Fluid Management Strategies in Heart Failure

Nancy M. Albert
Crit Care Nurse 2012;32:20-32 doi: 10.4037/ccn2012877
2012 American Association of Critical-Care Nurses Published online http://www.cconline.org Personal use only. For copyright permission information: http://ccn.aacnjournals.org/cgi/external_ref?link_type=PERMISSIONDIRECT

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Critical Care Nurse is the official peer-reviewed clinical journal of the American Association of Critical-Care Nurses, published bi-monthly by The InnoVision Group 101 Columbia, Aliso Viejo, CA 92656. Telephone: (800) 899-1712, (949) 362-2050, ext. 532. Fax: (949) 362-2049. Copyright 2012 by AACN. All rights reserved.

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Cover Article

Fluid Management Strategies in Heart Failure

Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC
In patients with chronic heart failure, fluid retention (or hypervolemia) is often the stimulus for acute decompensated heart failure that requires hospitalization. The pathophysiology of fluid retention is complex and involves both hemodynamic and clinical congestion. Signs and symptoms of both hemodynamic and clinical congestion should be assessed serially during hospitalization. Core heart failure drug and cardiac device therapies should be provided, and ultrafiltration may be warranted. Critical care, intermediate care, and telemetry nurses have roles in both assessment and management of patients hospitalized with acute decompensated heart failure and fluid retention. Nurse administrators and managers have heightened their attention to fluid retention because the Medicare performance measure known as the risk-standardized 30-day all-cause readmission rate after heart failure hospitalization can be attenuated by fluid management strategies initiated by nurses during a patients hospitalization. (Critical Care Nurse. 2012;32[2]:20-32,34)

CEContinuing Education
This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives: 1. Describe the pathophysiological processes related to fluid overload (hypervolemia) in heart failure 2. Recognize the signs, symptoms and diagnostic information needed to determine hypervolemia in heart failure 3. Identify strategies to manage hypervolemia associated with decompensated heart failure during hospitalization and after discharge

2012 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2012877

he term heart failure is defined as a clinical syndrome of decreased exercise tolerance and fluid retention due to structural heart disease (eg, cardiomyopathy or valvular disorders). Acute decompensated heart failure denotes development of progressive signs and symptoms of distress that require hospitalization in patients with a previous diagnosis of heart failure.1 Although many markers of acute decompensated heart failure are related to fluid retention,2 patients

may not have classic signs and symptoms of clinical congestion, such as respiratory distress, crackles, interstitial/alveolar edema, elevated jugular venous pressure or jugular venous distension, findings on chest radiographs, and an S3 heart sound. Patients may have hemodynamic congestion, defined as an increase in left ventricular filling and/or intravascular pressures.3 Hemodynamic congestion is a form of fluid retention that occurs earlier than does clinical congestion and indicates that the clinical manifestations of fluid retention may be imminent.3 Even when signs and symptoms of clinical congestion are relieved, patients may still have hemodynamic congestion that could lead to progression of heart failure and worsening prognosis.3 Thus, optimal assessment of fluid status and management of both hemodynamic and clinical congestion are integral components of nursing care. Congestion in any form is a hallmark of acute decompensated heart failure that stems from a cyclical detrimental process involving low
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cardiac output, arterial underfilling, activation of neurohormonal systems, and dysregulation between the heart and kidneys.4 Two large US heart failure registries, Acute Decompensated Heart Failure Registry (ADHERE)5 and Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF)6 collected data on the clinical features of patients hospitalized for acute decompensated heart failure. According to both registries, cardiogenic shock was uncommon, accounting for 2% or less of all cases. However, hypervolemic states were prevalent and often included dyspnea (89% and 90%, respectively), crackles (67% and 65%, respectively), and peripheral edema (66% and 65%, respectively) regardless of whether or not the ejection fraction was less than 40% (indicating systolic left ventricular dysfunction) or normal (indicating heart failure with preserved ejection fraction, or diastolic dysfunction). In this review, I briefly describe the complex pathophysiological processes of hypervolemia in hospitalized patients with decompensated heart failure and discuss fluid management strategies, many of which can be nurse-led or nurse-facilitated. Critical care, intermediate care, telemetry, and general care nurses have many opportunities to assess patients fluid status, correct hypervolemia, Author

and ensure that fluid management strategies are in place before a patient is discharged. Patients must also understand their roles in assessing, monitoring, and treating hypervolemia at home to optimize health-related clinical outcomes.

Pathophysiology of Hypervolemia
In patients with normal hemodynamic, neurohormonal, cardiac, and renal processes, an increase in total blood volume is associated with an increase in renal levels of sodium and water excretion4,7 (Figure 1). Renal excretion of sodium and water is due to a series of reflexes that maintain normal total body volume when atrial pressure increases. Thus, any increase in atrial pressure leads to a diminished release of arginine vasopressin (antidiuretic hormone), increased release of atrial natriuretic peptide, and decreased renal sympathetic tone.8 However, in patients with acute decompensated heart failure, total blood volume is not the determinant of renal excretion of sodium and water; the integrity of arterial circulation is a key factor in euvolemia.4 Patients with heart failure have either decreased cardiac output that causes underfilling of the arterial circulation or high cardiac output that prompts systemic arterial vasodilatation and underfilling of the arterial circulation.4 In order to

Nancy M. Albert is the senior director, Nursing Research and Innovation, Nursing Institute, and a clinical nurse specialist in the George M. and Linda H. Kaufman Center for Heart Failure at the Cleveland Clinic Foundation, Cleveland, Ohio.
Corresponding author: Nancy M. Albert, PhD, CCNS, CHFN, CCRN, NE-BC, FAHA, FCCM, 9500 Euclid Ave, Mail code J3-4, Cleveland, OH 44195 (e-mail: albertn@ccf.org). To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org.

compensate, total blood volume is increased by expansion of blood volume in the venous circulation and systemic vascular resistance (afterload) increases.9 Increased afterload combined with impaired systolic performance also leads to an acute increase in left ventricular enddiastolic pressure. An acute increase in left ventricular end-diastolic and pulmonary venous pressures causes an increase of pressure in the alveoli. When the absorptive capabilities of the alveoli cells are overwhelmed, pulmonary congestion occurs.9 Further, in acute decompensated heart failure, normal reflexes stimulated by increased atrial pressure are blunted by reflexes initiated in the high-pressure arterial circulation. For example, an increase in total blood volume associated with decompensated heart failure prompts activation of the reninangiotensin-aldosterone system, leading to production of angiotensin II.3 Angiotensin II has many physiological effects, including peripheral and renal vasoconstriction (to restore arterial pressure and improve cardiac output), increased thirst, and stimulation of the sympathetic nervous system. Angiotensin II increases synthesis of aldosterone, leading to renal reabsorption of sodium and sodium retention.8,10 Activation of the sympathetic nervous system leads to elevated plasma levels of norepinephrine that stimulate -receptors in the nephron, enhancing reabsorption of sodium in the proximal tubules.8,10 In addition, -receptors in the juxtaglomerular apparatus stimulate the renin-angiotensinaldosterone system, further enhancing proximal tubular reabsorption of sodium.8 Normally,

