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ACEP Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Acute Heart Failure.

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Presentation on theme: "ACEP Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Acute Heart Failure."— Presentation transcript:

1 ACEP Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department with Acute Heart Failure Syndromes Brian McMichael, M.D. PGY-1, Emergency Medicine Wayne State University/Detroit Medical Center (Detroit Receiving Hospital) Brian McMichael, M.D. PGY-1, Emergency Medicine Wayne State University/Detroit Medical Center (Detroit Receiving Hospital)

2 Objectives Give an overview of the pathophysiology of responses that lead to the common final pathway of acute heart failure (AHF) syndromes. Present key treatment modalities for AHF. Present the findings of the ACEP Clinical Policy Consider rational interventional approaches that take into account evidence and the particularities of patient history and physical upon presentation. Give an overview of the pathophysiology of responses that lead to the common final pathway of acute heart failure (AHF) syndromes. Present key treatment modalities for AHF. Present the findings of the ACEP Clinical Policy Consider rational interventional approaches that take into account evidence and the particularities of patient history and physical upon presentation.

3 Goals Participants will be able to understand the four core questions of the ACEP Clinical Policy Participants will be able to understand the best supported conclusions to the four core questions Participants will be able to formulate treatment approaches likely to be most effective for a given history and physical of patient scenarios. Participants will be able to understand the four core questions of the ACEP Clinical Policy Participants will be able to understand the best supported conclusions to the four core questions Participants will be able to formulate treatment approaches likely to be most effective for a given history and physical of patient scenarios.

4 Perspective Prevalence: 5,000,000 –~ 2 % of total US population Incidence: 550,000 –Approaches 10 per 1000 for those > 65 yrs Prevalence: 5,000,000 –~ 2 % of total US population Incidence: 550,000 –Approaches 10 per 1000 for those > 65 yrs American Heart Association. Heart Disease and Stroke Statistics Update.

5 Prevalence by Age and Gender American Heart Association. Heart Disease and Stroke Statistics Update.

6 Perspective: Hospital Care Total hospital discharges in 2001: 995,000 –164 % increase from 1979 –Most common DRG among pts > 65 Total hospital discharges in 2001: 995,000 –164 % increase from 1979 –Most common DRG among pts > 65 American Heart Association. Heart Disease and Stroke Statistics Update.

7 Who is at Risk for Heart Failure Development? 1,2 Overall, lifetime risk is 1 in 5 for those > 40 yrs HTN and CAD are primary risk factors –Risk to 1 in 9 for males and 1 in 6 for females without hx of CAD –HTN antedates disease onset in 75% Chronic BP 160/100: risk ~ 1 in 4 Chronic BP < 140/90: risk ~ 1 in 8 Overall, lifetime risk is 1 in 5 for those > 40 yrs HTN and CAD are primary risk factors –Risk to 1 in 9 for males and 1 in 6 for females without hx of CAD –HTN antedates disease onset in 75% Chronic BP 160/100: risk ~ 1 in 4 Chronic BP < 140/90: risk ~ 1 in 8 1 Lloyd-Jones DM, et al. Circulation. 2002;106: Levy D, et al. JAMA 1996;275(20):

8 Disproportionate Risk for African-Americans % excess rate of new-onset HF Younger age with more advanced disease at initial presentation More rapid progression from asymptomatic to symptomatic phase 50-75% excess rate of new-onset HF Younger age with more advanced disease at initial presentation More rapid progression from asymptomatic to symptomatic phase 1 McCullough PA, et al. J Am Coll Cardiol 2002;39(1): Yancy CW. Curr Cardiol Rep 2002;4(3): Yancy CW. Curr Cardiol Rep 2001;3(3): Bourassa MG, et al. J Am Coll Cardiol 1993;22(4 Suppl A):14A-9A. 5 Afzal A, et al. Clin Cardiol 1999;22(12):791-4.

