Myths in Heart Failure: Part I – ED Evaluation

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK)


A 62-year-old male presents with significant dyspnea with exertion and lower extremity edema. He has a prior history of heart disease, hypertension, and hyperlipidemia, but no known diabetes or heart failure. He has not seen a physician in over 5 years. He is hypertensive on exam, but the rest of his vital signs, including respiratory rate and saturation, are normal. You detect bibasilar rales and 2+ pitting edema bilaterally.  Seems pretty straightforward…standard heart failure, right? Do you need a BNP? What role does renal function play? What imaging test should you obtain?  


Acute heart failure is one of the most causes of hospitalization in the U.S. for those > 65 years, accounting for over 650,000 ED visits annually in the U.S.1-7   Close to 80% of patients with AHF are first evaluated in the ED.5-7  There are many ways patients may present with AHF, including gradual decline with worsening symptoms over several weeks, hypertensive pulmonary edema, or cardiogenic shock.

Though we see HF daily and there are several sets of guidelines available,8-12  there are several myths and misconceptions in HF evaluation and management. Part I will address these myths/misconceptions in evaluation of acute HF. Part II will look at treatment.

Myth #1 – Natriuretic peptide testing should be routinely used to rule out or rule in acute heart failure.

B-type natriuretic peptide (BNP) and NT-proBNP are the typical natriuretic peptides obtained on laboratory testing. Natriuretic peptides are produced in the cardiac musculature due to myocyte stretch and function in volume and sodium homeostasis.8,10,13  Myocyte stretch releases proBNP, a precursor molecule, which is enzymatically cleaved to NT-proBNP and BNP.13-17  Both increase sodium and water excretion, increase peripheral vasodilation, and decrease activity of the renin angiotensin aldosterone system (RAAS).8,10  BNP’s half-life approximates 20 minutes, and NT-proBNP’s half-life is 3-6 times the half-life of BNP.13-17

These molecules are often used in AHF. An American College of Emergency Physicians (ACEP) clinical policy provides level B recommendations that with BNP < 100 pg/mL or NT-proBNP < 300 pg/mL, AHF is unlikely, while for BNP > 500 pg/mL or NT-proBNP > 1,000 pg/mL, AHF is likely.8  The 2017 American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Failure Society of America (HFSA) guideline updates provide a Level IA recommendation that natriuretic peptides are useful to support the diagnosis or exclusion of AHF, similar to the 2013 guidelines.9,10  However, the literature behind their use in the ED is controversial.

Pearl #1 – Natriuretic peptides should only be used in combination with clinical evaluation. Other causes of elevated BNP should be considered.

Close to 1/4 of patients with dyspnea will not have definitive levels of natriuretic peptides that help clinicians.13-20 An early study evaluating BNP in 1586 patients suggested the biomarker was more accurate than history or exam, with a sensitivity of 90% for BNP > 100 pg/mL and specificity 76%.18  However, emergency physicians were correct in diagnosing AHF in 95% of cases if they were sure of the diagnosis! If emergency physicians did not think AHF was the cause of symptoms, they were right in 92% of cases.18  A separate study found that BNP 100 pg/mL had a sensitivity of 90% and specificity 73%, compared to emergency physicians with sensitivity of 49% and specificity 96%.19  Study authors state BNP may have corrected physician diagnosis, but there is no discussion for patients in whom BNP was incorrect. The gold standard was cardiology diagnosis, which was 90% accurate in diagnosis, but cardiologists disagreed on diagnosis 11% of the time.19