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Normal cardiac output and effective arterial blood volume + fluid overload

Distal tubule sodium reabsorption Atrial natriuretic peptide Extracellular fluid volume

Plasma renin, aldosterone, norepinephrine, and arginine vasopressin

Glomerular filtration rate

Proximal tubule sodium reabsorption

Enhanced sodium and water delivery to the distal tubule

Renal sodium and water excretion

No edema formation and other signs and symptoms of fluid overload

Figure 1 Events in adults with normal cardiac output and effective blood volume when fluid overload occurs.
Adapted from Schrier,7 with permission.

atrial natriuretic peptide increases glomerular filtration rate and excretion of water and sodium; however, in advanced heart failure, these effects are attenuated by renal vasoconstriction and a reduction in sodium delivery to the distal nephron. Arginine vasopressin is released as a result of arterial underfilling. Arginine vasopressin increases plasma and urine osmolalities and leads to

peripheral arterial vasoconstriction and water reabsorption in the cells of the distal tubule and collecting duct in the kidney, promoting hyponatremia.8 Figure 2 provides a global depiction of interacting events and responses that occur in patients with reduced cardiac output and fluid overload.7,10 Thus, activation of neurohormonal systems leads to worsening

retention of sodium and water that contributes to pulmonary congestion, hyponatremia, and edema. Ultimately, a vicious cycle occurs, with activation of neurohormonal systems leading to worsening cardiac function and further stimulation of neurohormonal systems.4 In addition to the pathophysiological processes of acute decompensated heart failure set in motion when

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Le f

In

mode ial re card o y m lar rload icu r t afte n e e s tv ea cr

ling

Left ven tricu lar m yo I n c reas cardi Heart failure with e a al r low cardiac output e fte rlo mod and arterial e underfilling + Fluid overload (high preload)*

ad

g lin

Activation of the arterial baroreceptors

Nonosmotic vasopressor stimulation

Stimulation of sympathetic nervous system

Activation of the renin-angiotensionaldosterone system

Renal water retention

Peripheral arterial resistance

Renal vascular resistance

Renal sodium retention

Renal sodium and water excretion

* Hemodynamic congestion.

Edema and other signs and symptoms of fluid overload

Figure 2 Events in adults with low cardiac output and ineffective blood volume (arterial underfilling) when fluid overload occurs (high preload).
Adapted from Schrier,7 with permission.

total blood volume increases because of arterial underfilling, increased left ventricular filling (diastolic) pressure and myocardial stretch (left ventricular dilatation) are also powerful mechanisms of neurohormonal activation and hypervolemia that can further impair cardiac function.2

Assessment of Hypervolemia
Accurate assessment of hypervolemia is important, because freedom from hypervolemia after

hospitalization has been associated with improvement in long-term clinical outcomes. Lucas et al11 assessed patients 4 to 6 weeks after hospital discharge for 5 signs of hypervolemia: orthopnea, peripheral edema, weight gain, need to increase baseline diuretic dose, and jugular venous distension. Patients with any 3 of the 5 signs 6 weeks after discharge had a 3-fold increase in mortality at 2 years after the index hospitalization. In another study,12 investigators defined clinical exacerbation of heart

failure as the occurrence of at least 2 of the following: new or worsening edema, increased body weight, worsened dyspnea, worsened orthopnea, worsened paroxysmal nocturnal dyspnea, and increased jugular venous distension, all of which are indications of hypervolemia. In 189 outpatients with heart failure, episodes of clinical exacerbation were assessed over time. More episodes of clinical exacerbation were associated with an increased rate of hospitalization for heart failure, an increased risk of

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mortality over a 2-year period, and a greater likelihood of lower quality of life, lower functional status, and poorer exercise tolerance. In other studies,13,14 repeated hospitalizations for heart failure decompensation were associated with all-cause mortality, even after adjustments for patients characteristics. Moreover, hemodynamic congestion is not benign. In one study,15 increased blood volume was associated with increased pulmonary artery wedge pressure and increased risk for death or urgent heart transplantation at 1 year. Although assessment of hypervolemia is important, some nuances are worth mentioning. First, although some signs and symptoms (weight gain, nocturia, elevated jugular venous pressure, lower extremity edema, positive hepatojugular reflux, paroxysmal nocturnal dyspnea, and crackles) were significant predictors of decompensated heart failure in patients treated in an emergency department, the overall sensitivity (the probability that signs or symptoms assessed were present in patients who actually had worsening heart failure) of each sign or symptom was low, even though specificity (the probability that signs or symptoms were absent in patients without worsening heart failure) was high.16 Thus, signs and symptoms commonly associated with decompensated heart failure were not helpful in diagnosing heart failure as the current problem. Invasive hemodynamic monitoring may be needed to assess intracardiac pressures.1 Second, Mueller et al16 characterized daily dyspnea, edema, and

body weight in patients with heart failure for 1 month, and Albert et al17 determined if signs and symptoms differed between ambulatory and hospitalized patients. Although dyspnea was positively and significantly associated with edema, changes in body weight were not routinely associated with dyspnea or edema.18 Hence, although changes in body weight might be associated with hospitalization for heart failure16,17,19 and repeat hospitalization for worsening heart failure,20 weight gain may not occur in patients with acute decompensated heart failure.21,22 Lack of association of body weight with dyspnea or edema could have many causes, including failure to monitor a patients weight, offset of weight gain from fluid by weight loss from cachexia, and minimal weight gain because of diminished appetite due to ascites.17 Finally, hemodynamic congestion may not be associated with physical findings of hypervolemia. In a study15 of ambulatory nonedematous patients, physical findings of hypervolemia were infrequent and were not associated with increased blood volume. In patients with acutely decompensated heart failure, pulmonary artery wedge pressures can be elevated even though crackles and edema are absent or infrequent, and jugular venous pressures may not be elevated.23,24 The biomarker B-type natriuretic peptide (BNP) may not be an ideal marker of volume status. In one study,25 levels of BNP increased with worsening heart failure and correlated with New York Heart Association functional class. However, in another study,26 after treatment, patients hemodynamic parameters

correlated better with changes in blood volume than with changes in BNP values. Although the sample size was small, the researchers26 thought that BNP values changed more slowly than did blood volume and were better for showing longterm rather than instantaneous volume status. Likewise, ONeill et al27 found that BNP levels were not accurate predictors of serial hemodynamic changes in hospitalized patients with advanced heart failure. Even though an initial decrease in BNP levels was associated with early improvement in hemodynamic parameters, a change in BNP level was not associated with a change in pulmonary artery wedge pressure. Research results1,8 reinforce the need to use more than 1 method to assess initial volume status, to determine the effectiveness of therapies, and to inform clinical decisions.