9 Disproportionate Risk May be explained by divergence in etiology 1-3 –Hypertensive cardiomyopathy in AA –Ischemic cardiomyopathy in Caucasians May be explained by divergence in etiology 1-3 –Hypertensive cardiomyopathy in AA –Ischemic cardiomyopathy in Caucasians 1 Bourassa MG, et al. J Am Coll Cardiol 1993;22(4 Suppl A):14A-9A. 2 Alexander M, et al. JAMA 1995;274(13): Mathew J, et al. Am J Cardiol 1996;78(12):

10 DMC Statistics Total ED visits for HF Site ALL YEARS DRH1,0441,0551,2431,1511,1251,1176,735 HARPER ,599 HVSH ,681 SGH1,5891,6091,5041,4391,3751,4758,991 TOTAL3,7103,8813,9263,8813,7763,83223,006

11 Perspective: Bottom Line American Heart Association. Heart Disease and Stroke Statistics Update Coronary Heart Disease Stroke Hypertensive Disease Heart Failure Billions of Dollars

12 What is Heart Failure ? Syndrome defined by inadequate cardiac performance –Primarily a reflection of ventricular dysfunction Diminished inotropy (systolic ~ 55 %) Diminished compliance (diastolic ~ 45 %) –Exacerbated by changes in volume status Syndrome defined by inadequate cardiac performance –Primarily a reflection of ventricular dysfunction Diminished inotropy (systolic ~ 55 %) Diminished compliance (diastolic ~ 45 %) –Exacerbated by changes in volume status

13 Starling Curve LV End-Diastolic Volume (or Pressure) StrokeVolume Normal response Baseline Heart failure

14 Normal Pressure-Volume Loop LV Volume LV Pressure SV Compliance Inotropy 4. AV Closes 3. AV Opens 2. MV Closes 1. MV Opens

15 Normal Pressure-Volume Loop LV Volume LV Pressure EDVESV SV Compliance Inotropy EDP

16 Systolic Dysfunction LV Volume LV Pressure

17 Diastolic Dysfunction LV Volume LV Pressure

18 More on Etiology of Cardiac Dysfunction Systolic –Males –Impaired contractility –Chamber dilated –Eccentric hypertrophy –Cardiomegaly noted –Ischemic in nature –Audible S 3 Limited ability to differentiate based solely on clinical parameters 1 Diastolic –Elderly females –Impaired compliance –Chamber narrowed –Concentric hypertrophy –Cardiomegaly absent –Hypertensive in nature –Audible S 4 1 Thomas et al. Am J Med 2002;112:

19 General Principles Focus is on clinical presentation not etiology 1,2 –Common denominator = LVEDP –End result = congestion Balance specificity with sensitivity –Rule-out vs. rule-in approach 1 Gheorghiade et al. Circulation 2005;112: Friedewald et al. Am J Cardiol 2007;10:

20 Basic Pathophysiology Cardiac dysfunction leads to diminished output with arterial underfilling –Baroreceptor activation Carotid sinus Left ventricle Aortic arch – glomerular filtration rate Triggers compensatory response Cardiac dysfunction leads to diminished output with arterial underfilling –Baroreceptor activation Carotid sinus Left ventricle Aortic arch – glomerular filtration rate Triggers compensatory response

21 Basic Pathophysiology From: Schrier and Abraham. NEJM 1999;341:583.

22 Compensatory Response Enhanced sympathetic tone –Predominantly norepinephrine 1,2 –Improves circulatory integrity inotropy and chronotropy (β1) preload and afterload (α1) effective volume (α1) –Beneficial effects over time Receptor down-regulation and G-protein uncoupling Induction of myocyte toxicity 3,4 Enhanced sympathetic tone –Predominantly norepinephrine 1,2 –Improves circulatory integrity inotropy and chronotropy (β1) preload and afterload (α1) effective volume (α1) –Beneficial effects over time Receptor down-regulation and G-protein uncoupling Induction of myocyte toxicity 3,4 1 Braunwald et al. Proc R Soc Med 1965;58: Francis et al. Ann Intern Med 1984;101: Schrier et al. NEJM 1999;341: Mann et al. Circulation 1992;85:

23 Biochemical Response to Adrenergic Stimulation

24 Compensatory Response Stimulation of neurohormonal modulators –Renin-angiotensin-aldosterone system (RAAS) –ANP –Arginine vasopressin Cytokine release Stimulation of neurohormonal modulators –Renin-angiotensin-aldosterone system (RAAS) –ANP –Arginine vasopressin Cytokine release

25 RAAS Renin Angiotensinogen Active angiotensin fragments: Ang III, Ang IV, Ang 1-7 Angiotensin II Angiotensin I ACE (Lung, etc) Chymase, other proteases Protease Direct effects of AT II Bradykinin Inactive kinins

26 Angiotensin-II Vasoconstriction –Efferent > afferent arteriolar constriction Results in GFR Promotion of sodium reabsorption –Direct effect on proximal tubule –Indirect through stimulation of aldosterone release Dipsogenic response Cardiac (and vascular) remodeling Vasoconstriction –Efferent > afferent arteriolar constriction Results in GFR Promotion of sodium reabsorption –Direct effect on proximal tubule –Indirect through stimulation of aldosterone release Dipsogenic response Cardiac (and vascular) remodeling