The RED-HOT study evaluated BNP use and 90-day mortality and readmission and found BNP demonstrated an area under the curve of 0.67 (poor correlation).20   One meta-analysis suggested a pooled sensitivity of 95% and pooled specificity of 63% if a cutoff of 100 ng/L was utilized, while NT-proBNP cutoff of 300 ng/L demonstrated pooled sensitivity and specificity 99% and 43%, respectively.21  Another meta-analysis found a sensitivity and specificity of 93.5% and 52.9%, respectively, for BNP, and 90.4% and 38.2%, for NT-proBNP, respectively.22  Though the study states BNP outperformed history and exam findings, the studies that were included had significant weakness including use of cardiologist opinion as gold standard for diagnosis, and few of the included studies evaluated emergency physician judgment and evaluation.22  Remember that phrase, garbage in equals garbage out?… Observational data suggest natriuretic peptides have high sensitivities for AHF diagnosis, but poor to moderate specificity. Higher cutoff values increase specificity, but lower sensitivity. If emergency physicians are not certain in diagnosing AHF exacerbation, natriuretic peptides have less accuracy. It is not clear that these biomarkers can outperform clinician judgment.

What about randomized controlled trial (RCT) data? A 2004 study suggests fewer admissions and decreased cost with natriuretic peptide use; no differences in mortality or readmission rates were found. This study did not blind physicians managing patients, and objective outcomes were no different when utilizing BNP.23   Another study, the IMPROVE-CHF study, evaluated NT-proBNP, finding decreased length of stay (0.7 hours) and decreased cost. However, results show no differences in admissions or readmissions, along with a nonsignificant increase in mortality with NT-proBNP.24  When used in isolation, BNP did not improve diagnostic accuracy, but when added to history and exam, a marginal improvement was present. A separate study found decreased hospital length of stay by 2 days, but no change in ED length of stay or admission rate.25  More recent RCTs suggest no difference in clinical outcomes such as mortality, readmission, or hospital stay.26-30

One major issue is that a large number of other etiologies can elevate natriuretic peptide levels including coronary syndromes, valvular heart disease, pericardial disease, atrial fibrillation, cardiac surgery, cardioversion, older age, anemia, renal failure, pulmonary hypertension, critical illness, sepsis, and burns.21-23  Thus, the test is not specific. Body weight/body mass index (BMI) and gender can affect BNP levels as well.31,32 Elevated BMI actually decreases natriuretic levels.

If used in isolation, BNP may outperform other history and examination features in diagnosis of AHF. However, we rarely, if ever, use tests in isolation. These biomarkers do not outperform overall clinical impression and gestalt. Studies evaluating natriuretic peptides suggest they do not change patient-centered outcomes such as mortality, though they may be associated with reduction in cost and length of stay (admission rates are controversial).26-30  The literature evaluating natriuretic peptides is rife with poor blinding and bias, as well as a variety of different cutoff levels.  For an even deeper dive on BNP, see this First10EM post.


Myth #2 – Renal function assessment is of low yield in the evaluation of AHF.

We typically order a variety of labs in the evaluation of these patients. Troponin is one important assessment, as an elevation in troponin is associated with worse outcomes in AHF.9-12 Another important test is renal function, which is also associated with AHF outcomes.9-12

Pearl #2 – Renal function assessment provides valuable information for disease prognosis and severity in AHF.

Complex cardiac, renal, and vascular interactions occur in AHF, with renal impairment limiting sodium and fluid excretion and increasing activation of the renin-angiotensin-aldosterone system (RAAS).9-12,33  Data suggest kidney injury is common in patients presenting with AHF, with 15%-20% of patients demonstrating Cr > 2.0 mg/dL,34-39 and approximately 25%-31% of patients with glomerular filtration rate (GFR) < 60 mL/min.39-44   Renal function is an important laboratory measurement in AHF, as worsening renal function is associated with short and long-term mortality, increased length of stay, and increased rate of return visit/hospitalization.44-48  AHF may also result in renal injury or further decrease renal function (potentially causing cardiorenal syndrome).42,44,45  Each 10 mL/min decrease in GFR is associated with a 7% increase in mortality.48,49  One meta-analysis reports that annual mortality rates for AHF approach 26% for patients without renal disease, 41% with patients with any form of renal impairment, and 51% in patients with moderate or severe renal dysfunction.48  Forman et al. reported that patients with worsening renal disease possess a 7.5 times higher relative risk ratio for mortality in-hospital.41

Pearl #3 – Serum Cr is limited in assessing renal dysfunction in patients presenting acutely with AHF, and BUN is an important predictor of mortality in AHF.