Fluid Management Strategies

The guidelines of the American College of Cardiology and American Heart Association1 and the Heart Failure Society of America28 include recommendations for management of patients with chronic heart failure during acute episodes that require hospitalization. The recommendations should be followed to ensure optimal management with evidencebased therapies. During both hospitalization and outpatient care, the aims of fluid management strategies for left ventricular systolic dysfunction and left ventricular dysfunction with preserved ejection fraction are relief of signs and symptoms of hypervolemia, stabilization of hemodynamic status without further

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damage of cardiac myocytes, and minimization of preventable recurrences of hypervolemia that require hospitalization for heart failure decompensation.1,28 In patients with hypervolemia, signs and symptoms are the tip of the iceberg in regard to congestion. Pathophysiological changes in hypervolemia include low cardiac output, arterial underfilling, elevation in left ventricular diastolic pressures, and neuroendocrine activation. Thus, managing hemodynamic congestion manifested by increased left ventricular filling pressure but no constellation of signs and symptoms is just as important as managing clinical congestion. Core medications for heart failure and cardiac resynchronization therapies are first-line strategies for managing hypervolemia because the interventions attenuate neurohormonal activation and prevent progression, or promote reversal, of left ventricular remodeling that can worsen congestion.1,28 Unless contraindicated, all patients should take an angiotensinconverting enzyme inhibitor (eg, lisinopril, enalapril, or captopril) or angiotensin II receptor blocker (eg, valsartan or candesartan) and a -blocker (eg, carvedilol, metoprolol succinate, or bisoprolol). Patients hospitalized with advanced systolic heart failure often meet indications for an aldosterone antagonist (eg, spironolactone or eplerenone) or hydralazine-and-nitrate combination therapy and cardiac resynchronization therapy.1,28 Finally, when patients have hypoperfusion and diuretic-resistant elevations in cardiac filling pressures, intravenous inotropic or vasopressor therapies

are indicated to maintain systemic perfusion and preserve or improve end-organ performance.1 Loop diuretics are the hallmark pharmacological treatment for hypervolemia.5 Because oral agents, especially furosemide, have irregular intestinal absorption and can have altered pharmacokinetics and pharmacodynamics, intravenous administration is preferred during the early part of hospital therapy.8 When administered intravenously, loop diuretics rapidly relieve signs and symptoms of pulmonary congestion by lowering left ventricular filling pressures.1 Initially, loop diuretics should be administered at a dose that is higher than the total daily outpatient dosage. Urine output and signs and symptoms of hypervolemia must be serially assessed so that the dosage of a diuretic can be titrated to a patients needs.1 Adverse events associated with use of diuretics include electrolyte imbalances (hypokalemia and hypomagnesemia) leading to serious dysrhythmias, hypotension (especially when vasodilator therapy is used concomitantly), and worsening renal function.8 Electrolyte levels, hemodynamic parameters, and

overall fluid volume status must be carefully monitored and managed. Diuretic resistance is common in patients with advanced heart failure because of hypertrophy of distal tubule epithelial cells,29 increased activation of the renin-angiotensinaldosterone system,30 and decreased glomerular filtration rate.7 Strategies to overcome diuretic resistance are provided in Table 1. Some therapies developed to directly or indirectly relieve hypervolemia were promising in early research but did not improve shortand long-term quality of life, morbidity, and mortality in large-scale randomized controlled trials. A1 adenosine receptor antagonists,31 vasopressin receptor antagonists,32 and levosimenden33 resulted in removal of excess fluid or improved cardiac output in heart failure in clinical trials but were not approved by the Food and Drug Administration because the medications did not decrease the number of hospitalizations for heart failure or mortality rates. Likewise, early clinical outcomes did not differ between treatment groups in acutely decompensated, hospitalized patients with heart failure and stable hemodynamic

Table 1

Strategies to overcome diuretic resistancea

1. Infuse the agent as a continuous intravenous infusion: for example, furosemide at 5-40 mg/h or bumetanide at 0.1-0.5 mg/h 2. Administer 2 diuretic agents at the same time: for example, a loop diuretic and an agent that blocks the distal tubule Intravenous chlorothiazide (500-1000 mg), given 30 minutes before administration of an intravenous loop diuretic Oral metolazone (2.5-10 mg) given with an oral loop agent 3. Rotating loop diuretic agents: for example, switching or alternating between oral furosemide and torsemide
a No large, randomized trials that provide evidence of the effectiveness of these strategies have been done. Based on data from Jessup et al1 and the Heart Failure Society of America.28

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status who were randomized to continuous intravenous infusion of milrinone or placebo.34 More patients sustained hypotension requiring intervention and had new atrial arrhythmias in the milrinone group. Further, use of milrinone in patients who had worsening renal function (increasing serum levels of urea nitrogen) during hospitalization did not have improved outcomes despite minor improvements in renal function.35 As a therapeutic procedure, ultrafiltration is the mechanical removal of fluid from the vasculature. Whole blood passes across a

the amount of sodium in the water component of plasma.36 In addition, diuretic therapy can cause hypovolemia, which enhances renal secretion of renin and activation of neurohormones. In ultrafiltration, fluid is removed from the blood at the same rate at which fluid is reabsorbed from the edematous interstitium; therefore, prolonged intravascular hypovolemia does not occur and neurohormonal activation is not stimulated.37 Ultrafiltration became a more clinically relevant option after a portable, peripheral venovenous system became available and the

Other disadvantages of ultrafiltration therapy are patients costs, need for training nurses in the procedure, nurse staffing, excessive volume removal (resulting in hypotension and worsening prerenal azotemia), and catheter-related or system complications, such as infection, thrombosis, air embolism, or hemorrhage due to disconnection of the venous return catheter.40 To date, peripheral ultrafiltration has not been better than aggressive intravenous diuretic therapy in improving signs and symptoms, causing weight loss, or preventing complications.

