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Critical Care Nurse. 2004;24: 14-29
Copyright © 2004 by the American Association of Critical-Care Nurses.
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Cover Article
CE Article

Evidence-Based Practice for Acute Decompensated Heart Failure

Nancy M. Albert, RN, MSN, CCNS, CCRN, CNA
 Cathy A. Eastwood, RN, MN
 Michelle L. Edwards, RN, MSN, FNP, ACNP

Nancy M. Albert is certified as a clinical nurse specialist and has a dual role of director of nursing research in the division of nursing and clinical nurse specialist at the George M. and Linda H. Kaufman Center for Heart Failure of the Cleveland Clinic Foundation, Cleveland, Ohio. She codeveloped heart failure programs along the continuum of care, including emergency care, critical care, and acute care, at the Cleveland Clinic Foundation.

Cathy A. Eastwood graduated with a master of nursing degree from the University of Calgary, Canada, after specializing in the care of patients with heart failure. She developed and managed the outpatient heart failure center and oversaw the flow of inpatients with heart failure at St. Luke’s Episcopal Hospital, Houston, Tex. Currently, she is a lecturer at Memorial University of Newfoundland, School of Nursing, in St. John’s, Newfoundland, Canada.

Michelle L. Edwards earned a master of science degree in nursing from the University of Alabama at Birmingham and is a board-certified family and acute care nurse practitioner. She practiced several years in critical care, specializing in the care of cardiovascular patients. She currently is a cardiology nurse practitioner/outcomes manager at St. Luke’s Episcopal Hospital.

To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.

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. Identify the core drug therapies for decompensated heart failure
  2. Describe the role of B-type natriuretic peptide in decompensated heart failure
  3. Explain the pharmacological management of decompensated heart failure

Each year, chronic left ventricular systolic and diastolic dysfunction, or heart failure, causes 1 million hospitalizations in the United States.1 Heart failure is the most common Medicare diagnosis related group at discharge1,2 and is associated with poor survival and quality of life. In addition, cost of care is high; in 1998, Medicare paid out $3.6 billion for care related to heart failure.1

The Acute Decompensated Heart Failure National Registry (ADHERE)3 recently reported data on 14716 patients hospitalized for heart failure in the United States (Tables 1Go and 2Go). Generally, patients admitted to the hospital for heart failure were elderly, were female, had a history of heart failure, and were unable to carry out activities of daily living without exercise intolerance. The most common symptom was dyspnea, which was most often associated with other signs and symptoms of fluid retention. Comorbid conditions were common, and patients were equally likely to be admitted with systolic dysfunction (reduced ventricular contractility; ejection fraction ≤0.40) or diastolic dysfunction (impaired ventricular relaxation or ventricular stiffness that decreases the ventricle’s ability to fill). One quarter of patients were rehospitalized within 6 months of a previous hospitalization, and Medicare was the primary hospital payor. Most patients spent time in the emergency department before admission as an inpatient, and the most common level of initial care was telemetry. Median length of stay was 4.4 days.3


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  		Table 1 Characteristics of patients, clinical signs and symptoms, and hospital placement: data from the Acute Decompensated Heart Failure National Registry3

 

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  		Table 2 Outpatient medications before hospitalization and medications at discharge: data from the Acute Decompensated Heart Failure National Registry3

 
The ADHERE data are similar to data from other studies4,5 in which investigators found an equal split of patients with impaired and preserved left ventricular systolic function, signifying hospitalization of patients with systolic dysfunction and patients with diastolic dysfunction. The primary mechanism of diastolic dysfunction that led to signs and symptoms was impaired ventricular relaxation, which was associated with increased age, obesity, hypertension, and cardiovascular disease.4 In addition, ADHERE data were comparable to data from other reports6–8 in that retention of fluid and sodium, as evidenced by admitting signs and symptoms, was a primary factor in hospitalization. This knowledge provides an opportunity for care improvement that can be championed by nurses, because hospitalization for fluid and sodium retention in patients with systolic or diastolic dysfunction may be avoidable, especially when such retention is due to patients’ failure to adhere to medication regimens or self-care instructions.

