biomarkers, B-natriuretic peptides, decompensated, heart failure, nursing management



  1. Varughese, Sheeba MSN, RN, CNS, CCRN, APRN,BC


Heart failure, a debilitating complex clinical syndrome, affects nearly 5 million people in the United States and presents a heavy socioeconomic burden. Neurohormonal abnormalities contribute to the pathophysiology of heart failure. Acute decompensated heart failure (ADHF) has emerged as a major health problem associated with poor prognosis, increased costs related to care, reduced quality of life, and frequent readmissions. Symptoms of ADHF are primarily related to congestion and/or low perfusion states. The use of biomakers such as B-natriuretic peptides is useful in distinguishing between cardiac and noncardiac causes of symptoms. Treatment for ADHF begins with identification and treatment of precipitating factors for acute decompensation. Initial goal of therapy is focused on symptom management followed by interventions that delay disease progression, reduce readmission, and prolong survival.


Article Content

HEART FAILURE (HF) is a progressive, complex clinical syndrome resulting from structural and/or functional cardiac disorders that impair systolic and/or diastolic function. A series of neurohormonal mechanisms are integrated into this syndrome and impacts the overall outcomes associated with the disease. Acute decompensated heart failure (ADHF) has emerged as a major health problem associated with poor prognosis, increased costs related to care, and frequent readmissions.1,4,5


Heart failure is a growing health problem and affects nearly 5 million people in the United States.4 Nearly 550,000 new patients are diagnosed each year.4 The incidence of HF is highest among those who are aged 65 years or older.4 Despite modern therapies, the expected 5-year mortality is approximately 50%6 and the incidence of sudden cardiac death is 6 to 9 times the rate of the general population.4


More Medicare dollars are spent for the diagnosis and management of HF than for any other disease. In 2006, it was estimated that expenses related to HF would reach $29.6 billion.4 The majority of these expenses ($15.4 billion) are directly related to hospitalized care.4 Each year, HF is a contributor of approximately 1 million hospitalizations.6 From 1979 to 2003, the number of hospital discharges related to HF increased by 174%.4


The rise in HF has been attributed to several factors, including the increasing proportion of elderly individuals in the population, improved short-term survival of patients with myocardial infarction, and heightened awareness of HF resulting in increased diagnosis and reporting.7 Approximately 80% of patients hospitalized with HF are older than 65 years.4 The incidence of HF is rising in both men and women.4


The hospitalized HF population consists of a mixed group of patients with low and preserved left ventricular ejection fraction (LVEF). Recent data from the Acute Decompensated Heart Failure National Registry (ADHERE) suggest that 40% of patients hospitalized for ADHF have normal systolic function,8 72% have history of hypertension, and 29% have chronic renal insufficiency.5 However, congestion is the dominant feature in all ADHF hospitalizations.5


Several factors that may predispose a patient to experience ADHF with or without worsening of underlying cardiac structure or function have been identified.1 Exacerbation of comorbid factors such as a worsening of renal function, persistent neurohormonal activation, and progressive deterioration in myocardial function all plays a role in ADHF.1 In addition, failure to adhere to prescribed medication and treatment plan or an inadequate medical regimen may also contribute to decompensation.1Table 1 outlines some potential exacerbating factors that may lead to ADHF.

Table 1 - Click to enlarge in new windowTable 1. Exacerbating factors that may lead to decompensation


Heart failure is a complex syndrome in which myocardial injury results in a fall in left ventricular (LV) performance.11 This can be due to a systolic or diastolic dysfunction resulting in a drop in perfusion. The body recognizes this and attempts to compensate through neurohormonal activation. The neurohormonal activation involves the renin-angiotensin-aldosterone system, sympathetic nervous system, endothelin, vasopressin, cytokines, and natriuretic peptides (Table 2).11 When the compensatory mechanisms are unable to positively impact perfusion, symptoms prevail. Over time, these compensatory mechanisms lead to remodeling and progressive worsening of myocardial function and apoptosis (programmed cell death).11 The result is the increased morbidity and mortality that is associated with HF.