recommendations and advocate for patients during daily rounds with physicians and pharmacy care providers.
hemofilter (a semipermeable membrane) to yield plasma water in response to a pressure gradient created by the filtrate compartments and hydrostatic pressures in blood and also by oncotic pressure produced by plasma proteins.36 The ultrafiltration device extracts blood from and then returns it to the venous circulation via separate access points with large venous catheters (known as a venovenous technique) and an extracorporeal blood pump. Vascular catheters can be placed in the femoral, internal jugular, or subclavian veins and in large peripheral veins. The procedure can be performed only once, continuously or intermittently. Unlike the situation in fluid removal with diuretics, which is primarily hypotonic, the sodium content in the ultrafiltrate is equal to results of a multicenter, randomized, controlled research trial38 corroborated the usefulness of the treatment. When peripheral ultrafiltration was compared with diuretic therapy in patients with acute decompensated heart failure, patients treated with ultrafiltration had greater weight loss, decreased need for vasoactive drugs, and reduced 90-day rate of rehospitalization.38 However, in a small single-center study39 in patients with very advanced heart failure and diuretic resistance, ultrafiltration was associated with variable fluid removal, and renal function worsened in 45% of patients during therapy. Overall, in 3 of 5 trials of peripheral ultrafiltration with a portable system, readmission was not improved in 3 studies, and signs and symptoms were significantly reduced in only 1 study.40 Interdisciplinary nurse-physician or nurse-led programs, initiated and maintained in a variety of environments of care, did not prevent worsening hypervolemia associated with rehospitalization. Education before hospital discharge41-43; counseling43-46; and follow-up programs after discharge,47,48 including transition-tohome,43,46 telephone, and other forms of remote monitoring48,49 programs, were associated with adherence to prescribed therapies and fewer rehospitalizations after discharge. However, most strategies used to minimize preventable hypervolemia and subsequent morbidity and mortality were not well described and therefore are hard to replicate. Investigators provided a global overview of programs but did not provide details of key components,

Nurses must understand medically appropriate care

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Table 2

New York Heart Association functional classificationa and examples

Definition Ordinary physical activity does not cause symptoms Ordinary physical activity may be slightly limited by symptoms but no symptoms at rest Physical activity is markedly limited because of symptoms Physical activity cannot be carried out without symptoms; symptoms occur at rest Example A: Stair climbing Example B: Personal grooming A: Patient can climb 2 full flights (basement to second floor) with out symptoms developing B: Patient is not limited A: Symptoms occur after climbing 1 full flight (12 regular steps) or 8 steps while carrying 10.8 kg (24 lb) B: Symptoms occur during or after washing, dressing, preparing meals, but patient does not need to stop A: Patient cannot climb 1 full flight without stopping B: Symptoms occur during washing, dressing, or preparing meals; patient needs to take a break A: Patient cannot climb more than 1 or a few steps without taking a break because of symptoms B: Symptoms occur when patient initiates personal grooming behaviors

Functional status I, Asymptomatic

II, Mild

III, Moderate

IV, Severe

a Signs

and symptoms: dyspnea, fatigue, chest pain, palpitations.

the depth or breadth of content delivered (program intensity), or assessment methods used to determine and enhance patients understanding. Additionally, not all programs were effective in preventing hospitalizations, even if patients had improvement in knowledge or self-care.48-51

Nursing Implications
Assessment

Because of the nuances of hypervolemia assessment in heart failure, nurses must not base decisions on volume status on a single method of assessment or on only a few variables. Physical signs and symptoms must be assessed along with patients subjective perceptions of clinical changes in status, such as worsening exercise intolerance or changes in New York Heart Association functional class (Table 2). A valuable assessment variable for hypervolemia may be history of recent hospitalization for heart failure. Nurses should ask patients about recent hospital events, especially if patients use more

than a single health care center to meet health needs. Specific issues and tips for assessing hypervolemia are provided in Table 3. In lieu of invasive hemodynamic monitoring to measure intracardiac pressures and definitively determine hemodynamic congestion, clinicians can be trained to use other technology. Portable, handheld, pocketsized ultrasound machines can be used to determine left ventricular function, detect pericardial effusions, predict intravenous fluid responsiveness, and identify important valvular defects.64,65 For patients with implantable cardioverter defibrillators that also measure intrathoracic impedance, impedance data (on intrathoracic fluid) can be downloaded by using a wand system similar to that used to download pacemaker data. The impedance report provides data about the presence of thoracic congestion. In a study66 of 23 patients, impedance values measured by using an implantable cardioverter defibrillator were compared with pulmonary

artery wedge pressures measured noninvasively by using echocardiography. The results indicated a strong correlation between high wedge pressure and low intrathoracic impedance.
Fluid Management

Currently, a gap exists between clinical expectations for use of evidence-based treatment recommendations and actual practice. Disparities are prevalent in the quality of care in heart failure at both the patient67-69 and hospital level.67,68,70 Nurses must understand medically appropriate care recommendations and advocate for patients during daily rounds with physicians and pharmacy care providers. Nurses should participate in quality improvement programs that focus on monitoring the adherence of health care providers use of heart failure medications chosen on the basis of research evidence and recommendations for use of cardiac devices. Nurses should also participate in quality improvement programs that focus

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Table 3

Hypervolemia assessment issues and tips

Issue 1: Insensitivity of common signs and symptoms of heart failure15-17 Ask multiple questions, in a variety of ways, to obtain a well-rounded picture of the incidence and level (mild, moderate, or severe) of signs and symptoms. - For example, when assessing dyspnea, do not just ask if it had worsened before the patient came to the hospital or outpatient clinic. Patients may decrease activity level to prevent worsening of dyspnea. Ask what activities the patient has given up or is doing more slowly or less frequently because of dyspnea. Ask if caregivers have changed behaviors to minimize patients dyspnea. Obtain an individualized history of events that might be the reason for new or worsening signs and symptoms of hypervolemia. - For example, if a patient complains of difficulty sleeping, you might learn that he or she has nocturia. Once the problem is identified, ask the patient about Change in dietary behaviors (eating away from home or a change in purchasing practices) Change in food preparation (new meal planner or cook) Recent nonadherence to medications for heart failure New or worsening thirst leading to increased fluid intake Use of ibuprofen or other over-the-counter drugs that cause sodium and water retention Use noninvasive and internal monitoring features of cardiac devices to aid in assessment when elevations in pulmonary artery wedge pressure cannot be directly assessed.52 - When measurement of thoracic impedance is available as a feature of an implantable cardioverter-defibrillator device, assess thoracic impedance levels.53 - If respiratory distress or clinical evidence of impaired perfusion and intracardiac filling pressures cannot be assessed clinically, use invasive hemodynamic monitoring.1 Issue 2: Neuroendocrine activation leading to hypervolemia could be due to nonoptimal medication regimen or medication nonadherence.1,28,54 Obtain medication reconciliation related to therapies used before hospitalization. - Report findings and patients rationale for not taking medications as prescribed. - Report core medications not prescribed for heart failure. - Report identified contraindications to medications for heart failure. - Report medications not for heart failure that could worsen heart failure. Issue 3: Nonadherence to self-care program for heart failure may have multiple, patient-specific causes that may be related to or beyond knowledge and skills deficits.26,55-58 Carefully assess patients rationale for nonadherence. Consider economic issues (transportation or costs of care), social issues (caregiver support, loneliness),57 psychological issues (depression, anxiety),58 and cognition issues.59 Assess health literacy.60 Assess number of heart failure health care provider services as patients may be receiving mixed or confusing advice.61 Issue 4: Be aware of laboratory and clinical parameters that may be helpful in determining hypervolemia, renal dysfunction that aggravates hypervolemia,8 or other medical conditions associated with decreased cardiac output and neuroendocrine activation leading to hypervolemia.1,28,62,63 Assess creatinine clearance (estimated glomerular filtration rate). Assess increases ion serum levels of urea nitrogen and creatinine during hospitalization. Assess hemoglobin level for presence of anemia that could be due to hemodilution. Assess serum sodium level for hyponatremia, which is a marker of an increase in plasma levels of arginine vasopressin (and water retention). Assess for elevated blood pressure that may be associated with stimulation of the sympathetic nervous system. Assess QRS duration 120 ms associated with cardiac dyssynchronization that can lead to mitral regurgitation and pulmonary congestion as well as hypervolemia from neuroendocrine activation associated with poor cardiac performance. Assess serum levels of troponins I and T, which are highly sensitive markers of myocardial injury. Elevated values (troponin I >1 g/L or troponin T >0.1 g/L) could indicate cardiac myocyte damage as the precipitant of hypervolemia. Assess worsening burden of comorbid conditions that could cause acute deterioration in renal function (eg, worsening diabetes or hypertension).