In this article, we discuss evidence-based practices for managing patients with acutely decompensated heart failure because in-hospital actions may facilitate an improved experience for patients after hospitalization. The intent is to provide management goals and actions associated with the most common clinical manifestation, fluid retention, and not to focus on management of cardiogenic shock, profound hypoperfusion, or complex decompensation (severe hyper-volemia, hypoperfusion, and acidosis or other conditions such as pneumonia). Assessment of patients, management strategies, and education of patients are highlighted. Myths associated with acute care management are discussed so that nurses will be more aware of appropriate interventions that are safe and effective. Heart failure management has progressed rapidly in recent years. Ultimately, nurses must be proactive in ensuring that their behaviors are based on current evidence.


   Heightened Expectations for Evidence-Based Care
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 Heightened Expectations for...
Assessment of Patients
 Myths and Realities of...
 References
 
Nurses are challenged to plan and provide care that promotes the best possible clinical and health-related outcomes. The Joint Commission on Accreditation of Healthcare Organizations9 recently established 4 core measures in the acute management of patients with heart failure to promote adherence to basic standards of evidence-based care (Table 3Go). Because of the large number of patients and the high cost of care associated with hospital readmissions, acute and critical care nurses must develop and implement strategies that are associated with improved outcomes for patients and hospitals. In addition, in 2001, the American College of Cardiology (ACC) and the American Heart Association (AHA) published practice guidelines10 for adults with chronic heart failure. These guidelines provide caregivers with recommendations for nonacute care and include the rationale and level of evidence for support of each management strategy. Table 4Go provides a list of management strategies, including core drug therapies, that should be a part of each patient’s treatment plan at discharge after an admission for decompensated heart failure stemming from volume overload.10,11


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  		Table 3 The 4 core measures of the Joint Commission on Accreditation of Healthcare Organizations

 

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  		Table 4 Practice guidelines that apply to stage C* patients

 
If the medication expectations listed in Table 4Go are compared with the actual medication therapies before hospitalization and at discharge indicated in the ADHERE data (Table 2Go), a need for change is evident. New efforts must be undertaken to promote use of consensus guidelines and therapies to meet the overall goal of managing heart failure: promoting regression and preventing progression of left ventricular enlargement (remodeling) to decrease disease progression and improve survival.11–14 See Figure 1Go and Table 5Go for definition and description of consequences of ventricular remodeling.



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  		Figure 1 Ventricular remodeling. Cross-sectional view of left and right ventricles: a, normal; b, concentric hypertrophy; and c, eccentric hypertrophy.

 

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  		Table 5 Ventricular remodeling: definition and consequences

 
No standardized evidence-based guidelines are available to direct acute care; however, randomized, placebo-controlled research studies provide strong support for actions that are effective and safe. In addition, many actions promoted in the current guidelines for long-term outpatient management of heart failure can be translated to the acute setting and provide a uniform plan of care based on large, multicenter, randomized research studies that focus on the primary management goal of preventing progression of heart failure.10

Nurses can facilitate some practical assessment and management strategies that apply to patients admitted to the hospital with a primary diagnosis of heart failure who are not in cardiogenic shock or do not have profound hypoperfusion or complex decompensation. Implementation of the following strategies might require a change in the philosophy of care, further education, and continuous quality monitoring to ensure that evidence-based strategies are used regardless of the type of physician, a patient’s placement (telemetry or nonmonitored bed), a nurse’s background (cardiac, heart failure, or generalist), or a hospital’s resources.


   Assessment of Patients
Top
 Heightened Expectations for...
 Assessment of Patients
Myths and Realities of...
 References
 
Before planning interventions for a patient hospitalized with heart failure, the healthcare team must conduct a systematic assessment that includes identification of the cause of the heart failure, aggravating factors, potential risk factors that may influence survival and quality of life, and current clinical status. Patients’ comorbid conditions, especially active chronic conditions, may act as exacerbating factors (Table 6Go), affecting the planning of patients’ care and influencing the timing and intensity of therapies. The treatment plan must include modification of correctable causes of decompensation. Examples include education for sodium indiscretion, alcohol abstinence programs for overconsumption of alcohol, or revascularization strategies for hibernating myocardium (ie, viable but under-perfused myocardial tissue with decreased contractility). In addition, risks related to heart failure must be considered, such as the need for anticoagulation to prevent embolic events or the need for an implantable cardioverter-defibrillator to prevent sudden cardiac death, so that appropriate consultations and therapies are discussed and initiated before patients are discharged from the hospital.