Table 2 - Click to enlarge in new windowTable 2. Neurohormonal response

Heart failure can be due to systolic or diastolic dysfunction. Systolic dysfunction results from impaired ventricular contractility, resulting in reduced ventricular emptying, elevated diastolic filling pressures, ventricular dilatation, and reduction in stroke volume and cardiac output.3,11 The most common cause of systolic dysfunction is myocardial ischemia/infarction, coronary artery disease, and hypertensive heart disease. Less common causes include valvular heart disease and dilated cardiomyopathy. Systolic dysfunction is associated with an LVEF of less than 45%.13


Diastolic dysfunction causes impairment in ventricular relaxation, which results in resistance to filling of the ventricle.15 This impairment can result in elevated diastolic filling pressures. The contractility of the myocardium may be normal, resulting in a near-normal LVEF.15 However, the stiffened left ventricle impedes normal ventricular filling, which can result in a reduction of cardiac output.15 The most common causes of diastolic dysfunction include ventricular hypertrophy due to chronic hypertension, myocardial ischemia or infarction, coronary artery disease, diabetes, and aging.15



Functional status is an important assessment that is made for HF patients. The New York Heart Association (NYHA) functional classification system is utilized to make this assessment. It assists in classifying HF patients into 1 of 4 classes that are related to the degree of functional limitations imposed by HF symptoms (Table 3).1 The most severe NYHA functional class is class IV, where a patient experiences symptoms of HF that limit functional status even at rest.1 The other classification system is the American College of Cardiology/ American Heart Association (ACC/AHA) staging system for HF.1,2 It encompasses 4 stages of heart failure (Table 4).2 Stages A and B are asymptomatic stages. Patients who are at risk for developing HF are in these 2 stages. Stage C is symptomatic HF, which is responsive to treatment. Stage D is end-stage refractory HF. In 2005, The ACC/AHA Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult was published.2 These guidelines provide recommendations for nonacute care and include both rationale and level of evidence for the support of each management strategy identified for each stage of HF. Recommended therapies focus on modifying or suppressing the neurohormonal processes and preventing or delaying the disease progression.2

Table 4 - Click to enlarge in new windowTable 4. ACC/AHA stages of heart failure
Table 3 - Click to enlarge in new windowTable 3. The New York Heart Association classification of heart failure


Although in HF management the priority of treatment is related to delaying disease progression and prolonging survival,2 during ADHF hospitalizations, the initial priorities of treatment are related to symptom management.1,9 This initial treatment strategy for ADHF involves a 3-step process. The first step is a search for potential reversible factors that may be the cause of the exacerbation (Table 1).9 Second, an evaluation of symptoms related to congestion and/or low perfusion is completed.9 The symptoms that are being evaluated are related to functional status. The use of the hemodynamic profile (Fig 1) may be helpful in accomplishing this step. The last step is the determination of appropriate treatment strategies based on the assessment findings.9

Figure 1 - Click to enlarge in new windowFigure 1. Two-minute assessment of hemodynamic profile. Hemodynamic profiles for patients with heart failure. Most patients can be classified in a rapid bedside assessment according to the signs and symptoms shown. This classification helps guide the use of initial therapy. Reprinted with permission from Dr Stevenson.

Several triggers or exacerbating factors that predispose a patient with HF to experience worsened symptoms and the development of ADHF have been identified (Table 1).9,10 It is important to evaluate the ADHF patient for the presence of any of these reversible factors and attempt to address them as quickly as possible.9,10 A common factor is atrial arrhythmias where the rapid ventricular response may contribute to exacerbation. Systemic hypertension is another exacerbating factor seen with ADHF admissions.1,5 Other factors include implications from comorbidities, new ischemic event, heavy alcohol consumption, infection, medication interactions, and lack of compliance with the prescribed treatment plan.9,10


Evaluation of symptoms is the next step in the treatment plan. The major symptoms of ADHF include shortness of breath, congestion, and fatigue.1 Unfortunately, these symptoms are not specific to only ADHF. They can be seen with other conditions such as chronic pulmonary disorders, or infections. Therefore, differential diagnosis becomes essential.


