitivity of 90%, a specificity of 76%, and a positive predictive value of 83% for the diagnosis of heart failure in symptomatic patients. In general, the higher the BNP level, the more specific the test result is for underlying heart failure.
Clinicians must be aware, however, that not all elevations in BNP result from heart failure. Other conditions, including some that typically present with dyspnea, may elevate BNP levels. These include cor pulmonale (BNP levels of 200 to 500 pg/ml), primary pulmonary hypertension (200 to 500 pg/ml), acute pulmonary embolism (150 to 500 pg/ml), acute coronary syndromes (40 to 400 pg/ml), acute myocardial infarction (MI, 40 to 1300 pg/ml), and end-stage renal disease (80 to more than 1300 pg/ml).
The plasma concentration of BNP falls after effective pharmacologic treatment of heart failure. In patients with known heart failure, comparing their BNP level with their "dry” level can aid in determining whether acute dyspnea is due to heart failure or some other etiology. Serial BNP monitoring in the hospital, particularly in the intensive care unit, is less likely to be helpful because BNP may not correlate well with pulmonary capillary wedge pressure in these patients. Also, current evidence is not yet sufficient to establish whether the use of BNP measurements to titrate therapy will improve long-term outcomes.
Bedside echocardiography, if available, is a highly valuable tool for the evaluation of dyspnea when the diagnosis is not apparent from other, less expensive tests. In addition to providing immediate information about EF, an echocardiogram can help determine global cardiac function and wall motion and the presence or absence of valvular and pericardial disease. Exercise echocardiography can reveal underlying coronary artery disease by visualizing ischemic wall motion abnormalities.
GOALS OF THERAPY
Once the diagnosis of heart failure is established, prompt initiation of therapy prevents further decompensation and reduces hospital stays. Remarkably, however, median length of inpatient stay for this condition remains fairly long despite advances in heart failure diagnosis and management—around 4.3 days. In one national registry, door-to-diuretic time was 7.8 hours.
Clinicians evaluating ADHF start by assessing the perfusion and volume status of the patient. The majority of patients in ADHF are “wet,” and the sickest are cold and wet. Dry patients may be dry because of excessive diuresis or occasionally right ventricular infarction. The immediate goals of therapy in ADHF are to restore oxygenation and organ perfusion and to treat volume overload, if present.
Subsequent hospital management should focus on initiation or modification of a maintenance regimen and patient education to prevent early readmission and improve symptoms.
A sample management algorithm for ADHF is shown below.
management strategies
Medication interventions for ADHF include vasodilators (diuretics, nitrates, and morphine) and inotropes.
Diuretics. Intravenous (IV) loop diuretics have better bioavailability and a more rapid onset than oral agents. They provide prompt symptomatic relief, decreasing pulmonary and peripheral edema, and may have pulmonary vasodilatory properties as well. Starting doses of furosemide are usually 40 mg IV or the patient’s oral dose of furosemide administered intravenously (for example, an 80-mg oral dose would translate to a dose of 80 mg intravenously). Intravenous furosemide is roughly twice as potent as the same oral dose. In critically ill patients, repeat doses may be administered as frequently as every 20 to 30 minutes until urine output is established, hypotension develops, or the ceiling dose is reached. Most clinicians will double each subsequent dose until the maximum dosage is reached or urine output is satisfactory. Cautious addition of a thiazide diuretic (such as metolazone) may be helpful if the loop diuretic alone is ineffective.
It is critically important to follow the patient’s intake and output and serum electrolytes carefully. A baseline weight is also helpful. The risks involved in diuretic therapy include electrolyte disturbances, arrhythmias, and worsening renal function. Perhaps because of increased neurohormonal activation, high doses have been associated with increased mortality. Therefore, diuretics should not be used alone as monotherapy for heart failure.
Nitrates. Nitrates produce rapid symptomatic relief in patients with acute exacerbation of heart failure. Through a mechanism involving nitric oxide and cyclic guanosine monophosphate (GMP), these agents induce arterial and venous vasodilation. Although relatively safe, nitroglycerin may produce or exacerbate hypotension, and it often causes a headache. Many clinicians use topical nitrates for initial therapy and switch to IV therapy only if the patient’s response is not satisfactory. Because both topical nitroglycerin (nitropaste) and IV nitroglycerin may be rapidly discontinued if severe hypotension develops, they are the acute therapy of choice. Intravenous nitroglycerin (at an initial dose 5 µg/min) is titrated to the desired blood pressure, symptomatic relief, and diuresis.