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  		Table 6 Exacerbating factors in chronic heart failure that lead to decompensation

 
Hemodynamic Status: Volume and Perfusion
Volume and perfusion status provide useful clues to a patient’s cardiac performance and help shape the treatment plan. Nurse caregivers must frequently reassess the patient’s hemodynamic status to determine volume and perfusion status. Volume status is determined by assessing if the patient is wet, dry, or has a balanced fluid level (ie, has hypervolemia, hypovolemia, or euvolemia, respectively), and perfusion is assessed by determining if the patient is cold, cool/lukewarm, or warm (ie, has perfusion that is very low, slightly low, or normal, respectively). Evidence of congestion includes the signs of neck vein distension, elevated pressure in the right internal jugular vein, positive abdominal-jugular neck vein reflex, edema, ascites, and crackles (rarely) and the symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.15 Nurses must be careful not to count on the presence of crackles as an indicator of congestion because chronic movement of fluid into the interstitium (common in patients with a history of chronic heart failure) is associated with increased lymphatic drainage so that crackles are absent and the alveoli remain relatively dry.16

Evidence of very low perfusion includes symptomatic hypotension, especially in patients receiving angiotensin-converting enzyme (ACE) inhibitors, cool extremities (arms and legs, not just hands and feet), mental obtundation or constant sleepiness, worsening renal function (elevation in serum levels of creatinine and urea nitrogen), hyponatremia, narrow pulse pressure, and, most important, a proportional pulse pressure of 25% or less.15,16 Acute care nurses should be educated in calculating proportional pulse pressure. The calculation is simple to do and can provide valuable information about cardiac contractility and perfusion, especially when trends over time are assessed.

The formula to determine proportional pulse pressure is (systolic blood pressure - diastolic blood pressure)/systolic blood pressure, resulting in a proportion or percentage.16 An example of a calculation of proportional pulse pressure is (108 –66)/108 = 42/108 = 0.389 or 39%.

In a hemodynamic study16 of 50 patients with a history of heart failure, 91% of patients with a proportional pulse pressure of 25% or lower had a cardiac index (calculated as cardiac output in liters per minute divided by body surface area in square meters) of less than 2.2; however, systolic and mean arterial blood pressure were poorly correlated with cardiac index or stroke volume index. In a study17 of hemodynamic profiles (wet, dry, cold, and warm) and clinical characteristics of advanced heart failure, a low proportional pulse pressure was the only predictor of wet patients, and among wet patients, proportional pulse pressure was the only predictor of patients in the cold category. A patient’s hemodynamic profile should influence initiation of pharmacological and other treatment strategies and also guide the adjustment of therapies during the hospitalization.

Of note, patients who are admitted in a congestive or wet state with a high preload (passive stretch of myocardial fibers; reflects left ventricular end-diastolic pressure and volume) often have a high afterload (pressure the heart must pump against; reflects systemic vascular resistance, systolic stress, and systolic impedance) that impairs stroke volume and is reflected as a cool or lukewarm perfusion state. When hemodynamic measurements were recorded in 750 patients with heart failure before tailored therapy at a large university teaching hospital, the mean pulmonary artery occlusive pressure was 26 mm Hg (normal is 4–12 mm Hg; in heart failure treatment, the goal is 8–15 mm Hg) and the mean systemic vascular resistance was 1640 dynes•sec•cm–5 (normal is 800–1200 dynes•sec•cm–5),15 reflecting a vasoconstricted state and the need for vasodilator therapy in addition to diuresis and natriuresis (sodium excretion).

