Presented By Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN

Transcription

1 Presented By Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN

2 I m not telling you it is going to be easy, I m telling you it is going to be worth it. ~ Art Williams 3 Definition Heart Failure is a complex clinical syndrome resulting from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject 4 2

3 Definitions 5 Definition of Heart Failure Classification Heart Failure with Reduced Ejection Fraction (HFrEF) Ejection Fraction Description 40% Also referred to as systolic HF. Heart Failure with Preserved Ejection Fraction (HFpEF) 50% Also referred to as diastolic HF. III. HFpEF, Borderline 41% - 49% These patients fall into a borderline or intermediate group. IV. HFpEF Improved >40% A subset of patients who previously had HFrEF. 6 3

4 Stages, Phenotypes and Treatment of HF At Risk for Heart Failure Heart Failure STAGE A At high risk for HF but without structural heart disease or symptoms of HF STAGE B Structural heart disease but without signs or symptoms of HF STAGE C Structural heart disease with prior or current symptoms of HF STAGE D Refractory HF e.g., Patients with: HTN Atherosclerotic disease DM Obesity Metabolic syndrome or Patients Using cardiotoxins With family history of cardiomyopathy Structural heart disease e.g., Patients with: Previous MI LV remodeling including LVH and low EF Asymptomatic valvular disease Development of symptoms of HF e.g., Patients with: Known structural heart disease and HF signs and symptoms Refractory symptoms of HF at rest, despite GDMT e.g., Patients with: Marked HF symptoms at rest Recurrent hospitalizations despite GDMT HFpEF HFrEF THERAPY Goals Heart healthy lifestyle Prevent vascular, coronary disease Prevent LV structural abnormalities Drugs ACEI or ARB in appropriate patients for vascular disease or DM Statins as appropriate THERAPY Goals Prevent HF symptoms Prevent further cardiac remodeling Drugs ACEI or ARB as appropriate Beta blockers as appropriate In selected patients ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Prevent hospitalization Prevent mortality Strategies Identification of comorbidities Treatment Diuresis to relieve symptoms of congestion Follow guideline driven indications for comorbidities, e.g., HTN, AF, CAD, DM Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Patient education Prevent hospitalization Prevent mortality Drugs for routine use Diuretics for fluid retention ACEI or ARB Beta blockers Aldosterone antagonists Drugs for use in selected patients Hydralazine/isosorbide dinitrate ACEI and ARB Digoxin In selected patients CRT ICD Revascularization or valvular surgery as appropriate THERAPY Goals Control symptoms Improve HRQOL Reduce hospital readmissions Establish patient s endof-life goals Options Advanced care measures Heart transplant Chronic inotropes Temporary or permanent MCS Experimental surgery or drugs Palliative care and hospice ICD deactivation 7 Classification of Heart Failure New York Heart Association 8 4

5 Stages / Classification of Heart Failure 9 Acute Decompensated Heart Failure (ADHF) Sudden or gradual onset of the signs and symptoms of heart failure requiring unplanned office visits, emergency room visits, or hospitalizations. Associated with pulmonary and systemic congestion due to increased left and right heart filling pressures. Acute Decompensated HF represents a sentinel prognostic event. Readmission rate predicted to be 50% at 6 months year mortality of approximately 30% of ADHF admissions 5

6 The Numbers Data from the National Ambulatory Medical Care (NAMCS) and the National Hospital Ambulatory Medical Care Survey (NHAMCS), symptoms that necessitate early intervention is a common occurrence. Nearly 658,000 annual ED encounters primarily for acute HF in the United States a figure that represents almost 20% of the total HF-specific ambulatory care delivered each year Nearly 80% of those treated for acute HF syndromes are admitted to the ED. 11 Common Precipitating Factors of ADHF Non adherence with Medications Dietary sodium intake Fluid intake Acute MI Arrhythmias Atrial fibrillation (30%) Persistent hypertension Recent addition of negative inotrope Pulmonary embolism Nonsteroidal antiinflammatory drugs Excessive alcohol or drug use Endocrine abnormality Concurrent infection New anemia 12 6