Most patients will display evidence of volume overload as manifested by signs and symptoms of congestion or elevated filling pressures.4,8 These signs and symptoms may include weight gain, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, rales, pleural effusion, pulmonary edema, hypoxemia, third heart sound, worsening regurgitation of mitral valve, generalized edema, elevated jugular venous pressure (JVP), hepatic enlargement, ascites, and hepatojugular reflux.1,5,9


In chronic HF, orthopnea and elevated JVP are the 2 primary symptoms or findings of elevated filling pressure.16 Rales are absent in the majority of patients with chronically elevated filling pressures because the chronic movement of fluid into the pulmonary interstitium is associated with increased pulmonary lymphatic drainage.9


The other signs and symptoms of ADHF are related to inadequate perfusion. Symptoms of low perfusion are nonspecific and may include complaints of lack of energy and fatigue, mental status changes, or weakness.9 The complaints of daytime sleepiness or difficulty concentrating may be reflective of disturbed sleep patterns, severely reduced perfusion to the brain, or depression.9 The signs of hypoperfusion may include narrow pulse pressure, pulsus alternans, cool extremities, hypotension, or renal dysfunction.9 A quick estimate of cardiac index is the proportional pulse pressure. If this value is less than 25%, the estimated cardiac index is below 2.2 L/min.16 The formula to determine proportional pulse pressure is given below.15

Equation (Uncited) - Click to enlarge in new windowEquation (Uncited)

As was previously mentioned, signs and symptoms associated with ADHF are not specific to only cardiac disorders, and so making a differential diagnosis is important. The clinical diagnosis of HF is based on history, physical examination, and diagnostic testing. Tests done at the time of admission may include chest radiograph, arterial blood gas, liver function tests, hematologic series, electrocardiogram, echocardiogram, basic metabolic profile, and a B-natriuretic peptide (BNP) assay.2


The BNP assay can be utilized as an aid to establish the diagnosis, estimate prognosis, and monitor the response to therapy of patients with ADHF.17,18 The BNP is a cardiac hormone secreted by the ventricular myocytes in response to wall stretch. The results of this assay may be especially useful when the diagnosis of HF is uncertain because of other comorbid factors.1 The Breathing Not Properly Study provided important evidence supporting the clinical use of BNP in the assessment of patients presenting with possible HF.19,20 The results of this study indicate that the diagnostic accuracy of BNP, using a cutoff value of 100 pg/mL, was 83% when compared to the assessment made by independent cardiologists, whereas the negative predictive value of BNP for HF, when levels were less than 50 pg/mL, was 96%.19,20 Therefore, assessment of BNP assay may serve as a useful tool in the diagnosis of a patient presenting with HF symptoms.


To continue further symptom evaluation, the hemodynamic profile (Fig 1) may be utilized.9 The hemodynamic profile has 4 subsets relating to the presence or absence of 2 fundamental abnormalities in HF: congestion and hypoperfusion.9 A patient who has congestion is profiled as being "wet," whereas a patient without congestion is profiled as being "dry." Inadequate perfusion leads to the patient being profiled as being "cold," whereas a patient with adequate perfusion is profiled as being "warm."9 A patient can be rapidly assessed according to these criteria and classified into 1 of 4 subsets (warm and dry, warm and wet, cold and wet, and cold and dry).9 Most patients presenting with ADHF experience congestion without low perfusion (warm and wet). Severely decompensated patients may present with both congestion and low perfusion (cold and wet).9


For those patients in whom the initial hemodynamic profile is unclear or early responses to treatment are not as anticipated, invasive hemodynamic monitoring may be a useful tool. Invasive hemodynamic measurement in the form of a pulmonary artery catheter may be utilized in tailoring therapy for the ADHF patient21 but the use of these catheters is associated with several risks for the patient, including infection, bleeding, and vessel damage.22,23