Nesiritide (synthetic BNP) has also been studied for the treatment of ADHF. Its mechanism of action is not completely understood, but it appears to involve cyclic GMP and nitric oxide, with hemodynamic effects similar to nitrovasodilators. However, recent data suggesting increased mortality and worsening renal function with this medication has tempered initial enthusiasm for its use. It is also expensive.
Nitroprusside, a very potent vasodilator, is generally reserved for pulmonary edema in the presence of severe hypertension or cases in which dramatic afterload reduction (acute aortic regurgitation, for example) is required.
Morphine. Besides producing both venous and arteriolar vasodilation, morphine has analgesic and anxiolytic properties. Patients experience rapid symptomatic relief from acute dyspnea with administration of IV morphine. Relief of anxiety ameliorates the adverse effects of endogenous catecholamines. Doses of 2 to 4 mg IV should be administered, titrated to patient comfort. Significant hypotension and suppression of respiratory drive are possible, so cautious administration of small doses at frequent intervals, if necessary, is advised.
Inotropes. Patients with hypotension and acute pulmonary edema are generally in cardiogenic shock, which is associated with a very high mortality. Therapy may consist of pressors (dopamine and dobutamine for systolic pressures in the 70 to 100 mm Hg range and norepinephrine for lower pressures), intra-aortic balloon pump placement, or urgent cardiac catheterization or bypass surgery.
Dobutamine is primarily a beta-1 agonist that increases myocardial contractility, improving cardiac output, with only a slight decrease in systemic vascular resistance. The starting dose is 2.5 mcg/kg/min, increased slowly to 10 to 20 µg/kg/min as tolerated. Dopamine, administered at 3 to 10 µg/kg/min, stimulates beta-1 receptors and also has alpha agonist activity, causing vasoconstriction, which is only desirable when hypotension is present. Norepinephrine is a potent alpha-1 and beta-1 agonist. The initial rate is 0.5 to 1 µg/min, titrated to the desired blood pressure response; 8 to 30 µg/min is the usual range.
Potential complications with all inotropes include arrhythmias, myocardial ischemia, and exacerbation of heart failure.
CONTROLLING ARRHYTHMIAS
Atrial fibrillation commonly accompanies ADHF, sometimes as its cause and sometimes as an effect. Loss of atrial kick and decreased left ventricular filling time both contribute to decreased cardiac output. As with most arrhythmias, when hypotension or shock is present, primary management is electrical cardioversion according to advanced cardiac life support protocols. Rate control may also be accomplished with a short half-life IV beta blocker (such as esmolol) or cautious use of the calcium channel blocker diltiazem. In these cases, the benefits of rate control usually exceed the risks associated with negative inotropy.
Digoxin (1-mg loading dose over 12 to 24 hours) also slows the heart rate and supports cardiac output, but not as quickly as esmolol or diltiazem. Digoxin and diltiazem may be used together, although caution should be observed because of the potential for high-grade atrioventricular (AV) block.
Ventricular tachycardia with heart failure usually requires electrical cardioversion and initiation of anti-arrhythmic therapy (with amiodarone or lidocaine, for example).
NONPHARMACOLOGIC MEASURES
Nonpharmacologic interventions in heart failure treatments include oxygen, bilevel positive airway pressure (BiPAP), and intubation. If adequate oxygenation cannot be maintained with supplemental oxygen via a nasal or face mask, noninvasive positive pressure ventilation (especially BiPAP) offers a number of physiologic benefits, including decreased preload and afterload. In several trials and subsequent meta-analyses, BiPAP has been shown to reduce the need for endotracheal intubation and ICU admission and to decrease mortality. The greatest benefit appears to be seen in patients with hypercapnic respiratory failure.
Bilevel positive airway pressure generally requires a conscious and cooperative patient. Its benefits are usually apparent within 30 to 60 minutes. Patients whose oxygenation fails to improve within one to two hours of pharmacologic management and BiPAP should be intubated.
Critically ill patients with a cardiac index below 2 L/min/m2, those with systemic hypotension, and those with pulmonary capillary wedge pressures above 18 mm Hg despite maximal pharmacologic measures may benefit from mechanical support. The two generally available options are intra-aortic balloon pump placement and use of a short-term left ventricular assist device. The mortality rate is very high in these circumstances, and it is unclear to what extent 30-day survival is improved in patients treated emergently with these therapies.
HOSPITAL MANAGEMENT
Criteria for hospitalization of the patient in ADHF are listed in the table below. Some patients who respond promptly to diuretics and have an identifiable, nonurgent cause for decompensation (for example, excessive salt intake) may not require hospitalization. Inpatient management of ADHF focuses on reversing the acute illness, determining the cause of the exacerbation in order to prevent recurrence, adjusting medications, and educating the patient in self-management.