7 Potential Contributing Precipitating Factors and/or Comorbidities ACS / coronary ischemia (troponins typically elevated with ADHF) Severe hypertension Atrial or ventricular arrhythmias Infections Pulmonary emboli Renal failure Medical or dietary compliance Valvular heart disease New onset anemia 13 Hospitalization Recommended Evidence of severe ADHF, including: Hypotension Worsening renal function Altered mentation Dyspnea at rest Typically reflected by resting tachypnea Less commonly reflected by oxygen saturation <90% Hemodynamically significant arrhythmia - including new onset of rapid atrial fibrillation Acute coronary syndromes 14 7

8 Hospitalization Should be Considered Worsened congestion: Even without dyspnea Signs and symptoms of pulmonary or systemic congestion Even in the absence of weight gain Major electrolyte disturbance Associated comorbid conditions Pneumonia Pulmonary embolus Diabetic ketoacidosis Symptoms suggestive of transient ischemic accident or stroke Repeated ICD firings Previously undiagnosed HF with signs and symptoms of systemic or pulmonary congestion 15 Treatment Goals Improve symptoms, especially congestion and low-output symptoms Optimize volume status Identify etiology Identify and address precipitating factors Optimize chronic oral therapy Minimize side effects Identify patients who might benefit from revascularization Identify patients who might benefit from device therapy Identify risk of thromboembolism and need for anticoagulant therapy Educate patients concerning medications and self management of HF Consider and, where possible, initiate a disease management program 16 8

9 Diagnosis Based on signs and symptoms B-type natriuretic peptide (BNP) or N-terminal pro-b-type natriuretic peptide (NT-proBNP) Good to assess in patients with dyspnea being evaluated for HF Should not be used as the sole tool to diagnose HF Must be used in concert with signs and symptoms Special consideration with renal insufficiency and obesity. Low values rule out HF 17 Causes of Elevated Naturetic Peptide Levels Cardiac Noncardiac Heart failure, including RV syndromes Acute coronary syndrome Heart muscle disease, including LVH Valvular heart disease Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Anemia Advancing Age Renal failure Pulmonary: obstructive sleep apnea, severe pneumonia, pulmonary hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults, including cancer chemotherapy and envenomation 18 9

10 3 Clinical Presentations Patient 1: Volume overload (Backwards Failure) Patient 2: Profound depression of cardiac output hypoperfusion (Forwards Failure) Patient 3: Signs and symptoms of both fluid overload and hypoperfusion (cardiogenic shock) 19 Evaluation Guides Treatment Decisions Determine Volume Status Perfusion Status Role of / or presence of precipitating factors and/or comorbidities Ejection fraction HFpEF HFrEF 20 10

11 Forwards Flow: CI, Skin temp (warm or cold) Hypoperfusion vs. Volume Overload Hypoperfusion Narrow pulse pressure Resting tachycardia Cool Skin Altered mentation Decreased urine output Increased BUN/Creatinine Cheyne Stokes Respirations Intravascular Volume Overload Elevated jugular venous pressure Hepatojugular reflex Orthopnea Dyspnea Crackles Weight gain Peripheral edema S3 21 Hemodynamic and Clinical Subsets Normal Hemodynamics (I) No pulmonary congestion: PWP < 18; Dry lungs No hypoperfusion: CI > 2.2; Warm skin Backwards Failure (II) Pulmonary congestion PWP > 18; Wet lungs No hypoperfusion CI > 2.2; Warm skin Forwards Failure (III) No pulmonary congestion PWP < 18; Dry lungs Hypoperfusion CI < 2.2; Cold skin The Shock Box (IV) Pulmonary congestion PWP > 18; Wet lungs Hypoperfusion CI < 2.2; Cold skin Preload: PWP, lung sounds (dry or wet) 22 11

12 Forward Flow: Cardiac Index Skin temp (warm or cold) Treatment for Acute Decompensated Heart Failure Congestion with Adequate Perfusion Subset II Reduce Preload Hypoperfusion with No Congestion Subset III Increase contractility Assure adequate preload Hypoperfusion with Congestion Subset IV Reduce Afterload 23 Changing Preload: Moves patient along the current curve 5 4 Warm and Dry Preload Cold and Wet 24 12

13 Forwards Flow: CI, Skin temp (warm or cold) Forwards Flow: CI, Skin temp (warm or cold) Changing Contractility: moves patient to a higher curve Preload: PWP, lung sounds (dry or wet) 25 Changing Afterload:: moves patient up and to the left (improves forwards flow and reduces preload) Preload: PWP, lung sounds (dry or wet) 26 13

