David S. Roffman, PharmD, BCPS/AQ Cardiology Professor Pharmacy Practice and Science

Management of Acute Decompensated Heart Failure

Washington Metropolitan Society of Health-System Pharmacists

September 28, 2013Rockville Maryland

David S. Roffman, PharmD, BCPS/AQ CardiologyProfessor

Pharmacy Practice and ScienceSchool of Pharmacy

University of Maryland

Financial Disclosures for David S. Financial Disclosures for David S. Roffman, PharmDRoffman, PharmD

Nothing to discloseNothing to disclose

Learning Objectives

At the completion of the lecture, the participants will be able to:

1. Describe the typical presentation of acute decompensated heart failure (ADHF)2. List the therapeutic objectives associated with pharmacologic therapy for ADHF3. State the indications, adverse effects, and monitoring parameters for the use of inotropes, vasodilators, pressors, and loop diuretics in the treatment of ADHF

4. Describe emerging pharmacotherapeutic options for ADHF

2013 ACCF/AHA Guideline for the Management of Heart Failure

A Report of the American College of Cardiology A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Foundation/American Heart Association Task Force on

Practice GuidelinesPractice Guidelines

Heart Failure GuidelinesHeart Failure Guidelines

http://circ.ahajournals.org/content/early/2013/06/03/CIR.0b013e31829e8776.citation

Class IClass I Benefit >>> RiskBenefit >>> Risk

Procedure/ Procedure/ Treatment Treatment SHOULD SHOULD be be performed/ performed/ administeredadministered

Class IIaClass IIa Benefit >> RiskBenefit >> RiskAdditional studies Additional studies with focused with focused objectives neededobjectives needed

IT IS REASONABLE IT IS REASONABLE to perform to perform procedure/administeprocedure/administer treatmentr treatment

Class IIbClass IIb Benefit ≥ RiskBenefit ≥ RiskAdditional studies Additional studies with broad objectives with broad objectives needed; Additional needed; Additional registry data would registry data would be helpfulbe helpful

Procedure/Treatment Procedure/Treatment MAY BE MAY BE CONSIDERED CONSIDERED

Class IIIClass III Risk ≥ BenefitRisk ≥ BenefitNo additional studies No additional studies neededneeded

Procedure/Treatment Procedure/Treatment shouldshould NOT NOT be be performed/administeperformed/administeredred SINCE IT IS SINCE IT IS NOT HELPFUL AND NOT HELPFUL AND MAY BE HARMFULMAY BE HARMFUL

Level A:Level A: Data derived from multiple randomized clinical trials or meta-analyses Data derived from multiple randomized clinical trials or meta-analyses

Multiple populations evaluatedMultiple populations evaluated

Level B:Level B: Data derived from a single randomized trial or nonrandomized studies Data derived from a single randomized trial or nonrandomized studies

Limited populations evaluatedLimited populations evaluated

Level C:Level C: Only consensus of experts opinion, case studies, or standard of care Only consensus of experts opinion, case studies, or standard of care

Very limited populations evaluatedVery limited populations evaluated

Applying Classification of Recommendations and Level of Evidence

Level of Evidence:

Definitions of HFrEF and HFpEF


Clinical Profiles of Hospitalized HF Patients

Volume overloadVolume overload– pulmonary/systemic vascular pulmonary/systemic vascular

congestioncongestion– precipitated by acute BP increaseprecipitated by acute BP increase

Profound depression of COProfound depression of CO– hypotensionhypotension– renal insufficiencyrenal insufficiency– shock syndromeshock syndrome

Signs/symptoms of bothSigns/symptoms of both

The diagnosis of heart failure is primarily based on signs and symptoms derived from a thorough history and physical exam. Clinicians should determine the following:

a. adequacy of systemic perfusion;b. volume status;c. the contribution of precipitating factors and/or co-morbidities d. if the heart failure is new onset or an exacerbation of chronic disease; ande. whether it is associated with preserved, normal, or reduced ejection fraction.

Chest radiographs, echocardiogram, and echocardiography are key tests in this assessment.