Once the acute decompensation is stabilized, attention should be directed to underlying, potentially treatable causes. Was acute ischemia present that might be addressed by a medication adjustment or stent insertion? Was the issue medication error or noncompliance? Was the patient on an optimal outpatient medication regimen?
Medical management of heart failure has transformed the condition from a virtual death sentence to a chronic illness for many patients. The cornerstones of therapy are angiotensin-converting enzyme (ACE) inhibitors and beta blockers. Both unequivocally improve patient symptoms, prevent and reverse left ventricular remodeling, and reduce morbidity and mortality from the condition. Most clinicians begin therapy with an ACE inhibitor, but under certain circumstances (such as ischemic cardiomyopathy and tachycardia) the patient might benefit from a beta blocker as first-line therapy.
ACE INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS
The 2005 ACC/AHA guidelines call for ACE inhibitor use across the entire spectrum of heart failure: in any patient with symptomatic heart failure, in asymptomatic ventricular dysfunction with a left ventricular EF below 35% to 40%, and in all patients post-MI. These recommendations are based on extensive data showing a 23% reduction in all-cause mortality and a 35% reduction in cardiovascular death or hospitalization. Although ACE inhibitors may have somewhat less efficacy in African-Americans (or perhaps higher doses may be necessary to achieve desired effects), the ACC/AHA guidelines continue to recommend the use of these drugs in this population.
It is best to start ACE inhibitor therapy at a low dose, which can then be titrated as tolerated toward the target dose (see table below). Patients may be euvolemic or hypervolemic at the time of initiation, but use caution if the systolic blood pressure is less than 90 mm Hg. Renal function and serum potassium levels should be checked after one to two weeks. These drugs should not be used without concomitant diuretic therapy.
Adverse effects of ACE inhibitors may include hypotension (particularly after the first dose), worsening renal function, hyperkalemia, cough, angioedema, rash, ageusia, and neutropenia. Cough is the most common side effect and is likely related to the accumulation of bradykinin. It may attenuate over time, so patients should be encouraged to continue the medication for a while before switching to a different drug. If the cough is not tolerable, an angiotensin receptor blocker (ARB) is indicated. These drugs appear to offer many (but not all) of the benefits of ACE inhibitors, including a reduction in mortality and hospitalization.
Nonaspirin nonsteroidal anti-inflammatory medications (NSAIDs) antagonize the beneficial effects of ACE inhibitors. Their use in heart failure is relatively contraindicated.
USE OF BETA BLOCKERS
Widespread adoption of beta blocker use in heart failure has been somewhat slower than for ACE inhibitors, perhaps because they require a slower, more cautious approach. Nonetheless, beta blockers are at least as efficacious in reducing morbidity and mortality from systolic dysfunction heart failure as ACE inhibitors. Chronic sympathetic overactivation in heart failure leads inexorably to sodium retention via the renin-angiotensin-aldosterone system (RAAS), myocyte hypertrophy and injury, and left ventricular remodeling; it also causes fatal arrhythmias. Beta blockers restore the density of beta-1 receptors (reverse down-regulation), inhibit cardiotoxicity of catecholamines, reduce neurohormonal activation and heart rate, and exhibit antihypertensive and antiarrhythmic properties.
Clinical benefits of beta blockers include reduced hospitalizations, decreased incidence of sudden death, and improved overall survival. Unfortunately, these drugs improve symptoms of heart failure only over the long term. They often worsen symptoms transiently, requiring a higher dose of a diuretic and sometimes a lower dose of an ACE inhibitor to maintain patient well-being. Within a few months of initiation of therapy, however, the survival benefit becomes statistically apparent.
Beta blocker therapy should be initiated in euvolemic, clinically stable patients. Starting the medication during a hospital stay for heart failure may be appropriate after the patient’s condition has stabilized. Three beta blockers (carvedilol, metoprolol, and bisoprolol) have been established as clearly effective, so therapy should include one of these. Carvedilol is a nonselective beta blocker with alpha-1 antagonist properties; metoprolol and bisoprolol are beta-1 selective agents. Generic metoprolol tartrate is inexpensive but must be taken twice daily. Brand metoprolol succinate is somewhat more expensive and is taken only once daily. It is likely that the clinical differences among the medications are not significant, so the physician should choose the agent with which he is most familiar and that is affordable to the patient.