27 Aldosterone Sodium (and water) reabsorption at collecting ducts –Typical effect on extracellular volume ~ 2 L –Regulated by intrinsic feedback 1 Based on distal sodium delivery Altered in heart failure; results in sodium and fluid retention Diminishes arterial compliance Stimulates myocyte collagen synthesis 2 Sodium (and water) reabsorption at collecting ducts –Typical effect on extracellular volume ~ 2 L –Regulated by intrinsic feedback 1 Based on distal sodium delivery Altered in heart failure; results in sodium and fluid retention Diminishes arterial compliance Stimulates myocyte collagen synthesis 2 1 Schrier et al. NEJM 1999;341: Cohn et al. J Am Coll Cardiol 2000;35:

28 Arginine Vasopressin Vasoconstriction (V 1A receptor) Antidiuresis (V 2 receptor) –Occurs in collecting ducts –Induces synthesis and translocation of aquaporin-2 water channels Suppressed by atrial stretch receptors –Impaired in heart failure, with free-water retention Vasoconstriction (V 1A receptor) Antidiuresis (V 2 receptor) –Occurs in collecting ducts –Induces synthesis and translocation of aquaporin-2 water channels Suppressed by atrial stretch receptors –Impaired in heart failure, with free-water retention Nielsen et al. Proc Natl Acad Sci USA 1995;92:

29 Cytokine Mediators 1,2 Proinflammatory –Triggered by myocardial inflammation –? role of endotoxin from hypoperfused intestines Tumor necrosis factor (TNF-α) Transforming growth factor β (TGF- β) Interleukins (IL-1,2 and 6) Intracellular adhesion molecules (ICAM) Vasoactive –Endothelin (ET) Proinflammatory –Triggered by myocardial inflammation –? role of endotoxin from hypoperfused intestines Tumor necrosis factor (TNF-α) Transforming growth factor β (TGF- β) Interleukins (IL-1,2 and 6) Intracellular adhesion molecules (ICAM) Vasoactive –Endothelin (ET) 1 Anker et al. Heart 2004;90: Aukurst et al. Autoimmunity Reviews 2004;3:221-7.

30 Endothelin: Receptors & Effects ET A (upregulated) –Vasoconstriction (pulmonary HTN) –Smooth muscle and myocyte hypertrophy – inotropy and chronotropy – sodium and water retention ET B (downregulated) –Vasodilation – aldosterone production – ET-1 clearance and autocrine regulation ET A (upregulated) –Vasoconstriction (pulmonary HTN) –Smooth muscle and myocyte hypertrophy – inotropy and chronotropy – sodium and water retention ET B (downregulated) –Vasodilation – aldosterone production – ET-1 clearance and autocrine regulation Spieker et al. J Am Coll Cardiol 2001;37:

31 Ventricular Remodeling Gradual response to initial insult, circulating factors and oxidative stress Cycle leading to progressive dysfunction Gradual response to initial insult, circulating factors and oxidative stress Cycle leading to progressive dysfunction Insult with myocyte necrosis Hypertrophy of remaining cells Fibroblast proliferation with collagen synthesis Collagen degradation with progressive fibrosis Myocyte apoptosis Cohn et al. J Am Coll Cardiol 2000;35:

32 Ventricular Remodeling: Translational Model Hunter and Chien. NEJM 1999;341:

33 From: Jessup et al. N Engl J Med 2003;348: Myocyte elongation Infarct Related Remodeling

34 Ischemic Remodeling Wall thinning may cause chordae retraction –Result = ischemic mitral valve requrgitation Wall thinning may cause chordae retraction –Result = ischemic mitral valve requrgitation Bursi et al. Am J Med 2006;119:

35 From: Jessup et al. N Engl J Med 2003;348: Eccentric Hypertrophy Concentric Hypertrophy Non-infarct Related Remodeling

36 Counter Regulation Stimulation of natriuretic peptide system –A-type or atrial (ANP) and B-type or brain (BNP) most important –Produce diuresis, natriuresis and vasodilation Release of coenzyme Q 10 –Enhances mitochondrial function Stimulation of natriuretic peptide system –A-type or atrial (ANP) and B-type or brain (BNP) most important –Produce diuresis, natriuresis and vasodilation Release of coenzyme Q 10 –Enhances mitochondrial function