14 Acute Decompensated Heart Failure Reduce Preload Diuretics Venous Vasodilators Low dose NTG Neseritide Ultrafiltration Increase Contractility Positive Inotropes Dobutamine Milronone Dopamine Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide Intra aortic balloon pump 27 Pharmacological Options for Decreasing Preload Stop or decrease fluid Diuretics Venous Vasodilators A loop diuretic such as furosemide eliminates circulating volume Intravenous nitroglycerin, neseritide, or morphine sulfate (Venous vasodilatation pools blood away from the heart and decreases preload) ACE Inhibitors or Angiotensin II Receptor Blockers (ARBs) Interrupt renin- Angiotensin- aldosterone system. (RAAS). Aldosterone secretion is decreased and there is less sodium and water retention. ACE inhibitors end in pril / ARBs end in sartan Aldosterone antagonists Spironolactone or epleranone Directly block aldosterone and there is decreased sodium and water retention

15 Reduce Preload Loop Diuretics IV not PO Early intervention - ED Dose high enough to relieve signs and symptoms of congestion Should equal or exceed chronic oral dose Caution for signs of over diuresis Hypotension: check orthostatics Worsening renal failure Monitor E-lytes (potassium, magnesium, sodium) Arrhythmias Muscle cramps Monitor for gout Frequent reassessment 29 Diuretics and Renal Function Role of venous congestion in worsening renal function Role of volume depletion / hypotension and worsening renal function 30 15

16 Cardiorenal Syndrome Moderate to severe renal dysfunction with fluid overload Continue to treat with diuretics In severe fluid overload renal dysfunction my improve with continued treatment May need to hold ACE I secondary to AKI Venous congestion plays a role in worsening renal function (not just hypoperfusion) 31 Mullens, W., Abrahams, Z., Francis, G. S., Sokos, G., Taylor, D. O., Starling, R. C.,... & Tang, W. W. (2009). Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. Journal of the American College of Cardiology, 53(7), We observed in our patient population with low-output decompensated HF that besides the presence of intrinsic renal insufficiency, venous congestion was the strongest hemodynamic determinant for the development of WRF. In contrast, impaired CI on admission and improvement in CI after intensive medical therapy had a limited contribution to WRF

17 Damman, K., van Deursen, V. M., Navis, G., Voors, A. A., van Veldhuisen, D. J., & Hillege, H. L. (2009). Increased central venous pressure is associated with impaired renal function and mortality in a broad spectrum of patients with cardiovascular disease. Journal of the American College of Cardiology, 53(7), Increased CVP is associated with impaired renal function and independently related to allcause mortality in a broad spectrum of patients with cardiovascular disease. 33 Loop Diuretics Bumetanide (Bumex) Furosemide (Lasix) Torsemide (Demadex) Equivalents Furosemide 40 mg Max dose 600 mg /day Torsemide 20 mg Max dose 200 mg /day Bumetanide 1 mg Max dose 10 mg /day Dosing Adequate to relieve symptoms Start equal or greater than home maintenance dose 34 17

18 More on Loop Diuretics DOSE Trial NEJM: Felker et al., 2011 No significant difference in symptoms or renal function between continuous drip versus intermittent dosing Non significant trend toward improvement in symptoms with high dose (IV at 2.5 x PO dose) versus low dose; (IV at same as PO dose) no change in renal function 35 Differences in Loop Diuretics Bumetanide Furosemide Torsemide Lack of randomized control data with comparison to furosemide. BID Dosing when GFR is low 2 randomized trials comparing Torsemide and Furosemide N=471 Better pharmacokinetic profile (oral bioavailability) than furosemide but turosemide has evidence of more efficacy and more safety. (Wargo &Banta, 2009) Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. (DiNicolantonio, 2012) 36 18

19 Vasodilator Therapy Preload Reduction Venous Vasodilators Afterload Reduction Arterial Vasodilators Three Primary Drugs NTG IV Primary Venous Vasodilator Neseritide Mixed Nitroprusside Predominantly Arterial Vasodilator There are no data that suggest that intravenous vasodilators improve outcomes in the patient hospitalized with HF Use of intravenous vasodilators is limited to the relief of dyspnea in the hospitalized HF patient with intact blood pressure. Yancy et al, Nitroglycerin Mixed venous and arterial vasodilator Dosage < 1mcg/kg/min = venous vasodilator Dosage > 1mcg/kg/min = arterial and venous vasodilator Primarily used as venodilator to quickly reduce preload Sublingual tablets provide high enough dosage to dilate arteries and veins 38 19