Diagnostic Tests
In addition to results of tests done at the time of admission (chest radiographs, arterial blood gas levels, liver function tests, hematologic tests, electrocardiograms, basic metabolic profile) and findings on physical examination, the results of point-of-care assays of serum levels of natriuretic peptides can be used to guide treatment in patients with acute decompensated heart failure (Figure 2Go). B-type natriuretic peptide (BNP) is secreted mainly from the ventricular myocardium in response to elevations in end-diastolic pressure and ventricular volume expansion.18 Not only can rapid measurement of BNP aid in diagnosis of heart failure,19–23 but BNP level can also be used to assess clinical status and the effectiveness of therapies during an admission for acute decompensation.24



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  		Figure 2 Acute decompensated systolic heart failure (SHF) or diastolic heart failure (DHF) in patients with chronic heart failure: initial treatment of Abbreviations: BNP, B-type natriuretic peptide; EKG, electrocardiographic; INR, international normalized ratio; IV, intravenous; PT, prothrombin time. *Treatment decisions based on serum BNP results in acute decompensated heart failure DO NOT apply to patients with chronic, stable heart failure who are not acutely dyspneic. {dagger}Profiles: patient is wet, dry, or has a balanced fluid level (ie, has hypervolemia, hypovolemia, or euvolemia, respectively), and is cold, cool/lukewarm, or warm (ie, has perfusion that is very low, slightly low, or normal, respectively).

 
Point-of-care BNP testing can be a useful adjunct in determining which patients are receiving effective care, which patients are not progressing on the current treatment plan, and which patients might be candidates for end-of-life care. Nurses should consider all components of assessment of patients (etiology, aggravating factors, risks, and clinical status) when communicating and collaborating with members of the healthcare team so that patients have the best opportunity for care strategies that optimize outcomes and promote comfort.


   Myths and Realities of Management
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 Heightened Expectations for...
 Assessment of Patients
 Myths and Realities of...
References
 
An algorithm provides a systematic approach to decision making as patients with chronic heart failure are assessed and managed during an acute exacerbation (Figure 2Go). The myths associated with management of acute heart failure are replaced with evidence-based actions that contribute to the best possible outcomes.

Myth 1: The Goals of Treatment for Acute and Chronic Heart Failure Are Different
One of the hurdles in management of heart failure is to overcome the myth that the goals of managing acute decompensated and stable heart failure are different. Today, it is important to gear therapies toward reversal of ventricular remodeling. Reversing ventricular remodeling is important regardless of whether patients are in stable condition or in a decompen-sated state. Historically, the primary goal of treatment of acute decompensated heart failure was to quickly reduce the circulating fluid volume to relieve patients of the pulmonary and peripheral edema. Diuretics dyspnea in the emergency department. have long been the standard type of drug used for decreasing volume and improving hemodynamic status and signs and symptoms.25 Through research studies, however, it was learned that acute intravenous diuretic therapy was associated with many hazards, including increased mortality. Non–potassium-sparing diuretic therapy was associated with an increased risk of arrhythmic (sudden) death, increased cardiac mortality, aggravated renal dysfunction, further activation of the reninangiotensin and sympathetic nervous systems with a concomitant increase in systemic vascular resistance that was compounded by a decrease in cardiac output from a reduction in preload, and electrolyte imbalances that caused muscle weakness, depression, reduced contractility (from reduced conductivity), and peripheral vasoconstriction.26–31 In patients with acute decompensation, preventing or limiting further activation of neuroendocrine systems by using strategies that target excess intravascular and extravascular volume and vascular resistance will help meet the overall goals of preventing progression of and promoting reversal of ventricular remodeling.

Myth 2: Managing Fluid Overload Equals Use of Diuretics
Administration of intravenous and oral loop diuretic agents is an important therapy aimed at decreasing preload (through initial venodilatation and then through diuresis and natriuresis) and ultimately relieving signs and symptoms, but these agents should not be used alone to improve overall morbidity and survival in patients with heart failure. In order to address increased afterload associated with both exacerbation of heart failure and intravenous loop diuretic therapy, pharmacological therapies must include agents that reduce neuroendocrine activation and vasoconstriction because these mechanisms can worsen the heart failure syndrome by worsening ventricular remodeling.

