management of acute heart failure and cardiogenic shock · 2018-04-03 · management of acute heart...

2/29/2016

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Management of Acute Heart Failure and Cardiogenic Shock

www.fshp.org

Brittany D. Bissell, Pharm.D.PGY-2 Critical Care Pharmacy Resident

Jackson Memorial Hospital | Miami, Florida

DISCLOSURE STATEMENT

I have no actual or potential conflicts of interest in relation to this presentation.

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TECHNICIAN OBJECTIVES

• Explain management principles for left ventricular failure

• Describe treatment options for end-stage heart failure

• List pharmacologic therapies for cardiogenic shock

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PHARMACIST OBJECTIVES

• Assess the hemodynamic dysregulation implicated in the pathophysiology of heart failure

• Develop recommendations for preload optimization

• Investigate evidence for current options for the management of cardiogenic shock

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PATHOPHYSIOLOGY OF

ACUTE HEART FAILURE

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Afterload mismatch

Insulting Event

PATHOPHYSIOLOGY

Fluid Overload

Neurohormonal Activation

Diastolic Dysfunction

Afterload Mismatch

Cotter, et al. Am Heart J. 2008;155(1):9-18.

• Cardiac changes– Decreased stroke volume (SV)

– Increased end-diastolic pressure

• Vascular changes– Increased systemic vascular resistance

– Increased venous pressure

– Decreased arterial pressure

– Decreased compliance

HEMODYNAMIC DYSREGULATION

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CARDIAC PHYSIOLOGY

Sinoatrial node automaticity

Vagal innervation

Sympathetic activity and catecholamines8

Inotropy: Contractile force

Afterload: Resistance against ejection

Preload: Pre-contraction stretch of cardiac myocyte

Heart Rate Stroke Volume

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IMPROVING STROKE VOLUME

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Decreased Afterload↓ Systemic vascular resistance↓Aortic pressure

Increased Preload

↑Aortic Pressure↓ Heart Rate ↑Atrial Contractility ↑ Central Venous Pressure↑ Ventricular Compliance

Increased Inotropy

↑ Catecholamines↓ Vagal Inhibition↑ Sympathetic Activation↑Afterload↑ Heart Rate

EDV = End Diastolic Volume | ESV = End Systolic Volume

CARDIAC FUNCTION PARAMETERS

• Central venous pressure (CVP)

– Representative of right ventricular end diastolic pressure / preload

– Normal: 2 - 6 mmHg

• Cardiac index (CI)

– Correction of cardiac output for body surface area

– Normal: 2.5 - 4.0 L/min/m2

• Systemic vascular resistance index (SVRI)

– Resistance of blood flow by systemic vasculature corrected for surface area

– Normal: 800 - 1200 dynes - sec/cm-5

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ACUTE MANAGEMENT

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Preload optimization

Afterload optimization

Inotropic support

Congestion

Poor Systemic Perfusion

• Jugular vein distension• Hepatomegaly• Peripheral edema• Pulmonary edema

• Cold extremities• Alteration in mental status• Decreased urine output• Elevated lactate

Patient Evaluation

Mebazza, et al. Intensive Care Med. 2016 Feb;42(2):147-63.

ACUTE MANAGEMENT

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ACUTE HEART FAILURE

CONGESTION CONGESTION & LOW OUTPUT

MILDMODERATE-

SEVERE

SBP >90 SBP <90

DobutamineVasopressors

MilrinoneDobutamine

IV furosemide Furosemide infusion

plus nitroglycerin

Howlett. Can J Cardiol. 2011;27(3):284-95.

MILD-MODERATE

SEVERE

Consider PA line

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PRELOAD

OPTIMIZATION

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OPTIMIZATION OF PRELOAD

DIURETICS DOPAMINEHYPERTONIC

SALINEULTRAFILTRATION

LOOP DIURETIC RESISTANCE

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Ter Maaten, et al. Nat Rev Cardiol. 2015;12(3):184-92.

