Fellows School: Acute Heart Failure

Brent C. Lampert, DO

Aug 4, 2014

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Outline

Definitions

Incidence

Diagnosis

Treatment Diuretics, vasodilators, inotropes, UF, advanced

therapies Transition to discharge

RHC interpretation

Terminology

AHF Acute decompensated HF (ADHF) Acute on chronic systolic / diastolic HF Acute biventricular HF Acute HF syndrome Acute decompensation of chronic HF HFpEF HFrEF AHA 2013 HF Guidelines

GDMT

Heart Failure

Affects ~ 6 million people in the U.S.

Expected to increase > 25% by 2030

60,000 deaths per year directly attributed to HF

Half of patients die w/in 5 yrs of diagnosis

Costs $34.4 billion annually in the U.S.

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Go, et al. Circulation 2013.Heidenriech, et al. Circulation 2011

Hospital Discharges for HF by sex

Introduction: AHF

Definition: new, gradual, or rapidly worsening heart failure signs & symptoms requiring urgent therapy

1 million annual admissions in US: HF as primary diagnosis

3 million annual admissions in US: HF as primary or secondary dx

Gheorhiade M, et al. JACC 2009

Heart Failure Rehospitalizations

30 day rehospitalization rate 27% in Medicare patients

40% due to HF (at OSU within 7 days)

Higher early follow-up rate (in 7 days of discharge) associated with reduced 30 day event rates

Median Survival Decreases after HF Hospitalizations

Miller L. JACC. 2013

Etiologies of HF

Ischemia (#1)

Hypertension (#2)

Valvular

Inflammatory Myocarditis, infectious,

autoimmune.

Medications Chemotherapy,

chloroquin

Toxins Ethanol, cocaine

Deposition Amyloid,

hemochromatosis

Rheumatologic

Endocrine disorders

Neuromuscular disease

Miscellaneous Peripartum, tachycardia-

related,familial, sleep apnea, sarcoid.

Idiopathic (#3)

Common Factors Precipitating the HF Hospitalization Noncompliance

Myocardial ischemia / infarction

Hypertension

Atrial fibrillation / arrhythmia

Addition of negative inotropic drugs (verapamil/diltiazem, β-blockers)

Pulmonary embolus

NSAID’s

Excessive ETOH / drugs

Endocrine abnormalities

Concurrent infections (Pneumonia, viral illness)

ADHF Diagnosis - Presentation

No single finding conclusive for diagnosing Most common symptoms: progressive dyspnea,

fatigue, cough, orthopnea, PND, edema, and/or weight gain

PE: Tachypnea Tachycardia Crackles or wheezing (“cardiac asthma”) Extra cardiac sounds (S3 and/or S4) Elevated jugular venous pressure (use central lines

for CVP) Edema Nausea / poor appetite

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AHF: Clinical Parameters

ADHERE(150,000 pts)

OPTIMIZE-HF(48,612 pts)

EURO HF(11,327 pts)

Any Dyspnea 89 90 70

Rest Dyspnea 34 45 40

Fatigue 32 23 35

Rales 68 65 N/A

Pulm. edema 66 65 23

Systolic BP

<90 2 <8 <1

90-140 48 44 70

>140 50 48 29

Fonarow GC. Rev Cardiovasc. Med. 2003Gheorghiade M. JAMA 2008Cleland JGF. Eur Heart J 2003

ADHF Diagnosis - Presentation

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Table 9.2 Modified Framingham Criteria for the Diagnosis of Congestive Heart Failure

Major Criteria Minor Criteria

Paroxysmal nocturnal dyspnea or orthopnea Neck vein distention Crackles / Rales Acute pulmonary edema S3 gallop Central venous pressure >16 cm H2O Weight loss >4.5 kg in 5 days in response to treatment Echocardiographic left ventricular dysfunction

Bilateral ankle edema Pleural effusion Nocturnal cough Dyspnea on exertion Hepatomegaly Tachycardia (heart rate>120 beats/min) Weight loss >4.5 kg in 5 days caused by heart failure where factors other than treatment of CHF could have contributed to weight loss

*For diagnosis of heart failure, 2 major criteria or 1 major criteria and 2 minor criteria are needed. Source: McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441-1446.

ADHF Diagnosis - Testing

EKG to identify underlying causes (LVH, MI, afib)

CXR may reveal pulmonary vascular congestion, but normal chest x-raydoes not exclude ADHF

CBC to identify anemia or infection

Chemistries to evaluate for renal dysfunction

Cardiac biomarkers if ischemia is suspected

BNP useful when the diagnosis is uncertain > 400 pg/mL predictive of heart failure as cause of dyspnea < 100 pg/mL have a very high negative predictive value for

heart failure as a cause of dyspnea

Echocardiography in all patients with new onset heart failure

LHC in patients with suspected ACS

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Hemodynamic Profile Assessment

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ADHF – Initial treatment

Focus on hemodynamic & volume abnormalities and correct precipitating factors (ischemia/arrhythmias)

Diuretics, diuretics, diuretics! Start w/equal or greater dose of loop diuretic (IV) than outpatient

regimen (furosemide - NOT BUMEX) Short half-life; requires multiple doses or continuous infusion IV continuous infusion & bolus dosing have similar efficacy Be cognizant of detrimental effects on renal blood flow, GFR,

electrolytes, neurohormones

Volume status, evidence of congestion, daily I/O, daily wts, potassium and creatinine frequently assessed

Low sodium diet (2 g daily or less) and fluid restriction (at least <2 L daily) should be considered

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Ellison. Cardiology. 2001;96:132-143.