Though renal dysfunction is typically assessed using serum Cr, this measurement is influenced by a significant number of factors such as age, muscle mass, and concomitant medications, and Cr is not sensitive for renal dysfunction.44,49-54  Changes in serum Cr are dependent on baseline kidney function.52,53  Marked decreases in GFR may cause small changes in serum Cr in the first 24-48 hours of renal injury.33,44-49,52,53  Serum Cr is not always associated with renal injury, as it functions as an assessment of renal function rather than injury. Relying on this test in early presenters with AHF (< 24-48 hours) is not recommended, as Cr may not significantly elevate.33,46-49,52,53  However, BUN may be elevated. BUN is reabsorbed in the renal tubules, unlike Cr, and BUN levels are related to RAAS activity, sodium reabsorption, nitrogen production, and protein metabolism.47,52-59  BUN is an important predictor of mortality and morbidity in patients with AHF.54,55  Levels>43 mg/dL are associated with poor outcome.9-12,40  BUN or Cr elevation is associated with poor outcome in AHF, though BUN may be more accurate.


Myth #3 – Chest radiograph is the go-to imaging assessment in AHF exacerbation.

Chest X-ray is one of the most common assessments in AHF, especially in the patient with shortness of breath.8-12,22  However, chest X-ray findings are not definitive and vary.22  Kerley B-lines have a sensitivity of 9.2% and specificity 98.8%, interstitial edema sensitivity 31.1% and specificity 95.1%, cephalization sensitivity 44.7% and specificity 94.6%, alveolar edema sensitivity 5.7% and specificity 98.9%, pulmonary edema sensitivity 56.9% and specificity 89.2%, pleural effusion sensitivity 16.3% and specificity 92.8%, and cardiomegaly sensitivity 74.7% and specificity 61.7% for AHF.22  Close to 20% of chest X-rays demonstrate no findings of AHF, but the test does have value in suggesting another cause of symptoms.9-12,22

Pearl #4 – A more valuable means of diagnosis for pulmonary edema associated with AHF is ultrasound.

Yes, it’s time for some ultrasound love. Point of care ultrasound (POCUS) is an important tool in diagnosis and management of many critical conditions, including AHF. POCUS can provide a rapid and reliable diagnosis, while also evaluating for other conditions.  US assessment typically evaluates several components, including the lungs, heart, and inferior vena cava (IVC).22,60,61  US alone with the presence of >3 B lines in >2 bilateral thoracic lung zones has a +LR of 7.4, sensitivity approaching over 90%, and specificity 92.7% for pulmonary edema, while the absence of B lines has a -LR of 0.16.22,62-64  The number of B lines also correlates with AHF severity.65,66  Intravascular volume assessment can take into account IVC diameter and collapsibility.22,60  However, specific numbers vary for IVC collapsibility index, including 20%-50%. An IVC that collapses < 33% is associated with sensitivity close to 80% for volume overload, with specificity 81%-87%.66-69  However, keep in mind that IVC assessment is complicated by many other conditions (tricuspid regurgitation, pulmonary hypertension (pulmonary embolism), and right ventricular myocardial infarction).22,67-69  US also provides an evaluation of cardiac function, which can be completed by measuring the inward movement of the interventricular septum and inferior wall of the LV in systole and degree of excursion of the anterior mitral valve leaflet in diastole.22,60,61  Detecting reduction in LV function has a sensitivity of 77-83% and specificity 74-90%.22,66,67  There are several other assessments including E-point septal separation (EPSS) and diastolic filling restrictive pattern with pulsed Doppler analysis (typically a specialist test). An EPSS measurement > 7 mm suggests ejection fraction (EF) < 50%.70-72  This emDocs post has some great information on EPSS.  The key to remember is that lung US plays a vital role in assessment for pulmonary edema with B lines, along with global cardiac function.22,62-64

B lines in the presence of pulmonary edema


Key Points

– A variety of misconceptions are present concerning the ED evaluation and management of AHF.