37 CHF and Na+ Retention

38 Counter Regulation Release of endogenous vasodilators –Prostacyclin and prostaglandin E –Bradykinin –Nitric oxide (NO) Produced from L-arginine by NO synthetase –Soluble or bound form (endothelial cells) Induces smooth muscle relaxation via cGMP Tenuous balance Release of endogenous vasodilators –Prostacyclin and prostaglandin E –Bradykinin –Nitric oxide (NO) Produced from L-arginine by NO synthetase –Soluble or bound form (endothelial cells) Induces smooth muscle relaxation via cGMP Tenuous balance

39 Nitric Oxide Balance Hare, JM. NEJM 2004;351:

40 Contributory Cellular Mechanisms Disruptions of cytoskeletal and contractile proteins 1 Sodium channel ion channel mutations 2 –SCN5A associated with dilated cardiomyopathy K ATP regulatory subunit defects 3 Altered intracellular calcium cycling 4,5 Disruptions of cytoskeletal and contractile proteins 1 Sodium channel ion channel mutations 2 –SCN5A associated with dilated cardiomyopathy K ATP regulatory subunit defects 3 Altered intracellular calcium cycling 4,5 1 Schonberger and Seidman. Am J Hum Genet 2001;69: Olson et al. JAMA 2005;293: Bienengraeber et al. Nat Genet 2004;36: Schmitt et al. Science 2003;299: Wehrens et al. Science 2004;304:292-6.

41 Calcium Cycle Modulation Renlund, DG. N Engl J Med 2004;351:

42 Heart Failure Presentations Fatigue Right-sided features –Peripheral edema –Ascites Left-sided features –Dyspnea (exertional or nocturnal) –Rales –Acute cardiogenic pulmonary edema (ACPE) Fatigue Right-sided features –Peripheral edema –Ascites Left-sided features –Dyspnea (exertional or nocturnal) –Rales –Acute cardiogenic pulmonary edema (ACPE)

43 CardioRenal Syndrome Heart failure plus –Chronic renal insufficiency –Worsening renal function during treatment 25% or > increase in Cr or BUN –Difficult diuresis w/o worsening renal function –ACE (-) intolerance from hypotension or hyperkalemia Often complicated by anemia Heart failure plus –Chronic renal insufficiency –Worsening renal function during treatment 25% or > increase in Cr or BUN –Difficult diuresis w/o worsening renal function –ACE (-) intolerance from hypotension or hyperkalemia Often complicated by anemia

44 Diagnosis of Heart Failure Can be difficult on clinical basis alone –Limited sensitivity of physical examination 1,2 –Electrocardiogram often not helpful 3,4 –Common chest x-ray findings unreliable and often non-predictive 5 Cepahalization Cardiomegaly Interstitial edema Can be difficult on clinical basis alone –Limited sensitivity of physical examination 1,2 –Electrocardiogram often not helpful 3,4 –Common chest x-ray findings unreliable and often non-predictive 5 Cepahalization Cardiomegaly Interstitial edema 1 Stevenson et al. JAMA 1989;261: Badgett et al. JAMA 1997;277: Davie et al. BMJ 1996;312: Gillespie et al. BMJ 1997;314: Badgett et al. J Gen Intern Med 1996;11:

45 Diagnosis of Heart Failure Difficult based on common variables –Limited sensitivity of physical examination 1,2 –Electrocardiogram often not helpful 3,4 Atrial fibrillation may be found in up to 1/3 Interventricular conduction delays in 1/4 –Common chest x-ray findings unreliable and often non-predictive 5,6 Normal in ~ 20% reliance on serum markers 1 Stevenson et al. JAMA 1989;261: Badgett et al. JAMA 1997;277: Davie et al. BMJ 1996;312: Gillespie et al. BMJ 1997;314: Badgettet al. J Gen Intern Med 1996;11: Collins et al. Ann Emerg Med 2006;47;13-8.

