They may forget your name, but they will never forget how you made them feel.

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1 Relax and Learn at the Farm 2013 Presented By DNP, RN, CCNS, CCRN-CMC, CHFN Cardiovascular Nursing Education Associations 1 They may forget your name, but they will never forget how you made them feel. -Maya Angelou 2 1

2 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. 3 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 4 2

3 3 Clinical Presentations Patient 1: Volume overload with acute increase in chronic hypertension (Backward Failure) Patient 2: Profound depression of cardiac output manifested by hypotension, renal insufficiency, and or a shock syndrome (Forward Failure) Patient 3: Signs and symptoms of both fluid overload and shock. 5 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 6 3

4 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 7 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 8 4

5 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. 9 Classification of Heart Failure New York Heart Association Class I Class II Class III Class IV Cardiac disease no resulting limitation in physical activity. Cardiac disease with slight limitation of physical activity. Cardiac disease with marked limitation on physical activity. Cardiac disease resulting in inability to carry out any physical activity without discomfort. Ordinary activity free of fatigue, palpitation, dyspnea or anginal pain. Comfortable at rest but ordinary activity results in fatigue, palpitations, dyspnea, or anginal pain. Comfortable at rest but less than ordinary activity results in fatigue, palpitations, dyspnea, or anginal pain. May have symptoms of cardiac insufficiency at rest. 10 5

6 New York Heart Association Further Sub Classification Class IIIB Dyspnea with less than one block walking Class IV At rest With ADLs 11 Evaluation Guides Treatment Decisions Determine Volume Status Perfusion Status Role of / or presence of precipitating factors and/or comorbidities Ejection fraction HFPEF HFREF 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 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 14 7

8 Using Left Ventricular Function Curves to Drive Therapy 15 Hemodynamic and Clinical Subsets Forwards Flow: CI, Skin temp (warm or cold) Normal Hemodynamics (I) No pulmonary congestion: PWP < 18; Dry lungs No hypoperfusion: CI > 2.2; Warm skin Forwards Failure (III) No pulmonary congestion PWP < 18; Dry lungs Hypoperfusion CI < 2.2; Cold skin Backwards Failure (II) Pulmonary congestion PWP > 18; Wet lungs No hypoperfusion CI > 2.2; Warm skin The Shock Box (IV) Pulmonary congestion PWP > 18; Wet lungs Hypoperfusion CI < 2.2; Cold skin Preload: PWP, lung sounds (dry or wet) 16 8

9 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 Subset IV Reduce Afterload Hypoperfusion with Congestion 17 Left Ventricular Function Curves 5 4 Forwards flow: CI, skin temp (warm or cold) Preload: PAOP, SVV, lung sounds, S3, etc. ) 18 9

10 Changing Preload: Moves patient along the current curve Forwards Flow: Cardiac Index Skin temp (warm or cold) Preload 19 Changing Contractility: moves patient to a higher curve 5 4 CI Preload 20 10

11 Changing Afterload: Move patient up and to the left: improves forwards flow and reduces preload 5 Forwards Flow: Cardiac Index Skin temp (warm or cold) Must have adequate BP SVR must be elevated Preload 21 Acute Decompensated Heart Failure Reduce Preload Diuretics Loop Other Venous vasodilators Low dose Nitroglycerin Neseritide Ultrafiltration Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide Intra aortic balloon pump 22 Increase Contractility Positive Inotropes Dobutamine Milronone Dopamine 11

12 Changing Preload: Moves patient along the current curve Forward Flow: Cardiac Index Skin temp (warm or cold) Warm and Dry Preload Cold and Wet 23 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

13 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 25 Diuretics and Renal Function Role of venous congestion in worsening renal function Role of volume depletion / hypotension and worsening renal function 26 13

14 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) 27 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 28 14

15 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 29 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) 30 15

16 Vasodilator Therapy Preload Reduction Venous Vasodilators Afterload Reduction Arterial Vasodilators Three Primary Drugs NTG IV Primary Venous Vasodilator Neseritide Mixed Nitroprusside Predominantly ArterialVasodilator 31 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 32 16

17 Uses: Acute MI, unstable angina, CHF Side Effects: H/A, Hypotension, flushing Nitroglycerin 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 33 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 34 17

18 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 35 Nesiritide (Natrecor) Patient must have systolic BP > 90 mmhg 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

19 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: 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 difference. 37 ASCEND HF Trial Effect of Nesiritide in Patients with Acute Decompensated Heart Failure O'Connor et al. July ,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

20 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 Nitroprusside 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 39 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 40 20

21 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 Consider ultrafiltration Diuretic Resistance Reasons High sodium levels NSAIDs Severe renal impairment Renal hypoperfusion 41 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

22 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 Subset IV Reduce Afterload Hypoperfusion with Congestion 43 Changing Contractility: moves patient to a higher curve 5 4 CI Preload 44 22

23 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 Pharmacological Options for Increasing Contractility Inotrope is the termed used for medications used to increase contractility Sympathomimetics stimulating the β1 receptors of the sympathetic nervous system Phosodiesterase Inhibitors (PDE Inhibitors) Cardiac Glycoside Dobutamine: most commonly used because it is predominant beta one stimulator Other sympathomimetics may have inotropic properties even if not used primarily for an inotropic purpose Milrinone Is used as an intravenous inotrope but also has arterial vasodilator properties Digoxin weak inotrope and is never used intravenously to support left ventricular dysfunction. Exerts weak inotropic properties when given orally

24 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 47 Phosphodiesterase Inhibitors: Non Sympathomimetic Inotropes Used as an Inotrope Preload Reduction Also has BUT.. Afterload Reduction 48 24

25 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 49 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 50 25

26 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 51 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

27 53 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 Subset IV Reduce Afterload Hypoperfusion with Congestion 54 27

28 Changing Afterload: Move patient up and to the left: improves forwards flow and reduces preload 5 Forwards Flow: Cardiac Index Skin temp (warm or cold) Must have adequate BP SVR must be elevated Preload 55 Acute Decompensated Heart Failure Reduce Preload Diuretics Loop Other Venous vasodilators Low dose Nitroglycerin Neseritide Ultrafiltration Reduce Afterload Arterial vasodilators High dose Nitroglycerin Nitroprusside Neseritide Intra aortic balloon pump 56 Increase Contractility Positive Inotropes Dobutamine Milronone Dopamine 28

29 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 filed for CE Mark approval Feb 25, 2013 Breakthrough therapy designation by FDA June Additional Care Issues 58 29

30 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 59 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 60 30

31 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 61 Oxygen BiPap/CPAP 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

32 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 63 Mechanical Circulatory Support in ADHF Bridge to transplant (BBT) for those who are transplant eligible Destination therapy (DT) for those who are not transplant eligible. 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 64 32

33 65 Intra Aortic Balloon Pump Most often 1 st step in cardiogenic shock treatment Minimially invasive The IAB is a volume displacement device Decreases LV afterload Increases coronary perfusion 66 33

34 Impella Bridge to Recovery 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 34

35 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 69 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 70 35

36 I m not telling you it is going to be easy, I m telling you it is going to be worth it. ~ Art Williams 71 BE THE BEST THAT YOU CAN BE EVERY DAY. YOUR PATIENTS ARE COUNTING ON IT! 72 36

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