webinar 1 make the diagnosis : acute heart failure

1. Webinar #1Make the Diagnosis : Acute Heart Failure

2. Faculty Members Justin A. Ezekowitz, MBBCh MSc FRCPC Assistant Professor, University of Alberta Director, Heart Function Clinic, Mazankowski Alberta Heart Institute Robert S. McKelvie, MD PhD FRCPC Professor of Medicine, Division of Cardiology, McMaster University Medical Director, Heart Failure Program, Hamilton Health Sciences Medical Director, Cardiac Health and Rehabilitation Program, Hamilton Health Sciences � Jonathan G. Howlett, MD FRCPC FACC FSCAI Clinical Professor of Medicine University of Calgary and Foothills Medical Centre

3. Faculty Disclosures Justin A. Ezekowitz: available online at www.vigour.ualberta.ca Robert S. McKelvie: Honoraria and research funding from BMS, Sanofi Aventis, Astra Zeneca Jonathan G. Howlett: Honoraria and research funding from Merck, AstraZeneca, Pfizer, Servier, Novartis, Schering

4. Session #1: Make the Diagnosis: Acute Heart FailureDate: Wednesday January 13th 2010Time: 1200-1300 hours EST Session #2: Treatment of AHFDate: Wednesday January 27th 2010Time: 1200-1300 hours EST Session #3: Transition of AHF to home and Chronic HFDate: Wednesday February 10th 2010Time: 1200-1300 hours EST Session #4: Chronic HF problem managementDate: Wednesday February 24th 2010Time: 1200-1300 hours EST

5. Program Outline 12:00 Welcome and Introductions 12:05 Case Presentation ? The Value of the History and Physical ? Other Standard Tests ? Practical Imaging 12:50 Q&A period 13:00 Closing Remarks 

6. Learning Objectives Understand the burden of HF in Canada Learn how to diagnose HF with �basic� information Learn about other diagnostic tests useful when heart failure is on the differential

7. What is heart failure? Chronic Heart Failure (CHF): Heart failure is a complex syndrome in which abnormal heart function results in, or increases the subsequent risk of, clinical symptoms and signs of low cardiac output and/or pulmonary or systemic congestion. Acute Heart Failure Syndrome (AHF): �gradual or rapid change in heart failure signs and symptoms resulting in the need for urgent therapy�

8. Case - Presentation 70 year old male presents to your ED Worsening SOB for 2 to 3 months + orthopnea but no PND Possible weight gain Associated leg swelling History of hypertension, no MI/DM Retired steel mill worker, former smoker Medications: �Some blue one, a white diamond one and a round one�

9. Case - Examination Vitals at triage: HR 108 bpm; BP 146/82 mmHg, RR 22, O2sat 90%ra Initial Exam JVP elevated, +S3, 2/6 systolic murmur Crackles bilateral lung fields, mild wheeze Mild obesity, ?ascites 2+ lower extremity edema, pulses 1+=

10. QUESTIONS #1

11. How does AHF present? However before we look too far ahead into the future, let us first deal with misconceptions of the present. A common misconception is that most AHF patients have poor systolic function and that a low output state is common. In fact, half of these patients have normal LVEF and the vast majority are normotensive or hypertensive on arrival. These folks would be best treated with diuretics and vasodilators. The classic �low output� patient that would need an inotrope/mechanical support/VADs is rare and comprise only 2% of the population. Equally important is the observation that three-quarters of these patients have worsening chronic HF suggesting the need for aggressive use of standard HF therapies. De novo HF: ACS is most frequent cause. In Europe in a large prospective database, the incidence of ACS was 30% and 6.2% had positive troponin in ADHERE.However before we look too far ahead into the future, let us first deal with misconceptions of the present. A common misconception is that most AHF patients have poor systolic function and that a low output state is common. In fact, half of these patients have normal LVEF and the vast majority are normotensive or hypertensive on arrival. These folks would be best treated with diuretics and vasodilators. The classic �low output� patient that would need an inotrope/mechanical support/VADs is rare and comprise only 2% of the population. Equally important is the observation that three-quarters of these patients have worsening chronic HF suggesting the need for aggressive use of standard HF therapies. De novo HF: ACS is most frequent cause. In Europe in a large prospective database, the incidence of ACS was 30% and 6.2% had positive troponin in ADHERE.

12. Clinical Presentations of Heart Failure Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45.Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45.

13. Physical exam JVP elevated Enlarged apical impulse S3 Murmur of mitral regurgitation Peripheral edema Other: HJR Ascites

14. Is history and exam enough?

15. Case The patient is put on a telemetry monitor in the ED, and �routine� work-up is started ED MD orders ECG, CXR, Labs IV lasix x1 Calls you (as admitting MD of the day) for consult and consideration of admission You review his ECG electronically and decide it is abnormal but nil acute

16. ECG in heart failure Rarely normal LVH, intraventricular conduction delay and LBBB are common PVC�s, atrial arrhythmias are common