46 Criterion Diagnosis of Heart Failure Framingham –Most commonly used –Defines cases as questionable, probable or definite HF –Definite requires 2 major or 1 major and 2 minor criteria National Health and Nutrition Examination Surveys (NHANES) Boston European Society of Cardiology

47 Framingham Criteria 1,2 Major Criteria Clinical PND Orthopnea JVP Hepatojugular reflux Rales S 3 gallop Chest x-ray Cardiomegaly Pulmonary edema Minor Criteria Ankle edema Night cough Dyspnea on exertion Hepatomegaly Pleural effusion HR 120 Wt loss 4.5 kg in 5 d Considered major criterion when occurring in response to diuretics 1 McKee et al. NEJM 1971;285: Kannel et al. Arch Intern Med 1999;159:

48 Clinical Diagnostic Accuracy Wang et al. JAMA 2005;294:

49 Exam Findings Do Matter Drazneret al. NEJM 2001;345:

50 Acoustic Cardiography

51 Gallop Murmur Mnemonics S3 Montreal SLOSH'-ing-in SLOSH'-ing-in SLOSH'-ing-in S1 S2 S3 S1 S2 S3 S1 S2 S3 Kentucky/Tennessee? (you decide) S4 Toronto a-STIFF'-wall a-STIFF'-wall a-STIFF'-wall S4 S1 S2 S4 S1 S2 S4 S1 S2 Kentucky/Tennessee? (you decide)

52 Acoustic Cardiography: Test Characteristics Marcus et al. JAMA 2005;295:

53 Ear of the Beholder? Marcus et al. Arch Intern Med 2006;166:

54 CXR and ECG Wang et al. JAMA 2005;294:

55 Serum Markers Natriureticpeptides –ANP –N-ANP –BNP –NT-proBNP Norepinephrine Endothelin Proinflammatorycytokines –TNF-α, IL-1β, IL-6

56 BNP Level > 100 pg/ml more accurate than clinical criteria for diagnosis –BNP: 83 % –Framingham: 73 % –NHANES: 67 % Robust independent predictive value Maisel et al. NEJM 2002;347:161-7.

57 ROC Curve (BNP) Maiselet al. NEJM 100 pg/ml cut off: Sens 90 % Spec 76 PPV 79 NPV 89

58 BNP: Pooled Operating Characteristics Wang et al. JAMA 2005;294:

59 Should You Obtain a BNP for High Probability Pts ? Correlates with disease severity and provides prognostic information 1,2 –BNP > 480 pg/ml 51 % with HF event at 6 mos Rate only 2.5 % when < 230 pg/ml –BNP > 700 pg/ml HR (death or admit) = 15.2 Enables serial comparison 3 –Inc. risk of death when remains high 97 pg/ml 1 Harrison et al. Ann Emerg Med 2002;39: Logeart et al. J Am Coll Cardiol 2004;43: Latini et al. Am J Med 2006;119:70.e23-30.

60 BNP: Using Your Results Utilization improves clinical judgment 1 –Degree dependent on pre- test probability –Effect greatest for intermediate pts Best use: acute dyspnea –Reliably differentiates HF from lung disease 2 –Can reduce admissions, ICU use and LOS 3 1 McCollough et al. Circulation 2002;106: Morrison et al. J Am Coll Cardiol 2002;39: Mueller et al. NEJM 2004;350:

61 BNP: Things to Consider May be lower than expected with –Flash pulmonary edema –Diastolic dysfunction Mild elevation ( pg/ml) found with other conditions –Cor Pulmonale –PE –COPD –Pulmonary HTN

62 Other Natriuretic Peptides ANP and N-ANP –Correlates with LVEF, but lower sensitivity and NPV than BNP 1 NT-proBNP –Similar overall accuracy to BNP –May be better predictor of LV dysfunction 2,3 Wall motion index < 1.2or LVEF < 40 % –Useful as a marker of therapeutic effectiveness 4 1 Collins et al. Ann Emerg Med 2003;41: Talwar et al. Eur Heart J 1999;20: Hammerer-Lecher et al. Clin Chim Acta 2001;310: Troughton et al. Lancet 2000;355:

63 NT-proBNP Moe et al. Circulation 2007;115:

64 Natriuretic Peptide Caveats Relative increase in women Inverse relationship with BMI Krauser et al. Am Heart J 2005;

65 Natriuretic Peptide Caveats Daniels et al. Am Heart J 2006;151:

66 Natriuretic Peptide Caveats Higher with renal dysfunction McCollough et al. Am J Kidney Dis 2003;41: Anwaruddin et al. JACC 2006;47:91-7. Optimal cut-point = 200 pg/ml Optimal cut-point = 1200 pg/ml

67 Echocardiography Gold standard Functional and structural information –Ejection fraction –Wall motion –Tissue doppler and harmonics –Chamber size –LV wall thickness and mass –Regurgitant mitral valve diameter Utility in acute setting is unclear

68 Echocardiography Provides long-term prognostic information –Annual mortality with EF 10 %: ~ 29 % ! Enables diagnosis of HF etiology 1 –Systolic dysfunction: EF < 50 % –Diastolic dysfunction: EF 50 % with impaired relaxation and elevation of filling pressures Doppler tissue imaging at mitral annulus 1 Bursi et al. JAMA 2006;296:

69 CHF Treatment Modalities

70 Diuretics Limited evidence, but used empirically Loop agents most common –Initial diuresis at 30 min 1 Peak effect at 2-4 hrs Maximal with mg furosemide Avg in-hospital net diuresis > 4 L 2 –Vasodilatory effect at 15 min 3 Latent constriction through RAAS and adrenergic activation 4 – efficacy in combination with thiazides Limited evidence, but used empirically Loop agents most common –Initial diuresis at 30 min 1 Peak effect at 2-4 hrs Maximal with mg furosemide Avg in-hospital net diuresis > 4 L 2 –Vasodilatory effect at 15 min 3 Latent constriction through RAAS and adrenergic activation 4 – efficacy in combination with thiazides 1 Brater DC. NEJM 1998; 339: Steimle et al. Circulation 1997;96: Dikshit et al. NEJM 1973;288: Francis et al. Ann Intern Med 1985;103:1-6.

71 Nitrates Recognized benefit since mid-1970s Produces rapid in PCWP with clinical improvement 1 At lower doses, preload reduction through venodilation 2 Arterial dilation with afterload reduction at higher IV doses ( 250 mcg/min) 2,3 –Dose-effect relationship –More pronounced with resistance 4 Recognized benefit since mid-1970s Produces rapid in PCWP with clinical improvement 1 At lower doses, preload reduction through venodilation 2 Arterial dilation with afterload reduction at higher IV doses ( 250 mcg/min) 2,3 –Dose-effect relationship –More pronounced with resistance 4 1 Bussmann et al. Am L Cardiol 1978;41: Imhof et al. Eur J Clin Pharmacol 1980;18: Herling IM. Am Heart J 1984;108: Haber et al. J Am Coll Cardiol 1993;22:251-7.

72 Nitroprusside Effective in refractory ACPE with SVR Enables concurrent venous and arterial dilation Requires arterial line placement for proper titration Produces reflex tachycardia Potential for cyanide toxicity –Minimized by use of thiosulfate Effective in refractory ACPE with SVR Enables concurrent venous and arterial dilation Requires arterial line placement for proper titration Produces reflex tachycardia Potential for cyanide toxicity –Minimized by use of thiosulfate Guiha et al. NEJM 1974;291:

73 Nesiritide Exogenous BNP Rapid onset –Peak effect in min Elimination half-life = 18 min Dosing –2 mcg/kg bolus –Infusion at 0.01 mcg/kg/min (titration to a max of 0.03 mcg/kg/min) Safe with dose dependent in PCWP Exogenous BNP Rapid onset –Peak effect in min Elimination half-life = 18 min Dosing –2 mcg/kg bolus –Infusion at 0.01 mcg/kg/min (titration to a max of 0.03 mcg/kg/min) Safe with dose dependent in PCWP Colucci et al. NEJM 2000;343:

74 ACE Inhibitors Limited data on use in acute setting Sublingual captopril (25 mg) 1,2 –Diminished rate of intubation (9 vs 20 %) –Improved dyspnea scores at 30 min –Early improvements in SVI and CI IV enalaprilat 3 –Improved hemodynamics with 1 mg infusion –No data on bolus dosing Limited data on use in acute setting Sublingual captopril (25 mg) 1,2 –Diminished rate of intubation (9 vs 20 %) –Improved dyspnea scores at 30 min –Early improvements in SVI and CI IV enalaprilat 3 –Improved hemodynamics with 1 mg infusion –No data on bolus dosing 1 Haude et al. Int J Cadiol 1990;27: Hamilton et al. Acad Emerg Med 1996;3: Annane et al. Cirulation 1996;94:

75 Inotropic Agents Usually reserved for those with CO Dobutamine 1,2 –Increases ventricular ectopy and myocardial oxygen demand Milrinone 3,4 –Prolonged LOS and 60-day mortality More pronounced with ischemic etiology in-hospital mortality for both versus NTG and nesiritide 5 Usually reserved for those with CO Dobutamine 1,2 –Increases ventricular ectopy and myocardial oxygen demand Milrinone 3,4 –Prolonged LOS and 60-day mortality More pronounced with ischemic etiology in-hospital mortality for both versus NTG and nesiritide 5 1 Leier et al. Circulation 1977;56: Burger et al. Am J Cardiol 2001;88: Cuffe et al. JAMA 2002;287: Felker et al. J Am Coll Cardiol 2003;41: Abraham et al. J Card Fail 2003; 9:S81.