on the understanding of patients and patients families of education received, adherence to early (7-day) follow-up care, and adherence to the nonpharmacological plan of care. Nurses should participate on interdisciplinary collaborative teams to implement strategies to

improve quality of care and conformity with recommended guidelines for management of heart failure. The need is great for nurses to develop and participate in programs that ease the transition of patients and informal caregivers from hospital to home and focus on

disease management. Nurse-led initiatives can facilitate safe and effective care before patients are discharged, increase awareness of patients and informal caregivers barriers to optimal self-care, and prepare patients and informal caregivers to adhere to the plan of care.

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Patients nonadherence to methods for managing heart failure has been associated with acute decompensated heart failure leading to hospitalization.71-73 Nonadherence to diet, medication, or fluid restriction was cited as a reason for readmission by 25% of patients and 26% of informal caregivers.72 However, only 14% of cardiologists and 13% of heart failure nurses thought nonadherence was the primary reason for hospitalization.72 Cardiologists and heart failure nurses were more likely to cite other diseases, nonoptimal medical regimens, knowledge deficits, and delay in seeking help as reasons for hospitalization. Among participants in the study,72 33% of patients and 23% of heart failure nurses cited improving adherence to heart failure therapies as the primary intervention to prevent readmissions. Adequate professional help was identified by 35% of family caregivers as the most important intervention. Cardiologists identified 2 primary interventions as equally important: improving adherence and adequate professional help. Nurses have an opportunity and a responsibility to help patients improve adherence to regimens for managing heart failure. Research results highlight the need for greater vigilance in optimal assessment of possible causes of patients nonadherence with the heart failure plan of care so that an individualized approach can be

developed. Nurses must ensure consistency of hospital-based education and counseling related to fluid management (weight monitoring, fluid restriction when ordered, and low-sodium diet). Nurses must also ensure consistency in the delivery of interventions to manage heart failure (including those targeting clinicians and informal caregivers) and in assessment of the effectiveness of the interventions by studying clinical outcomes and cost of care so that deficiencies can be corrected. Attention to emerging knowledge and evidence-based practices is paramount to a successful program focused on patients, patients families and patients informal caregivers. Revised national guideline recommendations and new research that provides important and generalizable findings should be the basis for standards of clinical care.

Nurse-led or nurse-facilitated education, counseling, and follow-up programs after discharge from the hospital promote patients and caregivers knowledge and expectations for adherence to heart failure selfcare. During acute decompensated heart failure, nursing care that conforms to the recommendations of evidence-based guidelines to reconcile and prevent hypervolemia may promote improved outcomes. CCN

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Financial Disclosures
None reported.

References
1. Jessup M, Abraham WT, Casey DE, et al; 2009 Writing Group to Review New Evidence and Update the 2005 Guideline for the Management of Patients with Chronic Heart Failure Writing on Behalf of the 2005 Heart Failure Writing Committee. 2009 Focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation. Circulation. 2009; 119(14):1977-2016. 2. Metra M, Dei Cas L, Bristow MR. The pathophysiology of acute heart failureit is a lot about fluid accumulation. Am Heart J. 2008; 155:1-5. 3. Gheorghiade M, Filippatos G, De Luca L, Burnett J. Congestion in acute heart failure syndromes: an essential target of evaluation and treatment. Am J Med. 2006;119(12 suppl 1):S3-S10. 4. Chen HH, Schrier RW. Pathophysiology of volume overload in acute heart failure syndromes. Am J Med. 2006;119(12 suppl 1): S11-S16. 5. Adams KF Jr, Fonarow GC, Emerman CL, et al; ADHERE Scientific Advisory Committee and Investigators. Characteristics and outcomes of patients hospitalized for heart failure in the United States: rationale, design, and preliminary observations from the first 100 000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE). Am Heart J. 2005;149:209-216. 6. Gheorghiade M, Abraham WT, Albert NM, et al; OPTIMIZE-HF Investigators and Coordinators. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. JAMA. 2006;296:2217-2226.

Summary
Hypervolemia (both hemodynamic and clinical congestion) is an import predictor of worsening heart failure, morbidity leading to hospitalization for heart failure, and mortality. Hypervolemia can be difficult to recognize when common signs and symptoms of clinical congestion are not manifested during an acute congestive exacerbation. Clinical congestion often occurs later than elevated left ventricular filling pressure (hemodynamic congestion) does, necessitating use of multiple measures and methods of monitoring hypervolemia. Nurse-led or nurse-facilitated delivery of interventions to manage heart failure may decrease practice gaps associated with worsening heart failure due to hypervolemia.

To learn more about caring for heart failure patients, read Caregiving for Patients With Heart Failure: Impact on Patients Families by Hwang et al in the American Journal of Critical Care, 2011;20: 431-442. Available at www.ajcconline.org.