– BNP should only be used in conjunction with clinical gestalt and cannot be used in isolation on a reliable basis.

– There are many other conditions that can elevate BNP, and obesity can actually decrease BNP.

Renal function, including Cr and BUN, are important assessments in the patient with AHF exacerbation. Elevation in these tests are associated with poor outcome.

– Though chest x-ray is considered the go-to imaging test, ultrasound is better for evaluating for the presence of pulmonary edema.


References/Further Reading

  1. Roger VL. Epidemiology of heart failure. Circ Res 2013;113:646–59.
  2. Bui AL, Horwich TB, Fonarow GC. Epidemiology and risk profile of heart failure. Nat Rev Cardiol 2011;8:30–41.
  3. Collins SP, Storrow AB. Acute heart failure risk stratification: can we define low risk? Heart Fail Clin. 2009;5:75–83.
  4. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Blaha MJ, et al. Heart disease and stroke statistics—2014 update: a report from the American Heart Association. Circulation. 2014;129:e28–292.
  5. Storrow AB, Jenkins CA, Self WH, et al. The burden of acute heart failure on U.S. emergency departments. JACC Heart Fail 2014;2(3):269–77.
  6. Pang PS, Collins SP. Acute heart failure in the emergency department: just a one night stand? Acad Emerg Med 2017;24(3):385–7.
  7. Pang PS, Collins SP, Miro O, et al. The role of the emergency department in the management of acute heart failure: an international perspective on education and research. Eur Heart J Acute Cardiovasc Care 2017;6(5):421–9.
  8. Silvers SM, Howell JM, Kosowsky JM, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med 2007;49:627–69.
  9. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American college of cardiology foundation/American heart association task force on practice guidelines. J Am Coll Cardiol 2013;62:147–239.
  10. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA Focused Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure. JACC. 2017;70(6):776-803.
  11. Hunt SA, Abraham WT, Chin MH, et al. ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society. 2005;112:e154–e235.
  12. McMurray JJ, Adamopoulos S, Anker SD, et al. ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2012: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012 of the European Society of Cardiology. Developed in collaboration with the heart failure association (HFA) of the ESC. Eur Heart J 2012;33:1787–847.
  13. Haug C, Metzele A, Kochs M, et al. Plasma brain natriuretic peptide and atrial natriuretic peptide concentrations correlate with left ventricular end-diastolic pressure. Clin Cardiol 1993;16(7):553-557.
  14. Darbar D, Davidson NC, Gillespie N, et al. Diagnostic value of B-type natriuretic peptide concentrations in patients with acute myocardial infarction. Am J Cardiol 1996;78(3):284-7.
  15. Omland T, Aakvaag A, Bonarjee VVS, et al. Plasma brain natriuretic peptide as an indicator of left ventricular systolic function and long-term survival after acute myocardial infarction. Comparison with plasma atrial natriuretic peptide and N-terminal proatrial natriuretic peptide. Circulation 1996;93:1963-9.
  16. Valli N, Gobinet A, Bordenave L. Review of 10 years of the clinical use of brain natriuretic peptide in cardiology. J Lab Clin Med 1999;134(5):437-444.
  17. Maeda K, Tsutamoto T, Wada A, et al. High levels of plasma brain natriuretic peptide and interleukin-6 after optimized treatment for heart failure are independent risk factors for morbidity and mortality with congestive heart failure. J Am Coll Cardiol 2000;36:1587-93.