Diuretics and ACE Inhibitor Therapy
Although only limited data are available, when an ACE inhibitor was combined with loop diuretics, the combination therapy reduced the pressor (vasoconstriction) response of diuretics.32 ACE inhibitors reduced the increase in plasma angiotensin II, thus decreasing the sympathetic activation (and associated deterioration in left ventricular pump function) that preceded the diuretic action of diuretics.32

ACE inhibitors ultimately decreased reabsorption of sodium in the distal tubule and decreased aldosterone stimulation in the adrenal glands.33,34 Many randomized, controlled research studies were conducted from the early 1980s through the mid-1990s that added an ACE inhibitor to diuretic therapy in patients with mild to severe heart failure, as summarized in the consensus guidelines.10 Researchers reported improvements in exercise tolerance, ejection fraction, and survival along with decreased rehospitalization rates.10 Therefore, diuretics are necessary to relieve signs and symptoms but should be used with ACE inhibitor therapy for survival benefit and to counterbalance the alterations in renal and adrenal mechanisms responsible for sodium and water retention. Nurses must proactively recommend increases in dosage of ACE inhibitors based on the ACC/AHA practice guidelines10 during the acute hospitalization period so that patients’ dosing regimens are on target before the patients are discharged from the hospital.

Diuretics and Intravenous Vasodilator Therapy
When patients are admitted with a wet and lukewarm/cool or cold profile without indications of profound hypoperfusion, a combination of intravenous diuretics and vasodilator therapy leads to improved acute outcomes, without the need for inotropic agents (Figure 2Go). Many studies were conducted in the late 1970s and early 1980s in patients with New York Heart Association functional class IV decompensated heart failure to study the effectiveness of intravenous diuretic and vasodilator (nitroprusside and nitroglycerin) therapy in reducing filling pressures (preload) and systemic vascular resistance (afterload) and improving cardiac output. The results indicated that nitroprusside was a clinically effective and powerful agent for reducing afterload that also decreased ventricular systolic and diastolic volumes and improved ventricular diastolic properties. It provided rapid symptomatic relief for patients and improved, stabilized, and optimized hemodynamic parameters.35–39

Intravenous nitroglycerin is known predominantly as an agent for reducing preload. However, at high doses, intravenous nitroglycerin reduces systemic and pulmonary vascular resistance. In patients with decompensated chronic heart failure, nitroglycerin was less powerful than nitroprusside in reducing afterload but was effective in reducing preload, increasing cardiac output, and controlling signs and symptoms and hemodynamic derangements.40–42 Table 7Go is a summary of the dose ranges, actions, and indications of vasoactive medications used in the management of patients with acute decompensated heart failure.43


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  		Table 7 Intravenous vasoactive medications indicated in acute decompensated heart failure43

 
As the overall goal of managing patients with heart failure has shifted from improving hemodynamic status to improving neuroendocrine abnormalities in the hope that ventricular remodeling will be favorably affected, researchers have studied the effectiveness of intravenous vasodilator therapy in modulating the neuroendocrine axis. In a recent study44 of 34 patients with decompensated heart failure who received intravenous diuretics and vasodilator therapies (nitroprusside and ACE inhibitors) to reduce preload and afterload, neurohormonal activation (endothelin, norepine phrine, and BNP levels) decreased rapidly and was associated with improved hemodynamic status. Similar to results of studies conducted in previous decades, in this study,44 the mean cardiac index increased from 1.70 before treatment to 2.58 after treatment. Pulmonary artery occlusive pressure decreased from a mean of 31 to 18 mm Hg, and systemic vascular resistance decreased from a mean of 1780 to 1109 dynes•sec•cm–5 from before to after treatment. This research provided further evidence that hemodynamic parameters in patients at rest were significantly modulated by improving preload and afterload, rather than by using agents that increased contractility and cardiac workload. In addition, decreased activation of neuroendocrine hormones might improve short- and long-term outcomes.