17. Case You then review his CXR�

19. QUESTIONS #2

20. The lab tests Renal: Creatinine can be elevated due to AHF (improves with Rx) Pre-renal azotemia: decreased renal perfusion Anemia (20% of patients): worse prognosis Hyponatremia - dilutional from increased ADH Abnormal liver enzymes Hepatic congestion: increased bilirubin, ALP, PT INR Hepatic ischemia: increased transaminases other labs: SPEP/UPEP, ferritin, TSH, HbA1c etc

21. Troponin elevation common and linked to mortality

22. Case Creatinine 152 �mol/L (eGFR = 43 mls/min) BUN 18 mmol/L Na 138, K 4.5, Hb 120 g/L TroponinI 0.21 (ULN 0.15)

23. QUESTIONS #3

24. What is B-Type Natriuretic Peptide (BNP)? Found in the cardiac ventricles Released in response to stretch and increased volume in the ventricles BNP levels related to: Left ventricular end-diastolic pressure NYHA classification BNP is found in the cardiac ventricles and is released in direct response to stretch and increased volume in the ventricles. The utility of BNP in staging the severity of disease has been documented through its relationship to left ventricular end-diastolic pressure and NYHA classification. This information will now be reviewed. BNP is found in the cardiac ventricles and is released in direct response to stretch and increased volume in the ventricles. The utility of BNP in staging the severity of disease has been documented through its relationship to left ventricular end-diastolic pressure and NYHA classification. This information will now be reviewed.

25. BNP � Storage and Secretion

26. BNP: Physiologic effects BNP has multiple beneficial effects, including decreased wall stress in the cardiac myocyte and peripheral artery vasodilation. hBNP also exhibits antifibrotic properties and increases endothelial function in the peripheral artery. BNP has multiple beneficial effects, including decreased wall stress in the cardiac myocyte and peripheral artery vasodilation. hBNP also exhibits antifibrotic properties and increases endothelial function in the peripheral artery.

27. QUESTIONS #4

28. How uncertain are we in the ED?

29. Does BNP add to clinical assessment?

30. Sure you can order it � but is it cost-effective?

31. BNP (CCS 2007) BNP/NT-proBNP � should be measured to � confirm or rule out a diagnosis of heart failure in the acute or ambulatory care setting in patients in whom the clinical diagnosis is in doubt. (class I, level A)

32. Case Regardless of your choice, the patient had a BNP drawn: BNP 934 pg/ml Does that help? By what criteria do you decide if a patient has HF other than clinical gestalt? Boston criteria, Framingham criteria, Carlson, PRIDE score all used infrequently but can help focus differential Dx

33. AHF Dx Scoring systems

34. QUESTIONS #5

35. Echocardiography �Confirm� diagnosis with transthoracic echocardiography LV dimensions and ejection fraction Systolic versus diastolic function Valvular disease Pulmonary hypertension All patients, Class 1C

36. Echo images

37. I don�t need an echo, I can tell their EF by looking at them!

38. Case Good quality images LVEF 32% LVEDD 59 mm LVH RVEF 34% Borderline RV dilation RVSP 44 mmHg Valves: MR 2+ (moderate central jet) Mild TR Anterior and inferior hypokinesis

39. QUESTIONS #6

40. When to Order a CMR scan for a Patient with HF Poor acoustic windows on echocardiography �Borderline cases� on echocardiography Viability and perfusion assessment Tissue characterization for cardiomyopathy etiology Early monitoring of treatment response Evaluation of patients with dual pathologies

41. MRI images

42. Coronary angiogram Cath done: LVEDP 22 mmHg LAD � 70% mid Cx � 50%, OM 50% RCA dominant � 50% PDA Decision to treat the CAD

43. Heart Failure Etiology Systolic � Usually LV dilation IHD/CAD Alcohol Cocaine Diabetic Drug-Induced (eg adriamycin) Idiopathic Peripartum Myocarditis Preterminal Valvular Disease Congenital Heart Disease

44. Common causes of HF decompensation Medication non-compliance Excessive salt intake Infections Atrial fibrillation or flutter Ischemia/infarction Hypertension

45. Case resolution You are comfortable with the diagnosis of AHF. You decide to admit him to the ward rather than the ICU/CCU. What are the odds of him dying in hospital? 1% 2% 5% 10% 20% 50%

46. In-hospital and 30-day mortality models ADHERE = 5.6% EFFECT score = 60 = 0.5%

47. Seattle HF Model (outpatient)

48. Diagnosis of HF Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45. Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45.

49. Practical Tips in HF Diagnosis HF can be diagnosed without a history or current evidence of volume overload. Thus, the term �heart failure� is generally preferred over �congestive heart failure� A normal LVEF does not exclude HF as a diagnosis (e.g.: HF with preserved systolic function � PSF) First admission is the opportunity to establish etiology Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45. Reference: 1. Arnold JMO et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006:diagnosis and management. Can J Cardiol 2006;22(1):23-45.

50. Key points History and physical guides the Dx and Rx Find the cause (e.g CAD) and the trigger (e.g. salt intake) ECG, labs, CXR, ECHO on all suspected HF patients BNP can be useful Advanced imaging (especially CMR) can aid Dx Use validated risk scores where possible

51. End of Case

52. QUESTIONS

53. For additional references, resources and tools, please visit our website: www.hfcc.ca