  18. Maisel AS, Krishnaswamy P, Nowak RM, et al.Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. The New England journal of medicine. 2002; 347(3):161-7.
  19. McCullough PA, Nowak RM, McCord J. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002; 106(4):416-22.
  20. Maisel A, Hollander JE, Guss D. Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT). A multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath. Journal of the American College of Cardiology. 2004; 44(6):1328-33.
  21. Roberts E, Ludman AJ, Dworzynski K. The diagnostic accuracy of the natriuretic peptides in heart failure: systematic review and diagnostic meta-analysis in the acute care setting. BMJ (Clinical research ed.). 2015; 350:h910.
  22. Martindale JL, Wakai A, Collins SP. Diagnosing Acute Heart Failure in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine. 2016; 23(3):223-42.
  23. Mueller C, Scholer A, Laule-Kilian K. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea. The New England journal of medicine. 2004; 350(7):647-54.
  24. Moe GW, Howlett J, Januzzi JL, Zowall H. N-terminal pro-B-type natriuretic peptide testing improves the management of patients with suspected acute heart failure: primary results of the Canadian prospective randomized multicenter IMPROVE-CHF study. Circulation. 2007; 115(24):3103-10.
  25. Rutten JH, Steyerberg EW, Boomsma F. N-terminal pro-brain natriuretic peptide testing in the emergency department: beneficial effects on hospitalization, costs, and outcome. American heart journal. 2008; 156(1):71-7.
  26. Schneider HG, Lam L, Lokuge A. B-type natriuretic peptide testing, clinical outcomes, and health services use in emergency department patients with dyspnea: a randomized trial. Annals of internal medicine. 2009; 150(6):365-71.
  27. Singer AJ, Birkhahn RH, Guss D. Rapid Emergency Department Heart Failure Outpatients Trial (REDHOT II): a randomized controlled trial of the effect of serial B-type natriuretic peptide testing on patient management. Circulation. Heart failure. 2009; 2(4):287-93.
  28. Boldanova T, Noveanu M, Breidthardt T. Impact of history of heart failure on diagnostic and prognostic value of BNP: results from the B-type Natriuretic Peptide for Acute Shortness of Breath Evaluation (BASEL) study. International journal of cardiology. 2010; 142(3):265-72.
  29. Meisel SR, Januzzi JL, Medvedovski M. Pre-admission NT-proBNP improves diagnostic yield and risk stratification – the NT-proBNP for EValuation of dyspnoeic patients in the Emergency Room and hospital (BNP4EVER) study. European heart journal. Acute cardiovascular care. 2012; 1(2):99-108.
  30. Steinhart BD, Levy P, Vandenberghe H. A Randomized Control Trial Using a Validated Prediction Model for Diagnosing Acute Heart Failure in Undifferentiated Dyspneic Emergency Department Patients-Results of the GASP4Ar Study. Journal of cardiac failure. 2017; 23(2):145-152.
  31. Ray P, Arthaud M, Birolleau S, et al. Comparison of brain natriuretic peptide and probrain natriuretic peptide in the diagnosis of cardiogenic pulmonary edema in patients aged 65 and older. J Am Geriatr Soc 2005;53(4):643-8.
  32. Mueller T, Gegenhuber A, Poelz W, et al. Diagnostic accuracy of B type natriuretic peptide and amino terminal proBNP in the emergency diagnosis of heart failure. Heart 2005;91(5):606-12.
  33. Han SW, Ryu KH. Renal Dysfunction in Acute Heart Failure. Korean Circulation Journal. 2011;41(10):565-574.
  34. Adams KF, Jr, Fonarow GC, Emerman CL, et al. 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.