The Hospitalized Patient

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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIIIDiagnosis of HF

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII

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It is recommended that the following common potential precipitating factors for acute HF be identified as recognition of these comorbidities, is critical to guide therapy:

• acute coronary syndromes/coronary ischemia• severe hypertension• atrial and ventricular arrhythmias• infections• pulmonary emboli• renal failure• medical or dietary noncompliance


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III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII Precipitating Factors for Acute HF

Concentrations of BNP or NT-proBNP should be measured in patients being evaluated for dyspnea in which the contribution of HF is not known. Final diagnosis requires interpreting these results in the context of all available clinical data and ought not to be considered a stand-alone test.


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Acute coronary syndrome precipitating HF hospitalization should be promptly identified by electrocardiogram and cardiac troponin testing, and treated, as appropriate to the overall condition and prognosis of the patient.


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Patients Being Evaluated for Dyspnea

Therapeutic Objectives for Acute Decompensated Heart

Failure Improve survival?Improve survival? Resolve pulmonary vascular Resolve pulmonary vascular

congestioncongestion Preserve end organ performancePreserve end organ performance Achieve previous baseline heart failure Achieve previous baseline heart failure

status (NYHA Classification)status (NYHA Classification) Reduce the risk of rehospitalizationReduce the risk of rehospitalization

Recommended Therapies for Hospitalized HF Patients


Recommended Therapies for Hospitalized HF Patients


Patients admitted with HF and with evidence of significant fluid overload should be treated with intravenous loop diuretics. Therapy should begin in the emergency department or outpatient clinic without delay, as early intervention may be associated with better outcomes for patients hospitalized with decompensated HF (Level of Evidence: B).

If patients are already receiving loop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose. Urine output and signs and symptoms of congestion should be serially assessed, and diuretic dose should be titrated accordingly to relieve symptoms and to reduce extracellular fluid volume excess. (Level of Evidence: C).

The Hospitalized Patient Treatment With Intravenous Loop Diuretics


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Diuretic Therapy in ADHF

Hunt et.al. 2009. J Am Coll Cardiol 53;15:1-90



Intensifying the Diuretic Regimen

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When diuresis is inadequate to relieve congestion, as evidence by clinical evaluation, the diuretic regimen should be intensified using either:

a. higher doses of loop diuretics;b. addition of a second diuretic (such

as metolazone, spironolactone or intravenous chlorthiazide) or

c. Continuous infusion of a loop diuretic.

Ultrafiltration is reasonable for patients with refractory congestion not responding to medical therapy.


III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIIIIntravenous inotropic drugs such as dopamine, dobutamine or milrinone might be reasonable for those patients presenting with documented severe systolic dysfunction, low blood pressure and evidence of low cardiac output, with or without congestion, to maintain systemic perfusion and preserve end-organ performance.

Ultrafiltration and Intravenous Inoptropic Drugs

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Effect of HF treatment should be monitored with careful measurement of fluid intake and output; vital signs; body weight, determined at the same time each day; clinical signs (supine and standing) and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of intravenous diuretics or active titration of HF medications.



Monitoring and Measuring Fluid Intake and Output

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Diuretic Strategies in Patients with Acute Decompensated

Heart Failure

A. A. Bolus dosing more effectiveB. Continuous infusion more effectiveC. Higher dose more effective than lower doseD. Both B and C are correct

Diuretic Strategies in Patients with Acute Decompensated

Heart Failure

In a prospective, double-blind, randomized trial, we assigned 308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high dose (2.5 times the previous oral dose). The protocol allowed specified dose adjustments after 48 hours. The co-primary end points were patients’ global assessment of symptoms, quantified as the area under the curve (AUC) of the score on a visual-analogue scale over the course of 72 hours, and the change in the serum creatinine level from baseline to 72 hours.