20 Nesiritide (Natrecor) Recombinant form of human B type natriuretic peptide (BNP) BNP allows the heart to participate in the regulation of vascular tone and extracellular volume status BNP is a naturally occurring cardiac neurohormone secreted by the heart in the body s response to heart failure The BNP system and the renin-angiotensin system counteract each other in heart failure BNP levels are elevated in heart failure 39 Nesiritide (Natrecor) Balanced arterial and venous vasodilatation Causes rapid reduction in right and left sided ventricular filling pressures (preload reduction) Reduces afterload Indicated for acutely decompensated heart failure patients who have dyspnea at rest 40 20

21 Nesiritide (Natrecor) Patient must have systolic BP > 90 mmhg Longer half-life resulting in more persistent hypothension PAOP should be estimated to be > 20 mmhg Given by IV bolus and maintenance infusion (bolus to be taken from reconstituted IV bag and not from vial) Infusion is usually hours Monitor BP closely during administration. 41 Nesiritide: Where do we stand? Sackner-Bernstein et al., Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA 2005, 293: trials randomized double-blind study of patients with ADHF 485 patients were randomized to nesiritide and 377 to control therapy. Death within 30 days tended to occur more often among patients randomized to nesiritide therapy (35 [7.2%] of 485 vs 15 [4.0%] of 377 patients. No statistically significant difference

22 ASCEND HF Trial Effect of Nesiritide in Patients with Acute Decompensated Heart Failure O'Connor et al. July Randomized 7,141 patients Nesiritide was not associated with an increase or a decrease in the rate of death and re-hospitalization. It was not associated with a worsening of renal function, but it was associated with an increase in rates of hypotension. Neseritide cannot be recommended for routine use. 43 Nitroprusside Mixed venous and arterial dilator (primarily arterial including pulmonary bed) Decreases BP, SVR, PVR, PAOP, RAP Uses: Hypertensive crisis CHF Acute Mitral Regurgitation Other Indications for Afterload Reduction Side Effects: Hypotension Thiocyanate toxicity: tinnitus, blurred vision, delirium, seizures, muscle twitching, absent reflexes, dilated pupils [several days high doses] Nursing Considerations: Onset: 1-2 minutes Duration: 1-10 minutes Monitor BP carefullyarterial line encouraged 44 22

23 Reduce Preload Venous Vasodilators Persistent failure with aggressive diuresis and standard oral therapies NTG Neseritide Nitroprusside Especially helpful with severe hypertension or severe MR For rapid symptom relief in acute pulmonary edema with hypertension NTG / Nitroprusside Do not give with hypotension 45 If No Improvement With Preload Reduction Na and fluid restrict Increase dose of loop diuretic Continuous infusion of loop diuretic Add 2 nd diuretic PO Maximize loop diuretic Metalazone Spironolactone OR IV chlorothiazide Low dose dopamine Consider ultrafiltration Diuretic Resistance Reasons High sodium levels NSAIDs Severe renal impairment Renal hypoperfusion 46 23

24 Ultrafiltration Ultrafiltration may be considered for patients with obvious volume overload to alleviate congestive symptoms and fluid weight (Class Iib Level of Evidence: B) Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy. (Class Iib Level of Evidence: C) 47 UNLOAD Trial Veno-venus ultrafiltration (UF) vs standard IV diuretic therapy for hypervolemic HF 200 patients randomized UF with statistical significance for: greater weight loss (48 hours), greater fluid loss (48 hours), less 90-day resource utilization for HF. No statistically significant difference in dyspnea scores or creatinine levels (safety endpoint) Ultrafiltration CARESS-HF Trial Treatment of ADHF, worsening renal function, persistent congestion with stepped pharmacologic approach vs ultrafiltration 188 patients randomized UF: inferior to pharmacologic therapy and associated with adverse events