A newer vasodilator, nesiritide, is indicated for reducing dyspnea and improving hemodynamic status in patients with acute decompensated heart failure. Nesiritide, a recombinant form of human BNP, has actions identical to those of the endogenous BNP molecule.45 Nesiritide produced balanced arterial and venous vasodilatation that resulted in rapid reduction in ventricular filling pressures. This reduction was manifested clinically as a dose-dependent decrease in pulmonary artery occlusive pressure, pulmonary artery pressures, and systemic blood pressure.46 Nesiritide caused diuresis and natriuresis by suppressing the reninangiotensin-aldosterone system.47

When intravenous nesiritide was compared with intravenous nitroglycerin during the first 72 hours of signs and symptoms in patients hospitalized with acute heart failure,47 the results favored nesiritide. Nesiritide produced a significantly quicker and greater reduction in pulmonary artery occlusive pressure than did nitroglycerin. Patients reported and caregivers measured a greater reduction in dyspnea when the patients received nesiritide rather than nitro-glycerin. The combined actions of vasodilatation, diuresis, and natriuresis led to preload and afterload reduction to achieve the goal of enhanced cardiac output and reduced pulmonary and systemic congestion. The investigators47 concluded that nesiritide should be the drug of choice in patients admitted with a wet and cool to cold hemodynamic profile because it was less potent and less toxic than intravenous nitroprusside and more easily administered than intravenous nitroglycerin. During the first 24 hours of infusion, neither symptomatic nor asymptomatic hypotension differed significantly between patients receiving intravenous nitroglycerin, patients receiving nesiritide, and control subjects.47 During the research trial, hypotension, which was dose-dependent, was easily assessed with regular monitoring of blood pressure (ie, noninvasively every 15 minutes for an hour, then every 4 hours). Thus, infusion of nesiritide does not require placement of an arterial catheter for blood pressure monitoring and admission to a critical care unit (as nitroprusside infusion does) or telemetry monitoring.

Diuretics and ß-Blocker Therapy
ß-Blocker therapy also affects mechanisms in the kidneys and the renin-angiotensin system. ß-Blockers are the only oral medications in the core pharmacological therapy for heart failure that decrease renin release, thereby indirectly decreasing proximal reabsorption of sodium (by decreasing angiotensin II levels).34 When a nonselective ß-blocker/{alpha}-blocker such as carvedilol is used, renal blood flow may improve from a reduction in renal vascular resistance.34 Nurses should not assume that an acute exacerbation of heart failure requires termination of treatment with or decrease in dosage of ß-blockers. In actuality, maintenance of ß-blockers (and eventual increase to target dosage once hypervolemia is controlled, based on AHA/ACC practice guidelines)10 may actually improve signs and symptoms and quality of life by antagonizing mechanisms that cause excessive sodium and water retention.

Myth 3: Low Systolic Blood Pressure Requires Treatment With Intravenous Inotropic Agents
Some myths are associated with interventions when patients with heart failure have low systolic blood pressure. One belief is that a systolic blood pressure of less than 90 mm Hg requires intravenous infusion of inotropic agents. Unless the hypotension is severe (systolic blood pressure <80 mm Hg), it is important to assess for indications of hypoperfusion and not to rely just on systolic blood pressure readings when determining whether intravenous inotropic agents are needed. Is the patient mentally obtunded or oliguric? Does the patient have cold arms or legs or long-lasting orthostasis (ie, dizziness and lightheadedness that lasts longer than 15 minutes after a change in body position from lying to sitting or standing)? Is the proportional pulse pressure less than 25%? In combination, these signs are more reflective of profound hypoperfusion and low cardiac output than is systolic blood pressure.16 Patients who do not have these signs generally tolerate ACE inhibitor, ß-blocker, and diuretic therapies, especially when the dosing scheme is staggered so that therapies do not reach peak effectiveness at the same time.

It is important to consider that a lower systolic blood pressure reflects lower myocardial wall tension (stress) and afterload. Afterload reduction decreases activation of the neuroendocrine axis to promote regression of cardiac remodeling and improve clinical outcomes. Nurses must educate patients about the benefits of maintaining a low systolic blood pressure and adhering to core pharmacological therapies that decrease neuroendocrine activation and decrease blood pressure.