Bioimpedance cardiography is a noninvasive alternative to hemodynamic monitoring that is now available and being evaluated. This technology enables the calculation of hemodynamic values (eg, stroke volume, cardiac output, cardiac index, and systemic vascular resistance) based on the impedance of flow of electricity through the chest wall.23 Results from the study conducted by Albert et al indicate that impedance cardiography provides accurate measurements of cardiac output and cardiac index when compared with the invasive bolus thermodilution method.23 This noninvasive method may lead to timely interventions, resulting in clinical improvement and a shorter stay in the intensive care unit.23


Once adequate information is obtained regarding the patient, it is time to employ a treatment strategy. Although improving the signs and symptoms (related to congestion and hypoperfusion) is the principal immediate goal, treatments should be applied in a way that limits adverse effects of treatment and reduces the risk of morbidity.1,9 The Heart Failure Society of America (HFSA) has developed some comprehensive practice guidelines for the management of patients with ADHF. The treatment goals identified by the HFSA practice guidelines include optimizing volume status, identifying etiology, identifying precipitating factors, optimizing chronic oral therapy, minimizing side effects, identifying patients who may benefit from revascularization, educating patients concerning medications and self-assessment of HF, and considering initiating a disease management program.1


Adequate perfusion, no evidence of congestion

A patient who is warm and dry according to the hemodynamic profile9 is one who does not reflect evidence of elevated filling pressures or hypoperfusion. The goal of therapy for the patient is focused on disease management and prevention of disease progression.9 This patient generally does not fit the criteria for ADHF. Treatment strategies for this subgroup of patients are directed by the 2005 AHA/ACC guidelines.2


Evidence of congestion, adequate perfusion

A patient who presents as wet and warm has signs and symptoms of congestion but perfusion appears to be adequate.9 Therapy needs to be directed at dealing with congestion. If they are already on angiotensin-converting enzyme (ACE) inhibitors, their diuretic regimen needs to be enhanced.2,9 By the time these patients present in the acute care setting, some may have already been treated on an outpatient basis to manage their congestion.9 Hospitalization occurs when there is inadequate relief of symptoms. In this context, the addition of intravenous loop diuretics or supplementation with other diuretics can be utilized to achieve symptom relief.1 Initial improvement in symptoms can also be accelerated by intravenous vasodilators such as nitroglycerin (Nitrospan and Nitrostat) or natrecor (Nesiritide).25 Intravenous inotropes are generally not utilized unless evidence of fluid overload persists because of poor response to intravenous diuretics or diminished renal function.1,9,26


Diuretics have been the standard of therapy for the management of the congested ADHF patients because of their ability to rapidly decrease volume overload and congestion.1,27 Complications associated with diuretic use have also been reported. These complications include reduced glomerular filtration rate, neurohormonal activation, and diuretic resistance.1,27-33 The neurohormonal activation results in further vasoconstriction. Other concerns are related to the fact that diuretics create electrolyte imbalances (eg, hypokalemia), which may contribute to the development of potentially fatal arrhythmias.28-33 These adverse effects are thought to increase mortality within the HF patient population.27 The HFSA recommendations are that diuretics should be administered at a dose that produces sufficient diuresis to relieve congestion and to achieve optimal volume status. This treatment strategy should be done without inducing an excessively rapid reduction in volume, whereby symptomatic hypotension and/or worsening renal function is created.1 Patients should be closely monitored for adverse effects, electrolyte imbalances, intake and output, and weight status.1 In addition, sodium and fluid restriction may also need to be instituted.