Dose Response Curves for Loop Diuretics in ADHF Are Altered

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18

16

14

12

10

8

6

4

2

0

[Furosemide], µg/mL

0.01 0.1 1 10 100

Normal

CRF

CHFSecretory

Defect

DecreasedMaximalResponse

FE

Na ,%

Fractional Na Excretion

increased NH reduced renal perfusion poor absorption receptor unresponsive

Most Common Intravenous Medications

0

10

20

30

40

50

60

70

80

90

100

Pat

ient

s (%

)

IV Diuretic Dobutamine Dopamine Milrinone Nesiritide Nitroglycerin Nitroprusside

IV Vasoactive Meds

88%

6% 6%10%

3% 1%

10%

ADHERE® Registry. Benchmark Report. 2004.

All Enrolled Discharges (n=105,388) October 2001–January 2004

Acute HF – Options When Initial Diuretics Fail Is there persistent “congestion” ?

Careful exam (JVP), labs, BNP May need invasive hemodynamics

Continuous infusion of furosemide 5-40 mg/hr

Add thiazide (distal tubule diuretic) Ultrafiltration Additional Vasoactive therapy Inotropes Advanced therapies

Thiazide diuretics – “Booster”

• HCTZ

• Metolazone

• Long ½ life

• Does not need to be administered 30 min prior

• Significant electrolyte disturbances

• Chlorothiazide (Diuril)

• IV

• $$$

Ultrafiltration for Acute Heart Failure

Useful in patients w/ ADHF + renal insufficiency or diuretic resistance

Advantages: adjustable fluid removal rates, no effect on electrolytes, decreased neurohormonal activity

CARESS-HF 188 pts w/ ADHF, worsened renal function Stepped pharmacologic care (loop

diuretics, metolazone, selective inotropes or vasodilators) vs. UF

No difference in weight loss UF with increased Cr and more adverse

events

Vasodilators

Rapid resolution of congestive symptoms, angina, HTN

Most patients will have high SVR (MAP/CO)

Improve SV, C.O., right and left sided filling pressures without increase HR

Nitroglycerin, Nesiritide, Nitroprusside

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Vasodilators - Nitroglycerin

Reduces LV filling pressures primarily through venodilation

Variable effect on SVR (depends on degree of elevation)

Improves myocardial blood flow (coronaries, LVEDP, HR)

Start at 5-10 mcg/min and can titrate rapidly to effect (as high as 400 mcg/min)

Attention to intravascular volume (resistance in those with high RAP) and hypotension in those with low IVV, RV dysfunction, diastolic HF

Short half life

Tachyphylaxis can occur within hours

Avoid with PDE inhibitors

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Vasodilators - Nitroprusside

Potent vasodilator with balanced venous & arterial effects Short half-life (effects are gone w/in 10 minutes) Rapidly reduces filling pressures, MVO2, valve

regurgitation Rapidly increases SV Significant increase in HR (or drop in BP) should stop

infusion Typically use with invasive hemodynamics Potential for cyanide toxicity (rare) – limit to 48 hours Dose starts at 0.5 mcg/kg/min and titrate to

hemodynamic effect Q 3-5 minutes.

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Vasodilators - Nesiritide

Recombinant human BNP Venous and arterial dilation. Reduces BP, filling

pressures and mild increase in CO; no increase in HR

Limited evidence for “natriuretic” effect in clinical studies. Does not replace diuretics.

Start at 0.005 – 0.01 mcg/kg/min; +/- bolus. Limited dose titration necessary. Long half-life.

As with all vasoactive therapies, must monitor BP, symptoms, renal function closely (multiple times per day)

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Conclusions:Mild benefit in dyspneaNo effect on outcomesNo adverse effect on renal functionIncreased hypotension

O’Connor et al. NEJM 2011

ADHF Treatment - Inotropes

Milrinone and dobutamine For “cold” patients with evidence of hypoperfusion Short-term therapy to maintain systemic perfusion

and preserve end-organ performance until definitive therapy (revascularization, MCS, Transplant) or palliative therapy

Require continuous rhythm and frequent BP monitoring

Symptomatic hypotension or tachyarrhythmias should prompt consideration of dose reduction or discontinuing

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ADHF Treatment - Milrinone

PDE inhibitor that increases myocardial inotropy by inhibiting degradation of cyclic AMP