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7. Schrier RW. Body fluid volume regulation in health and disease: a unifying hypothesis. Ann Intern Med. 1990;113(2):155-159. 8. Sarraf M, Masoumi A, Schrier RW. Cardiorenal syndrome in acute decompensated heart failure. Clin J Am Soc Nephrol. 2009;4: 2013-2026. 9. Cotter G, Felker M, Adams KF, Milo-Cotter O, OConnor CM. The pathophysiology of acute heart failureis it all about fluid accumulation? Am Heart J. 2008;155(1):9-18. 10. Cadnapaphornchai MA, Gurevich AK, Weinberger HD, Schrier RW. Pathophysiology of sodium and water retention in heart failure. Cardiology. 2001;96:122-131. 11. Lucas C, Johnson W, Hamilton MA, et al. Freedom from congestion predicts good survival despite previous class IV symptoms of heart failure. Am Heart J. 2000;140:840-847. 12. Sayers SL, Riegel B, Goldberg LR, Coyne JC, Samaha FF. Clinical exacerbations as a surrogate end point in heart failure research. Heart Lung. 2008;37:28-35. 13. Setoguchi S, Stevenson LW, Schneeweiss S. Repeated hospitalizations predict mortality in the community population with heart failure. Am Heart J. 2007;154:260-266. 14. Lee DS, Austin PC, Stukel TA, et al. Dosedependent impact of recurrent cardiac events on mortality in patients with heart failure. Am J Med. 2009;122:162-169. 15. Androne AS, Hryniewicz K, Hudaihed A, Mancini D, Lamanca J, Katz SD. Relation of unrecognized hypervolemia in chronic heart failure to clinical status, hemodynamics, and patient outcomes. Am J Cardiol. 2004;93:1254-1259. 16. Mueller C, Frana B, Rodriguez D, LauleKilian K, Perruchoud AP. Emergency diagnosis of congestive heart failure: impact of signs and symptoms. Can J Cardiol. 2005; 21:921-924. 17. Albert NM, Trochelman K, Li J, Lin S. Heart failure signs and symptoms: are you asking the right questions? Am J Crit Care. 2010; 19(5):443-452. 18. Webel AR, Frazier SK, Moser DK, Lennie TA. Daily variability in dyspnea, edema and body weight in heart failure patients. Eur J Cardiovasc Nurs. 2007;6:60-65. 19. Chaudhry SI, Wang Y, Concato J, Gill TM, Krumholz HM. Patterns of weight change preceding hospitalization for heart failure. Circulation. 2007;116:1549-1554. 20. Blair JE, Khan S, Konstam MA, et al; for EVEREST Investigators. Weight changes after hospitalization for worsening heart failure and subsequent re-hospitalization and mortality in the EVEREST trial. Eur Heart J. 2009;30:1666-1673. 21. Zhang J, Goode KM, Cuddihy PE, Cleland JG; TEN-HMS Investigators. Predicting hospitalization due to worsening heart failure using daily weight measurement: analysis of the Trans-European Network-Home-Care Management System (TEN-HMS) study. Eur J Heart Fail. 2009;11(4):420-427. 22. Mehta RH, Rogers JG, Hasselblad V, et al. Association of weight change with subsequent outcomes in patients hospitalized with acute decompensated heart failure. Am J Cardiol. 2009;103:76-81. 23. Mahdyoon H, Klein R, Eyler W, Lakier JB, Chakko SC, Gheorghiade M. Radiographic pulmonary congestion in end-stage congestive heart failure. Am J Cardiol. 1989;63: 625-627.

24. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989;261:884-888. 25. Maisel AS, Krishnaswamy P, Nowak RM, et al; Breathing Not Properly Multinational Study Investigators. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347(3):161-167. 26. James KB, Troughton RW, Feldschuh J, Soltis D, Thomas D, Fouad-Tarazi F. Blood volume and brain natriuretic peptide in congestive heart failure: a pilot study. Am Heart J. 2005;150:984.e1-984.e6. 27. ONeill JO, Bott-Silverman CE, McRae AT, et al. B-type natriuretic peptide levels are not a surrogate marker for invasive hemodynamics during management of patients with severe heart failure. Am Heart J. 2005; 149:363-369. 28. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010;16(6):e1-e194. 29. Liang KV, Williams AW, Greene EL, Redfield MM. Acute decompensated heart failure and the cardiorenal syndrome. Crit Care Med. 2008;36(1 suppl):S75-S88. 30. Wang DJ, Gottlieb SS. Diuretics: still the mainstay of treatment. Crit Care Med. 2008; 36(1 suppl):S89-S94. 31. Massie BM, OConnor CM, Metra M, et al; PROTECT Investigators and Committees. Rolofylline, an adenosine A1-receptor antagonist, in acute heart failure. N Engl J Med. 2010;363:1419-1428. 32. O'Connor CM, Miller AB, Blair JE, et al; Efficacy of Vasopressin Antagonism in heart Failure Outcome Study with Tolvaptan (EVEREST) investigators. Causes of death and rehospitalization in patients hospitalized with worsening heart failure and reduced left ventricular ejection fraction: results from Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) program. Am Heart J. 2010;159:841-849. 33. Mebazaa A, Nieminen MS, Packer M, et al; SURVIVE Investigators. Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE Randomized Trial. JAMA. 2007;297:1883-1891. 34. Cuffe MS, Califf RM, Adams KF Jr, et al; Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002;287(12):1541-1547. 35. Klein L, Massie BM, Leimberger JD, et al; OPTIME-CHF Investigators. Admission or changes in renal function during hospitalization for worsening heart failure predict postdischarge survival: results from the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF). Circ Heart Fail. 2008;1:25-33. 36. Ronco C, Ricci Z, Bellomo R, Bedogni F. Extracorporeal ultrafiltration for the treatment of overhydration and congestive heart failure. Cardiology. 2001;96:155-168. 37. Marenzi GC, Lauri G, Grazi M, et al, Circulatory response to fluid overload removal by extracorporeal ultrafiltration in refractory