Alternative therapies

DIURETIC RESISTANCE MANAGEMENT

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DOSE: No differences in responsewith continuous infusion

Dose-dependent mortality with furosemide over 300 mg

Diuretic Response0.5 L net fluid outputOr 0.4 kg weight loss

HYPERTONIC

SALINEDOPAMINE ULTRAFILTRATION


LOOP DIURETIC

INTRAVENOUS LOOP

ALTERNATIVE LOOP

COMBINATION

THERAPY

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CHOICE OF DIURETIC

STANDARD THERAPY = FUROSEMIDE

TORSEMIDE

• Liver clearance and increased bioavailability

• Correction of collagen cross-linking and left ventricular stiffness

• Decreased sympathetic nerve response and remodeling

• Significant improvement in NYHA class compared to furosemide

• Decreased mortality compared to furosemide

Ter Maaten, et al. Nat Rev Cardiol. 2015;12(3):184-92.Di Somma, et al. Rev Esp Cardiol. 2015;68(8):706-13.

COMBINATION THERAPY

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DOPAMINE

•5 mcg/kg/min with furosemide 5 mg/hour•As effective as furosemide 20 mg/hour with decrease in worsened renal function

DAD-HF

•2 mcg/kg/minute•No effect on urine volume or cystatin C

ROSE

•5 mcg/kg/minute•No difference in urine output or mortality

DAD-HF II

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HYPERTONIC SALINE

• Mobilization of extravascular fluid into the intravascular space

• Increases cardiac output, renal blood flow, and quick excretion

• SMAC-HF Trial

– 150 mL of hypertonic saline twice daily

– Increased diuresis

– Decreased creatinine

– Reduction in hospitalization and readmission

– Decreased mortality

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ULTRAFILTRATION

RAPID-CHF

• 8 hour ultrafiltration versus pharmacologic treatment

• Increased fluid removal

• No difference in 24-hour weight loss

UNLOAD

• Ultrafiltration versus intravenous diuretics

• Increased fluid removal

• No difference in dyspnea

• Decrease in rehospitalization and hospital visits

CARRESS-HF

• Fixed-rate ultrafiltration versus stepwise diuretics

• Increased serum creatinine

• Increased adverse events

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Semipermeable membrane yields iso-osmotic ultrafiltrate

Added benefit of removal of myocardial depressant cytokines


AFTERLOAD

OPTIMIZATION

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OPTIMIZATION OF AFTERLOAD

NITRATES NESIRITIDE CLEVIDIPINE

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NITRATE THERAPY

Nitroglycerin

•5- 200 mcg/min

•Primarily venodilation with coronary vasodilation

•Decreased rates of endotracheal intubation and ICU admission

•Tachyphylaxis problematic

Nitroprusside

•0.25 - 3 mcg/kg/min

•Primarily arterial with some venous vasodilation

•Retrospective study evidence

•Concern in renal dysfunction


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NESIRITIDE

– Arterial and venous vasodilation with natriuretic effects

– Significant improvement in cardiac output and dyspnea

– Increased short-term mortality and symptomatic hypotension

CLEVIDIPINE

– Selective arterial vasodilation

– 2 - 32 mg/hour

– Rapid reduction in blood pressure without worsening of heart failure

– Higher rates of target blood pressure and dyspnea improvement compared to standard of care

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NITRATE ALTERNATIVES

Mebazza, et al. Intensive Care Med. 2016 Feb;42(2):147-63.Di Somma, et al. Rev Esp Cardiol. 2015;68(8):706-13.