  35. Cleland JG, Swedberg K, Cohen-Solal A, et al. The Euro Heart Failure Survey of the EUROHEART survey programme: a survey on the quality of care among patients with heart failure in Europe: the Study Group on Diagnosis of the Working Group on Heart Failure of the European Society of Cardiology: the Medicines Evaluation Group Centre for Health Economics University of York. Eur J Heart Fail. 2000;2:123–132.
  36. Zannad F, Mebazaa A, Juillière Y, et al. Clinical profile, contemporary management and one-year mortality in patients with severe acute heart failure syndromes: the EFICA Study. Eur J Heart Fail. 2006;8:697–705.
  37. O’Meara E, Chong KS, Gardner RS, et al. The modification of diet in renal disease (MDRD) equations provide valid estimations of glomerular filtration rates in patients with advanced heart failure. Eur J Heart Fail. 2006;8:63–67.
  38. Choi DJ, Han S, Jeon ES, et al. Characteristics, Outcomes and Predictors of Long-Term Mortality for Patients Hospitalized for Acute Heart Failure: A Report From the Korean Heart Failure Registry. Korean Circ J. 2011;41:363–371.
  39. Nohria A, Hasselblad V, Stebbins A, et al. Cardiorenal interactions: insights from the ESCAPE trial. J Am Coll Cardiol. 2008;51:1268–1274.
  40. Fonarow GC, Adams KF Jr, Abraham WT, et al. Risk stratifica­tion for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA 2005; 293:572-80.
  41. Forman DE, Butler J, Wang Y, et al. Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure. J Am Coll Cardiol. 2004;43:61–67.
  42. Damman K, Navis G, Voors AA, et al. Worsening renal function and prognosis in heart failure: systematic review and meta-analysis. J Card Fail. 2007;13:599–608.
  43. Cowie MR, Komajda M, Murray-Thomas T, Underwood J, Ticho B POSH Investigators. Prevalence and impact of worsening renal function in patients hospitalized with decompensated heart failure: results of the prospective outcomes study in heart failure (POSH) Eur Heart J. 2006;27:1216–1222.
  44. Metra M, Nodari S, Parrinello G, et al. Worsening renal function in patients hospitalised for acute heart failure: clinical implications and prognostic significance. Eur J Heart Fail. 2008;10:188–195.
  45. Gottlieb SS, Abraham W, Butler J, et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J Card Fail. 2002;8:136–141.
  46. Schrier RW. Role of diminished renal function in cardiovascular mortality: marker or pathogenetic factor? J Am Coll Cardiol. 2006;47:1–8.
  47. Klein L, Massie BM, Leimberger JD, et al. 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.
  48. Smith GL, Lichtman JH, Bracken MB, et al. Renal impairment and outcomes in heart failure: systematic review and meta-analysis. J Am Coll Cardiol 2006;47:1987-96.
  49. Hillege HL, Nitsch D, Pfeffer MA, et al. Renal function as a predictor of outcome in a broad spectrum of patients with heart failure. Circulation 2006;113:671-8.
  50. Haase-Fielitz A, Bellomo R, Devarajan P, et al. Novel and conventional serum biomarkers predicting acute kidney injury in adult cardiac surgery: a prospective cohort study. Crit Care Med. 2009;37:553–560.
  51. Bonventre JV, Vaidya VS, Schmouder R, Feig P, Dieterle F. Next-generation biomarkers for detecting kidney toxicity. Nat Biotechnol. 2010;28:436–440.
  52. Stevens LA, Coresh J, Greene T, Levey AS. Assessing kidney function: measured and estimated glomerular filtration rate. N Engl J Med. 2006;354:2473–2483.
  53. Waikar SS, Bonventre JV. Creatinine kinetics and the definition of acute kidney injury. J Am Soc Nephrol. 2009;20:672–679.
  54. Filippatos G, Rossi J, Lloyd-Jones DM, et al. Prognostic value of blood urea nitrogen in patients hospitalized with worsening heart failure: insights from the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Chronic Heart Failure (ACTIV in CHF) study. J Card Fail. 2007;13:360–364.