Mechanical methods of fluid removal are also being actively investigated as a potential alternative to pharmacologic diuresis.34,35 In a study conducted by Costanzo et al, early ultrafiltration in patients admitted with fluid overload and diuretic resistance in reduced length of stay (compared to the length of stay indicated for ADHF patients in ADHERE database), aggressive fluid withdrawal (approximately 8500 mL), sustained drop in plasma BNP, and reduced hospitalizations within 30 days.35 Ultrafiltration was not associated with worsening renal failure, electrolyte abnormalities, or symptomatic hypotension.35 Clinical benefits persisted at 3 months after the treatment.35


Natrecor (exogenous BNP) is one of the agents that may be used in a patient who exhibits congestion but adequate perfusion (warm and wet). It has a combined action of vasodilation, diuresis, and natriuresis.36 These effects lead to a reduction in preload, afterload, and congestion.36 Natrecor has no inotropic effects and thus does not increase myocardial oxygen demand. It is contraindicated in patients with symptomatic hypotension and cardiogenic shock.37 In ADHF, the counterregulatory effects of endogenous BNP (BNP produced by myocytes) are not sufficient; therefore, natrecor may be administered to achieve the desired physiologic effect. The most common side effect of natrecor therapy is dose-related hypotension.36,37 If this occurs, the natrecor dose should be reduced or discontinued and measures to support blood pressure (eg, intravenous fluids, changes in body position) should be instituted.37 Recent findings relating natrecor to increased incidence of renal dysfunction and mortality may impact the use of natrecor in the ADHF patient population.38,39


Evidence of congestion and low perfusion

Patients who present with congestion and low perfusion (wet and cold) require interventions to improve perfusion and reduce congestion.9 For these patients, it is usually necessary to impact perfusion issues first and then the congestion issues.9 [beta]-Blockers and ACE inhibitors may need to be withdrawn until stabilization is achieved, especially if the patient is experiencing symptomatic hypotension.9 For many patients, low cardiac output is associated with high systemic vascular resistance and predictable improvement may be experienced with vasodilator therapy alone.9 There is considerable controversy about the relative role of vasodilators and inotropic-vasodilator agents such as dobutamine (dobutrex), low-dose dopamine (Intropin), and milrinone (Primacor).12,40 The investigators from Vasodilation in the Management of Acute CHF (VMAC) study concluded that natrecor may be the drug of choice in these patients because it is less potent and less toxic than intravenous nitroprusside (Nipride) and more easily administered than intravenous nitroglycerin.36


It is well understood that contractility is a determinant of cardiac output and when cardiac output is low, clinicians often consider utilizing an inotrope first. It is important to also remember that increased afterload impacts cardiac output. Since vasodilators are very effective in reducing afterload, it is a group of drugs that may be considered within this group of patients.1,9


Medications such as nitroprusside, nitroglycerin, and natrecor can be used to reduce afterload and thereby improve cardiac output, organ perfusion, and diuresis. It is definitely a challenge to use these agents in patients who start out hypotensive, even if asymptomatic.9


The routine use of intravenous inotropes (eg, dobutamine or milrinone) in HF may be detrimental.2,26 However, in select ADHF patients, inotropes may be administered to relieve symptoms and improve end-organ function.1,26 These patients are characterized by LV dilation, reduced LVEF, diminished systemic perfusion, and symptomatic hypotension.1 Inotropes are also utilized when initial hemodynamic status is unclear and temporary stability is needed until a more definitive profile can be determined.9,26 Concomitant use of [beta]-blockers and inotropes that are beta agonists (eg, dobutamine) are also controversial since both groups of drugs compete for the same beta receptor. The response to dobutamine is inhibited in patients receiving high doses of [beta]-blockers.41


Low perfusion and no evidence of congestion

Patients who present with low perfusion and no clinical evidence of congestion (cold and dry) reflect a very small subgroup of the ADHF patients.9 These patients may be stable clinically and often do not present with urgent symptoms.9 Unappreciated congestion may exist and requires further evaluation to determine.9 Treatment strategies for this subgroup will focus on improving the low perfusion state.1,9