In contrast with the use of beta blockers for the treatment of hypertension, the initial dose for heart failure should be as low as possible. Dose titration should occur no more frequently than every two weeks and should proceed slowly. Patients need to be advised that they may feel somewhat worse for a few weeks after starting to take the medication. They should also be told to call the prescribing physician if they develop any signs or symptoms of fluid retention (such as dyspnea, edema, or weight gain).
There are few contraindications to the use of beta blockers. Symptomatic bradycardia or high-grade AV block, if present, should delay starting beta blocker therapy until a pacemaker has been implanted. Symptomatic bradycardia that occurs while the patient is on beta blocker therapy should prompt consideration of a pacemaker rather than discontinuation of the drug. Inadequately controlled asthma is a contraindication to beta blocker therapy, but cautious initiation of a beta-1 selective agent (such as metoprolol) may be attempted in patients whose asthma is stabilized. Diabetes is not a contraindication to beta blocker therapy.
DIGOXIN AND ALDOSTERONE ANTAGONISTS
Digoxin inhibits cellular sodium-potassium ATPase and improves myocardial contractility. It also promotes natriuresis and modulates various neurohumoral axes. Unlike ACE inhibitors and beta blockers, however, digoxin does not reduce overall mortality from heart failure, but it does alleviate symptoms of heart failure and reduces hospitalizations. Recent data suggest that digoxin’s neurohumoral effects may be more important than its direct inotropic properties. These effects are attainable with low doses, at serum levels well below the traditional therapeutic range of 0.8 to 2.0 mcg/dl.
It would be appropriate to add digoxin when patients do not have a satisfactory clinical response to an ACE inhibitor, beta blocker, and diuretic combination. Another accepted indication is in patients with atrial fibrillation, to slow AV conduction and thus heart rate.
Digoxin’s low therapeutic/toxic ratio makes its safe use sometimes challenging, especially in patients with renal insufficiency and those who may become dehydrated. To minimize the risk of toxicity, serum levels should be maintained below 1.1 mcg/dl and normokalemia should be ensured.
As noted earlier, chronic activation of the RAAS is responsible for some of the symptoms of heart failure and for its progression. Aldosterone causes sodium and water retention (leading to edema), potassium and magnesium wastage (precipitating arrhythmias), and collagen deposition (causing fibrosis of the myocardium and arterial walls). Aldosterone antagonists oppose and reverse many of these effects. Adding an aldosterone antagonist like spironolactone should be considered in patients with an EF below 35% and a New York Heart Association (NYHA) class III or IV heart failure. (These patients would already be on an ACE inhibitor and a loop diuretic.) Low doses of an aldosterone antagonist decrease mortality 30% in this population over two to three years.
Aldosterone antagonists should not be used if hyperkalemia or renal insufficiency is present. The starting dose for spironolactone is 25 mg daily; for eplerenone it is 25 mg daily, titrated to 50 mg after a month. Serum potassium levels should be monitored at frequent intervals. If they rise above 5.5 mmol/L, the dosing interval should be increased to every 48 hours. If potassium levels are low or stable, increasing the spironolactone dose to 50 mg daily should be considered.
NITRATES AND HYDRALAZINE
Hydralazine and nitrates are vasodilators. Studies from the 1970s and ’80s suggested a mortality benefit with a combination of the nitrate isosorbide dinitrate (ISDN) and hydralazine (HDRLZ). Post-hoc analysis of these trials suggested that African-Americans might particularly benefit from this combination of drugs. A proprietary fixed combination product (BiDil) has recently been approved by the FDA after a recent study in African-Americans showed an incremental benefit in mortality, reduction in hospitalizations, and improved quality of life, even when added to a regimen of ACE inhibitors and beta blockers. The 2005 AHA/ACC guidelines suggest that the combination of HDRLZ and a nitrate is “reasonable” for patients with a low EF and persistent symptoms who are already taking an ACE inhibitor and a beta blocker.
The African-American Heart Failure Trial treatment group that was given BiDil had its dose titrated to one tablet of HDRLZ 75 mg plus ISDN 40 mg, administered three times daily. It is uncertain but likely that the medications given separately (much less expensive as generics) will be equally effective.
DIASTOLIC DYSFUNCTION
Diastolic dysfunction heart failure (DDHF) is diagnosed when patients present with symptoms of heart failure but are found to have an EF of more than 40%. The condition is particularly prevalent in the elderly, hypertensive individuals, diabetic patients, those with chronic renal insufficiency, and women. Pathophysiology reflects a stiff left ventricle that is unable to relax sufficiently during diastole and thus transmitting high left-sided pressure to the pulmonary veins. Ischemia is often present. A BNP level does not reliably distinguish between systolic and diastolic dysfunction, although very high levels are more common in systolic dysfunction.