Felker GM, Lee KL, Bull DA, et.al., N Engl J Med 2011;364:797-805


Diuretic Strategies in Patients with Acute Decompensated Heart Failure









Fluid and Sodium Restriction in Acute Decompensated Heart

Failure

Fluid and sodium restriction in Fluid and sodium restriction in ADHF patients improves weight loss ADHF patients improves weight loss and clinicaal stability in and clinicaal stability in hospitalized ADHF patientshospitalized ADHF patients

– A. TrueA. True– B. FalseB. False

Aggressive Fluid and Sodium Restrictionin Acute Decompensated Heart Failure

A Randomized Clinical Trial

To compare the effects of a fluid-restricted To compare the effects of a fluid-restricted (maximum fluid intake, 800 mL/d) and sodium (maximum fluid intake, 800 mL/d) and sodium restricted (maximum dietary intake, 800 mg/d) restricted (maximum dietary intake, 800 mg/d) diet (intervention group [IG]) vs. a diet with no diet (intervention group [IG]) vs. a diet with no such restrictions (control group [CG]) on weight such restrictions (control group [CG]) on weight loss and clinical stability during a 3-day period loss and clinical stability during a 3-day period in patients hospitalized with ADHFin patients hospitalized with ADHF

JAMA Intern Med. 2013;173(12):1058-1064



JAMA Intern Med. 2013;173(12):1058-1064



JAMA Intern Med. 2013;173(12):1058-1064



JAMA Intern Med. 2013;173(12):1058-1064


In all patients hospitalized with HF, both with preserved and low ejection fraction, transition should be made from intravenous to oral diuretic therapy with careful attention to oral diuretic dosing and monitoring of electrolytes. With all medication changes, the patient should be monitored for supine and upright hypotension and worsening renal function and HF signs/symptoms.


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Invasive hemodynamic monitoring should be performed to guide therapy in patients who are in respiratory distress or with clinical evidence of impaired perfusion in whom the adequacy or excess of intracardiac filling pressures cannot be determined from clinical assessment.

In patients with clinical evidence of hypotension associated with hypoperfusion and obvious evidence of elevated cardiac filling pressures (e.g., elevated jugular venous pressure; elevated pulmonary artery wedge pressure), intravenous inotropic or vasopressor drugs should be administered to maintain systemic perfusion and preserve end-organ performance while more definitive therapy is considered.




Preserving End-Organ Performance

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Intravenous Inotropic Agents Used in ADHF


Inotropic Support in Acute Heart Failure

In the presence of significant In the presence of significant hypotension, dopamine may enhance hypotension, dopamine may enhance both blood pressure and peripheral both blood pressure and peripheral organ perfusion.organ perfusion.

Dopamine, in pressor doses (greater Dopamine, in pressor doses (greater than 5 mcg/kg/min), increases than 5 mcg/kg/min), increases myocardial oxygen demand and myocardial oxygen demand and potentially limits augmentation of potentially limits augmentation of peripheral perfusion via peripheral peripheral perfusion via peripheral vasoconstrictionvasoconstriction

Issues with Intravenous Inotropes

Initial choice of therapyInitial choice of therapy WeaningWeaning Patient related variablesPatient related variables Differences in efficacyDifferences in efficacy Adverse effect profileAdverse effect profile Survival dataSurvival data ““Long-term” infusionsLong-term” infusions

Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptoms despite empiric adjustment of standard therapies, and

a. whose fluid status, perfusion, or systemic orpulmonary vascular resistances are uncertain;b. whose systolic pressure remains low, pr is associated with symptoms, despite initialtherapy;c. whose renal function is worsening with therapy;d. who require parenteral vasoactive agents; ore. who may need consideration for advanced device therapy or transplantation.


I IIa IIb IIIInvasive Hemodynamic Monitoring

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Routine use of invasive hemodynamic monitoring in normotensive patients with acute decompensated HF and congestion with symptomatic response to diuretics and vasodilators is not recommended.

Use of parenteral inotropes in normotensive patients with acute decompensated HF without evidence of decreased organ perfusion is not recommended.


III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIII

III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIII

Parenteral Inotropes

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Vasodilator Support in Acute Heart Failure

Nitroglycerin, nitroprusside, and Nitroglycerin, nitroprusside, and nesiritide, have been demonstrated nesiritide, have been demonstrated to improve symptoms and to improve symptoms and hemodynamics in acute heart hemodynamics in acute heart failure.failure.


Nitroprusside infusions (initial Nitroprusside infusions (initial dose 0.1 mcg/kg/min) improve dose 0.1 mcg/kg/min) improve symptoms of pulmonary symptoms of pulmonary congestion, and signs of congestion, and signs of peripheral perfusion.peripheral perfusion.