INOTROPIC SUPPORT

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CARDIOGENIC SHOCK

• Less than 5% of acute heart failure cases

• 80% of cases secondary to acute coronary syndromes with or without mechanical complications

• 40% short-term mortality rates

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ACUTE MANAGEMENT

CARDIOGENIC

SHOCK

CATH LAB OR

SURGERY

RESPIRATORY

DISTRESSHYPOPERFUSION

NONINVASIVE

VENTILATION

INVASIVE

MONITORING

INOTROPES ±VASOPRESSORS

MECHANICAL

SUPPORT

RENAL

REPLACEMENT

INVASIVE

VENTILATION

IDENTIFY CAUSE


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POSITIVE PRESSURE VENTILATION

• Decreased …

– Transthoracic pulmonary pressure decreases LV afterload

– Venous return decreases preload

– Breathing efforts decreases metabolic demand

– Hypoxia decreases pulmonary vasoconstriction

• Studies show increased cardiac output, decreased pulmonary pressures, improved oxygenation, increased ventilator weaning, and increased survival

BIPAP CPAP INVASIVE

Positive end-expiratory pressure (PEEP) = Aveolar pressure above atmospheric pressure after expiration

Wiesen, et al. Heart. 2013;99(24):1812-7.

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INOTROPIC SUPPORT

DOPAMINE DOBUTAMINE MILRINONE

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DOSE-DEPENDENCY OF DOPAMINE

Low doses (<5 mcg/kg/minute) vasodilate, including coronary and renal arteries

• Increased renal perfusion not seen in cohort studies

Intermediate doses (5 - 10 mcg/kg/minute) produce inotropic and chronotropic effects

High doses (>10 mcg/kg/minute) induce vasoconstriction and increases in afterload

Tariq, et al. Int J Mol Sci. 2015;16(12):29060-8.

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DOPAMINE


1679 patients receiving dopamine 2– 20 mcg/kg/minute or norepinephrine 0.02-0.19 mcg/kg/minute for shock

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DOBUTAMINE

• Dose range: 5-20 mcg/kg/minute

• β effects improve myocardial contractility and output

• Increased left ventricular end diastolic pressure

• May induce hypotension

• Risk of eosinophilic myocarditis and arrhythmias

• Increased myocardial oxygen demand


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MILRINONE

Inhibits phosphodiesterase-3, preventing cAMP degradation

Positive inotrope activity independent of β stimulation

Reduction of pulmonary artery pressure

Significantly higher rates of hypotension compared to placebo

Dose range: 0.25 - 0.75 mcg/kg/min


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MILRINONE

Felker, et al. . J Am Coll Cardiol. 2003;41(6):997-1003

949 patients receiving milrinone or placebo for

48-72 hours

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MILRINONE

Abraham, et al. J Am Coll Cardiol. 2005;46(1):57-64.

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MECHANICAL

CIRCULATORY SUPPORT

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MECHANICAL CIRCULATORY SUPPORT

INTRA-AORTIC

BALLOON PUMP

(IABP)

VENTRICULAR

ASSIST DEVICE

(VAD)

EXTRACORPOREAL

MEMBRANE

OXYGENATION

(ECMO)

Inflation facilitates coronary perfusion with increased diastolic pressure

Deflation augments left ventricular (LV) ejection through negative pressure

MECHANICAL CIRCULATORY SUPPORT

Long-term support of cardiac output

Blood removed from left ventricle and returned to ascending aorta

Pulmonary artery return for right ventricular support

Extracorporeal controller and power supply

Blood removed from femoral vein or inferior vena cava

Blood returned to right heart or femoral artery

Separate modes for goal outcomes

Subramaniam, et al. Best Pract Res Clin Anaesthesiol. 2015;29(2):203-27.Pratt, et al. Crit Care Med. 2014; 42:158–168Russell, et al. Circulation. 2009;120(23):2352-7.