76 Inotropic Agents Levosimendan –Novel calcium sensitizer Contractility improvement w/o O 2 consumption –Opens K-ATP channel –Dose-response relationship with in CO/SV and in PCWP 1,2 –Dosing: IV bolus (6 to 24 mcg/kg) followed by infusion (0.05 to 0.2 mcg/kg/min) –Trial data promising Levosimendan –Novel calcium sensitizer Contractility improvement w/o O 2 consumption –Opens K-ATP channel –Dose-response relationship with in CO/SV and in PCWP 1,2 –Dosing: IV bolus (6 to 24 mcg/kg) followed by infusion (0.05 to 0.2 mcg/kg/min) –Trial data promising 1 Nieminen et al. J Am Coll Cardiol. 2000;36: Slawsky et al. Circulation 2000;102:

77 Morphine Sulfate Commonly used; limited supporting data Unclear derivation of beneficial effects –Venodilation –Afterload reduction –Respiratory relaxation Evidence suggesting association with adverse outcomes 1,2 – need for intubation and ICU admission Commonly used; limited supporting data Unclear derivation of beneficial effects –Venodilation –Afterload reduction –Respiratory relaxation Evidence suggesting association with adverse outcomes 1,2 – need for intubation and ICU admission 1 Hoffman et al. Chest 1987;92: Sacchetti et al. Am J Emerg Med 1999;17:571-4.

78 Non-invasive Ventilation Consider if poor response at 30 min –CPAP: continuous positive airway pressure 1,2 Reduction in need for ETI by 26 % Trend towards survival –BiPAP: bilevel positive airway pressure 3,4,5 time to symptom resolution (30 vs. 105 min) intubation rate (~ 23 %) One prospective comparison trial 6 – MI rate with BiPAP Consider if poor response at 30 min –CPAP: continuous positive airway pressure 1,2 Reduction in need for ETI by 26 % Trend towards survival –BiPAP: bilevel positive airway pressure 3,4,5 time to symptom resolution (30 vs. 105 min) intubation rate (~ 23 %) One prospective comparison trial 6 – MI rate with BiPAP 1 Berstein et al. NEJM 1991;325: Pang et al. Chest 1998;114: Masip et al. Lancet 2000;356: Levitt MA. J Emerg Med 2001;21: Nava et al. Am J Resp Crit Care Med 2003;168: Mehta et al. Crit Care Med 1997;620-8.

79 EBM Literature Classification Schema

80 EBM Recommendation Levels Level A –Generally accepted principles for Pt management that reflect a high degree of clinical certainty (i.e., based on Class I or overwhelming, directly pertinent Class II evidence ) Level B –Recommendations for Pt management that may identify a particular strategy of range of strategies that reflect moderate clinical certainty (i.e., based on directly pertinent Class II evidence, directly pertinent decision analysis, or strong Class III consensus) Level C –Other strategies for patient management that are based on preliminary evidence, or in the absence of any published literature, based on panel consensus Level A –Generally accepted principles for Pt management that reflect a high degree of clinical certainty (i.e., based on Class I or overwhelming, directly pertinent Class II evidence ) Level B –Recommendations for Pt management that may identify a particular strategy of range of strategies that reflect moderate clinical certainty (i.e., based on directly pertinent Class II evidence, directly pertinent decision analysis, or strong Class III consensus) Level C –Other strategies for patient management that are based on preliminary evidence, or in the absence of any published literature, based on panel consensus

81 ACEP Clinical Guideline Questions 1.Does a B-type natriuretic polypeptide (BNP) or NT-ProBNP measurement improve the diagnostic accuracy over standard clinical judgment in the assessment of possible acute heart failure syndromes in the ED? 2.Is there a role for noninvasive positive-pressure ventilatory support in the ED management of patients with acute heart failure syndromes and respiratory distress? 3.Should vasodilator therapy (eg, nitrates, nesiritide, and ACE inhibitors) be prescribed in the ED management of patients with acute heart failure syndromes? 4.Should diuretic therapy be prescribed in the ED management of patients with acute heart failure syndromes? 1.Does a B-type natriuretic polypeptide (BNP) or NT-ProBNP measurement improve the diagnostic accuracy over standard clinical judgment in the assessment of possible acute heart failure syndromes in the ED? 2.Is there a role for noninvasive positive-pressure ventilatory support in the ED management of patients with acute heart failure syndromes and respiratory distress? 3.Should vasodilator therapy (eg, nitrates, nesiritide, and ACE inhibitors) be prescribed in the ED management of patients with acute heart failure syndromes? 4.Should diuretic therapy be prescribed in the ED management of patients with acute heart failure syndromes?