Additionally, use of intravenous inotropic agents is not supported in patients in an acute setting except as temporary treatment of diuretic-refractory complex decompensation.48 Intravenous inotropic therapies (continuous or intermittent infusion of milrinone or dobutamine) have been associated with increased mortality when used in patients requiring inotropic support, even though these agents improve hemodynamic status10 (Table 7Go). In an effort to learn if a short-term infusion (48 hours) might lead to short- or intermediate-term improvements in patients hospitalized for exacerbation of heart failure who had a wet and cool to cold profile but in whom intravenous inotropic support was not essential, the study called Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-HF) was conducted.49 Investigators randomized patients to receive short-term intravenous milrinone or placebo. The 2 groups did not differ significantly in hospital and 60-day posthospitalization mortality or in the median number of days patients were hospitalized for cardiovascular causes in the first 60 days after discharge. In addition, sustained hypotension or new atrial arrhythmias were significantly more likely to develop in the patients receiving milrinone than in the patients receiving placebo. The results of this research, that receiving an inotropic agent without clear evidence of significant hemodynamic compromise does not enhance clinical or economic outcomes, led to a tempering of the use of intravenous inotropic agents unless absolutely warranted.

Further, concomitant use of ß-blocker (ß-antagonist) and intravenous dobutamine (ß-agonist) therapies is controversial. The pharmacological response of dobutamine is inhibited in patients receiving high doses of ß-blockers because both drugs compete for the same ß-adrenergic receptors.48 This conflict is especially apparent with carvedilol because it blocks both ß1 and ß2 receptors.48,50

Myth 4: ACE Inhibitors and ß-Blocker Therapies Should Be Temporarily Decreased or Discontinued During Decompensation
Another belief is that ACE inhibitors and ß-blocker therapies must be decreased or discontinued or should not be initiated when the patient’s blood pressure is low. These agents help suppress maladaptive neuroendocrine responses that lead to increased wall stress, ventricular hypertrophy, and worsening cardiac remodeling and cardiac output.51 Unless symptomatic low blood pressure occurs or intravenous vasodilator agents are used, core oral therapies used to manage patients with chronic heart failure should be maintained whenever possible. Blood pressure may not decrease or the reduction may be self-limiting when vasodilator (ACE inhibitor or angiotensin-receptor blocker) and ß-blocker therapies are initiated and maintained in patients with a low baseline blood pressure (85–90 mm Hg). If blood pressure decreases but indications of hypoperfusion are absent, nurses should assess patients for hypovolemia (from overdiuresis). In addition, nurses must communicate expected effects of core agents for treating heart failure to patients so that patients are prepared for potential dizziness or other symptoms associated with drug actions and interactions and understand the self-limiting nature of these changes.52

Myth 5: Once Core Therapies Are Unsuccessful, They Should Not Be Tried Again
Some may believe that once ACE inhibitor or ß-blocker therapy is unsuccessful in a patient because of low blood pressure, these therapies should not be tried again. Assessment and correction of mechanisms that cause low blood pressure (such as initiating ACE inhibition when the serum level of sodium is less than 130 mmol/L) may make the preceding statement a false claim. Core pharmacological therapies known to improve health-related outcomes can be successfully implemented without episodes of low blood pressure in most patients, as evidenced by low dropout rates in randomized controlled studies. The acute care episode is a perfect setting for trying ACE inhibitors or ß-blockers again, when appropriate, because patients can be carefully monitored and resources are readily available. Low-dose, shorter-acting agents in each drug class (such as captopril and carvedilol) are the drugs of choice in patients with a history of low blood pressure.

Nursing Considerations
In addition to assessment of patients, nursing actions that are central to patients’ outcomes are administration of medications, evaluation of treatment effectiveness, and education and ongoing communication with patients, patients’ families, and the healthcare team. If a patient’s dyspnea improves but weight loss, urination, intake and output, or proportional pulse pressure do not improve, nurses must be assertive in providing timely communication of these findings to peers and the physician team because delays can diminish high-quality care, hinder achievement of clinical goals, and harm the hospital financially. Table 8Go outlines nursing actions and goals that reflect critical thinking and foster communication when managing patients with heart failure.