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congestive heart failure. J Am Coll Cardiol. 2001;38:963-968. Costanzo MR, Guglin ME, Saltzberg MT, et al; UNLOAD trial investigators. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007; 49:675-683. Liang KV, Hiniker AR, Williams AW, Karon BL, Greene EL, Redfield MM. Use of a novel ultrafiltration device as a treatment strategy for diuretic resistant, refractory heart failure: initial clinical experience in a single center. J Card Fail. 2006;12(9):707-714. Shin JT, Dec GW. Ultrafiltration should not replace diuretics for the initial treatment of acute decompensated heart failure. Circ Heart Fail. 2009;2:505-511. Koelling TM, Johnson ML, Cody RJ, Aaronson KD. Discharge education improves clinical outcomes in patients with chronic heart failure. Circulation. 2005;111(5):179-185. Caldwell MA, Peters KJ, Dracup KA. A simplified education program improves knowledge, self-care behavior, and disease severity in heart failure patients in rural settings. Am Heart J. 2005;150:983e7-983e12. Anderson C, Deepak BV, Amoateng-Adjepong Y, Zarich S. Benefits of comprehensive inpatient education and discharge planning combined with outpatient support in elderly patients with congestive heart failure. Congest Heart Fail. 2005;11(6):315-321. Blue L, Lang E, McMurray JJ, et al. Randomised controlled trial of specialist nurse intervention in heart failure. BMJ. 2001;225:715718. Soran OZ, Pna IL, Lamas GA, et al. A randomized clinical trial of the clinical effects of enhanced heart failure monitoring using a computer-based telephonic monitoring system in older minorities and women. J Card Fail. 2008;14:711-717. Naylor MD, Brooten DA, Campbell RL, Maislin G, McCauley KM, Schwartz JS. Transitional care of older adults hospitalized with heart failure: a randomized, controlled trial. J Am Geriatr Soc. 2004;52:675-684. Kasper EK, Gerstenblith G, Hefter G, et al. A randomized trial of the efficacy of multidisciplinary care in heart failure outpatients at high risk of hospital readmission. J Am Coll Cardiol. 2002;39:471-480. Klersy C, Di Silvestri A, Gabutti G, Regoli F, Auricchio A. A meta-analysis of remote monitoring of heart failure patients. J Am Coll Cardiol. 2009;54:1683-1694. Ferrante D, Varini S, Macchia A, et al. Longterm results after a telephone intervention in chronic heart failure. J Am Coll Cardiol. 2010; 56:372-378. Albert NM, Buchsbaum R, Li J. Randomized study of the effect of video education on heart failure healthcare utilization, symptoms, and self-care behaviors. Patient Educ Couns. 2007;69(1-3):129-139. Artinian NT, Harden JK, Kronenberg MW, et al. Pilot study of a Web-based compliance monitoring device for patients with congestive heart failure. Heart Lung. 2003;32(4): 226-233. Whellan DJ, Ousdigian KT, Al-Khatib SM, et al; PARTNERS study investigators. Combined heart failure device diagnostics identify patients at higher risk of subsequent heart failure hospitalizations: results from PARTNERS HF (Program to Access and

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Review Trending Information and Evaluate Correlation to Symptoms in Patients With Heart Failure) study. J Am Coll Cardiol. 2010; 55(17):1803-1810. Catanzariti D, Lunati M, Landolina M, et al; Italian Clinical Service Optivol-CRT group. Monitoring intrathoracic impedance with an implantable defibrillator reduces hospitalizations in patients with heart failure. Pacing Clin Electrophysiol. 2009;32(3):363-70. Welsh JD, Heiser RM, Schooler MP, et al. Characteristics and treatment of patients with heart failure in the emergency department. J Emerg Nurs. 2002;28(2):126-131. White MM, Howie-Esquivel J, Caldwell MA. Improving heart failure symptom recognition: a diary analysis. J Cardiovasc Nurs. 2010; 25(1):7-12. Sheahan SL, Fields B. Sodium dietary restriction, knowledge, beliefs, and decisionmaking behavior of older females. J Am Acad Nurse Pract. 2008;20(4):217-224. Rosland AM, Heisler M, Choi HJ, Silveira MJ, Piette JD. Family influences on selfmanagement among functionally independent adults with diabetes or heart failure: do family members hinder as much as they help? Chronic Illn. 2010;6(1):22-33. Morgan AL, Masoudi FA, Havranek EP, et al; for the Cardiovascular Outcomes Research Consortium (CORC). Difficulty taking medications, depression, and health status in heart failure patients. J Card Fail. 2006;12(1): 54-60. Heckman GA, Patterson CJ, Demers C, St Onge J, Turpie ID, McKelvie RS. Heart failure and cognitive impairment: challenges and opportunities. Clin Interv Aging. 2007; 2(2):209-218. Evangelista LS, Rasmusson KD, Laramee AS, et al. Health literacy and the patient with heart failureimplications for patient care and research: a consensus statement of the Heart Failure Society of America. J Card Fail. 2010;16(1):9-16. Remme WJ, McMurray JJ, Hobbs FD, et al; SHAPE study group. Awareness and perception of heart failure among European cardiologists, internists, geriatricians, and primary care physicians. Eur Heart J. 2008; 29(14):1739-1752. Jhanjee R, Templeton GA, Sattiraju S, et al. Relationship of paroxysmal atrial tachyarrhythmias to volume overload: assessment by implanted transpulmonary impedance monitoring. Circ Arrhythm Electrophysiol. 2009;2(5):488-494. Koide K, Yoshikawa T, Nagatomo Y, et al. Elevated troponin T on discharge predicts poor outcome of decompensated heart failure. Heart Vessels. 2010;25(3):217-222. Khasawneh FA, Smalligan RD. Focused transthoracic echocardiography. Postgrad Med. 2010;122(3):230-237. Culp BC, Mock JD, Chiles CD, Culp WC. The pocket echocardiograph: validation and feasibility. Echocardiography. 2010;27(7): 759764. doi:10.1111/j.1540-8175.2009.01125.x. Maines M, Catanzariti D, Cirrincione C, Valsecchi S, Comisso J, Vergara G. Intrathoracic impedance and pulmonary wedge pressure for the detection of heart failure deterioration. Europace. 2010;12(5):680-685. Albert NM, Yancy CW, Liang L, et al. Use of aldosterone antagonists in heart failure. JAMA. 2009;302:1658-1665.

68. Horwich TB, Hernandez AF, Liang L, et al; Get With the Guidelines steering committee and hospitals. Weekend hospital admission and discharge for heart failure: association with quality of care and clinical outcomes. Am Heart J. 2009;158:451-458. 69. Fonarow GC, Abraham WT, Albert NM, et al; OPTIMIZE-HF investigators and hospitals. Age- and gender-related differences in quality of care and outcomes of patients hospitalized with heart failure (from OPTIMIZE-HF). Am J Cardiol. 2009;104:107-115. 70. Ambardekar AV, Fonarow GC, Dai D, et al; Get With The Guidelines steering committee and hospitals. Quality of care and inhospital outcomes in patients with coronary heart disease in rural and urban hospitals (from Get With the Guidelines-Coronary Artery Disease Program). Am J Cardiol. 2010;105:139-143. 71. Fonarow GC, Abraham WT, Albert NM, et al; OPTIMIZE-HF investigators and hospitals. Factors identified as precipitating hospital admissions for heart failure and clinical outcomes: findings from OPTIMIZE-HF. Arch Intern Med. 2008;168(8):847-854. 72. Annema C, Luttik ML, Jaarsma T. Reasons for readmission in heart failure: perspectives of patients, caregivers, cardiologists, and heart failure nurses. Heart Lung. 2009; 38:427-434. 73. Klapholz M, Maurer M, Lowe AM, et al; New York Heart Failure Consortium. Hospitalization for heart failure in the presence of a normal left ventricular ejection fraction: results of the New York Heart Failure Registry. J Am Coll Cardiol. 2004;43:1432-1438.