Titration of infusion rate is initailly Titration of infusion rate is initailly based on invasive hemodynamic based on invasive hemodynamic monitoring.monitoring.


Nitroprusside patient variables:Nitroprusside patient variables:– Chronic liver diseaseChronic liver disease– Renal insufficiencyRenal insufficiency– Blood pressureBlood pressure– Malnourished patientsMalnourished patients


Nitroprusside toxicities:Nitroprusside toxicities:– Cyanide intoxication: metabolic Cyanide intoxication: metabolic

acidosisacidosis– Thiocyanate toxicity: Hyper-reflexia, Thiocyanate toxicity: Hyper-reflexia,

seizures, altered mental status. seizures, altered mental status. Serum concentration assay availableSerum concentration assay available


Nitroglycerin infusion may be Nitroglycerin infusion may be preferred in patients an active or preferred in patients an active or recent history of ischemia.recent history of ischemia.

Nitroglycerin is a less potent Nitroglycerin is a less potent arteriolar dilator than arteriolar dilator than nitroprussidenitroprusside


Nesiritide is a brain naturetic peptide (BNP) Nesiritide is a brain naturetic peptide (BNP) which has significant vasodilator effects.which has significant vasodilator effects.

Dosing regimen, 0.2 mcg/kg bolus followed Dosing regimen, 0.2 mcg/kg bolus followed by 0.01 mcg/kg/min continuous infusionby 0.01 mcg/kg/min continuous infusion

Reduces LV filling pressure, variable effect on Reduces LV filling pressure, variable effect on CO, urine output, sodium excretionCO, urine output, sodium excretion

Better than diuretics for dyspneaBetter than diuretics for dyspnea Longer t ½ than nitroglycerin or Longer t ½ than nitroglycerin or

nitroprussidenitroprusside Adverse renal outcomesAdverse renal outcomes

History of New Treatments in ADHF

1988: Milrinone approved based 1988: Milrinone approved based on small hemodynamic studieson small hemodynamic studies

2000: Levosimendan approved in 2000: Levosimendan approved in Sweden then 40 countriesSweden then 40 countries

2001: Nesiritide based on 489 2001: Nesiritide based on 489 patient VMAC trialpatient VMAC trial

Research on Drugs for Acute Heart Failure

PubMed search for “heart failure” (19,154)/”randomized controlled trials”(2176)/”acute disease”(61) for novel, intravenous treatments for acute heart failure

Search results: Levosimendan, nesiritide, rolofylline, tezosentan

Levosimendan (REVIVE I and II)

700 patients, placebo controlled700 patients, placebo controlled Primary endpoint: Clinical Primary endpoint: Clinical

composite based on patient composite based on patient global assessment during first 5 global assessment during first 5 days of treatment (positive)days of treatment (positive)

Increased ventricular/atrial Increased ventricular/atrial arrhythmias, symptomatic arrhythmias, symptomatic hypotension, early mortalityhypotension, early mortality

JCHF. 2013;1(2):103-111. doi:10.1016/j.jchf.2012.12.004

Levosimendan vs. Dobutamine (SURVIVE)

1327 patients1327 patients Primary endpoint: All cause Primary endpoint: All cause

mortality at 180 days not mortality at 180 days not achievedachieved

No secondary endpoints achievedNo secondary endpoints achieved Decreased BNPDecreased BNP

JAMA. 2007 May 2;297(17):1883-91

Nesiritide (ASCEND-HF)

Placebo controlled post approval Placebo controlled post approval trialtrial

Prespecified primary endpoint Prespecified primary endpoint (dyspnea relief) not met(dyspnea relief) not met

No beneficial effect on hospital No beneficial effect on hospital readmisiion, all-cause mortality, readmisiion, all-cause mortality, worsening renal functionworsening renal function

N Engl J Med 2011;365:32-43

Rolofylline (Protect)

2033 patients2033 patients Failed to meet primary clinical Failed to meet primary clinical

composite endpointcomposite endpoint No reduction in hospital No reduction in hospital

readmissionsreadmissions Complicated by seizures and Complicated by seizures and

strokestrokeN Engl J Med 2010; 363:1419-28

Tezosentan (VERITAS)

1448 patients1448 patients No improvement in dyspneaNo improvement in dyspnea No improvement in worsening No improvement in worsening

heart failure or death at 7 daysheart failure or death at 7 days No improvement in renal function, No improvement in renal function,

hospital readmission or mortalityhospital readmission or mortality

JAMA 2007;298:2009-19

Medications should be reconciled in every patient and adjusted as appropriate on admission to and discharge from the hospital.