25 Increase Contractility Inotropes Goal: Relief of symptoms and end organ perfusion Use in: Low output states Symptomatic hypotension or marginal blood pressure Despite good filling pressures No magic blood pressure look for symptoms Unresponsive / intolerant of IV vasodilators Diminished or worsening renal function Use vasodilators first as able Monitor closely for tachyarrhythmias and hypotension Not recommended if normotensive (ACC) 49 Dobutamine Synthetic Compound What receptors are stimulated: What are the resultant actions: Primarily β 1 Some alpha 1 receptor stimulation Some β 2 stimulation Modest β 2 (more β 2 than alpha 1 ) Increase contractility (+ inotrope) (β 1 ) Increase AV node conduction Modest vasodilation When and why do we use: Used as an inotrope (resultant preload reduction) with modest afterload reduction (ACC / AHA Guidelines for Heart Failure*) What are special nursing considerations: Onset 1 to 2 minutes; Peak 10 minutes Half-life 2 minutes Note: Blood pressure response is variable; β 2 causes vasodilatation; β 1 increases cardiac output and may increase BP 50 25

26 Phosphodiesterase Inhibitors: Non Sympathomimetic Inotropes Used as an Inotrope Preload Reduction Also has BUT.. Afterload Reduction 51 Milrinone (Primacor) Creates + inotropic effect by increasing availability of calcium Inhibits the degradation of cyclic AMP which is indirectly responsible for increasing the influx of calcium through the calcium channel Smooth muscle relaxant (venous and arterial vasodilator) Indications: Refractory heart failure (in combination with dobutamine) Left ventricular failure in MI Patients waiting transplant Side Effects: Ventricular arrhythmias, thrombocytopenia (new generation less) OPTIME Trial 52 26

27 OPTIME Trial Milrinone approved by FDA based on hemodynamic data Future trials need to include symptom relief and post discharge outcome data OPTIME Prospective trial, randomized, placebo controlled patients Patients had indication for but not all required inotrope for end organ perfusion. Results: No difference in LOS, No difference in subjective improvement Treatment failures more common in milrinone group due to hypotension, more atrial fibrillation in milrinone Not powered for mortality differences Conclusion: Hemodynamic improvement does not translate into clinical improvement 53 Dopamine Mimics endogenous dopamine; metabolic precursor of norepinephrine and epinephrine What receptors are stimulated: What are the resultant actions: When and why do we use: What are special nursing considerations: Dopaminergic at low doses ( mcg/kg/min) β 1 also at moderate doses ( mcg/kg/min) Pure alpha stimulation at high doses > 10mcg/kg/min Increase GFR at low doses Increase contractility at moderate doses (greater effects on contractility than heart rate) Vasoconstriction (alpha) at high doses Refractory hypotension / shock * Not indicated for routine treatment or prevention of acute renal failure Onset 1-2 minutes; Peak 10 minutes Maximal Large IV line or central line; Regitine (alpha blocker) for infiltrate 54 27

28 Comparison of Dopamine to Norepinephrine in Shock Backer et al. Multi Center Randomized Controlled Trial New England Journal of Medicine March 4 th 2010 There were no significant differences between the groups in the rate of death at 28 days or in the rates of death in the ICU, in the hospital, at 6 months, or at 12 months More patients with arrhythmia in the dopamine group Rate of death was higher in predefined subgroup analysis for patients with cardiogenic shock treated with dopamine. 55 Additional Care Issues 56 28

29 Invasive Monitoring Routine use not recommended When to consider: Refractory to initial therapy Volume status and cardiac filling pressures are unclear Pulmonary and systemic pressures unclear Clinically significant hypotension (SBP < 80 mm Hg) Worsening renal function 57 Foley Catheter Foley Catheter Not recommended routinely in heart failure If need to closely monitor hourly urine output Possible outlet obstruction High risk patients include those with BPH and or right sided volume overload 58 29

30 Fluid Restriction Dietary Sodium Restriction Water follows sodium If hyponatremic Serum sodium < 130 meq/l 2 liters per day Serum Sodium < 125 meq/l Stricter fluid restriction may be considered If persistent fluid overload Assure sodium restriction in conjunction with fluid restriction 59 Oxygen therapy is recommended if the patient exhibits hypoxemia If not hypoxemic no need for oxygen therapy Use of non-invasive positive pressure ventilation may be considered for severely dyspneic patients with clinical evidence of pulmonary edema