Cardiorenal syndrome is a condition seen in HF where renal and cardiac dysfunction coexists. As the disease of HF advances, a decline in the renal function is evident. Diuretics and other treatment modalities become less effective. Worsening cardiac function contributes to a further decline in renal function.31,42 The cardiorenal syndrome is one of the major factors leading to frequent inotropic infusions for diuretic resistant congestion. Upon initiation of inotropic infusion, symptoms of congestion are temporarily relieved. Once inotropic therapy is discontinued, the symptoms reappear.9


Multiple factors are involved in the development of renal failure in these patients. Renal failure may occur because of reduced renal perfusion, neurohormonal mediated vasoconstriction, medication side effects (eg, nonsteroidal anti-inflammatory agents), and/or comorbidities (eg, hypertension, diabetes).42 Renal insufficiency is a significant component of the morbidity and mortality associated with HF. The presence of cardiorenal syndrome signals a marked worsening of prognosis for the HF patient.42 This is one of the most common reasons why patients during late stages of HF have unrelieved symptoms, despite aggressive management.9,31,42



A 70-year-old man was admitted with symptoms of increasing dyspnea and fatigue. He stated that his activity level declined substantially over the past few weeks. This was his second admission in the past 3 months with a similar presentation. His history is significant for non-insulin-dependent diabetes, coronary artery disease, and chronic bronchitis. His ejection fraction during his last hospitalization was noted as being 20%. He was determined to be a New York Heart Association class IV. Upon physical examination, 2+ edema to the mid-calf region, jugular venous distention, weight gain of 10 lb since his last follow-up visit 2 weeks ago, and cold upper and lower extremities bilaterally were evident. His BNP assay was 1000 pg/mL. His current medications were ACE inhibitor, loop diuretic, [beta]-blocker, antiarrhythmic, and bronchodilators.


This patient was presenting with signs and symptoms of ADHF. According to the hemodynamic profile, this patient was cold and wet. Evaluation for exacerbating factors revealed that he had a respiratory tract infection. He was started on antibiotics and breathing treatments. His symptoms of congestion and low perfusion were addressed on the basis of the cold and wet profile discussed earlier. Patient education was begun in the intensive care unit and continued throughout his hospitalization.



Nurses are challenged to have a thorough knowledge base related to the disease state of HF and the eliciting factors that impact readmissions for ADHF. For patients admitted to the intensive care unit, appropriate assessment of signs and symptoms of congestion and hypoperfusion is essential. It is important to utilize diagnostic tools such as the BNP assay to decipher the presented symptoms as it relates to HF versus other comorbid factors. The use of the hemodynamic profile is helpful in developing treatment strategies. To evaluate the effectiveness of the treatment plan, an understanding of what the anticipated outcomes should be is necessary. Since readmissions are frequent within this patient population, prevention strategies should be evaluated and employed. Effective treatment plans are dependent on ongoing communication and collaboration by all members of the healthcare team.12


In 2002, the Joint Commission on Accreditation of Healthcare Organizations developed the HF core measure set.43 The 4 standardized core measures set for hospitalized HF patients are documentation of discharge instruction in 6 areas (medication management, diet, activity and exercise, signs and symptoms of worsening condition, weight monitoring, and when to contact a healthcare provider), assessment of LV function, use of an ACE inhibitor or angiotensin receptor blocker in patients with LV dysfunction, and smoking cessation counseling.43 The healthcare team needs to be aware of these core measures and address each element throughout the hospitalization for all HF patients.



Patients hospitalized with ADHF are complex and clinically challenging. Hospitalizations related to ADHF are associated with poor prognosis, increased costs, and reduced quality of life. The use of biomakers such as B-natriuretic peptides is useful in distinguishing between cardiac and noncardiac causes of symptoms. Early identification and management of precipitating factors is vital in the successful management of these patients. The hemodynamic profile serves as a useful tool to rapidly assess patients presenting with ADHF symptoms. Interventions should focus on symptom management, preventing readmissions, delaying disease progression, and prolonging survival. Nurses have an integral role in this process.