In patients with reduced ejection fraction experiencing a symptomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blocker therapy, it is recommended that these therapies be continued in most patients in the absence of hemodynamic instability or contraindications.


Reconciling and Adjusting Medications

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Serelaxin

Recombinant human relaxin-2 (peptide that regulates maternal adaptations to pregnancy)

Increased arterial compliance, cardiac output, renal blood flow.

Suggested benefit on dyspnea and post-discharge clinical outcomes in patients admitted with evidence of congestion, normal to elevated blood pressure, mild to moderate renal dysfunction.

Serelaxin (RELAX-AHF)

Prospective, randomized, double-blind, Prospective, randomized, double-blind, placebo-controlled, parallel group trial placebo-controlled, parallel group trial 1161 patients comparing serelaxin to 1161 patients comparing serelaxin to placebo.placebo.

The RELAX-AHF trial tested the hypothesis that serelaxin-treated patients would have greater dyspnea relief compared with patients treated with standard care and placebo

Lancet 2013; 381: 29–39

Serelaxin (RELAX-AHF)Inclusion Criteria

Acute heart failure within past 16 hours, Acute heart failure within past 16 hours, Dyspnea at rest or minimal exertionDyspnea at rest or minimal exertion

Pulmonary congestion on CXRPulmonary congestion on CXR BNP BNP >> 350 ng/L, NT-proBNP > 1400

ng/L GFR 30 – 75 ml/min/1.73 m2

Systolic BP > 125 mm Hg Treated with > 40 mg iv furosemide

Lancet 2013; 381: 29–39

RELAX-AHF Trial

RELAX-AHF Trial

Lancet 2013; 381: 29–39

RELAX-AHF Trial

Lancet 2013; 381: 29–39

Serelaxin

June 2013: FDA grants serelaxin “breakthrough-June 2013: FDA grants serelaxin “breakthrough-therapy” designation based on RELAX-HF Trialtherapy” designation based on RELAX-HF Trial

Breakthrough designation therapy reserved for Breakthrough designation therapy reserved for the development or review of drugs seen as the development or review of drugs seen as poteentiaal game changers for serious and life-poteentiaal game changers for serious and life-threatening conditions that have preliminary threatening conditions that have preliminary evidence in at least one clinically significant evidence in at least one clinically significant endpoint over other available therapiesendpoint over other available therapies

Other Investigational Drugs for AHF

TRV027– Β-arrestin-biased AT1R ligand, competitively inhibits G-protein

signaling– Reduces MAP, increases cardiac contractility, maintains stroke

volume, preserves GFR– Anti-apoptotic effect

Ularitide– Synthetic foem of urodilatin (naturetic peptide produced by

kidneys)– Binds to specific naturetic peptide receptors, imcreasing

intracellular cyclic GMP– Relaxes smooth muscle cells, vasodilation and increased renal

blood flow– Ongoing TRUE-AHF study: Symptoms, HF improvement, and

death

Other Investigational Drugs for AHF

Omecamtiv mecarbil– Selective cardiac myosin activator– ATOMIC-AHF was a randomized, double-blind, placebo-controlled Phase ATOMIC-AHF was a randomized, double-blind, placebo-controlled Phase

II clinical trial that enrolled 613 patients hospitalized with acute heart II clinical trial that enrolled 613 patients hospitalized with acute heart failure (AHF) treated for 48 hours with an intravenous formulation of failure (AHF) treated for 48 hours with an intravenous formulation of omecamtiv mecarbil or placebo and designed to evaluate the safety, omecamtiv mecarbil or placebo and designed to evaluate the safety, pharmacokinetics, pharmacodynamics, and potential efficacy of pharmacokinetics, pharmacodynamics, and potential efficacy of omecamtiv mecarbil in patients with AHFomecamtiv mecarbil in patients with AHF

