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Brian McMichael, M.D. PGY-1, Emergency Medicine

This presentation provides an overview of the pathophysiology of acute heart failure syndromes (AHF) and presents key treatment modalities for AHF. It discusses the findings of the ACEP clinical policy and considers rational interventional approaches based on evidence and patient history. The goals are to understand the core questions of the ACEP Clinical Policy, formulate effective treatment approaches, and understand the prevalence and risk factors of heart failure.

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Brian McMichael, M.D. PGY-1, Emergency Medicine

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  1. ACEP Clinical Policy: Critical Issues in the Evaluation and Managementof Adult Patients Presenting to the Emergency Department withAcute Heart Failure Syndromes 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.

  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.

  4. Perspective • 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 - 2004 Update.

  5. Prevalence by Age and Gender American Heart Association. Heart Disease and Stroke Statistics - 2006 Update.

  6. Perspective: Hospital Care • 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 - 2006 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 1 Lloyd-Jones DM, et al. Circulation. 2002;106:3068-72. 2 Levy D, et al. JAMA 1996;275(20):1557-62.

  8. Disproportionate Risk for African-Americans 1-5 • 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):60-9. 2 Yancy CW. Curr Cardiol Rep 2002;4(3):218-25. 3 Yancy CW. Curr Cardiol Rep 2001;3(3):191-7. 4 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 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):1037-42. 3 Mathew J, et al. Am J Cardiol 1996;78(12):1447-50.

  10. DMC Statistics • Total ED visits for HF 1999-2004

  11. 160 142.5 140 120 100 Billions of Dollars 63.5 80 57.9 60 29.6 40 20 0 Stroke Heart Failure Hypertensive Disease Coronary Heart Disease Perspective: Bottom Line American Heart Association. Heart Disease and Stroke Statistics - 2006 Update.

  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

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

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

  15. Normal Pressure-Volume Loop Inotropy LV Pressure Compliance SV EDP ESV EDV LV Volume

  16. Systolic Dysfunction LV Pressure LV Volume

  17. Diastolic Dysfunction LV Pressure LV Volume

  18. Systolic Males 50-70 Impaired contractility Chamber dilated Eccentric hypertrophy Cardiomegaly noted Ischemic in nature Audible S3 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 S4 More on Etiology of Cardiac Dysfunction 1 Thomas et al. Am J Med 2002;112:437-45.

  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;112:3958-68. 2 Friedewald et al. Am J Cardiol 2007;10:1145-52.

  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

  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 1 Braunwald et al. Proc R Soc Med 1965;58:1063-6. 2 Francis et al. Ann Intern Med 1984;101:370-7. 3 Schrier et al. NEJM 1999;341:577-84. 4 Mann et al. Circulation 1992;85:790-804.

  23. Biochemical Response to Adrenergic Stimulation

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

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

  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

  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 1 Schrier et al. NEJM 1999;341:577-84. 2Cohn et al. J Am Coll Cardiol 2000;35:569-582.

  28. Arginine Vasopressin • Vasoconstriction (V1A receptor) • Antidiuresis (V2 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;92:1013-7.

  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) 1 Anker et al. Heart 2004;90:464-70. 2 Aukurst et al. Autoimmunity Reviews 2004;3:221-7.

  30. Endothelin: Receptors & Effects • ETA (upregulated) • Vasoconstriction (pulmonary HTN) • Smooth muscle and myocyte hypertrophy • ↑ inotropy and chronotropy • ↑ sodium and water retention • ETB (downregulated) • Vasodilation • ↑ aldosterone production • ↑ ET-1 clearance and autocrine regulation Spieker et al. J Am Coll Cardiol 2001;37:1493-1505.

  31. Ventricular Remodeling • Gradual response to initial insult, circulating factors and oxidative stress • Cycle leading to progressive dysfunction Insult with myocyte necrosis Myocyte apoptosis Hypertrophy of remaining cells Collagen degradation with progressive fibrosis Fibroblast proliferation with collagen synthesis Cohn et al. J Am Coll Cardiol 2000;35:569-582.

  32. Ventricular Remodeling: Translational Model Hunter and Chien. NEJM 1999;341:1276-1283.

  33. Infarct Related Remodeling Myocyte elongation From: Jessup et al. N Engl J Med 2003;348:2007-2018.

  34. Ischemic Remodeling • Wall thinning may cause chordae retraction • Result = ischemic mitral valve requrgitation Bursi et al. Am J Med 2006;119:103-12.

  35. Non-infarct Related Remodeling “Concentric” Hypertrophy “Eccentric” Hypertrophy From: Jessup et al. N Engl J Med 2003;348:2007-2018.

  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 Q10 • 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

  39. Nitric Oxide Balance Hare, JM. NEJM 2004;351:2112-2114.

  40. Contributory Cellular Mechanisms • Disruptions of cytoskeletal and contractile proteins 1 • Sodium channel ion channel mutations 2 • SCN5A associated with dilated cardiomyopathy • KATP regulatory subunit defects 3 • Altered intracellular calcium cycling 4,5 1 Schonberger and Seidman. Am J Hum Genet 2001;69:249-60. 2 Olson et al. JAMA 2005;293:447-54. 3 Bienengraeber et al. Nat Genet 2004;36:382-87. 4 Schmitt et al. Science 2003;299:1410-3. 5 Wehrens et al. Science 2004;304:292-6.

  41. Calcium Cycle Modulation Renlund, DG. N Engl J Med 2004;351:849-851.

  42. Heart Failure Presentations • 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

  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 1 Stevenson et al. JAMA 1989;261:884-8 2 Badgett et al. JAMA 1997;277:1712-9. 3 Davie et al. BMJ 1996;312:222. 4 Gillespie et al. BMJ 1997;314:936-940. 5 Badgett et al. J Gen Intern Med 1996;11:625-634.

  45. Diagnosis of Heart Failure 1 Stevenson et al. JAMA 1989;261:884-8 2 Badgett et al. JAMA 1997;277:1712-9. 3Davie et al. BMJ 1996;312:222. 4 Gillespie et al. BMJ 1997;314:936-940. 5 Badgettet al. J Gen Intern Med 1996;11:625-634. 6 Collins et al. Ann Emerg Med 2006;47;13-8. • 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

  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 S3 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;285:1441-6. 2 Kannel et al. Arch Intern Med 1999;159:1197-1204.

  48. Clinical Diagnostic Accuracy Wang et al. JAMA 2005;294:1944-56.

  49. Exam Findings Do Matter Drazneret al. NEJM 2001;345:574-81.

  50. Acoustic Cardiography http://depts.washington.edu/physdx/heart/tech2.html

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