IABP INDICATIONS FOR USE

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Acute Coronary Syndromes•Cardiogenic shock in STEMI

•High-risk PCI or CABG

•STEMI and NSTEMI complications

•Refractory angina

Ventricular Arrhythmias

Refractory Heart Failure

Ihdayhid, et al. Curr Opin Cardiol. 2014, 29:285–292

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ANTICOAGULATION WITH IABP

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•Randomized controlled trial

•Heparin vs. placebo

•Ischemia 0.2 vs. 2.4%

•Bleeding 14.2 vs. 2.4%

2003

•Prospective cohort

•Heparin vs. selective

•Ischemia 0.5 vs. 0%

•Bleeding 38.5 vs. 25.4%

2008 •Retrospective study

•No anticoagulation

•Ischemia 3.4%

•Bleeding 4.2%

2012

Anticoagulation warranted for primary indications

Jiang, et al. J Zhejiang Univ Sci. 2003;4:607–11Cooper, et al. Acute Cardiac Care. 2008;10:214–20Kogan, et al. J Card Surg. 2012;27:434-437

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7 - Advanced NYHA III

6 - Exertion limited

5 - Exertion intolerant

4 - Resting symptoms

3 - Inotrope dependent

2 - Progressive decline

1 - Critical cardiogenic shock

Definitive Therapy Required

Months

Hours

Days

Feldman, et al. JHLT. 2013;32:157–187

INTERMACS HEART FAILURE PROFILES

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MECHANICAL SUPPORT

Kirklin, et al. JHLT. 2014 ; 33(10): 996-1008

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CRITERIA FOR IMPLANTATION

Peak oxygen consumption <14

mL/kg/minor

Inability to perform exercise

test

NYHA functional class IV

Left ventricular ejection fraction

<25%

Failed optimal management for

45/60 days or

7 days IABP-dependent or

14 days inotrope-dependent

Kirklin, et al. J Heart Lung Transplant. 2014;33:555–564

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MECHANICAL SUPPORT

Destination

Therapy (DT)

HEARTMATE II• Axial flow• Mechanical bearings• Larger in size• FDA approved for BTT: 75-90%

survival• FDA approved for DT: 58-61% survival• Increased hemolysis and thrombosis

HEARTWARE

• Centrifugal flow• Hydrodynamic bearings• Less experience with use• FDA approved for BTT: 90.7% survival• DT trial completed• Increased stroke and bleeding

Mancini, et al. Am Coll Cardiol. 2015;65:2542–55Lalonde, et al. J Card Surg. 2013;28:604–610

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ANTIPLATELET THERAPY

HEARTWARE ADVANCE TRIAL

• Aspirin (ASA)• Warfarin to INR 2-3• INR<2 or ASA ≤81 mg

associated with increased thrombotic events

• Pump exchange rates decreased 55% with increase to aspirin 325 mg

HEARTMATE II RETROSPECTIVE

COHORT

• Aspirin 325 mg• Warfarin to INR 2-3• ~50% dipyridamole use• Significantly higher bleeding

rates versus thrombotic events• Aspirin dose changed to 81 mg

Kreuziger . J Thromb Thrombolysis. 2015;39:337–344

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ANTICOAGULATION BRIDGING

Slaughter, et al. J Heart Lung Transplant. 2010;29, 616–624.

HEARTMATE II RETROSPECTIVE SUB-ANALYSIS

• Stratified by PTT values

• PTT <40 associated with significantly less transfusions

• No difference in stroke or pump thrombosis

• Post-operative heparin an independent risk factor for bleeding

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ANTICOAGULANT THERAPY

WARFARIN

DABIGATRAN

• Decreased major bleeding compared to warfarin (n=7)

• Increased thromboembolism in mechanical valve population

• Ongoing study (EudraCT: 2010-024534-38)

General Consensus: Warfarin after chest-tube removal days two to three

• Increased thrombosis with INR <1.5

• Increased bleeding with INR >2.5

• Wide range of INR goals

• 31-51% of time spent within goal

Kreuziger . J Thromb Thrombolysis. 2015;39:337–344

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EXTRACORPOREAL MEMBRANE

OXYGENATION (ECMO)

Returns to arterial system

CO2 and O2 exchange

Augmentation of cardiac output

Removes venous blood

Returns to venous system

CO2 and O2 exchange

Nonpulsatile flowPulsatile flow

VENOVENOUS (VV) VENOARTERIAL (VA)