– The primary efficacy endpoint of dyspnea symptom response was not The primary efficacy endpoint of dyspnea symptom response was not met; favorable trends between the dose and plasma concentration of met; favorable trends between the dose and plasma concentration of omecamtiv mecarbil and dyspnea response. The incidence of worsening omecamtiv mecarbil and dyspnea response. The incidence of worsening heart failure within seven days of initiating treatment appeared lower in heart failure within seven days of initiating treatment appeared lower in each of the cohorts on omecamtiv mecarbil. Rates of adverse events each of the cohorts on omecamtiv mecarbil. Rates of adverse events (AEs), serious AEs, adjudicated deaths and hospitalizations were similar (AEs), serious AEs, adjudicated deaths and hospitalizations were similar between omecamtiv mecarbil and placebo groups. Omecamtiv mecarbil between omecamtiv mecarbil and placebo groups. Omecamtiv mecarbil was not associated with an increased incidence of tachyarrhythmias nor was not associated with an increased incidence of tachyarrhythmias nor were heart rate or blood pressure adversely affected.were heart rate or blood pressure adversely affected.

Continuation of Outpatient ACE/ARB Therapy

Blood pressureBlood pressure Renal functionRenal function Volume dependencyVolume dependency Substitution of Substitution of

hydralazine/nitrateshydralazine/nitrates

Beta Blocker Use in ADHFBeta Blocker Use in ADHF

Foranow GC. J Am Coll Cardiol 2008;52:190-9

Beta Blockers in Acute Decompensated Heart Failure

Foranow GC. J Am Coll Cardiol 2008;52:190-9

The Hospitalized PatientIn patients hospitalized with HF with reduced ejection fraction not treated with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blocker therapy, initiation of these therapies is recommended in stable patients prior to hospital discharge.

Initiation of beta-blocker therapy is recommended after optimization of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stable patients. Particular caution should be used when initiating beta-blockers in patients who have required inotropes during their hospital course.


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In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such as intravenous nitroglycerin, nitroprusside or neseritide can be beneficial when added to diuretics and/or in those who do not respond to diuretics alone.

The Hospitalized Patient Severe Symptomatic Fluid Overload

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I IIa IIb III


Comprehensive written discharge instructions for all patients with a hospitalization for HF and their caregivers is strongly recommended, with special emphasis on the following 6 aspects of care: diet, discharge medications, with a special focus on adherence, persistence, and uptitration to recommended doses of ACE inhibitor/ARB and beta-blocker medication, activity level, follow-up appointments, weight monitoring, and what to do if HF symptoms worsen.


Reconciling and Adjusting Medications

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Recommendations for Hospital Discharge


Improvement of Guideline Beta-Blocker Improvement of Guideline Beta-Blocker Prescribing in Heart Failure: A Cluster-Prescribing in Heart Failure: A Cluster-

Randomized Pragmatic Trial of a Pharmacy Randomized Pragmatic Trial of a Pharmacy InterventionIntervention

We conducted a pragmatic cluster-randomized trial, where facilities (n 5 12) with patients (n 5 220) were the clusters. Eligible patients had a beta-blocker prescription that was not guideline concordant. Level 1 intervention included information to a pharmacist on facility guideline concordance. Level 2 also provided a list of patients not meeting guideline goals. Intervention and follow-up periods were each 6 months. Achievement of full concordance with recommendations was low (4%e5%) in both groups, primarily due to lack of tolerability. However, compared with level 1, the level 2 intervention was associated with 1.9-fold greater odds of improvement in prescribing (95% confidence interval [CI] 1.1e3.2). Level 2 patients also had greater odds of a higher dose (1.9, 95% CI 1.1e3.3). The intervention was aided by the patient lists provided, the electronic medical record system, and staff support..

Journal of Cardiac Failure Vol. 19 No. 8 2013

Acute Decompensated Heart Failure

Few well controlled trialsFew well controlled trials Little data to demonstrate Little data to demonstrate

improved morbidity/mortalityimproved morbidity/mortality Need for newer, more effective, Need for newer, more effective,

lower ADR-inducing agentslower ADR-inducing agents

Documents

David S. Roffman, PharmD, BCPS/AQ Cardiology Professor Pharmacy Practice and Science