1. Adams KF, Lindenfeld J, Arnold JMO, et al. Heart Failure Society of America (HFSA) 2006 comprehensive heart failure practice guideline. J Cardiac Fail. 2006;12(1):10-38. [Context Link]


2. ACC/AHA. Guideline update for the diagnosis and management of chronic HF in the adult. American Heart Association/American College of Cardiology. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult. 2005. Available at:[1]032. Accessed October 3, 2006. [Context Link]


3. Albert N. Heart failure: the pathophysiologic basis for current therapeutic concepts. Crit Care Nurse.1999;18(suppl):2-13. [Context Link]


4. American Heart Association. Heart Disease and Stoke Statistics-2006 Update. Washington, DC: American Heart Association; 2006. [Context Link]


5. Fonarow GC. The acute decompensated heart failure national registry (ADHERE): opportunities to improve care of patients hospitalized with acute decompensated heart failure. Rev Cardiovasc Med. 2003;4(7):S21-S30. [Context Link]


6. CDC Heart Failure Fact Sheet. Available at: Accessed October 2, 2006. [Context Link]


7. Skrabal MZ, Stading JA Behmer-Miller KA, Hilleman DE. Advances in the treatment of congestive heart failure: new approaches for an old disease. Pharmacotherapy. 2000;20:787-804. [Context Link]


8. Yancy CW, Lopatin M, Stevenson LW, De Marco T, Fonarow GC, ADHERE Scientific Advisory Committee and Investigators Clinical presentation, management, and in-hospital outcomes of patients admitted with acute decompensated heart failure with preserved systolic function: a report from the Acute Decompensated Heart Failure National Registry (ADHERE) database. J Am Coll Cardiol. 2006;47(1):76-84. [Context Link]


9. Nohria A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA. 2002;287(5):628-640. [Context Link]


10. Albert NM, Eastwood CA, Edwards ML. Evidence based practice for acute decompensated heart failure. Crit Care Nurse. 2004;24(6):14-26. [Context Link]


11. Shah M, Ali V, Lamba S, Abraham WT. Pathophysiology and clinical spectrum of acute congestive heart failure. Rev Cardiovasc Med. 2001;2(suppl 2):S2-S6. [Context Link]


12. Saul L, Shatzer M. B-type natriuretic peptide testing for detection of heart failure. Crit Care Nurs Q. 2003;26(1):35-39. [Context Link]


13. Chatterjee K. Neurohormonal activation in congestive heart failure and the role of vasopressin. Am J Cardiol. 2005;95(suppl):8B-13B. [Context Link]


14. Sharma R, Coats A, Anker SD. The role of inflammatory mediators in chronic heart failure: cytokine, nitric oxide, and edothelin-1. Int J Cardiol. 2000;72:175-186.


15. Piccini JP, Klein L, Gheorghiade M, Bonow RO. New insights into diastolic heart failure: role of diabetes mellitus. Am J Med. 2004;115(suppl):64S-75S. [Context Link]


16. Stevenson LW, Perloff JK. The limited reliability of physical signs of estimating hemodynamics in chronic heart failure. JAMA.1989;261:884-888. [Context Link]


17. Maisel AS, McCullough PA. Cardiac natriuretic peptides: a proteomic window to cardiac function and clinical management. Rev Cardiovasc Med. 2003;(suppl 4):S3-S12. [Context Link]


18. Silver MA, Maisel AS, Yancy CW, et al, and BNP Consensus Panel. A clinical approach for the, screening, treatment monitoring and therapeutic roles of natriuretic peptide in cardiovascular diseases. Congest Heart Fail. 2004;10(suppl 3):S1-S30. [Context Link]


19. Baughman, KL. B-type natriuretic peptide: a window to the heart. N Engl J Med. 2002;347:158-159. [Context Link]


20. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161-167. [Context Link]


21. Stevenson LW. Are hemodynamic goals viable in tailoring heart failure therapy? Hemodynamic goals are relevant. Circulation. 2006;113:1020-1027. [Context Link]