Reduces systemic and pulmonary vascular resistance (via inhibition of peripheral phosphodiesterase)

Improves left ventricular diastolic compliance (lusitropy)

Increases cardiac index and decreases left ventricular afterload and filling pressures

Can be given with B-blockers Typical dose: 0.25 – 0.75 mcg/kg/min

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ADHF Treatment - Dobutamine

Acts primarily on beta-1 adrenergic receptors, with minimal effects on beta-2 and alpha-1 receptors

Increases stroke volume and cardiac output Modest decreases in systemic vascular

resistance and pulmonary capillary wedge pressure

Consider decrease / withdrawal B-blockers ? Increased ventricular ectopy Typical dose: 2-20 mcg/kg/min

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ADHF Treatment - Inotropes

Continue until euvolemia is achieved, or definitive therapy delivered

Wean gradually to avoid effects of sudden withdrawal including precipitous decreases in cardiac output

Failure to wean should prompt consideration of additional advanced therapies

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ADHF Treatment – Advanced therapies

IABP is the most commonly used, easily placed, and least expensive support device

ECMO can provide cardiopulmonary support Temporary support for patients failing all other therapies Bypasses the pulmonary circulation and oxygenated blood

returns to the patient via an arterial or venous route Venovenous ECMO: primarily supports patients with

severe respiratory failure Venoarterial ECMO utilizes an extracorporeal pump to help

with hemodynamic support

Short term VADS can be placed percutaneously or surgically

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ADHF – Predictors of outcome

Most important predictor of short term outcomes is adequacy of diuresis prior to discharge

BNP, troponin predict in-hospital mortality

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Peacock F, et al. NEJM 2008

Fonarow et al. JACC 2007;49:1943-50

ADHF – Discharge criteria

Recommended for all Patients Should be considered

Exacerbating factors addressed Near optimal volume status observed Transition from intravenous to oral diuretic successfully completed Patient and family education completed, including clear discharge instructions Left ventricular ejection fraction (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 Follow-up clinic visit scheduled, usually for 7 to 10 days

Oral medication regimen stable for 24 hours No intravenous vasodilator or inotropic agent for 24 hours Ambulation before discharge to assess functional capacity after therapy Plans for postdischarge management (scale present in home, visiting nurse or telephone follow up generally no longer than 3 days after discharge) Referral for disease management, if available

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Source: Lindenfeld, J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Klapholz M, Moser DK, Rogers JG, Starling RC, Stevenson WG, Tang WHW, Teerlink JR, Walsh MN. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010;16:e1-e194.

ADHF - RHC

Value of RHC remains controversial Randomized ESCAPE trial showed no benefit (or

increased risk) of using RHC in mortality or days alive out of the hospital

Did not enroll all consecutive patients b/c many physicians would not enroll and risk a 50% chance of not having PA catheter

Routine RHC in HF not recommended; useful in subset of patients

2013 ACC/AHA heart failure guideline: perform in patients “with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate”

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ADHF - RHC

Filling pressures Cardiac output

TD Fick PA saturation

TPG Mean PAP – PCWP Normal value ≤ 12 mmHg

PVR PVR = Normal value is < 3 Wood units (or 240 dynes-sec-

cm-5)

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  Pressure, mmHg

Chamber Average Range

Right atrium 5 ± 2

Right ventricle

25/5 ± 5 / ± 2

Pulmonary artery

25/10 ± 5 / ± 2

Left atrium (PCWP)

10 ± 2

ADHF - RHC      PH associated with HF

  Heart Failure PAH “In proportion”

“Out of proportion”

RA (mmHg) Normal or ↑ Normal or ↑ Normal or ↑ Normal or ↑

RV (mmHg) Normal or ↑ ↑ ↑ ↑

Mean PA (mmHg)

Normal or ↑ ≥ 25 ≥ 25 ≥ 25

PCWP (mmHg) > 15 ≤ 15 > 15 > 15

CO (L/min) Normal or ↓ Normal or ↓ Normal or ↓ Normal or ↓

TPG (mmHg) Normal > 12 ≤ 12 > 12

PVR (Wood units)

Normal > 3 < 3 > 3

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ADHF - RHC

RA 10, PA 50/24 (33), PCWP 26

CO/CI 4.7/2.4, PA saturation 65%

Diagnosis?

Treatment?

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ADHF - RHC

RA 20, PA 50/24 (33), PCWP 26

CO/CI 4.7/2.4, PA saturation 65%

Diagnosis?

Treatment?

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ADHF - RHC

RA 20, PA 50/24 (33), PCWP 26

CO/CI 3.1/1.5, PA saturation 43%

Diagnosis?

Treatment?

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ADHF - RHC

RA 18, PA 84/25 (45), PCWP 10

CO 5.0/2.6, PA saturation 68%

Diagnosis

Treatment

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ADHF - RHC

RA 18, PA 84/25 (45), PCWP 36

CO 5.0/2.6, PA saturation 68%

Diagnosis

Treatment

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Questions

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