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Handouts Available at the Web Site Next Week: www.cardionursing.com Drawing at the end of todays program. Sneak peek of our book. Must be present to win. 1 Presented By Cynthia Webner DNP, RN, CCNS, CCRN-CMC, CHFN 2014 www.cardionursing.com 2 They may forget your name, but they will never forget how you made them feel. -Maya Angelou 3 Definitions 4 Definition of Heart Failure Classification Ejection Fraction I. Heart Failure with Reduced Ejection Fraction (HFrEF) ≤40% II. Heart Failure with Preserved Ejection Fraction (HFpEF) ≥50% a. HFpEF, Borderline 41% - 49% b. HFpEF Improved >40% Description Also referred to as systolic HF. Randomized clinical trials have mainly enrolled patients with HFrEF and it is only in these patients that efficacious therapies have been demonstrated to date. Also referred to as diastolic HF. Several different criteria have been used to further define HFpEF. The diagnosis of HFpEF is challenging because it is largely one of excluding other potential noncardiac causes of symptoms suggestive of HF. To date, efficacious therapies have not been identified. These patients fall into a borderline or intermediate group. Their characteristics, treatment patterns, and outcomes appear similar to those of patient with HFpEF. It has been recognized that a subset of patients with HFpEF previously had HFrEF. These patients with improvement or recovery in EF may be clinically distinct from those with persistently preserved or reduced EF. Further research is needed 5 to better characterize these patients. Stages, Phenotypes and Treatment of HF At Risk for Heart Failure Heart Failure STAGE A STAGE B STAGE C At high risk for HF but without structural heart disease or symptoms of HF Structural heart disease but without signs or symptoms of HF Structural heart disease with prior or current symptoms of 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 HFpEF 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 STAGE D Refractory HF 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 Refractory symptoms of HF at rest, despite GDMT e.g., Patients with: · Marked HF symptoms at rest · Recurrent hospitalizations despite GDMT HFrEF 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 6 Classification of Heart Failure New York Heart Association 7 Stages / Classification of Heart Failure 8 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. Rehospitalization rate predicted to be 50% at 6 months 1-year mortality of approximately 30% of ADHF admissions (ACCF/AHA 2013 HF Guidelines) 9 Common Precipitating Factors of ADHF Non adherence with Medications Dietary sodium intake Fluid intake Acute MI Arrhythmias Atrial fibrillation Persistent hypertension Recent addition of negative inotrope Pulmonary embolism Nonsteroidal antiinflammatory drugs Excessive alcohol or drug use Endocrine abnormality Concurrent infection New anemia 10 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 11 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 12 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 13 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 14 program 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. 15 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) 16 Evaluation Guides Treatment Decisions Determine Volume Status Perfusion Status Role of / or presence of precipitating factors and/or comorbidities Ejection fraction HFpEF HFrEF 17 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 18 Hemodynamic and Clinical Subsets Forwards Flow: CI, Skin temp (warm or cold) 5 Normal Hemodynamics (I) Backwards Failure (II) 3 No pulmonary congestion: • PWP < 18; Dry lungs No hypoperfusion: • CI > 2.2; Warm skin Pulmonary congestion • PWP > 18; Wet lungs No hypoperfusion • CI > 2.2; Warm skin 2 Forwards Failure (III) 1 No pulmonary congestion • PWP < 18; Dry lungs Hypoperfusion • CI < 2.2; Cold skin 4 The Shock Box (IV) Pulmonary congestion • PWP > 18; Wet lungs Hypoperfusion • CI < 2.2; Cold skin 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Preload: PWP, lung sounds (dry or wet) 19 20 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 21 Changing Preload: Moves patient along the current curve Forward Flow: Cardiac Index Skin temp (warm or cold) 5 Warm and Dry 4 3 2 1 Cold and Wet 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Preload 22 Changing Contractility: moves patient to a higher Forwards Flow: CI, Skin temp (warm or cold) curve 5 4 3 2 1 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Preload: PWP, lung sounds (dry or wet) 23 Changing Afterload:: moves patient up and to the left Forwards Flow: CI, Skin temp (warm or cold) (improves forwards flow and reduces preload) 5 4 3 2 1 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 Preload: PWP, lung sounds (dry or wet) 24 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 25 Pharmacological Options for Decreasing Preload Stop or decrease fluid Diuretics ▪ A loop diuretic such as furosemide eliminates circulating volume Venous Vasodilators ▪ 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. 26 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 27 Diuretics and Renal Function Role of venous congestion in worsening renal function Role of volume depletion / hypotension and worsening renal function 28 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) 29 Loop Diuretics Bumetanide (Bumex) Furosemide (Lasix) Torsemide (Demadex) Equivalents Furosemide 40 mg Torsemide 20 mg Bumetanide 1 mg Dosing Adequate to relieve symptoms Start equal or greater than home maintenance dose 30 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 31 renal function Differences in Loop Diuretics Furosemide Bumetanide Torsemide Lack of randomized control data with comparison to furosemide. Better pharmacokinetic profile (oral bioavailability) than furosemide but turosemide has evidence of more efficacy and more safety. (Wargo &Banta, 2009) BID Dosing when GFR is low 2 randomized trials comparing Torsemide and Furosemide N=471 Torsemide associated with reduction in HF and CV readmission in systolic HF with a trend towards reduction of all cause mortality. (DiNicolantonio, 2012) 32 Vasodilator Therapy Preload Reduction Venous Vasodilators Afterload Reduction Arterial Vasodilators Three Primary Drugs NTG IV Primary Venous Vasodilator Neseritide Mixed Nitroprusside Predominantly Arterial Vasodilator 33 Nitroglycerin Mixed venous and arterial vasodilator Dosage < 1mcg/kg/min = venous vasodilator Dosage > 1mcg/kg/min = arterial and venous vasodilator Sublingual tablets provide high enough dosage to dilate arteries and veins Caution with severe Aortic Stenosis Decreases activity of Heparin 34 Nitroglycerin Uses: Acute MI, unstable angina, CHF Side Effects: H/A, Hypotension, flushing Nursing Considerations: Contraindicated with Sildenefil like drugs Caution (all venous vasodilators) with: Hypertrophic cardiomyopathy, aortic stenosis, right ventricular MI Treat H/A with pain meds and decrease dose Onset IV: 1-2 minutes Duration: 3-5 minutes 35 Nesiritide (Natrecor) Recombinant form of human B type natriuretic peptide (BNP) BNP allows the heart to BNP is a naturally occurring cardiac neurohormone secreted by the heart in the body’s response to heart failure participate in the regulation of vascular tone and extracellular volume status The BNP system and the renin-angiotensin system counteract each other in heart failure BNP levels are elevated in heart failure 36 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 37 Nesiritide (Natrecor) Given by IV bolus Patient must have systolic BP > 90 mmHg and maintenance infusion (bolus to be taken from reconstituted IV bag and not from vial) PAOP should be estimated to be > 20 Infusion is usually 24mmHg 48 hours Monitor BP closely during administration. 38 Nesiritide: Where do we stand? Balanced venous and arterial vasodilator Sackner-Bernstein JD, Kowalski M, Fox M, Aaronson K: Short-term risk of death after treatment with nesiritide for decompensated heart failure: a pooled analysis of randomized controlled trials. JAMA 2005, 293:1900-1905. In the 3 trials, 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 39 difference. ASCEND HF Trial Effect of Nesiritide in Patients with Acute Decompensated Heart Failure O'Connor et al. July 7 2011 7,141 patients Randomized 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. 