Cove, etal. Crit Care. 2010;14(5):235Brodie, et al. N Engl J Med. 2011;365(20):1905-14

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Heparin Anticoagulation

• Historical standard with most evidence

• Xa and thrombin inhibition

• 40-80 units/kg once followed by 10-30 units/kg/hour

• 1-2 hour half-life

• Problematic in antithrombin deficiency and heparin-induced thrombocytopenia

•Antithrombin decreases with ECMO •Hemodilution & coagulation•Decreased heparin responsiveness•Sudden rise in plasma-free hemoglobin•FFP administration may overcome

Antithrombin (AT) Deficiency

•10% of patients with MCS•Positive antibodies in 60% of patients•Requires change in anticoagulation•Some circuit components heparin-

coated

Heparin-Induced Thrombocytopenia

Gadepalli, et al. Semin Pediatr Surg. 2015;24(1):8-11Esper, et al. Anesth Analg. 2014 ;118(4):731-43

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Anticoagulation Alternatives

Argatroban

• 0.25 - 1 mcg/kg/minute

• T1/2 39-51 min

• Evidence in case series only

• Significant thrombin decrease compared to heparin

• Higher bleeding rates seen – lower doses warranted

Bivalirudin

• 0.08-0.2 mg/kg/hour

• T1/2 0.25-3.5 hours

• Operative use more common

• Guideline HIT recommendation

• Metabolized by thrombin - levels depleted in areas of stasis

Gadepalli, et al. Semin Pediatr Surg. 2015;24(1):8-11Esper, et al. Anesth Analg. 2014 ;118(4):731-43

EMERGING

THERAPEUTIC OPTIONS

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LEVOSIMENDAN

Increased inotropy via increased calcium

sensitivity through troponin C binding

Increased vasodilation through potassium

channels and reduction of preload and afterload


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LEVOSIMENDAN

MORTALITY

LIDO Trial (n=203)• Increased cardiac output

and decreased PCWP• Lower 1- and 6-month

mortality

SURVIVE Trial (n=1327)• No mortality difference at

180 days

ADVERSE EVENTS

RUSSLAN Trial (n=504)• No association with

hypotension or clinically significant ischemia

REVIVE-II Trial (n=600)• Increased adverse events,

including hypotension and arrhythmias despite symptom improvement


ULARITIDE

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Synthetic form of urodilatin

with resistance to degradation

Diuresis

Natriuresis

Vasodilation

Hsiao, et al. Prog Cardiovasc Dis. 2016. [Epub ahead of print]

ULARITIDE

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SIRIUS I

• 15- and 30-ng/kg/min

• Improvement in dyspnea

• Decreased mortality

SIRIUS II

• 15- and 30-ng/kg/min

• Improved dyspnea

• Improvement pulmonary pressures

• Decreased hospitalization

• Decreased mortality

TRUE-AHF


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TRUE-AHF

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Co-Primary Outcome:

• Improved global assessment at 6, 24, and 48 hours without meeting criteria for worsening, including:

• Death within 48 hours

• Worsening of disease warranting intervention

• Worsening global assessment

Co-Primary Outcome:

• Freedom from cardiovascular mortality

Secondary Outcomes:

• N-terminal pro-BNP changes

• All-cause mortality and rehospitalization

• Cardiovascular rehospitaliation

Anker, et al. Eur Heart J. 2015;36(12):715-2

SERELAXIN

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Human recombinant form

of relaxin

Upregulator of endothelin B receptors and nitric oxide production

Inhibition of angiotensin II

and endothelin potentiates

systemic and renal vasodilation

Anti-inflammatory

and anti-fibrotic properties


RELAX-AHF

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Significantly reduced hospital stay, time to dyspnea improvement, and worsening of heart failure

Significant improvement in symptomatic visual analog scale

30 mcg/kg/day serelaxin versus placebo

Teerlink, et al, Lancet. 2013;381(9860):29-39.

RELAX-AHF

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Felker, et al. J Am Coll Cardiol. 2014 ;64(15):1591-8.