31 Other considerations Continue other evidence based practice medications Daily monitoring of volume status via Daily weights Fluid balance JVP Orthopnea Orthostatic pressures Activity tolerance Perceived dyspnea 61 Bridge to transplant (BBT) for those who are transplant eligible Destination therapy (DT) for those who are not transplant eligible. Bridge to Decision (BTD) Careful consideration for all therapies Some patients may be too ill with multisystem issues to benefit from MCS Some decisions are best made in the hands of the most experienced centers 62 31

32 63 Absolute and Relative Contraindications for Durable MCS Absolute Contraindications Irreversible hepatic disease Irreversible renal disease Irreversible neurological disease Major coagulopathy Right sided heart failure (unless candidate for biventricular support) Medical non-adherence Severe psychosocial limitations Source: Peura et al., 2012; Slaughter et al., * May be a relative contraindication Relative Contraindications * Hypertrophic, infiltrative, or restrictive cardiomyopathy Uncorrectable moderate or greater aortic insufficiency Age _80 y(for destination therapy) Obesity or malnutrition MS disease that impairs rehabilitation Active systemic infection Prolonged intubation Untreated malignancy Severe PVD Active substance abuse Impaired cognitive function Unmanaged psychiatric disorder Lack of social support 64 32

33 Temporary Assist Devices in Acute Shock / Bridge to Decision or Recovery IABP ECMO Percutaneously implanted MCS Impella Tandem Heart Surgically implanted extracorporeal MCS CentriMag Thoratec pvad II Abiomed BVS 5000 Abiomed AB Impella Pulls blood from the left ventricle and expels blood into the ascending aorta. Inserted via femoral artery, into the ascending aorta, across the valve and into the left ventricle. Produces CO of L/Min (2 different devices) 66 33

34 ECMO

35 Who Gets a Device Acutely Cardiac arrest with ongoing CPR Cardiogenic shock, IABP-dependent on inotropes and vasopressors Intra-operative failure to wean from cardiopulmonary bypass Bridge to a decision: indeterminate neurologic status or other significant co-morbidity (i.e., possible incurable malignancy) with critical clinical deterioration 69 Long Term Therapy Bridge to Transplant Extracorporeal MCS Thoratec pvad II Implantable MCS Heart Mate II HeartWare HVAD Total Artificial Heart CardioWest Abiomed: Abiocor II Destination Therapy Heart Mate II HeartWare HVAD Investigational Devices 70 35

36 Heart Mate II 71 HeartWare HVAD 72 36

37 Criteria for Discharge Exacerbating factors addressed Near optimal volume status achieved Transition from intravenous to oral diuretic successfully completed Patient and family education completed, including clear discharge instruction LVEF documented Smoking cessation counseling initiated Near optimal pharmacologic therapy achieved, including ACE inhibitor and beta-blocker (for patients with reduced LVEF), or intolerance documented 73 Follow-up clinic visit scheduled, usually for 7 to 10 d Criteria for Discharge Advanced HF Patient or recurrent admission Oral medication regimen stable for 24 h No intravenous vasodilator or inotropic agent for 24 h Ambulation before discharge to assess functional capacity after therapy Plans for post discharge management (scale present in home, visiting nurse or telephone follow up generally no longer than 3 d after discharge) Referral for disease management, if available 74 37

38 Advanced HF Decision Making 75 Prognostic Models Heart Failure Survival Score All cause mortalilty Seattle Heart Failure Model All cause mortality, urgent transplantation or LVAD implant depts.washington.edu.shfm EVEREST Risk Model Combined endpoint of mortality or persistently poor quality of life over the 6 months after discharge EFFECT 30-day and 1-year mortality ADHERE In-hospital mortality ESCAPE Discharge Score 6 month mortality 76 38

39 Risk Factors for Mortality > 2 Referral for Advanced Treatment >2 Prompt Referral for Advanced Rx Hospitalization for HF on oral HF therapy Inability to take ACEI/ARB/BB BUN> 45, Creat>2.5, CrCl< 45 cc/min BNP >4 x s upper limit of normal Na+ < 136 Malnutrition/Cachexia VO2 <55% predicted LVEDD >7.0 cm

40 79 End of Life Decision Palliative Care versus Hospice When should they be involved Making an assessment Having the discussion 80 40

41 81 BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! Handouts are available on the NTI Network today and will be available next week at