  55. Cauthen CA, Lipinski MJ, Abbate A, et al. Relation of blood urea nitrogen to long-term mortality in patients with heart failure. Am J Cardiol. 2008;101:1643–1647.
  56. Aronson D, Mittleman MA, Burger AJ. Elevated blood urea nitrogen level as a predictor of mortality in patients admitted for decompensated heart failure. Am J Med. 2004;116:466–473.
  57. Lindenfeld J, Schirier RW. Blood urea nitrogen: A marker for adverse effects of loop diuretics? J Am Coll Cardiol. 2011;58:383–385.
  58. Testani JM, Cappola TP, Brensinger CM, Shannon RP, Kimmel SE. Interaction between loop diuretic-associated mortality and blood urea nitrogen concentration in chronic heart failure. J Am Coll Cardiol. 2011;58:375–38.
  59. Schrier RW. Blood urea nitrogen and serum creatinine: not married in heart failure. Circ Heart Fail. 2008;1:2–5.
  60. Öhman J,Harjola VP, Karjalainen P, Lassus J. Rapid cardiothoracic ultrasound protocol for diagnosis of acute heart failure in the emergency department. Eur J Emerg Med. 2017 Oct 3. doi: 10.1097/MEJ.0000000000000499. [Epub ahead of print]
  61. Russell FM,Ehrman RR. A Modified Lung and Cardiac Ultrasound Protocol Saves Time and Rules in the Diagnosis of Acute Heart Failure. J Emerg Med. 2017 Jun;52(6):839-845.
  62. Jambrik Z, Monti S, Coppola V, et al. Usefulness of ultrasound lung comets as a nonradiologic sign of extravascular lung water. Am J Cardiol. 2004;93(10):1265-1270.
  63. Mallamaci F, Benedetto FA, Tripepi R, et al. Detection of pulmonary congestion by chest ultrasound in dialysis patients. JACC Cardiovasc Imaging. 2010;3(6):586-594.
  64. Anderson KL, Fields JM, Panebianco NL, et al. Inter-rater reliability of quantifying pleural B-lines using multiple counting methods. Ultrasound Med. 2013;32(1): 115-120.
  65. Agricola E, Bove T, Oppizzi M, et al. “Ultrasound comet-tail images”: a marker of pulmonary edema: a comparative study with wedge pressure and extravascular lung water. Chest. 2005;127(5):1690-1695.
  66. Anderson KL, Jenq KY, Fields JM, et al. Diagnosing heart failure among acutely dyspneic patientswith cardiac, inferior vena cava, and lung ultrasonography.Am J Emerg Med. 2013;31(8):1208-1214.
  67. Gil Martinez P, Mesado Martinez D,Curbelo Garcia J, et al. Amino-terminal pro-B-type natriureticpeptide, inferior vena cava ultrasound, and bioelectrical impedance analysis for the diagnosis of acute decompensated Am J Emerg Med. 2016;34(9):1817-1822.
  68. Kajimoto K, Madeen K, Nakayama T, et al. Rapid evaluation by lung-cardiac-inferior vena cava (LCI)integrated ultrasound for differentiating heart failure frompulmonary disease as the cause of acute dyspnea in theemergency setting. Cardiovasc Ultrasound. 2012;10(1):49.
  69. Miller JB, Sen A, Strote SR, et al. Inferior vena cava assessment in the bedside diagnosis of acute heart failure. Am J Emerg 2012;30(5):778.
  70. Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol. 2006;97(1):137-40.
  71. Nazerian P, Vanni S, Zanobetti M, et al. Diagnostic accuracy ofemergency Doppler echocardiography for identification ofacute left ventricular heart failure in patients with acute dyspnea: comparison withBoston criteria and N-terminal prohormone brain natriuretic peptide. Acad Emerg Med.2010;17(1):18-26.
  72. Russell FM, Ehrman RR, Cosby K, et al. Diagnosing acute heart failure in patients with undifferentiated dyspnea: a lung andcardiac ultrasound (LuCUS) protocol. Acad Emerg Med. 2015;22(2):182-191.

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