2/29/2016

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Medication correlation with decompensation

Half-life longer than initial

critical period

Paradoxical activation of sympathetic

nervous system

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BETA-BLOCKER CONSIDERATIONS

Jondeau , et al. JACC Heart Fail. 2015;3(8):654-6

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BETA-BLOCKER THERAPY

IN-HOSPITAL MORTALITY

Prins, et al. JACC Heart Fail. 2015;3(8):647-53.

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BETA-BLOCKER THERAPY

SHORT-TERM MORTALITY OR REHOSPITALIZATION

Prins, et al. JACC Heart Fail. 2015;3(8):647-53.

ASSESSMENT QUESTION

Increasing preload and/or inotropy are strategies for optimization of cardiac

output.

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2/29/2016

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A primary principle in the management of left heart failure is

reduction of venous congestion.

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ASSESSMENT QUESTION

The patient receives a HeartMate II ventricular assist device. The patient

should be bridged with heparin.

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ASSESSMENT QUESTION

Management of Acute Heart Failure and Cardiogenic Shock

www.fshp.org

Brittany D. Bissell, Pharm.D.PGY-2 Critical Care Pharmacy Resident

Jackson Memorial Hospital | Miami, Florida

• Abraham WT, Adams KF, Fonarow GC, et al. In-hospital mortality in patients with acute decompensated heart failure requiringintravenous vasoactive medications: an analysis from the Acute Decompensated Heart Failure National Registry (ADHERE). J Am CollCardiol. 2005;46(1):57-64.

• Anker SD, Ponikowski P, Mitrovic V, Peacock WF, Filippatos G. Ularitide for the treatment of acute decompensated heart failure: frompreclinical to clinical studies. Eur Heart J. 2015;36(12):715-2

• Brodie D, Bacchetta M. Extracorporeal membrane oxygenation for ARDS in adults. N Engl J Med. 2011;365(20):1905-14.• Cooper HA, Thompson E, Panza JA. The role of heparin anticoagulation during intra-aortic balloon counterpulsation in the coronary

care unit. Acute Cardiac Care 2008;10:214–20.• Cotter G, Felker GM, Adams KF, Milo-Cotter O, O'Connor CM. The pathophysiology of acute heart failure--is it all about fluid

accumulation? Am Heart J. 2008;155(1):9-18.• Cove ME, MacLaren G. Clinical review: mechanical circulatory support for cardiogenic shock complicating acute myocardial infarction.

Crit Care. 2010;14(5):235.• Di Somma S, Magrini L. Drug Therapy for Acute Heart Failure. Rev Esp Cardiol. 2015;68(8):706-13.• Esper SA, Levy JH, Waters JH, Welsby IJ. Extracorporeal membrane oxygenation in the adult: a review of anticoagulation monitoring

and transfusion. Anesth Analg. 2014;118(4):731-43• Feldman D, Pamboukian SV, Teuteberg JJ, et al. The 2013 International Society for Heart and Lung Transplantation Guidelines for

mechanical circulatory support: executive summary. J Heart Lung Transplant. 2013;32(2):157-87.• Felker GM, Benza RL, Chandler AB, et al. Heart failure etiology and response to milrinone in decompensated heart failure: results from

the OPTIME-CHF study. J Am Coll Cardiol. 2003;41(6):997-1003.• Felker GM, Teerlink JR, Butler J, et al. Effect of serelaxin on mode of death in acute heart failure: results from the RELAX-AHF study. J

Am Coll Cardiol. 2014 ;64(15):1591-8.• Gadepalli SK, Hirschl RB. Extracorporeal life support: updates and controversies. Semin Pediatr Surg. 2015;24(1):8-11.• Howlett JG. Acute heart failure: lessons learned so far. Can J Cardiol. 2011;27(3):284-95.• Hsiao R, Greenberg B. Contemporary Treatment of Acute Heart Failure. Prog Cardiovasc Dis. 2016 Jan 4. [Epub ahead of print]• Ihdayhid AR, Chopra S, Rankin J. Intra-aortic balloon pump: indications, efficacy, guidelines and future directions.Curr Opin Cardiol.