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CCN Fast Facts

Facts
In patients with chronic heart failure, fluid retention (or hypervolemia) is often the stimulus for acute decompensated heart failure that requires hospitalization. The pathophysiology of fluid retention is complex and involves both hemodynamic and clinical congestion. Signs and symptoms of both hemodynamic and clinical congestion should be assessed serially during hospitalization. Core heart failure drug and cardiac device therapies should be provided, and ultrafiltration may be warranted. Adherence to heart failure medications improves cardiac function, leading to improvement in volume status. During both hospitalization and outpatient care, the aims of fluid management strategies for left ventricular systolic dysfunction and left ventricular dysfunction with preserved ejection fraction are relief of signs and symptoms of hypervolemia, stabilization of hemodynamic status without further damage of cardiac myocytes, and minimization of preventable recurrences of hypervolemia that require hospitalization for heart failure decompensation.1,2 Strategies to overcome diuretic resistance are provided in the Table.

The journal for high acuity, progressive, and critical care

CriticalCareNurse

Fluid Management Strategies in Heart Failure

Because of the nuances of hypervolemia assessment in heart failure, nurses must not base decisions on volume status on a single method of assessment or on only a few variables. Physical signs and symptoms must be assessed along with patients subjective perceptions of clinical changes in status, such as worsening exercise intolerance or changes in New York Heart Association functional class. A valuable assessment variable for hypervolemia may be history of recent hospitalization for heart failure. Nurses should ask patients about recent hospital events, especially if patients use more than a single health care center to meet health needs. CCN
References
1. Jessup M, Abraham WT, Casey DE, et al; 2009 Writing Group to Review New Evidence and Update the 2005 Guideline for the Management of Patients with Chronic Heart Failure Writing on Behalf of the 2005 Heart Failure Writing Committee. 2009 Focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: Developed in Collaboration With the International Society for Heart and Lung Transplantation. Circulation. 2009;119(14):1977-2016. 2. Heart Failure Society of America, Lindenfeld J, Albert NM, et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010;16(6):e1-e194.

Table

Strategies to overcome diuretic resistancea

1. Infuse the agent as a continuous intravenous infusion: for example, furosemide at 5-40 mg/h or bumetanide at 0.1-0.5 mg/h 2. Administer 2 diuretic agents at the same time: for example, a loop diuretic and an agent that blocks the distal tubule Intravenous chlorothiazide (500-1000 mg), given 30 minutes before administration of an intravenous loop diuretic Oral metolazone (2.5-10 mg) given with an oral loop agent 3. Rotating loop diuretic agents: for example, switching or alternating between oral furosemide and torsemide
a No large, randomized trials that provide evidence of the effectiveness of these strategies have been done. Based on data from Jessup et al1 and the Heart Failure Society of America.2

Albert NM. Fluid management strategies in heart failure. Crit Care Nurse. 2012;32(2):20-32,34.

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CE Test Test ID C122: Fluid Management Strategies in Heart Failure Learning objectives: 1. Describe the pathophysiological processes related to fluid overload (hypervolemia) in heart failure 2. Recognize the signs, symptoms and diagnostic information needed to determine hypervolemia in heart failure 3. Identify strategies to manage hypervolemia associated with decompensated heart failure during hospitalization and after discharge
1. Which statement best defines features of heart failure due to structural heart disease? a. Orthopnea and sleep disordered breathing b. Decreased exercise tolerance and fluid retention c. Cough and orthopnea d. Hypovolemia and decreased exercise tolerance 2. What is the key factor to ensure euvolemia in heart failure patients? a. The integrity of the arterial circulation b. Normal kidney function c. Decreased levels of B-type natriuretic peptide d. Increased level of renin 3. Which of the following are physiological effects of angiotensin II? a. Activates peripheral vasoconstriction and sodium excretion b. Activates renal vasodilatation and sodium retention c. Inhibits the release of antidiuretic hormone and B-type natriuretic peptide d. Activates renal vasoconstriction and stimulates the sympathetic nervous system 4. What is the mechanism for the stimulation of the renin-angiotensinaldosterone system? a. Decrease in arterial volume b. Hyponatremia and antidiuretic hormone c. Production of cortisol by the adrenal gland d. -Receptors in juxtaglomerular apparatus of the kidney 5. Which factor has been associated with long-term improvement in heart failure patients? a. Drinking fluids to prevent thirst b. Freedom from hypervolemia after hospitalization c. Weight loss when overweight, obese, or extremely obese d. Keeping serum sodium levels between 130-135 mmol/L 6. What did multiple researchers find to be true regarding weight gain in acute decompensated heart failure? a. Weight gain was commonly reported when even mild dyspnea was present. b. Weight gain was associated with systolic dysfunction (ejection fraction of <40%). c. Weight gain may not occur in patients, even if dyspnea or edema are present. d. Weight gain was commonly observed in patients with edema.
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7. After initial treatment (first 24 hours) of hypervolemia in patients with acute decompensated heart failure, what laboratory value is not an accurate predictor of heart failure status? a. Potassium c. B-type natriuretic peptide b. Sodium d. Glomerular filtration rate 8. What medications should all patients with heart failure take, unless otherwise contraindicated? a. Digoxin, -blocker, and angiotensin-converting enzyme inhibitor b. Angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker and -blocker c. Aldosterone inhibitor, loop diuretic, and angiotensin-converting enzyme inhibitor d. -Blocker, thiazide diuretic, and hydralazine/nitrate combination 9. What class of medication is considered the hallmark pharmacological treatment for hypervolemia in heart failure? a. Angiotensin-converting enzyme inhibitor b. -Blocker c. Loop diuretic d. Aldosterone inhibitor 10. What adverse events are associated with the use of loop diuretics? a. Hypokalemia and hypomagnesemia b. Hypocalcemia and hyperkalemia c. Hyperphosphotemia and hyponatremia d. Hypermagnesemia and hypercalcemia 11. Which strategies were most effective for promoting adherence to prescribed therapies and preventing rehospitalization? a. Sending patients home with written self-care materials b. Ensuring patients know how to record daily weight and report changes c. Education before discharge and remote monitoring d. Diet class provided to family members after discharge 12. What percentage of patients and informal caregivers cited nonadherence to diet, medications, or fluid restriction as the reason for readmission? a. 46% and 38%, respectively c. 12% and 15%, respectively b. 14% and 46%, respectively d. 25% and 26%, respectively

Test answers: Mark only one box for your answer to each question. You may photocopy this form.

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Test ID: C122 Form expires: April 1, 2014 Contact hours: 1.0 Fee: AACN members, $0; nonmembers, $10 Passing score: 9 correct (75%) Synergy CERP: Category A Test writer: Diane Byrum, RN, MSN, CCRN, CCNS, FCCM

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