82 Patient Management Recommendations Question 1 Level A recommendations. None specified. Level B recommendations. The addition of a single BNP or NT-proBNP measurement can improve the diagnostic accuracy compared to standard clinical judgment alone in the diagnosis of acute heart failure syndrome among patients presenting to the ED with acute dyspnea. Use the following guidelines: – BNP <100 pg/dL or NT-proBNP <300 pg/dL failure syndrome unlikely (Approximate LR -0.1) – BNP >500 mg/dL or NT-proBNP >1,000 pg/dL heart failure syndrome likely (Approximate LR +6) Level C recommendations. None specified. Level A recommendations. None specified. Level B recommendations. The addition of a single BNP or NT-proBNP measurement can improve the diagnostic accuracy compared to standard clinical judgment alone in the diagnosis of acute heart failure syndrome among patients presenting to the ED with acute dyspnea. Use the following guidelines: – BNP <100 pg/dL or NT-proBNP <300 pg/dL failure syndrome unlikely (Approximate LR -0.1) – BNP >500 mg/dL or NT-proBNP >1,000 pg/dL heart failure syndrome likely (Approximate LR +6) Level C recommendations. None specified.

83 Patient Management Recommendations Question 2 Level A recommendations. None specified. Level B recommendations. Use 5 to 10 mm Hg CPAP by nasal or face mask as therapy for dyspneic patients with acute heart failure syndrome without hypotension or the need for emergent intubation to improve heart rate, respiratory rate, blood pressure, and reduce the need for intubation, and possibly reduce inhospital mortality. Level C recommendations. Consider using BiPAP as an alternative to CPAP for dyspneic patients with acute heart failure syndrome; however, data about the possible association between BiPAP and myocardial infarction remain unclear. Level A recommendations. None specified. Level B recommendations. Use 5 to 10 mm Hg CPAP by nasal or face mask as therapy for dyspneic patients with acute heart failure syndrome without hypotension or the need for emergent intubation to improve heart rate, respiratory rate, blood pressure, and reduce the need for intubation, and possibly reduce inhospital mortality. Level C recommendations. Consider using BiPAP as an alternative to CPAP for dyspneic patients with acute heart failure syndrome; however, data about the possible association between BiPAP and myocardial infarction remain unclear.

84 Patient Management Recommendations Question 3 Level A recommendations. None specified. Level B recommendations. Administer intravenous nitrate therapy to patients with acute heart failure syndromes and associated dyspnea. Level C recommendations. –1. Because of the lack of clear superiority of nesiritide over nitrates in acute heart failure syndrome and the current uncertainty regarding its safety, nesiritide generally should not be considered first line therapy for acute heart failure syndromes. –2. Angiotensin-converting enzyme (ACE) inhibitors may be used in the initial management of acute heart failure syndromes, although patients must be monitored for first dose hypotension. Level A recommendations. None specified. Level B recommendations. Administer intravenous nitrate therapy to patients with acute heart failure syndromes and associated dyspnea. Level C recommendations. –1. Because of the lack of clear superiority of nesiritide over nitrates in acute heart failure syndrome and the current uncertainty regarding its safety, nesiritide generally should not be considered first line therapy for acute heart failure syndromes. –2. Angiotensin-converting enzyme (ACE) inhibitors may be used in the initial management of acute heart failure syndromes, although patients must be monitored for first dose hypotension.

85 Patient Management Recommendations Question 4 Level A recommendations. None specified. Level B recommendations. Treat patients with moderate-to- severe pulmonary edema resulting from acute heart failure with furosemide in combination with nitrate therapy. Level C recommendations. 1. Aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation compared with aggressive nitrate monotherapy. 2. Diuretics should be administered judiciously, given the potential association between diuretics, worsening renal function, and the known association between worsening renal function at index hospitalization and long-term mortality. Level A recommendations. None specified. Level B recommendations. Treat patients with moderate-to- severe pulmonary edema resulting from acute heart failure with furosemide in combination with nitrate therapy. Level C recommendations. 1. Aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation compared with aggressive nitrate monotherapy. 2. Diuretics should be administered judiciously, given the potential association between diuretics, worsening renal function, and the known association between worsening renal function at index hospitalization and long-term mortality.

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