2014, 29:285–292• Jiang CY, Zhao LL, Wang JA, Mohammod B. Anticoagulation therapy in intra-aortic balloon counterpulsation: does IABP really need

anti-coagulation? J Zhejiang Univ Sci 2003;4:607–11.• Jondeau G, Milleron O. Beta-Blockers in Acute Heart Failure: Do They Cause Harm? JACC Heart Fail. 2015;3(8):654-6

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REFERENCES

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• Kirklin JK, Naftel DC, Pagani FD, et al. Sixth INTERMACS annual report: a 10,000-patient database. J Heart Lung Transplant.2014;33:555–564

• Kogan A, Preisman S, Sternik, et al. Heparin-free management of intra-aortic balloon pump after cardiac surgery. J Card Surg2012;27:434-437.

• Kreuziger LM. Management of anticoagulation and antiplatelet therapy in patients with left ventricular assist devices. J ThrombThrombolysis. 2015;39:337–344.

• Lalonde SD, Alba AC, Rigobon A, et al. Clinical Differences Between Continuous Flow Ventricular Assist Devices: A ComparisonBetween HeartMate II and HeartWare HVAD. 2013; J Card Surg, 28: 604–610

• Liu C, Liu K. Effects of glucocorticoids in potentiating diuresis in heart failure patients with diuretic resistance. J Card Fail.2014;20(9):625-9.

• Mancini D, Colombo PC. Left Ventricular Assist Devices: A Rapidly Evolving Alternative to Transplant. J Am Coll Cardiol.2015;65(23):2542-55

• Mebazaa A, Tolppanen H, Mueller C, et al. Acute heart failure and cardiogenic shock: a multidisciplinary practical guidance. IntensiveCare Med. 2016 Feb;42(2):147-63.

• Pratt AK, Shah NS, Boyce SW. Left ventricular assist device management in the ICU. Crit Care Med. 2014; 42:158–168• Prins KW, Neill JM, Tyler JO, Eckman PM, Duval S. Effects of Beta-Blocker Withdrawal in Acute Decompensated Heart Failure: A

Systematic Review and Meta-Analysis. JACC Heart Fail. 2015;3(8):647-53.• Russell SD, Rogers JG, Milano CA, et al. Renal and hepatic function improve in advanced heart failure patients during continuous-flow

support with the HeartMate II left ventricular assist device. Circulation. 2009;120(23):2352-7.• Slaughter MS, Naka Y, John R, et al. Post-operative heparin may not be required for transitioning patients with a HeartMate II left

ventricular assist system to long-term warfarin therapy. J Heart Lung Transplant. 2010;29, 616–624.• Subramaniam K. Mechanical circulatory support. Best Pract Res Clin Anaesthesiol. 2015;29(2):203-27.• Teerlink JR, Cotter G, Davison BA, et al. Serelaxin, recombinant human relaxin-2, for treatment of acute heart failure (RELAX-AHF): a

randomised, placebo-controlled trial. Lancet. 2013;381(9860):29-39.• Tariq S, Aronow WS. Use of Inotropic Agents in Treatment of Systolic Heart Failure. Int J Mol Sci. 2015;16(12):29060-8.• ter Maaten JM, Valente MA, Damman K, Hillege HL, Navis G, Voors AA. Diuretic response in acute heart failure-pathophysiology,

evaluation, and therapy. Nat Rev Cardiol. 2015;12(3):184-92.• Wiesen J, Ornstein M, Tonelli AR, Menon V, Ashton RW. State of the evidence: mechanical ventilation with PEEP in patients with

cardiogenic shock. Heart. 2013;99(24):1812-7.

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REFERENCES

management of acute heart failure and cardiogenic shock · 2018-04-03 · management of acute heart...

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