22. Branum K. Management of decompensated heart failure. AACN Clin Issues. 2003;14:498-511. [Context Link]


23. Albert NM, Hail MD, Li J, Young JB. Equivalence of the bioimpedance and thermodilution methods in measuring cardiac output in hospitalized patients with advanced, decompensated heart failure. Am J Crit Care. 2004;13(6):469-479. [Context Link]


24. Wadas TM. The implantable hemodynamic monitoring system. Crit Care Nurse. 2005;25(5):14-26.


25. Cody RJ. Clinical trials of diuretic therapy in heart failure: research directions and clinical considerations. J Am Coll Cardiol. 1993;22(suppl):65A-71A. [Context Link]


26. Felker GM, O'Connor CM. Inotropic therapy for heart failure: an evidence based approach. Am Heart J. 2001;142:393-401. [Context Link]


27. Slike B. Diuretic induced changes in symptoms and quality of life. Br Heart J. 1994;72(suppl):S57-S62. [Context Link]


28. Cooper HA, Dries DL, Davis CE, Shen YL, Domanski MJ. Diuretics and risk of arrhythmic death with left ventricular dysfunction. Circulation. 1999;100:1311-1315. [Context Link]


29. Satorstein L. Electrophysiological impact of diuretics in heart failure. Br Heart J. 1994;72(suppl):S54-S56. [Context Link]


30. Anand IS, Chugh SS. Mechanisms and management of renal dysfunction in heart failure. Curr Opin Cardiol. 1997;12(3):251-258. [Context Link]


31. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal dysfunction during intensive therapy for advanced heart failure. Am Heart J. 1999;138:285-290. [Context Link]


32. Eshaghian S, Horwich TB, Fonarow GC. Relation of loop diuretic dose to mortality in advanced heart failure. Am J Cardiol. 2006;97:1759-1764. [Context Link]


33. Krum H, Cameron P. Diuretics in the treatment of heart failure: mainstay of therapy or potential hazard? J Cardiol Fail. 2006;12(5):333-335. [Context Link]


34. Bart BA, Boyle A, Bank AJ, et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: the relief for acutely fluid-overloaded patients with decompensated congestive heart failure (RAPID-CHF) trial. J Am Coll Cardiol. 2005;46(11):2043-2051. [Context Link]


35. Costanzo MR, Saltzberg M, O'Sullivan J, Sobotka P. Early ultrafiltration in patients with decompensated heart failure and diuretic resistance. J Am Coll Cardiol. 2005;46(11):2047-2051. [Context Link]


36. Publication Committee for the VMAC Investigators (Vasodilation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controller trial [published correction appears in JAMA. 2002;288:577]. JAMA. 2002;287:1531-1540. [Context Link]


37. Scios Inc. Natrecor United States Prescribing Information. Fremont, Calif: Scios Inc; 2002. [Context Link]


38. Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K. Short-term risk of death after treatment with nesiritide for decompensated heart failure. A pooled analysis of randomized control trials. JAMA. 2005;293(15):1900-1905. [Context Link]


39. Sackner-Bernstein JD, Skopicki HA, Aaronson KD. Risk of worsening renal function with nesiritide in patients with acutely decompensated heart failure. Circulation. 2005;111:1487-1491. [Context Link]


40. Felker GM, O'Connor CM. Inotropic therapy for heart failure: an evidence-based approach. Am Heart J. 2001;142:393-401. [Context Link]


41. Bristow MR, Shakar SF, Linseman JV, Lowes BD. Inotropes and B-blockers: is there a need for new guidelines? J Cardiac Fail. 2001;7(2, suppl 1):8-12. [Context Link]


42. Heywood JT. The cardiorenal syndrome: lessons from the ADHERE database and treatment options. Heart Fail Rev. 2004;9:195-201. [Context Link]


43. Joint Commission on Accreditation of Healthcare Organizations. Overview of the heart failure core measures set 2002. Available at: Accessed October 3, 2006. [Context Link]