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  		Table 8 Nursing considerations: critical thinking and communication

 
Nurses often take an active role in prompting initiation and adjustment of medication therapies. Nurses must know the actions, dosing, and effects of heart failure medications and must promote decisions that will affect the overall goal of management of heart failure (reversal of cardiac remodeling). This goal can be achieved during the acute hospitalization by adding, maintaining, and increasing dosages of vasodilators (ACE inhibitors) and maintaining ß-blocker therapy per consensus recommendations. Nurses must not focus on pharmacological therapies that simply improve symptoms (eg, diuretics), because these therapies also increase cardiac workload, activate adverse neuroendocrine systems, and increase mortality. When in doubt about therapeutic priorities, it is always helpful to reassess the patient’s clinical status. When patients have congestion and inadequate organ or peripheral perfusion (cool/lukewarm to touch), intravenous diuretic and vasodilator therapy (along with maintenance of prehospital ß-blocker therapy) may decrease afterload and preload to improve perfusion and cardiac index. When profound hypoperfusion compromises organ function, an intravenous inotropic agent may be the preferred agent of choice (Figure 2Go). It is especially important for nurses not to withhold doses of vasodilators, ß-blockers, or diuretics because of a patient’s low blood pressure unless the patient has orthostatic hypotension or other signs and symptoms reflecting hypoperfusion or hypovolemia. Nurses must use multiple clinical parameters, not just blood pressure values, to determine that withholding drugs will benefit a patient’s clinical status.

Critical evaluation of each patient’s progress involves ongoing assessment of electrolyte and fluid status. Such assessment is especially important in managing patients with heart failure because activation of neuroendocrine systems, renal dysfunction, and current drug therapies may disrupt the fine balance of electrolytes and cause shifts in sodium, potassium, calcium, and magnesium.53 It is important for nurses to develop and use advanced measurement and cardiac auscultation skills to monitor fluid status (eg, assessment of jugular venous pressure and the presence or worsening of systolic murmurs and S3 or S4 heart sounds) because patients may still have intravascular volume overload after obvious interstitial fluid retention (crackles, edema) dissipates. Freedom from congestion in the early weeks after hospital discharge was an independent predictor of survival in patients hospitalized with New York Heart Association functional class IV symptoms.54 In order to prevent readmission and maintain clinical stability, patients who have evidence of clinical and subclinical congestion before discharge should be considered for aggressive follow-up (cardiologist specializing in heart failure) and interventions aimed at promoting euvolemia (eg, increased restriction in sodium diet or fluid intake, diuretic self-management program, heart failure nurse clinic).

Serum BNP values provide another mechanism for monitoring fluid status in the early hours after hospitalization and for assessing patients’ outcomes. In patients with symptomatic, functional class III or IV heart failure who were undergoing tailored therapy for their congested state, hourly changes in BNP levels were significantly correlated with hourly changes in pulmonary artery occlusive pressure.55 When BNP levels at initial hospital assessment and within 24 hours of discharge or death were compared as an outcome variable,24 successfully treated patients (as compared with patients who died during the index hospitalization or were readmitted within 30 days of discharge) had a mean decrease in BNP level of 216 pg/mL. Patients who were readmitted or died had levels that increased during the course of hospitalization.

Last, communication between healthcare providers and patients and patients’ families about the patients’ clinical status and management plan is essential. Proactively assessing the knowledge base of patients and their families to promote understanding of the current plan of care and asking if there are questions can aid communication and information sharing. Information sharing and ongoing communication with patients and their families enhances perceived control, potentially decreasing stress.56 This communication is especially important because loss of functional mobility and role changes that occur with the progression of heart failure lead to a perceived loss of control57 that can ultimately affect coping, lifestyle modifications, and behaviors. Examples of important factors to address in patients’ education are found in the first item in Table 3Go and in Table 4Go. It is well recognized that improving patients’ knowledge of heart failure and providing support, encouragement, and positive reinforcement of self-care behaviors improves outcomes in patients with heart failure.58


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