40 Nitroprusside Mixed venous and arterial dilator (primarily arterial) 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 41 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 42 If No Improvement With Preload Reduction Na and fluid restrict Increase dose of loop diuretic Continuous infusion of loop diuretic Add 2nd diuretic PO Maximize loop diuretic Metalazone Spironolactone Diuretic Resistance Reasons High sodium levels NSAIDs Severe renal impairment Renal hypoperfusion OR IV chlorothiazide Consider ultrafiltration 43 Ultrafiltration 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) 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. 44 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) 45 Synthetic Compound Dobutamine What receptors are stimulated: Primarily β1 Some alpha1 receptor stimulation Some β2 stimulation Modest β2 (more β2 than alpha1) What are the resultant actions: Increase contractility (+ inotrope) (β1) 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; β2 causes vasodilatation; β1 increases cardiac output46 and may increase BP Phosphodiesterase Inhibitors: Non Sympathomimetic Inotropes Used as an Inotrope Preload Reduction Also has…… BUT….. Afterload Reduction 47 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 48 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 951 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 49 Dopamine What receptors are stimulated: Mimics endogenous dopamine; metabolic precursor of norepinephrine and epinephrine Dopaminergic at low doses (0.5-2.0 mcg/kg/min) β1 also at moderate doses ( 2.0-10.0 mcg/kg/min) Pure alpha stimulation at high doses > 10mcg/kg/min What are the resultant Increase GFR at low doses actions: Increase contractility at moderate doses (greater effects on contractility than heart rate) Vasoconstriction (alpha) at high doses When and why do we use: Refractory hypotension / shock * Not indicated for routine treatment or prevention of acute renal failure What are special nursing considerations: Onset 1-2 minutes; Peak 10 minutes Maximal effects @20/mcg/kg/min Large IV line or central line; Regitine (alpha blocker) for infiltrate 50 Comparison of Dopamine to Norepinephrine in Shock Backer et al. Multi Center Randomized Controlled Trial New England Journal of Medicine March 4th 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. 51 Acute Decompensated Heart Failure Reduce Preload Diuretics Venous vasodilators Low dose Nitroglycerin Neseritide Increase Contractility Positive Inotropes Dobutamine Milronone Dopamine 52 Ultrafiltration Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide Intra aortic balloon pump Serelaxin RELAX –AHF Trail Presented AHA November 2012 Recombinant human relaxin-2, vasoactive peptide hormone Double blinded placebo controlled, randomized trial Standard care plus 48 hours of serelaxin or placebo 1161 patients Positive outcomes: Dyspnea relief Improvement in signs and symptoms of HF Reduction in LOS Decreased all cause and CV 180 day mortality (37% reduction in mortality) No impact on readmissions Europe Regulators - Denied approval January 2014 Breakthrough therapy designation by FDA – June 21 2013 53 Pending FDA approval Feb 13, 2014. Additional Care Issues 54 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 55 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 56 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 57 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. 58 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 59 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 60 Profile of Severe Heart Failure Profile 1: Cardiogenic Shock Profound hypotension despite rapidly escalating inotropic support; acidosis; “crash and burn” Profile 2: Progressive decline Declining function despite IV inotropes, possible worsening renal function; “sliding on inotropes” Profile 3: Stable but inotrope-dependent Continuous IV inotropes +/- IABP or other mechanical support, unable to be weaned Margarita Camacho MD, FACS Surgical Director - Cardiac Transplant and Mechanical Assist Device Program Barnabas Health Heart Centers at Newark Beth Israel Medical Center, Newark, NJ 61 Profile of Severe Heart Failure Profile 4: Resting Symptoms Daily congestion at rest or during ADL (activities of daily living) Profile 5: Exertion intolerant