The long-term prognosis for DDHF may be somewhat better than that for systolic dysfunction heart failure. The only clear outcome-focused evidence available for diastolic dysfunction establishes the need for good blood pressure control. Calcium channel blockers, which are contraindicated (with the exception of amlodipine) in systolic dysfunction, may be used for management of hypertension and ischemia in DDHF. Digoxin is not likely to be helpful in DDHF except when atrial fibrillation is present. Management of acute decompensation of DDHF does not differ significantly from systolic dysfunction.
OTHER MODALITIES
More and more patients are candidates for heart failure device therapy. Implantable technology includes cardiac pacing and defibrillation devices and direct left ventricular assist devices (LVADs).
Many patients with NYHA class III and IV heart failure have ventricular dyssynchrony, which results from an intraventricular conduction defect (usually a left bundle branch block). The nonsynchronous ventricular activation decreases ventricular filling and EF. Cardiac resynchronization via biventricular pacing produces simultaneous activation of both ventricles and improved left ventricular output. Using a transvenous approach, pacemaker leads are placed in the right atrium and ventricle and through the coronary sinus into a tributary of the great cardiac vein overlying the left ventricle.
Depending on the unit inserted, a variety of pacing options and defibrillator functions are possible. Referral should be considered for biventricular pacing in patients with NYHA class III (especially) or class IV (evidence of benefit less well-established) with an EF below 35% who are on optimal medical management for at least six months, with a QRS duration greater than 120 msec. Biventricular pacing improves heart failure symptoms in patients meeting the above criteria and probably also improves survival.
Arrhythmia is the major cause of death in heart failure patients, followed by pump failure. Medications (including amiodarone) do not prevent mortality. Implantable cardiac defibrillators (ICDs) do seem to provide a benefit, however, with relative risk reductions for all-cause mortality ranging from 23% to 54% over several years of use. Trials to date suggest ICDs benefit patients with either ischemic or nonischemic dilated cardiomyopathy, although the evidence is clearer for those with ischemic disease. Therefore, ICDs are recommended for primary prevention in patients with ischemic heart disease who are post-MI, with an EF below 30% and NYHA class II or III heart failure on optimal medical therapy and with an estimated survival time of more than one year, and for those with nonischemic heart disease with a low EF but not end-stage heart failure.
These devices are expensive. With the current cost of $40,000 to $50,000 for an ICD unit (including implantation expenses), Medicare could not afford to cover placement in all individuals who qualify based on the above criteria. It is likely that improved risk-scoring systems using more than just EF will be developed to guide selection of those patients most likely to benefit from ICD implantation.
Left ventricular assist devices take over the work of a failing ventricle, improving cardiac output. In certain very sick patients, an LVAD may reduce mortality from 75% at one year to 40%.
DOCUMENTATION STANDARDS
New standards published by JCAHO and the Center for Medicare and Medicaid Services require hospitals to implement and document measures designed to improve quality of care for heart failure patients. Growing evidence also supports the use of standard order sets and standardized discharge instructions. Physicians should advise their patients to take an active role in disease management, particularly in reporting changes in symptoms and daily weight promptly. For example, patients should report any gain of more than two pounds in one day or a gain of five pounds over baseline dry weight. Outpatient interventions, including a temporary increase in the diuretic dose, may prevent the need for hospitalization if patients participate in their own care. Patients should also be educated about their medications, recommended activity level, and the need for a low-salt diet prior to discharge.
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Suggested Reading
ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. American Heart Association (Web site). Available at: http://circ.ahajournals.org/cgi/reprint/112/12/e154. Accessed September 22, 2006.
Heart Failure Tools and Resources. Mountain Pacific Quality Health Foundation (Web site). Available at: http//www.mpqhf.org/mpqhf_web/clinicalfocusareas/heartdisease/
heartfailuretools.html.
Accessed November 27, 2006.
National Heart Care Quality Improvement Team: Cardiovascular Measures Annotated Clinical Bibliography,2005. Available at:http://www.medqic.org/dcs/ContentServer?cid=
1109274729924&pagename=Medqic%2FMQLiterature%2FLiteratureTemplate&c=MQLiterature. Accessed November 27, 2006.
Quality Improvement Literature in Heart Failure. MedQIC (Web site). Available at: http://www.medqic.org (click "Search for Literature" link, check "Heart Failure," click "search"). Accessed November 27, 2006.
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