Comfortable at rest or with ADL, but unable to engage in any other activity, living predominantly within house Profile 6: Exertion limited Comfortable at rest and with ADL. Profile 7: Advanced NYHA III Living comfortably with meaningful activity limited to mild physical exertion 62 63 Temporary Assist Devices in Acute Shock IABP ECMO Impella CentriMag Thoratec pVAD Abiomed AB 5000 Abiomed BVS 5000 64 Intra Aortic Balloon Pump 65 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 2.5 – 5.0 L/Min (2 different devices) 66 Bridge to Recovery Impella Mechanical Cirulatory Support Device “Percutaneous VAD” Minimally invasive Unloads ventricle reducing myocardial workload Produces 2.5 liters of cardiac output Recommended for up to 7 days 67 Bridge to Recovery ECMO Extracorporeal Membrane Oxygenation Used to treat medically refractory cardiogenic shock with poor oxygenation Provides biventricular support Not good for long term durability Used in a short term situation Requires perfusion support 68 69 Who Gets a Device Acutely Cardiac arrest with ongoing CPR Cardiogenic shock, IABP-dependent on inotropes and pressors 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 70 Cardiac Arrest with Ongoing CPR CentriMag AB5000 PVAD or IVAD Alternate: Impella 5.0 or Tandem Heart 71 Cardiogenic Shock, IABP Dependent on Inotropes and Pressors CentriMag Impella 5.0 Tandem Heart PVAD or IVAD 72 Intra-operative failure to wean from CP Bypass CentriMAG Tandem Heart or Impella 5.0 PVAD OR IVAD (if suspect patient will need longterm support) AB5000 (concerns about coagulopathy/increased hemolysis after long bypass runs 73 Bridge to Decision Bridge to a decision: indeterminate neurologic status or other significant co-morbidity (i.e., possible incurable malignancy) with critical clinical deterioration CentriMag AB5000 Impella 5.0 Tandem Heart 74 BiV Bridge to Transplant Thoratec pVAD Abiomed AB 5000 Abiomed BVS 5000 Heart Mate XVE Heart Mate II HeartWare HVAD Cardiowest Total Artificial Heart 75 Long Term Therapy BTT Thoratec pVAD Abiomed AB 5000 Abiomed BVS 5000 Heart Mate XVE Heart Mate II HeartWare HVAD DT Heart Mate XVE Heart Mate II HeartWare HVAD 76 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 77 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 78 Advanced HF Decision Making 79 Things to Think About Currently 2.4% of adult population affected with HF Over 11% of the expanding population is > 80 years 80 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 81 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 82 European Society of Cardiology Criteria for Advanced Chronic Heart Failure Moderate to severe symptoms of dyspnea and/or fatigue at rest or with minimal exertion (NYHA functional class III or IV) Episodes of fluid retention and/or reduced cardiac output Objective evidence of severe cardiac dysfunction demonstrated by at least 1 of the following: Left ventricular ejection fraction <30% Pseudonormal or restrictive mitral inflow pattern by Doppler High left and /or right ventricular filling pressures, or Elevated B-type natriuretic peptide Severe impairment of functional capacity as demonstrated by either inability to exercise, 6-min walk distance 300 m, or peak oxygen uptake <12 to 14 mL g-1 min-1 History of at least 1 hospitalization in the past 6 months 83 Characteristics should be present despite optimal medical therapy 84 85 End of Life Decision Palliative Care versus Hospice When should they be involved Making an assessment Having the discussion 86 +20% to 68% P=0.1566 -43% to -91% P<0.0001 -70% to -96% P<0.0001 87 Fonarow GC,Yancy CW. J Am Heart Assoc 2012;1:16-26. Number of Therapies (vs 0 or 1 therapy) Odds Ratio (95% confidence interval) 2 therapies 0.63 (0.47-0.85) (p=0.0026) 3 therapies 0.38 (0.29-0.51) (p<0.0001) 4 therapies 0.30 (0.23-0.41) (p<0.0001) 5, 6, or 7 therapies 0.31 (0.23-0.42) (p<0.0001) 0 0.5 1 1.5 Fonarow GC, … Yancy, C. J Am Heart Assoc 2012;1:16-26. 2 88 A Final Thought: We must not, in trying to think about how we can make a big difference, ignore the small daily differences we can make which, overtime, add up to big differences that we often cannot foresee. -Marian Wright Edelman 89 BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! 90